Overeating = Natural Response to Strict Dieting That Occurs Despite Increased Satiety Hormone Response to XXL-Meal

Overeating = Natural Response to Strict Dieting That Occurs Despite Increased Satiety Hormone Response to XXL-Meal

fasting hunger lose fat satiety satiety hormones starvation

This is not a photo from the full-text of the study, but it could be. After all the energy deficient diet was >90% below the maintenance intakes of the subjects. That's unfortunately much more severe than the average dieter's approach, but some of the things the scientists observed still have very general applications.

If you've ever dieted to make the cut in a sports with weight classes, you will know this insatiable hunger which climaxes on the last two days when you are down to a handful of  calories per day. It's a hunger that won't be satisfied even if you eat an extra 1000 kcal above maintenance.

Athletes competing in sports with weight classes may need to accept the post-dieting binge, but what about average Joes and Janes? Will a fasting day ruin the average dieters dieting efforts by making them eat more extra-calories on day 2 than they've economized the day before? A recent study from the US Army Research Institute of Environmental Medicine, in which scientists have attempted to stimulate and simulate this insatiable hunger in a tightly controlled experimental environment, may hold the answer.

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As Kristie L O'Connor et al. point out an altered secretion of appetite-mediating hormones is the #1 candidate to explain the common tendency for weight regain (Sumithran. 2013 | see Figure 1). This hypothesis is supported by several studies that have reported decreases in circulating leptin and insulin concentrations in response to weight loss that are disproportionately greater than contemporaneous reductions in fat mass (Mars. 2005; Blom. 2006; MacLean. 2006; Pasiakos. 2011; Sumithran. 2011). Other studies have documented blunted postprandial gastroenteropancreatic hormone responses after weight loss (Chan. 2004).

Figure 1: Selected pathways involved in body weight regulation (left) and tabular overview of physiological changes after diet-induced weight loss and their effect on energy intake and storage (right | Sumithran. 2013).

Scientists have speculated that these ill effects may be countered by eating diets with a low energy density and thus putting equivalent stress on the gastric mechanoreceptors in our guts. Unfortunately, this alone has turned out to be as ineffective as other attempts to minimize the adaptive response to energy restriction. On the other hand, the existing effects the volume of what we have will have on our satiety is something that has been overlooked in previous studies.

Figure 2: Study design. EB, energy balance; ED, energy deprivation; EE, energy expenditure; EI, energy intake; RMR, resting metabolic rate; TDEE, total daily energy expenditure; VAS, visual analogue scale (O'Connor. 2016).

Overall, our understanding of the complex relationship between what and how much we eat and how this affects our subjective satiety and corresponding hormone response is still very limited. To address this knowledge gap O'Conner et al. created 2 isovolumetric diets that differed in energy density but were otherwise comparable in taste, texture, and appearance that were fed to healthy young adults during a period of energy balance (EB) and a period of 90% energy deprivation (ED), in oder to "examine the physiologic effects of short-term ED on appetite-mediating hormones and appetite independent from reductions in diet volume" (O'Connor. 2016 | see Figure 2).

It is a common misunderstanding that you "must" lose your weight slowly: While most mainstream diet advise involves the recommendation that you shouldn't reduce your energy intake too significantly and that you must lose your weight slowly, the existing peer-reviewed experimental and observational evidence does not support the notion that (a) slow eight gain would support greater lean mass retention or (b) prevent weight regain. Learn why that's the case.

Figure 3: Overview of energy intake, deficits and macronutrient composition in the two study groups (O'Connor. 2016).

As the scientists had expected the energy deficit that was induced over two seperate 48-h periods during which the energy intake was matched to energy expenditure to maintain energy balance (EB) (-44 +/- 92 kcal/d) or yield less than 10% of the energy the subjects required (ED).

In conjunction with the low-to-medium intensity exercise regimen (0–65% VO2peak for 187 6 +/- 21 min/d) that burned an extra 1683 +/- 329 kcal/d, the ED group did thus end up having a whopping -3696 +/- 742-kcal/d deficit on each of the two days (!).

It is thus no wonder that the scientists observed a whole host of significant differences in the hormonal response to the "diet" (diet vs. fasting). One difference you probably know much better however, is depicted in Figure 4, which shows that the subjects in the ED group consumed not simply the amount of energy they needed on the subsequent ad-libitum meal condition, but an extra 811 kcal - and they still felt a significantly greater desire to eat right after and 180 minutes after the meal.

Figure 4: Energy intake on an ad-libitum (eat as much as you want) meal before and after the intervention (left)
and the corresponding desire to eat before and after the meal (right); the dotted line at 20 min in the right graph
indicates the time at which the ad-libitum meal was served (O'Connor. 2016).

Unfortunately, the complexity of the hormonal changes does not allow us to identify this one parameter we could target to counter this effect. With significantly reduced fasting insulin (256% 6 42%) and acyl ghrelin (260% 6 17%) concentrations, as well as leptin concentrations that decreased more during ED compared with EB (-47% 6 +/- 27% compared with -20% +/- 27%; P-interaction = 0.05), we have two three (expected) candidates that could explain the increased hunger and desire to eat before the ad-libitum meal. The increased postprandial insulin (57% +/- 63%; P < 0.001), GLP-1 (14% 6 28%; P = 0.04), and PP (54% +/- 52%; P < 0.001) areas under the curve (AUCs), as well as the reduced acyl ghrelin increase (-56% +/- 13%; P < 0.001) after ED compared with after EB, on the other hand, appear to contradict the lack of satiating effect of the 1834 kcal lunch in the 18–39 year-old healthy men and nonpregnant women who participated in the study at hand.

Intermittent Fasting Works, But is It Better Than "Regular" Dieting? What Do the Latest Reviews / Meta-Analyses Say? Find out in this SuppVersity Classic!

So what can be done? Well, the increase in appetite and desire to eat is probably a generally unavoidable effect of "starvation diets" and since this is what the study at hand focuses on, it is difficult to predict how pronounced the effect would have been if the ~3500kcal energy deficit, the subjects in the study at hand reached within just one day, would have been induced over the course of 3-5 days. A dieting approach like that would after all been much closer to what the average dieter does over the course of 3-5 days only to then overeat and fall off the wagon on the weekend. In addition, a lower calorie deficit may have (a) made it easier to identify what exactly it is that causes the rebound effect and may (b) have been insufficient to compensate for the binge.

This leads us directly to the most important result of the study at hand: As suboptimal as the diet may be, one significant and probably mostly underappreciated result of the study at hand is that - once again - the energy deficit you accumulate during a quasi-fast was not fully compensated for over the 36h follow up period. A fact that adds to the existing evidence in favor of cyclic diets as every-other-day fasting, where you cycle hunger and ad-libitum diet days | Comment!

References:

• Blom, Wendy AM, et al. "Fasting Ghrelin Does Not Predict Food Intake after Short‐term Energy Restriction." Obesity 14.5 (2006): 838-846.
• Chan, Jean L., et al. "Ghrelin levels are not regulated by recombinant leptin administration and/or three days of fasting in healthy subjects." The Journal of Clinical Endocrinology & Metabolism 89.1 (2004): 335-343.
• Egecioglu, Emil, et al. "PRECLINICAL STUDY: FULL ARTICLE: Ghrelin increases intake of rewarding food in rodents." Addiction biology 15.3 (2010): 304-311.
• MacLean, Paul S., et al. "Peripheral metabolic responses to prolonged weight reduction that promote rapid, efficient regain in obesity-prone rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290.6 (2006): R1577-R1588.
• Mars, Monica, et al. "Decreases in fasting leptin and insulin concentrations after acute energy restriction and subsequent compensation in food intake." The American journal of clinical nutrition 81.3 (2005): 570-577.
• O'Connor, et al. "Altered Appetite-Mediating Hormone Concentrations Precede Compensatory Overeating After Severe, Short-Term Energy Deprivation in Healthy Adults." Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions (2016).
• Pasiakos, Stefan M., et al. "Appetite and Endocrine Regulators of Energy Balance After 2 Days of Energy Restriction: Insulin, Leptin, Ghrelin, and DHEA‐S." Obesity 19.6 (2011): 1124-1130.
• Sumithran, Priya, et al. "Long-term persistence of hormonal adaptations to weight loss." New England Journal of Medicine 365.17 (2011): 1597-1604.
• Sumithran, Priya, and Joseph Proietto. "The defence of body weight: a physiological basis for weight regain after weight loss." Clinical Science 124.4 (2013): 231-241.

Fructose May Help Control Post-Exercise Cravings - Almost 30% Reduced Desire to Eat After 1h Low-Intensity "Cardio"

Fructose May Help Control Post-Exercise Cravings - Almost 30% Reduced Desire to Eat After 1h Low-Intensity "Cardio"

appetite breakfast exercise fructose health hiking hunger lose fat pre-workout walking

About to go for a walk? Have fructose for breakfast to keep the hunger at bay.

I know very well that fructose is the nutritional boogyman of the 21st century, but avoiding it altogether is about as unwarranted as consuming it by the pound is unhealthy. A recent study from the Department of Health and Physical Education at the Hong Kong Institute of Education and the Department of Sports Science and Physical Education at the Chinese University of Hong Kong does now show a new, hitherto unknown, or at least under-appreciated effect of fructose: The ingestion of a fructose containing, albeit not fructose only (not tested, though) breakfast will significantly reduce the desire to eat that will usually rise sharply after a 60 minute bout of "cardio" training in form of walking at 50% of one's individual VO2max.

Learn more about fructose at the SuppVersity

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As a SuppVersity reader you will know that low-intensity cardio, much more than HIT or HIIT (learn more), will trigger significant increases in hunger and one's desire to eat. To ameliorate this effect, you could - that's at least what the aforementioned study shows - simply replace part of the starchy or high GI carbs of your breakfast with high fructose fruits and/or other fructose containing food items.... that's at least - as  previously mentioned - what the study at hand suggests; a study in which Hong Kong researchers compared the effects of three isocaloric breakfasts with identical amounts of carbs (1.0 g/kg body weight) from different food sources with different GIs (41, 39, and 72) and fructose contents on the appetite scores of ten healthy young male volunteers (21.7 ± 1.5 yr, 20.9 ± 1.1 kg/m²) who had to rate different aspects of appetite every 30 min during the 2-hr postprandial period after the meal, as well as during the 1-hr recovery period that followed the 1h of brisk walking (46% VO2max) all subjects had do perform 2h after consuming the standardized breakfasts.

"Three isocaloric meals were used in the present study. [...] Briefly, all meals had similar macronutrients and provided 1.0 g∙kg−1 body weight CHO for each participant. The LGI meal was composed of cooked spaghetti, egg, and full-fat milk. The LGIF meal comprised rice vermicelli, egg, ham, and fructose. The HGI meal involved rice vermicelli, egg, ham, and glucose. In the LGIF and HGI meals, approximately 25% of energy was derived from the fructose or glucose beverage (nearly 25 g for a 60 kg person). The calculated GI values for the LGI, LGIF, and HGI breakfasts were 41, 39, and 72, respectively. All meals were freshly prepared in the morning of each main trial, and the preparation procedure was standardized."

As you can see in Figure 1 the three test-meals initially had very similar effects on the subjects' appetite ratings, i.e. their desire to eat, hunger, fullness, and perceived ability to eat.

Figure 1: Appetite Sub-Score. b: P < 0.05 vs. LGIF. LGI: Low-GI meal without fructose; LGIF: Low-GI meal including fructose beverage; HGI: High-GI meal (Sun. 2015).

Only the 25% fructose meal, however, kept the rapid increase (or decrease in the case of fullness) in all four parameters after the 1h of brisk walking (Rec-X in Figure 1) at bay. That's quite an interesting observation, even though one could argue that the study cannot serve as a definite litmus test, because it lacks a post-exercise test-meal where the practical significance of the reduced appetite scores was measured against the reduction in food intake in the fructose group.

But isn't fructose the appetite increasing, liver clogging devil? While it may be the devil in the books of a couple of researchers who have nothing else to publish, the specific effect of fructose on appetite are far from being proven to be good or bad. (Rodin. 1990 & 1991). While it appears as if the isolated consumption of high amounts of free fructose has negative effects on appetite control (Lowette. 2015); and still, there's  no debating that fructose has the general ability to blunt food intake compared to an isocaloric amount of glucose in healthy individuals, as it has been shown by Rodin in 1991 (see Figure on the left).

Irrespective of the previously mentioned methodological short-coming, it is, as the authors highlight, quite striking that "the increased fructose content in LGIF breakfast suppressed the appetite score, compared with isocaloric HGI and LGI breakfast" (Sun. 2015). Previously, scientists often argued that the satiety promoting effect of fructose must be mediated by the lower GI and correspondingly lower insulin spikes as well as reduced glucose excursions after fructose vs. glucose containing meals. The data in Figure 2, however, tells us that neither the insulin spikes (Figure 2, right) nor the glucose excursions (Figure 2, left) differed significantly between the LGI (low GI) and the LGIF (low GI + fructose) meals over the relevant last part of the study period - an observation which does by the way also show us that "[w]hen exercise is included as a co-intervention strategy, the effect of GI on appetite may be highly complex" (Sun. 2015) and in most cases relatively irrelevant.

Figure 2: Glucose and insulin response to the test meals; significant differences were observed for high GI (HGI) compared to the other meals and initially for the fructose meal, where the glucose levels increased slightly more rapidly than in the low GI (LGI) reference meal -  in spite of identical calculated GI values, by the way (Sun. 2015)

Previous studies show that even though exercise exerts the most profound effect on human energy expenditure, it seems that post-exercise energy intake is not affected by exercise itself (Blundell. 1999; Melzer. 2005). In that, a study by Stevenson et al appears to confirm the finding of the study at hand which is that there is no difference relevant appetite scores between HGI and LGI trials during the postprandial period if the time between breakfast and moderate intensity exercise is sufficiently long.

Figure 3: The appetite suppressing effects of fructose preloads in the absence of exercise have been known ever since Rodin's 1990 study on the effects of fructose vs. glucose and water preloads on food intakes (Rodin. 1990).

What's new with the present study, though, is that "eating an LGIF [25% fructose] breakfast resulted in decreased appetite scores compared with HGI breakfast and LGI breakfast [25% non-fructose carbs]" (Sun. 2015). This and the fact that this difference cannot be explained by the usual suspects, i.e. insulin and blood glucose levels leads Sun et al to emphasize that ...

"[t]he effect of fructose on appetite has been substantially investigated. Earlier studies have indicated that fructose beverages suppressed energy intake more than glucose beverages did (Rodin, 1990 and Rodin, 1991). The underlying mechanism has been attributed to the metabolism of fructose in the liver and the effect of insulin" (Sun. 2015).

In fact, scientists have previously speculated that fructose may affect appetite through slow and incomplete absorption. This effect, however, is eliminated when fructose is consumed with other CHOs (Anderson. 2003). As far as potential mechanisms are concerned, we are thus left with changes in satiety hormones and peptides like ghrelin, cholecystokinin, glucagon-like-peptide-1 and peptide-YY and/or direct or indirect effects on the gut-brain axis as potential mechanisms that would explain the results of Sun's study. Unfortunately, neither of these mechanism was assessed in their study.

Make you choice - cholesterol and regular sugar (left), or fat free and fructose-laden? In the end it all may not even matter. In spite of that, you shouldn't forget that fruit is not the enemy, isolated fructose in drinks is.

So, what's the verdict? I'd like to cite the original conclusion first, before adding my two cents: "It appears that fructose content in, rather than the GI of, a pre-exercise breakfast meals affect subjective appetite score during the recovery period after 1-hr of brisk walking" (Sun. 2015).

There's no doubt that this is right, but there are important qualifications with respect to the real-world significance of the results: Firstly, the absence of a post-recovery test meal, where the actual food intake would have been measured, is a major methodological problem of the study at hand. Even though changes in appetite of a similar magnitude will usually translate in changes in food intake, this is not a necessity. Therefore the actual food intake and the mechanism for the appetite suppression have to be elucidated in future trials.

In the mean time, I'd suggest you do your own test-run. If it works, fine. If not, you don't have to care about the results of follow-up studies, anyway. Why? Well, what works for the virtual average study participant does not necessarily have to work for you | Comment on Facebook!

References:

• Anderson, G. Harvey, and Dianne Woodend. "Effect of glycemic carbohydrates on short-term satiety and food intake." Nutrition Reviews 61.5 (2003): S17.
• Blundell, John E., and Neil A. King. "Physical activity and regulation of food intake: current evidence." Medicine and science in sports and exercise 31 (1999): S573-S583.
• Lowette, Katrien, et al. "Effects of high-fructose diets on central appetite signaling and cognitive function." Frontiers in nutrition 2 (2015).
• Melzer, Katarina, et al. "Effects of physical activity on food intake." Clinical nutrition 24.6 (2005): 885-895.
• Rodin, Judith. "Comparative effects of fructose, aspartame, glucose, and water preloads on calorie and macronutrient intake." The American journal of clinical nutrition 51.3 (1990): 428-435.
• Rodin, Judith. "Effects of pure sugar vs. mixed starch fructose loads on food intake." Appetite 17.3 (1991): 213-219.
• Sun, Feng-Hua, Stephen Heung-Sang Wong, and Zhi-Gang Liu. "Post-exercise appetite was affected by fructose content but not glycemic index of pre-exercise meals." Appetite 96 (2016): 481-486.