Choosing & Processing Foods for Satiety: The Science 101 for Regular Consumers and Food Industry Insiders

Don't worry, this is no article about "Frankenfood" like salami bananas, ...

According to the drugs.com definition, a "designer food" is "a dietary supplements or foodstuffs containing nutrients and various combinations of vitamins, minerals, and other substances considered by some to offer clinically significant benefit, often without adequate scientific proof of efficacy." If you don't want your designer foods (or your self-prepared foods and meals) to fall into the latter category of products without adequate scientific proof of efficacy, this article is for you, because it summarizes the science on an often overlooked quality of food: its structure, and the effect the latter will have on your and/or customers' satiety.

Learn more about the satiety effects of foods, supplements and exercise

Whey to Casein Ratio not a Satiety Factor

Binging is just a natural starvation response

More Protein Doesn't Always More Satiety

Fluids and solids - What's More Satiating?

Tryptophan, the Satiety Amino Acid?

Always Hungry? What's Triggering Your Craving?

In a recent review, Campbell et al. have aptly illustrated how both the product and the way(s) costumers eat it affect the individual satiety (see Figure 1).

Figure 1: Satiety is more complex than calories in vs. calories out - In fact, it's hardly about calories at all.

Allegedly, the separate roles of the initial food structure, structural transformations, oral processing,
and dynamic sensory perception in satiation (makes you stop eating) and satiety (reduces your incentive to have another meal | see blue box) have not been fully established, but hey: you've got to start somewhere when designing functional (satiating and satiety promoting) foods is #1 on your private or professional agenda. So here's what we know:

• food structure and texture contribute to satiation and satiety,
• time required for oral processing has been shown to influence satiation/satiety,

If we were able to integrate the interaction of food structure, texture, and oral processing on satiation/satiety this may help us to produce more satiating foods and thus help people lose weight. So how can we do that?  Vliet, van Aken, de Jongh, & Hamer (2009) classified foods as fitting into broad categories of:

1. fluids - fluids flow and have minimal or no yield stress (e.g. beverages like sodas or milk); 
2. semi-solids - semisolids are fluid-like, have a high yield stress, and deform or break without fracturing into pieces (e.g., pudding, yogurt, and bananas); 
3. soft solids - soft solids fracture into pieces but without sound (e.g., cooked egg white, some cheese and processed meats); and 
4. hard solids - hard solids fracture into pieces and emit sound during fracture (e.g., crackers, toast, nuts, apples, and carrots). 

Needless to say that these overall physical properties are (a) a result of the foods individual food structure and can (b) be modified to a certain degree and thus affect an individual food's satiety effect by either natural (e.g. fermentation, mixing, etc.) or artificial (e.g. enzymatic treatments, adding thickening agents, etc.) means.

But isn't that overrating the importance of texture?

Not really... After all, you must take into consideration that the texture of your foods will influence their satiating effect and your satiety (after the meal) by at least mechanisms, i.e.

• oral processing parameters which are directly influenced, as well as adjusted to accommodate changes in food texture throughout the chewing sequence and ...
• texture perception, which will influence your expectations of satiety, which - despite being a highly dynamic process that correlates with oral processing (chewing, etc.) will eventually have significant effects on the satiating and satiety effects of the foods you eat.

By turning a protein shake into a pudding with xanthan, for example, you will "force" yourself or your customers to consume the shake like a pudding: with a spoon. In addition, the mouthfeel of a pudding will leave them with the expectation that the product is more satiating than a watery whey protein shake - an expectation that usually turns into a self-fulfilling prophecy.

Table 1: Overview of the results of Campbell's review (2016); studies accompanied by a plus symbol (+) indicate that at least one measured marker of satiation/satiety was affected by texture

As Campbell et al. point out in their previously cited review, this has been shown in multiple study. Agrawal et al. (1998), for example, were one of the first to demonstrate the dependence of oral processing and thus your eating speed on intrinsic properties of food texture:

"Using a selection of cheeses, nuts, and carrots, the authors established a clear dependence of breakdown rate and activity of closing muscles on mechanical parameters – in this case, toughness and modulus of elasticity. More recent studies have expanded on this concept by utilizing a wider variety of foods varying in texture from fluids to soft and hard solids (Forde et al., 2013; Viskaal-van Dongen, Kok, & de Graaf, 2011). Though the foods were not characterized structurally, both Forde et al. (2013) and Viskaal-van Dongen et al. (2011) found significant differences in eating rates, ranging between 4 g/min for crisp foods such as rice cakes or tortilla chips, 100 g/min for soft cooked vegetables, and 650 g/min for thin beverages such as juice or soda. The total number of chews necessary to process 50 g samples ranged from 27 to 488 chews for mashed potatoes and tortilla chips, respectively while total oral processing time ranged from 27 s for canned tomatoes to 350 s for tortilla chips" (Cambell. 2016).

Now, I am probably not telling you something new, when I inform you that science shows that faster eating rates are associated with increased food intake. Thus the "real-world, real-food approach" (Campbell. 2016) indicates that foods requiring limited oral processing actions, such as liquids, semisolids, and soft, cooked solids, may be more easily over-consumed than hard or chewy solids, such as crackers, chips, or certain meats.

With its satiety-promoting effects soluble fiber will reduce the number of meals and prolong the intervals between meals on an ad-libitum diet. It will, however, not affect the satiating effect of an individual meal; meaning: if you are a binge eater whose extra body  fat is "acquired" from super-size meals, it's not going to get you lean.

Did you know that there's a difference between satiety and satiation? Satiety is what determines when and whether you're going to eat. Satiation is what tells your body that you can stop eating now.

Why would you care? Well, the answer can be found in a recent study on soluble fiber intakes, for example. While the latter will increase your satiety and thus reduce your meal frequency and the number of meals you will be consuming on an ad-libitum (eat when and how much you want), it won't affect your satiation. Practically speaking this means: Increasing the soluble fiber content of your diet is not going to magically prevent obesogenic binges - and, when all is said and done, 3x2000 kcal are as fattening as 6x1000kcal.

That doesn't sound so indisputable any longer, right? I mean we know that chips are not exactly more satiating than, say, chicken breasts. In this context, it is important to understand that pertinent studies measure eating rate by weight (g/min) rather than by total calorie intake (calories/minute). In our example, the chicken breast will yield higher eating speeds indicating that a higher amount (as in weight) of the product is being consumed per minute, but for a given amount of food, the caloric content of the chicken breasts is usually still significantly lower than that of potato chips, which is yet another example of the fact that you have to consider all variables (in this case, first and foremost texture, eating speed and relative energy density) and their interaction to predict the satiety and satiating effects of a meal.

But there's more to it than the difference between hard, soft and liquid. Even if you don't go beyond the structure (e.g. looking at the protein content of foods), modifying the microstructure with gelling protein-polysaccharides or reducing the creaminess by cutting down on fat will sign. affect the chewing rate and thus - at least theoretically - make foods more or less satiating.

So far so bad, because it's all theory!

I am not sure if you've tried low-fat cheese; but if you have, you will have notice that it chews and, unfortunately, tastes like cardboard and is thus hardly more satiating than regular cheese. To actually make reliable predictions about the satiating and satiety effect of various foods, it does, therefore, take real-world studies the design of which usually look as described by Campbell et al., recently:

" Measurements of satiation and satiety typically fall into three categories: subjective panelist ratings, physiological measurements, and ad libitum intake. Subjective panelist ratings of hunger and fullness, often in the form of a 100 mm visual analog scale (VAS), represent the most direct and simplistic measurement of hunger and fullness. These ratings are often corroborated by offering an ad libitum snack or meal and measuring how many calories the panelist consumes following consumption of a test food. One can also measure physiological biomarkers associated with metabolism, satiation, and satiety, including glucose, insulin, ghrelin, leptin, cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and gastric inhibitory peptide (de Graaf et al., 2004). Other physiological measurements include diet induced thermogenesis (Crovetti, Porrini, Santangelo, & Tesolin, 1997; Westerterp-Plantenga, Rolland, Wilson & Westerterp, 1999) and gastric emptying time (Blundell et al. 2010). While quantification of biomarkers provides an unbiased, physiological response, healthy panelists often exhibit wide ranges of biomarker concentrations and this biological variation can complicate interpretation of results. Combinations of the above measurements are more commonly utilized to account for biological and psychological variability" (Campbell. 2016).

From these studies, scientists have learned a lot. Not all of it was surprising. After all, we all have some knowledge of what is satiating and what is not. It is thus not a surprise that...

• protein is the most satiating macronutrient, carbohydrates come in as a distant second and fats are really trailing behind;

Table 2: Dietary fibre content of foods in commonly served portions (Slavin .1987).

• non-digestible carbohydrates are satiating, too  -  fiber (see Table 2) and resistant starches both fall into this category and are (rightly so) on the list of 'best-known satiety promoters'

That the satiating effect of protein is more or less independent of whether it is fast- or slow-digesting, on the other hand (see my recent article on whey and casein | read it), is something only a few people know. The same goes for the advantages of fiber with a high intrinsic viscosity – such as pectin, β-glucan, psyllium, guar gum, and alginate, which have been shown to have superior effects on individual's energy intake(s). Likewise on the list of often-overlooked satiety factors are...

• polyphenolic compounds - these plant molecules have been shown to form high affinity, non-covalent bonds with both food proteins and digestive enzyme, will thus slow digestion and nutrient absorption... and thus up the satiety effect of the product and/or limit the nutrient uptake from the foods (e.g. tannins in cocoa, fruits, tea, cinnamon, and peanuts have been shown to be 'carb blockers')

Figure 3: Even for high protein foods, turning a solid into a liquid significantly compromises its satiety effect as measured by the dietary energy consumed after an isocaloric protein preload in 40 obese & lean subjects (Mourao. 2016).

• grinding or homogenizing food - while solidifying is a tried and proven method to make a food more satiating, grinding, pureeing, homogenizing and co will decrease the satiety effects of foods such as a chunky fruit yogurt, chicken, etc. that will be less satiating when you puréed it and/or created a pie of it
• increasing food volume - that's not by switching from chocolate to zucchini; rather than that it's about turning a soup-like food into a foam and/or simply using water to add volume

Figure 4: Mean overall intake at a breakfast test meal (±SEM) in grams (a) and kilocalories (b) that was served after a preload with 2mm (filled) or 50 mm (open bars). * represents significance at P < 0.05 (Lett. 2016).

• modifying the lipid droplet size - emulsion with smaller droplets are more satiating than those with large(r) fat droplets (Lett. 2016)

Can xanthan reduce the glycemic response to "sweet treats" like this? Learn more in this SuppVersity Classic.

Ok, we know relatively little, but... the little we know leaves no question that satiety is not just about macros. After all, calories count and the amount of energy you will consume depends on more parameters than "your macros".

With that being said, the addition of fiber is already used extensively in the food industry. What is hardly noticed by consumers and producers alike, however, is that simply adding volume by stirring air / adding water (in)to a product will likewise add to the satiating effect of a given food; the same goes for water. In fact, up to now producers add air (e.g. ice-cream) and water (e.g. to ham) mostly to make the production cheaper. That this has satiating side effects, on the other hand, is rarely used on purpose | Comment!

References: 

• Campbell, Caroline L., Ty B. Wagoner, and E. Allen Foegeding. "Designing foods for satiety: The roles of food structure and oral processing in satiation and satiety." Food Structure (2016).
• Lett, Aaron M., Jennifer E. Norton, and Martin R. Yeomans. "Emulsion oil droplet size significantly affects satiety: A pre-ingestive approach." Appetite 96 (2016): 18-24.
• Mourao, D. M., et al. "Effects of food form on appetite and energy intake in lean and obese young adults." International journal of obesity 31.11 (2007): 1688-1695.
• Slavin, Joanne L. "Dietary fiber: classification, chemical analyses, and food sources." Journal of the American Dietetic Association 87.9 (1987): 1164-1171.

Minimal Amounts of Fish Peptide Hydrolysate Double Fat Loss Compared to Whey Isolate on Energy Restricted Diet

I certainly recommend eating fish. Whether I will be recommending fish hydrolysate supplements in the future, however, will have to be determined when additional studies with different baseline diets will have been published.

You may remember that I've written about fish protein hydrolysates / peptides before. Unlike today's article, however, previous articles dealt with the effects of fish protein in rodents. Intrigued by in vitro and animal studies showing that fish-derived peptides demonstrated antihypertensive (Hatanaka. 2009; Kim. 2012; Li. 2012; Ngo. 2011), antioxidant (Nazeer. 2012; Najafian. 2012), immunomodulating effects (Duarte. 2006), reparative properties in the intestine (Fitzgerald. 2005; Marchbank. 2008), and effects in reducing plasma cholesterol and triglycerides levels (Möller. 2008), a group of Italian researchers decided to investigated the effect of Slimpro(R), a supplement containing commercially available fish protein hydrolysate from blue whiting (Micromesistius poutassou), on body composition and on stimulating cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) secretion in 120, overweight, non-obese (25 kg/m² < BMI < 30 kg/m²), male (25%) and female (75%) subjects aged 18 - 55 year.

Do not underestimate fish as a protein source - fish is more than just omega-3!

Salmon Better Than Whey?

Cod protein for recovery

Krill = Super Protein?

Fish Kicks Casein's Ass

Fast vs. slow protein

5x More Than FDA Allows

Unlike the product that was used may suggest, the study was not sponsored by the supplement company. The authors received neither funding nor other external support and they also declare that they don't have a conflict of interest that may be related to patents or direct involvements in the industry. I guess it's important to point that out, even though fact that the scientists chose whey, i.e. an actually relevant control, instead of carbohydrates or just plain water, may have given away the lack of sponsorship, anyways.

Two weeks before the study started, subjects were asked to fill in an alimentary diary reporting their food preferences. A mild hypocaloric ( 300 kcal/day) diet was elaborated for each subject by a dietitian based on subject’s food preferences and habits as reported in the alimentary diary.

Figure 1: The low protein content of the diet is - as highlighted in the annotations to this graphical illustration of the macronutrient composition of the test diets - problematic, to say the least.

Approximately, 55% of energy intake was from carbohydrates, 25% from lipids, and the remaining 20% from proteins. Part of these 20% of protein were either 1.4g and 2.8g of fish protein or 1.4g of whey protein isolate as a control (I just assume that the dosage was 1.4g, because there was only one whey group), which were consumed in form of a flavored shake according to the following protocol:

"Both the active (one dose treatment arm) and the placebo products were taken as follows: ‘dilute the content of one sachet in a large glass of cool water (200 ml). Shake or stir with a spoon. Consume within 10 30 min before the main meal’. In the case of two-dose treatment arm, one sachet of the active product was taken 30 min before lunch and one sachet 30 min before dinner" (Nobile. 2016).

To be able to tell what could be responsible for advantages or disadvantages of the two treatments, the scientists assessed more than just body weight, fat mass (DXA scans), and safety of use as well as the secondary efficacy endpoints, extracellular water, and the circumference of waist, hips, and thighs. They also checked the CCK and GLP-1 levels in their subjects' blood. This is relevant, because this is how the fish hydrolysate is advertised on the manufacturers website:

"Taken daily before meals, Slimpro® increases the production of CCK and GLP-1 in the body, thus amplifying messages associated with a decrease of food intake. Promising results were reported from in vivo et in vitro trials of these molecules that may control food intake. Scientists have described this ingredient as a direct action on the hunger process" (Nobile. 2015).

As it is usually the case in studies like this, some patients were "lost". In this case, we're talking about a total count of eleven subjects who did not reappear for the follow-up check (One subject in the one-dose treatment arm, four subjects in the twodose treatment arm, and six subjects in the placebo treatment arm discontinued intervention because they were no longer interested to participate in the study). The results of the other subjects are plotted in Figure 2:

Figure 2: Changes in body composition after 45 and 90 days of dieting w/ the specific supplements (Nobile. 2016).

As you can see, double-dosing had astonishingly little effect on the subjects' ability to lose body fat. That's in contrast to switching from fish protein hydrolysate to whey protein isolate, which produced measurably, but not statistically reduced rates of fat loss and waist reductions.

Figure 3: Blood biomarker levels. (a) CCK blood levels and (b) GLP-1 blood levels. Intragroup (vs. D0) statistical analysis is reported upon the bars of the histogram. The lines report the intergroup (vs. placebo) statistical analysis. Statistical analysis is reported as follows: *p < 0.05, **p < 0.01, and ***p < 0.001. Data are mean +/- SE (Nobile. 2016).

And guess what: Even though the bars don't look like it, the asterisks over the bars tell you that these differences may be caused by the same differential expression of the satiety hormones CCK and GLP-1 in the fish hydrolysate vs. whey protein group that has been observed with other control protein in previous studies and is boldly advertised on the producer's website.

Great! Let's eat more fish... It stands out of question that the former is actually a very good idea (assuming you make the right fish choices). I have to warn you, though: Firstly, the fish protein consumed in the study at hand came from fish, but just like whey protein and milk, fish and fish protein hydrolysates will also have different effects.

Is Wild Caught Fish Always the Better Choice? With Sign. More N3 and Less Pollutants?  Learn more!

What is probably way more important, however, is the relative protein deficiency of the subjects. With only 20% of the diet being protein, the study participants hovered around at the meager level of the RDA. Since the effects of 1.4g of fish protein hydrolysate you throw on top of a low protein diet are probably very different from those of the same amount of fish protein consumed alongside 2g/kg of dietary and supplemental protein, I wouldn't guarantee and in fact even doubt that you would see a similar almost 100% increase in fat loss while dieting - and still,  the CCK and GLP-1 boosting effects of fish protein hydrolysates are intriguing | Comment on Facebook!

References:

• Duarte, Jairo, et al. "Immunomodulating capacity of commercial fish protein hydrolysate for diet supplementation." Immunobiology 211.5 (2006): 341-350.
• Hatanaka, Akimasa, et al. "Isolation and identification of antihypertensive peptides from antarctic krill tail meat hydrolysate." Journal of food science 74.4 (2009): H116-H120.
• Kim, Se-Kwon, Dai-Hung Ngo, and Thanh-Sang Vo. "Marine fish-derived bioactive peptides as potential antihypertensive agents." Adv Food Nutr Res 65 (2012): 249-260.
• Li, Ying, et al. "Purification of a novel angiotensin I-converting enzyme (ACE) inhibitory peptide with an antihypertensive effect from loach (Misgurnus anguillicaudatus)." Journal of agricultural and food chemistry 60.5 (2012): 1320-1325.
• Marchbank, T., et al. "Clinical trial: protective effect of a commercial fish protein hydrolysate against indomethacin (NSAID)‐induced small intestinal injury." Alimentary pharmacology & therapeutics 28.6 (2008): 799-804.
• Möller, Niels Peter, et al. "Bioactive peptides and proteins from foods: indication for health effects." European journal of nutrition 47.4 (2008): 171-182.
• Nazeer, R. A., NS Sampath Kumar, and R. Jai Ganesh. "In vitro and in vivo studies on the antioxidant activity of fish peptide isolated from the croaker (Otolithes ruber) muscle protein hydrolysate." Peptides 35.2 (2012): 261-268.
• Najafian, L., and Abd Salam Babji. "A review of fish-derived antioxidant and antimicrobial peptides: their production, assessment, and applications." Peptides 33.1 (2012): 178-185.
• Ngo, Dai-Hung, et al. "Free radical scavenging and angiotensin-I converting enzyme inhibitory peptides from Pacific cod (Gadus macrocephalus) skin gelatin." International journal of biological macromolecules 49.5 (2011): 1110-1116.

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

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.

Do you have to worry about fasting when your're dieting!?

Breakfast and Circadian Rhythm

Does Meal Timing Matter?

Habits Determine Effects of Fasting

Fasting Works for Obese, Too!?

Does the Break- Fast-Myth Break?

Breakfast? (Un?) Biased Review

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.

Taste Matters - Bypassing Taste Receptors Boosts Insulin & CCK Satiety Hormone Response to Food - Why Does That Happen & What Are the Implications, If There Are Any?

Infusions of nutrient solutions via a tube is often the last resort for doctors to save anorexic patients' lives - it's yet nothing anyone should do voluntarily for the satiety plus Spetter et al. observed.

As a SuppVersity Reader you are no stranger to "incretin hormones" and their release in response to the interaction of food with the taste receptors that are distributed all over your body. Against that background you will probably not be surprised to hear that Martjee S. Spetter and her colleagues from the University Medical Center Utrecht and the Wageningen University found that bypassing oral the stimulation of oral taste receptors decreases the satiety and alters the appetite hormone response to a given meal.

As the Dutch researchers point out, the interaction between oral and gastric signals is an important part of food intake regulation.

Artificial sweeteners have a reputation of making you hungry - find out if they do

Unsatiating Truth About Artif. Sweeteners?

Will Artificial Sweeteners Spike Insulin?

Sweeteners & the Gut Microbiome Each is Diff.

Sweeter Than Your Tongue Allows!

The Latest on the Sweetener Scare.

Sweeteners In- crease Sweet- ness Threshold

In that, Spetter et al. are not the first to obversve that bypassing the oral taste receptors may diminish the suppression of hunger and increases gastric emptying rate. The role of appetite hormones, like cholecystokinin-8 and ghrelin, in this process, however, is still unclear.

The objective of Spetter et al.'s latest study was thus to determine the contributions of gastric and oral stimulation to subsequent appetite and hormone responses and their effect on ad libitum intake.
The scientists recruited fourteen healthy male subjects (age 24.6 ± 3.8y, BMI 22.3 ± 1.6 kg/m²) who participated in their randomized, single-blinded, cross-over experiment with 3 treatmentsessions:

• Stomach distention, only: naso-gastric infusion of 500 mL/0 kJ water, 
• Stomach distention with caloric content: naso-gastric infusion of 500 mL/1770 kJ chocolate milk, and 
• Stomach distention with caloric content and oral exposure: oral administration of 500 mL/1770 kJ chocolate milk.

Due to the specific design of the experiment, the distention of the stomach, of which you've learned previously on the SuppVersity that it is a major contributor to the satiety response (see "True or False: High Volume + Nutrient + Low Energy Foods Keep You Lean." | learn more) was fully controlled in the study at hand.

Hunger & desire to eat increase significantly faster after isocaloric liquid vs. solid meals (Tieken. 2007)

No, the study at hand does not imply that you should tube feed yourself: If we take into account that Jones & Mattes observed only recently that the satiety response to liquid meals is generally impaired, even in lean individuals (obese individuals cannot compensate for energy from beverages or solid foods | Jones. 2014), the results may well be different for a solid meal that would be chewed, not just swallowed like the chocolate milk in the study at hand.

Take a look at the data from Tieken et al. (2007) on the left, for example. They found that a liquid meal providing 25% of the daily energy requirement provides a lower and less sustained suppression of hunger and desire to eat than an isocaloric solid meal.

The stomach distention, only, trial can thus serve as a baseline. If we assume that the taste receptors in the mouth were irrelevant and the satiety response would be controlled solely by the amount of type of nutrients that arrive in the stomach, there should be a difference between the control infusion with water and the infusion of chocolate milk, but there should be no difference between the infusion compared to the ingestion of the chocolate milk.

Figure 1: Fullness rating (top) and desire do eat (bottom) in response to infusion (light and dark grey bars) of water and chocolate milk, respectively vs. the ingestion of chocolate milk (dark bars; Spetter. 2014).

As you can see in Figure 1, the latter was not the case. While there were no differences in the fullness ratings (top) and desire to eat (bottom) between chocolate milk and water, when it was infused through the nose, the subjects felt significantly fuller and had a significantly lower desire to eat, when they drank the chocolate milk the way nature intended it.

Things never are as you would expect them to be

Now, everyone would expect that the decrease in desire to eat and the increased fullness in response to the regular (=oral) ingestion of chocolate milk would significantly reduce the energy intake on a subsequent meal, right?

Figure 2: In contrast to what the data in Figure 1 would suggest there was no significant difference between the effects the intra-nasally infused chocolate milk (CM) and the regularly consumed CM had on the ad-lib. intake on a subsequent meal  (Spetter.2014) - How can that be? Maybe the higher satiety hormones in the infusion trial (see Figure 3)

Well, as you can see in Figure 2 this is not the case. There is a reduction in energy intake, but in contrast to the comparison to the water infusion (right), the difference between the oral chocolate milk vs. the intra-nasally infused chocolate milk was not significant.

Figure 3: The increase in the satiety hormones insulin (top) and CCK-8 (bottom) is more pronounced, when the taste receptors in the oral cavity are bypassed (Spetter. 2014)

But why is the intra-nasally administered chocolate milk eventually more "satiating"? Well, if you take a closer look at the previously mentioned CCK-8 and insulin response (see Figure 3), you will see that the increase in these satiety hormones (yes, insulin increases satiety; cf. Anika. 1980; Vanderweele. 1994) is more pronounced, when the taste receptors in the oral cavity are bypassed and the chocolate milk is infused intra-nasally. For the ad-libitum meal that was served 45 minutes later, this increase was more important than the increased feeling of "fullness", let alone the highly subjective desire to eat" (Figure 2).

As Spetter et al. point out, this initially counter-intuitive result provides evidence for the "common but relatively poorly underpinned idea that learned associations between sensory signals and ensuing metabolic consequences serve to adapt hormone responses based on nutrient content" as it was previously observed by Zafra et al. (2006) and Power et al. (2008).

In view of the obesity problem, the results support the idea that a relative lack of oral stimulation, due to e.g. caloric beverage or other fast food consumption can result in overeating by weakening satiety (de Graaf. 2010), an effect of which Jones & Mattes have shown that it is impaired in obese individuals and reduced in lean and obese individuals, when the energy they consume comes from liquid foods, like shakes (Jones. 2014) | Comment on Facebook!

Reference:

• Anika, S. M., T. R. Houpt, and K. A. Houpt. "Insulin as a satiety hormone." Physiology & behavior 25.1 (1980): 21-23.
• de Graaf, Cees, and Frans J. Kok. "Slow food, fast food and the control of food intake." Nature Reviews Endocrinology 6.5 (2010): 290-293.
• Jones J.B., Mattes R.D. "Effects of learning and food form on energy intake and appetitive responses. Physiol Behav. 21 (2014):1-8.
• Power, Michael L., and Jay Schulkin. "Anticipatory physiological regulation in feeding biology: cephalic phase responses." Appetite 50.2 (2008): 194-206. 
• Tieken, S. M., et al. "Effects of solid versus liquid meal-replacement products of similar energy content on hunger, satiety, and appetite-regulating hormones in older adults." Hormone and metabolic research= Hormon-und Stoffwechselforschung= Hormones et metabolisme 39.5 (2007): 389.
• Vanderweele, Dennis A. "Insulin is a prandial satiety hormone." Physiology & behavior 56.3 (1994): 619-622.
• Zafra, María A., Filomena Molina, and Amadeo Puerto. "The neural/cephalic phase reflexes in the physiology of nutrition." Neuroscience & Biobehavioral Reviews 30.7 (2006): 1032-1044.

Not Exercise, But Dieting Makes You Hungry: Beneficial or No Effects on Appetite of Exercise in Lean & Obese. (Ab-) using Exercise to Make Up For Messy Diets Still a Bad Idea!

Will working out make you cheat on your diet, 'cause it leaves you drained and ravenous? Or is it even a stand-alone weight loss tool with satieting and anti-depressive effects?

As a SuppVersity reader you will probably be aware of the fact that the purported "appetite increasing" effects of exercise are non-existent. Against that background, you won't be surprised to hear that scientists from the Norwegian University of Science and Technology have recently been able to show that the alleged hunger-inducing effects of exercise didn't occur, in twelve overweight/obese volunteers who had to perform moderate or high intensity exercise, either.

The exercise sessions, which were spaced 1-week apart and to which the subjects were randomly assigned in a counter-balanced fashion lasted 1 hour and were - and this may be an important fact - performed after a standard breakfast.

You can learn more about workout routines at the SuppVersity

What's the Right Training 4 You?

Hypertrophy Blueprints

Fat Loss Support Blueprint

Strength Training Blueprints

Study Proves: Overtraining Exists

Recovering from the Athlete's Triad

After the subjects had been sweating in the gy, an ad libitum test lunch was served (that's 3h after breakfast) and fasting/postprandial plasma samples of insulin, acylated ghrelin (AG), polypeptide YY3-36 (PYY3-36) and glucagon-like peptide 1 (GLP-1) and subjective feelings of appetite were measured every 30 minutes for 3h. Nutrient and taste preferences were measured at the beginning and end of each condition using the Leeds Food Preference Questionnaire. In contrast to the "increased appetite" hypothesis, but much in line with what any sane individual would expect, the "[i]nsulin levels were significantly reduced while the GLP-1 levels increased during all exercise bouts".

Figure 1: Consumed and expended energy (in kcal) before and after the workout / laziness (Martins. 2014). Both exercise modalities induced a caloric deficit because the energy expenditure was not compensated for - In the course of the rest of the 24h this advantage vanished and the total energy balance no longer significantly negative in the exercise groups.

The effects on acelyted ghrelin depended on the exercise intensity and duration and was significant only in the MICC and HIIC, but not shorter S-HIIC, compared with control. Practically relevant effects on hunger or fullness ratings, the energy intake at the subsequent ad libitum meal and the food reward the obese subjects experienced were yet not observed.

And what about the lean guys? Does exercise make lean guys hungrier?

In general the results reseachers from the Loughborough University are about to present in a soon-to-be-published paper in the scientific journal "Appetite" clearly support the results Martins et al. observed in significantly heavier subjects.

Figure 2: PYY3-36 satiety hormone levels (pg/ml) after doing nothing (diet or control) or exercise (=pre-prandial) before, during and after ad libitum test meals (Deighton. 2014)

The weight (1) was yet not the only of a total of four differences: (2) The total amount of energy the subjects expended during their standardized exercise bout was higher 40% (350kcal for the lean guys vs. 250kcal for the obese guys in the Martins study), (3) the satiety hormone PYY3-36 increased significantly in response to exercise, and (4) the study had a second, a diet arm, in which skipping breakfast (163kcal) and skipping lunch (190kcal) both lead to significant increases in appetite and corresponding reductions in PYY3-36.

Losing weight does not have to ruin your metabolism if you follow this simple set of rules.

Bottom line: The fact that exercise didn't develop any appetite increasing effects in either the obese or the lean subjects in the Martins or Deighton study, respectively probably won't be convincing enough to shut all the critics of my recommendation to use exercise as an adjunct to dietary restriction in order to lose weight.

That's something I don't care about, anyway. What I do care about, though, is the fact that there are thousands of people out there who may read the message "burn 350kcal from exercise, don't get hungry and lose 1lbs of fat in 10 days" ... yeah, I know: No SuppVersity student would ever be so stupid, but just to make sure that none of the newbies get confused and end up in the black whole some people call the "athlete's triad", although, it befalls more weekend warriors than athletes these days: Do not work out to burn calories! Work out to steer the weight loss away from muscle and towards fat and (re-)read the rules you have to follow to make sure this strategy works.

Reference: 

• Martins, Catia, et al. "Effect of Moderate-and High-Intensity Acute Exercise on Appetite in Obese Individuals." Medicine and science in sports and exercise (2014).