Phosphorus, the Magic Bullet For Fat Loss and Against the YoYo-Effect? P. Restores Thermogenesis, Enhances Satiety

This is not the first study to suggest that as little as 12.5% of the suggested upper limit for phosphorus can make a big difference when it comes to weight loss and the ease of weight loss when you battle reduced diet-induced thermogenesis & increased appetite.

I guess those of you who have been reading every SuppVersity article will remember my January article "Phosphorus, an Anti-Obesity Agent? 3x375 mg With Each Meal Strip Almost 4 cm Off Obese Waists in Only 12 Weeks" (re-read it). You liked that one? Well, I guess you will also like the fact that the evidence that there's some use in phosphorus supplements is accumulating.

Recently, scientists from the Lebanese American University in Beirut, Lebanon (Bassil. 2016), have observed that "P supplementation recovers the blunted diet-induced thermogenesis in overweight and obese subjects and enhances their postprandial satiety" (Bassil. 2016).

Phosphates have also been touted as buffer for athletes, but apper less effective than NaHCO3:

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Yes, that's right: This means that phosphorus aka "P" supplementation will address two of the main reasons for weight regain aka the YoYo-effect - a diet- / weight-loss-induced reduction in diet-induced thermogenesis and a decrease of the satiety effects of the foods you consume.

Since diet-induced thermogenesis (DIT) is believed to be largely related to ATP production, which is dependent on phosphorus (P) availability, Bassil and Omar speculated that supplementing extra phosphorus to lean and overweight/obese healthy subjects should have beneficial effects on their diet-induced thermogenesis. Accordingly, they measured the latter with or without P in 10 lean and 13 overweight/obese adults in a double-blind randomized cross-over pilot study with a one week washout period that was meant to exclude any possible interference of the previous trial.

Figure 1:  Diet-induced thermogenesis after drinking 75 g glucose solution with and without phosphorus supplementation in lean and obese subjects. (A) Resting metabolic rate at baseline and over 3 h (180 min) after drinking 75 g glucose solution in lean and obese subjects with phosphorus (solid lines) or placebo (dashed lines); (B) Total area under the curve of RMR with phosphorus (solid bars) or placebo (dashed bars) in lean and obese subjects (Bassil. 2016).

The "problem" is that the subjects were healthy, sedentary non-smokers whose body weight had been stable for the past 3 months. As I will elaborate in the bottom line, the significance of the results for reduced-obese individuals, i.e. people who have lost a significant of body weight and are now facing an increased risk of yoyo-ing backup, is limited... but as I said: more about that later.

Correlation between daily dietary P intake and subjects' BMI (Bassil. 2016).

Additional evidence: Phosphorus intakes correlate negatively with BMI -- Next to the previously cited study by Ajoub, et al. (read more), the study at hand does also provide additional evidence that high(er) phosphorus intakes could have an obesity protective effect. After all, the data in the figure to the left clearly indicates that there is a linear, inverse correlation between obesity / BMI (in normal people a good measure of obesity) and the individual's habitual phosphorus intakes. Since fasting serum P is tightly controlled in healthy humans and is not affected by diet, so that the effect of dietary P is only evident post-prandially, this differential DIT response of lean and obese individuals (see Figure 1).

Speaking of explanations... a 2006 study by Mataix, et al. shows that Spaniards who consume more energy than they'd need have an increased risk of suboptimal phosphate intakes. The same goes for people with low education (Mataix. 2006). Both could point to phosphate intakes as a correlate not a cause of reduced obesity risks. Furthermore, we must not forget that US citizens with the highest phosphorus intakes happen to have an increased risk of mortality (Chang. 2014). This association with mortality risk, however, well be unrelated to phosphorus and a simple result of the high amounts of phosphates you will also find in processed foods. In this case, phosphorus would rather be a marker of increased junk food intake, which in turn could be the actual reason for an increase in mortality risk - an increased risk that may, however, eventually be a result of a messed up balance between phosphorus, calcium and magnesium.

I the study at hand, the DIT, as well as the subjects' resting metabolic rate, respiratory quotient, and substrate utilization (ratio of fat and glucose oxidation) were measured after a 10 h overnight fast at fasting and every 30 min for 3 h after subjects drank a standardized glucose solution, with P (500 mg from potassium phosphate, 23% monobasic and 18% dibasic | considering the results of previous studies, it is, by the way, unlikely that the potassium in KP did the trick) or placebo (cellulose) pills.

Figure 2: Subjective appetite scores of lean (gray) and obese (black) subjects, 3 h after drinking 75 g glucose solution with phosphorus (solid bars) or placebo (dashed bars) supplementation (Bassil. 2016).

To assess the subjects' hunger/satiety response, the researchers used the classic validated visual analog scale (VAS) questionnaires we all know from other studies - with quite intriguing results.

• Overweight/obese subjects had a blunted DIT with placebo. 
• P supplementation induced a 23% increase in their DIT area under the curve (p < 0.05).
• The increase in DIT was associated with an increase in carbohydrate oxidation. 
• All subjects, obese or lean had lower appetite following P supplementation.
• The decrease was expressed as a significantly (p = 0.02) lower desire to eat a meal (4.0 ± 0.7 cm) compared with placebo (5.8 ± 0.9 cm). 

At least during/before a diet, the co-consumption of phosphorus with glucose-containing meals could thus, as the scientists point out, be a valid means to recover the blunted diet-induced thermogenesis in overweight and obese subjects and enhances their postprandial satiety.

High phosphorus intakes and/or supplementation accelerated the fat loss in a previous study sign.

So, will this actually prevent the YoYo-effect? That is possible, but nothing the study at hand can prove. Rather than that, it provides new evidence of the usefulness of phosphorus supplements during weight loss interventions. A usefulness that has been previously confirmed by Ajoub, et al. (read more), but does not necessarily mean that the same beneficial effects will be observed in reduced-obese (=formerly obese) individuals whose DIT and appetite response have been shown to be significantly depressed in the post-dieting period. Until this study has been done, we still have the evidence of its usefulness for overweight individuals trying to shed body fat.

Everyone? Well, I guess another two qualifications have to be made: (a) If the effect is, indeed, as the scientists speculate, mediated by ATP, it is not unlikely that the benefits depend on the co-consumption of glucose or rather carbohydrates. Accordingly, low carbers may benefit less, maybe even not at all. And (b) low carbers have another "disadvantage" with respect to phosphorus supplementation: With plenty of the foods you see in the photo at the top-right, their phosphorus intake usually is already very high - increasing it, even more, may thus have no effect irrespective of the glucose intake. Plus: Eventually, you must keep an eye on the balance between phosphorus, calcium, and magnesium. While a healthy kidney helps to balance serum imbalances out, adding another 1,500 mg of phosphorus or 37,5% of the upper intake limit for phosphorus (4g/day) to your diet with the 500mg extra phosphorus you'd take with e.g. three daily meals could increase your long-term calcium and magnesium requirements to a certain degree - a degree that you will probably cover automatically if you get your phosphorus from foods, not supplements, because only the former (e.g. dairy) come packaged with all important co-factors | Comment!

References:

• Bassil, Maya S., and Omar A. Obeid. "Phosphorus Supplementation Recovers the Blunted Diet-Induced Thermogenesis of Overweight and Obese Adults: A Pilot Study." Nutrients 8.12 (2016): 801.
• Chang, Alex R., et al. "High dietary phosphorus intake is associated with all-cause mortality: results from NHANES III." The American journal of clinical nutrition 99.2 (2014): 320-327.
• Mataix, José, et al. "Factors influencing the intake and plasma levels of calcium, phosphorus and magnesium in southern Spain." European journal of nutrition 45.6 (2006): 349-354.

DIT: Four Fat-Burning Facts About the Effects of Calories, Macros + Meal Timing on the Thermogenic Effects of Foods

A dream has come true: You can burn more calories by eating more... unfortunately, the so-called "diet-induced thermogenesis" does not fully compensate the increased energy intake - you cannot eat yourself slim as "unfair" as some people think this was.

You all will have read that: eating a high protein meal first thing in the AM kickstarts your metabolic engine. But do you also know that this "kick" is worth - in terms of calories, for example? Do you know how the mix of carbohydrates, fats and proteins will affect your diet-induced thermogenesis? Can you tell if calories matter and whether the meal size and speed at which you consume a given meal will matter?

Well, today's SuppVersity article will not be able to answer all of these questions in a "once and for all" fashion, but being based on the latest systematic review by Quatela et al. (2016), it will still give you a good overview of the individual effects of differing energy intakes, macronutrient compositions, and eating patterns of meals on what scientists call your DIT, i.e. your "diet-induced thermogenesis" (DIT) in response to a std. meal.

While fasting will obviously not trigger DIT, it relates to the effects of meal frequency on DIT

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The previously hinted at review comprised 26 papers - all with a randomized crossover design capable of comparing the effects of two or more eating events on DIT. And here's what the authors found:

Higher energy intake increased DIT; in a mixed model meta-regression, for every 100 kJ increase in energy intake, DIT increased by 1.1 kJ/h (p < 0.001 | Quatela. 2016). 

There's, for example, the 1990 study by Kinabo and Durnin who found no effect of the macronutrient composition of the test meals they served either high-carbohydrate-low-fat (HCLF) with 70%, 19% and 11% of the energy content from carbohydrate, fat and protein, respectively, or a low-carbohydrate-high–fat (LCHF) with 24%, 65% and 11% to sixteen adult, non–obese female subjects.

Figure 1: Studies like Kinabo & Durnin (1999) show that low carb vs. low fat does not make a difference - what does matter for DIT (and that's statistically and practically sign.) is the total energy intake per meal.

Accordingly, the two scientists concluded that "[t]he present study suggests that TEF is significantly influenced by the energy content of a meal but not by meal composition" (Kinabo. 1990) - very similar observations, albeit not always with meals differing in their macronutrient composition, have been made by Hill et al. (1984), and Segal et al. (1990).

There's a 50% difference in the thermogenic response to a std. meal (720kcal; the other meal was 35% of the RMR and thus not identical for both groups) in lean vs. obese men - in fact, the obese don't show any stat. sign. DIT (Segal. 1990).

Beware of becoming obese - It will impair your DIT: Even if the last-mentioned study by Segal et al. (1990) confirms that higher energy intakes will yield higher degrees of post-prandial diet-induced thermogenesis (DIT), it is far more important that this study is the first in a recently expanding line of studies that shows that this effect of high-energy meals is blunted in the obese (see Figure on the left). And there's more: With a 9-10% increase in thermogenesis in lean men, the 5% increase in the obese subjects is small and statistically and practically non-significant enough to count as one of the many reasons why obese individuals cannot get away with occasional binges as easily as those who are still lean.

With 100 kcal extra producing on average a thermogenic effect of only 1 kcal/h you got to be careful, though. Eating more is not going to burn body fat! What the research does suggest, however, is a possible explanation for the efficacy of intermittent fasting, where you can consume at least one really satiating, highly thermogenic high energy meal per day.

Meals with a high protein or carbohydrate content had a higher DIT than high fat, although this effect was not always significant (Quatela. 2016). 

The next take home message takes us back to my claim from the introduction: you all will have heard about the beneficial metabolic effects of high protein breakfasts. And in contrast to what the take home message says about carbohydrates, the evidence that high(er) protein intakes yield higher levels of diet-induced thermogenesis has been found consistently (see green lines in the Table 1) .

Table 1: Colored version of an overview from the review by Quatela, et al. (2016) - yellow = study shows advantage for CHOs; gray = study didn't find effect of high carb vs. high fat; green = study shows advantage for protein.

The effects of eating high carb and low carbohydrate meals on thermogenesis, on the other hand, is less clear. While there are studies showing that "low carb = more DIT" (see yellow lines in Table 1), there are also studies which observed identical effects for both, high fat and high carb meals (see gray lines in Table 1). a certain amount / percentage of protein, that's what the data in Table 1 tells us, is not enough for an optimal DIT to occur.

What should also be mentioned, though, is the fact that there's ZERO evidence to the opposite, i.e. an acute increase in thermogenesis to high fat intakes, when the meal size / energy content is standardized and the protein content is kept the same... and no, the study by Riggs et al. (2007) is not an example that this statement was wrong. After all, the "high fat" group in Riggs' study also received increased amounts of protein. The effects on DIT the scientists observed may thus well be ascribed to the extra 10% protein, not to the increased fat and/or reduced carb content.

You better don't starve yourself either! While the previous red box has thought you about the ill consequences being obese will have on your body's ability to burn off extra calories, the previously mentioned study by Riggs et al. shows that being too thin, i.e. underweight (starved), appears to have the same effect. In their study a higher protein intake lead to an increase in DIT only in the normal- yet not in the under- and overweight women; and that the exact same lack of thermogenesis can be observed in weight-reduced formerly obese subjects has been observed by Schutz et al. (1894) more than 40 years ago.

Simply distinguishing between calories and macros, alone, however, is not sufficient to predict the real-world DIT effect of a given meal. This (hopefully) unsurprising revelation takes us right to the last two take home messages that relate to the DIT effect of certain micronutrients and the importance of meal frequency.

Meals with medium chain triglycerides, and meals high in PUFA had a significantly higher DIT than other fats (meta-analysis, p = 0.002 | Quatela. 2016). 

Yes, it is true MCT oils are not just rapidly metabolized, there's also good evidence that they can increase the diet-induced thermogenesis in mouse and, more importantly, man (Kasai. 2002a,b; Clegg. 2013 | discussed => here).

Figure 2: The thermogenic effect of a meal does also depend on the type of fat in it (Casas-Agustench. 2009)

In a similar vein, the likewise comparatively easily oxidized PUFAs have been found to increase DIT compared to both MUFAs, i.e. monounsaturated, and - even more so - SFA, i.e. saturated fats (Piers. 2002; Casas-Agustench. 2009)

Consuming a meal as a single bolus eating event compared to multiple small meals or snacks was associated with a significantly higher DIT (meta-analysis, p = 0.02 | Quatela. 2016).

The last of our four take home messages is one you have read in previous SuppVersity articles about the advantages and disadvantages of fasting and/or a lower meal frequency, before. If you compare the effects of consuming a standardized meal as a bolus event versus splitting the same meal into two (Kinabo. 1990), three (Vaz. 1995), four (Allirot. 2013) or six (Tai. 1991) smaller equal meals or snacks to be consumed throughout the morning, the bolus administration will always produce the highest thermogenic response.

Figure 3: Mean differences in DIT between bolus vs. frequent smaller meals (e.g. snacking | Quatela. 2016)

This effect, however, is not significant in the two small meals and three small meals conditions. And still, Quatela's meta-analysis of all four studies (see Figure 3) shows that "[t]he overall mean of the difference is positive, which means that the DIT was lower in the smaller frequent meals event trials compared to the bolus trial" (Quatela. 2016).

The degree of processing will likewise affect the thermogenic response to food (Barr. 2010).

And there's still more: Unprocessed foods are more thermogenic than processed foods (Barr. 2010). The same goes for eating fast vs. slow (slow increases DIT compared to fast eating). It should be mentioned though that at least for the latter variable, as well as the effect of and palatability the evidence is either insufficient, unclear or contradictory. That's why I would agree that only "the energy intake, macronutrient compo-sition, and eating pattern of the meal" (Quatela. 106) have a sufficiently proven practically relevant effect on DIT.

With that being said, I cannot let you go without reminding you that neither the extra 10kcal/h you expend if you add another 1000kcal to your meal nor 17% increase in DIT you can get from increasing a meal's protein content will strip an inch off your waist or decrease your body fat percentage by 0.1% - and comprehensive evidence on the long-term effects is still warranted (for meal frequency there's some; the same goes for high protein). Optimizing your DIT should thus be only one (and not the most important) strategy in your dieting toolbox  | Comment.

References:

• Barr, Sadie B., and Jonathan C. Wright. "Postprandial energy expenditure in whole-food and processed-food meals: implications for daily energy expenditure." Food & nutrition research 54 (2010).
• Casas-Agustench, Patricia, et al. "Acute effects of three high-fat meals with different fat saturations on energy expenditure, substrate oxidation and satiety." Clinical Nutrition 28.1 (2009): 39-45.
• Clegg, Miriam E., Mana Golsorkhi, and C. Jeya Henry. "Combined medium-chain triglyceride and chilli feeding increases diet-induced thermogenesis in normal-weight humans." European journal of nutrition 52.6 (2013): 1579-1585.
• Kasai, Michio, et al. "Comparison of diet-induced thermogenesis of foods containing medium-versus long-chain triacylglycerols." Journal of nutritional science and vitaminology 48.6 (2002a): 536-540.
• Kasai, Michio, et al. "Comparison of diet-induced thermogenesis of foods containing medium-versus long-chain triacylglycerols." Journal of nutritional science and vitaminology 48.6 (2002b): 536-540.
• Kinabo, J. L., and J. V. G. A. Durnin. "Thermic effect of food in man: effect of meal composition, and energy content." British Journal of Nutrition 64.01 (1990): 37-44.
• Kinabo, J. L., and J. V. Durnin. "Effect of meal frequency on the thermic effect of food in women." European journal of clinical nutrition 44.5 (1990): 389-395.
• Hill, James O., et al. "Meal size and thermic response to food in male subjects as a function of maximum aerobic capacity." Metabolism 33.8 (1984): 743-749.
• Piers, L. S., et al. "The influence of the type of dietary fat on postprandial fat oxidation rates: monounsaturated (olive oil) vs saturated fat (cream)." International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 26.6 (2002): 814-821.
• Quatela, Angelica, et al. "The Energy Content and Composition of Meals Consumed after an Overnight Fast and Their Effects on Diet Induced Thermogenesis: A Systematic Review, Meta-Analyses and Meta-Regressions." Nutrients 8.11 (2016): 670.
• Riggs, Amy Jo, Barry D. White, and Sareen S. Gropper. "Changes in energy expenditure associated with ingestion of high protein, high fat versus high protein, low fat meals among underweight, normal weight, and overweight females." Nutrition journal 6.1 (2007): 1.
• Schutz, Yves, et al. "Decreased glucose-induced thermogenesis after weight loss in obese subjects: a predisposing factor for relapse of obesity?." The American journal of clinical nutrition 39.3 (1984): 380-387.
• Tai, Mary M., Peter Castillo, and F. Xavier Pi-Sunyer. "Meal size and frequency: effect on the thermic effect of food." The American journal of clinical nutrition 54.5 (1991): 783-787.
• Thyfault, JOHN P., et al. "Postprandial metabolism in resistance-trained versus sedentary males." Medicine and science in sports and exercise 36.4 (2004): 709-716.
• Vaz, Mario, et al. "Postprandial sympatho-adrenal activity: its relation to metabolic and cardiovascular events and to changes in meal frequency." Clinical Science 89.4 (1995): 349-357.

How Chewing (Gum/Food) Affects Your Energy Expenditure: Gum + Slow Eating Triple 3h Diet Induced Thermogenesis

If chewing gums can help triple the diet-induced thermogenesis. Does this mean that your doctor will soon prescribe chewing gums instead of diet and exercise or even weight loss surgery?

Slow eating, which involves chewing food slowly and thoroughly, is - according to most research, at least - an effective strategy for controlling hunger level and energy intake in overweight or obesity (Andrade. 2008; Smit. 2011). And the fact that slow eating / chewing more frequently aids weight management even in the people who don't tend to overeat, may - as a recent study from the Tokyo Institute of Technology shows - be a consequence of more than just a reduction in energy intake.

As Hamada et al. show in two recent studies in Obesity, eating slowly will also ramp up the postprandial energy expenditure and fat oxidation aka the "diet-induced thermogenesis" (DIT) of healthy, normal-weight men and women without one of the pertinent eating disorders.

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From their previous research, the authors knew that "increasing DIT by slowing the eating speed can be difficult for individuals to accomplish, since the natural eating speed is acquired over a long period of time" (Hamada. 2016). In the latest follow up, the scientists sought to investigate, whether the postprandial gum chewing increases DIT via an increase in the splanchnic circulation in eleven healthy, normal-weight subjects [7 males and 4 females; age, 24 ± 1 years (mean ± SD); height, 164 ± 10 cm; weight, 56 ± 6 kg; and body fat, 18 ± 8%].

Figure 1: Diagram for outline of study protocol. VAS, measurement of visual analog scale (Hamada. 2016).

As the illustration of the study design in Figure 1 tells you, Hamada et al. chose a randomized crossover design. The subjects completed four trials on four different days, with consecutive trials separated by more than 3 days (see Figure 1).

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"The subjects arrived at the laboratory at 9:00 a.m. after having abstained from eating, consuming caffeinated or alcoholic beverages, and intense exercise since dinner on the previous night (i.e., they had fasted for more than 10 h). Each subject was seated on a chair in a semisupine position in a quiet room in which the temperature and humidity were controlled to within 25.0 +/- 0.48C and 50 +/- 4%, respectively. After allowing the subjects to adjust to the experimental setup for 20 min, baseline data of gas-exchange variables and the splanchnic circulation were recorded while resting for 20 min. The subjects completed a visual analog scale (VAS) questionnaire to assess their hunger before the test meal.

After the previously described baseline data measurements, the subjects chewed the 621-kcal test meal for as long as possible and as many times as possible in the slow-eating trials, while they consumed the same meal as rapidly as possible in the rapid-eating trials (details from Hamada. 2016):

• In the gum-chewing trials, they started chewing 1.5 g (3 kcal) of sugarless gum with a lime-mint flavor (Lotte, Japan) immediately after the meal and chewed this gum at a natural pace for 15 min. 
• In the non-gum-chewing control trials, they consumed 3 kcal of sugar with the meal instead of chewing the gum. 
• In each rapid-eating and slow-eating trial, they were instructed to eat the meal at a similar speed in the non-gum-chewing and gum-chewing trials. Gasexchange variables and the splanchnic circulation were recorded until 180 min after the meal (note: I am not going to discuss this data in detail, but if the scientists are right the increase in the amount of blood that's circulating in the organs of the splachnic bed, is more than a correlate of the increase in energy expenditure).

The four trials of combinations of rapid eating and non-gum chewing, rapid eating and gum chewing, slow eating and non-gum chewing, and slow eating and gum chewing were labeled as RN, RG, SN, and SG, respectively.

The test meal (photos are not from the study, but show the products that are listed in the methods section) had a macro composition of 13% protein, 28% fat, and 59% carbohydrate and was spaghetti carbonara with orange juice and a regular yogurt.

What was the test meal? Test meal The 621-kcal test meal (energy proportions: 13% protein, 28% fat, and 59% carbohydrate) consisted of carbonara spaghetti (452 kcal; Nippon Flour Mills, Japan), yogurt (59 kcal; Meiji, Japan), and orange juice (110 kcal; Kirin Beverage, Japan). The temperature of the meal was measured using an infrared thermometer (A&D, Japan), and the meal was provided at a controlled temperature (spaghetti, 58 +/- 1*C; yogurt, 7 +/- 1°C; orange juice, 7 +/- 1°C | You're wondering about the temperatures? Well, we know that cold food has a thermogenic effect. Accordingly, you have to tightly control the food temperature to avoid temperature differences to mess with your results.).

To make sure the number of chews was measured accurately, the scientists went so far to determine the number from a videotape recording of the subject’s face and from recordings of the electromyographic (EMG) activities of the chewing muscles obtained using a standard electrocardiograph (MEG-2100, Nihon Kohden, Japan).

"The chewing duration of the meal was assessed as the duration from the first bite to swallowing after the last bite of the meal. The number of chews was counted using a hand tally counter while watching the videotape recording. The obtained numbers were double-checked using the EMG recordings. The chewing duration and the number of chews were measured twice. There was a small difference (less than 2.8%) between the measurements, and so they were averaged. The total chewing duration and the total number of chews were defined as the summed data obtained during the periods of meal and gum chewing" (Hamada. 2016).

The accurate measurement of the eating speed and chewing frequency, along with the rigid control of hunger, when the subjects arrived at the lab (pre-hunger values did not differ), and the sophisticated analysis of the gas-exchange variables and DIT, are certainly strengths of the study at hand - a study, the results of which confirmed the researchers expectations: the diet induced thermogenesis (DIT) was significantly greater in the gum-chewing trials than in the non-gum-chewing trials for both rapid-eating and slow-eating trials.

Figure 2: Time courses of changes in gas-exchange variables and DIT in rapid-eating trials (RN vs. RG, left panels) and slow-eating trials (SN vs. SG, right panels). Hatched bars indicate the duration of gum chewing. Filled and open circles denote data for the non-gum-chewing and gum-chewing trials, respectively. VO _ 2, oxygen uptake; *P < 0.05, vs. resting baseline in each trial. # P < 0.05, difference between trials (Hamada. 2016).

Even though these results are good news for chewing gum producers, the revelation that the difference in DIT between rapid-eating and slow-eating trials was greater than that between non-gum-chewing and gum-chewing (compare left vs. right graphs in Figure 2) suggests that only a combination of both: slow eating (high number of chews) and post-meal chewing gum will maximize the thermogenic effect of (low protein) meals.

To chew or not to chew, that is not the question! While it appears to be out of question that deliberately chewing more thoroughly and thus eating slower will increase your respiratory exchange ratio (RER, a marker of fat oxidation) and diet induced thermogenesis (DIT) compared to bolting your food (compare left hand vs. right hand graphs in Figure 2), the important question we still have to answer is: How practically relevant is this statistically significant difference?

Figure 3: Diet-induced thermogenesis (DIT) and postprandial splanchnic blood flow (BF) accumulated over the 180-min period immediately after the meal. Filled and open bars indicate data for non-gum-chewing and gum-chewing trials, respectively. *P < 0.05, non-gum-chewing vs. gum-chewing trials. #P < 0.05, rapid-eating vs. slow-eating trials (Hamada. 2016).

To answer this question, we need the data in Figure 3, data which reveals that the difference between eating rapidly and chewing no gum, on the one, and eating slowly and chewing gum, on the other hand, is 350 cal/kg over 3h. That sounds huge, but only if you are not looking at the units closely. Since we're talking about calories, not kilocalories, the average 80 kg man would burn less than 30 kcal extra - that's bull? Well, that's about the same increase in DIT you can expect from a high protein vs. high carbohydrate meal if you extrapolate the data from a 2002 study by Carol Johnston et al. - an effect of which future studies must determine whether it adds to the effect of chewing more thoroughly and using a gum after your meals | Comment!

References:

• Andrade, Ana M., Geoffrey W. Greene, and Kathleen J. Melanson. "Eating slowly led to decreases in energy intake within meals in healthy women." Journal of the American Dietetic Association 108.7 (2008): 1186-1191.
• Hamada, Yuka, Hideaki Kashima, and Naoyuki Hayashi. "The number of chews and meal duration affect diet‐induced thermogenesis and splanchnic circulation." Obesity 22.5 (2014): E62-E69.
• Hamada, Yuka, Akane Miyaji, and Naoyuki Hayashi. "Effect of postprandial gum chewing on diet‐induced thermogenesis." Obesity (2016).
• Johnston, Carol S., Carol S. Day, and Pamela D. Swan. "Postprandial thermogenesis is increased 100% on a high-protein, low-fat diet versus a high-carbohydrate, low-fat diet in healthy, young women." Journal of the American College of Nutrition 21.1 (2002): 55-61.
• Smit, Hendrik Jan, et al. "Does prolonged chewing reduce food intake? Fletcherism revisited." Appetite 57.1 (2011): 295-298.

Regular Meals Promote Thermogenic Effect of Food - 22% to 50% Higher Postprandial Thermogenesis in Healthy Women

While the ads for many fat burners tell you just that, thermogenesis is not the #1 determinant of whether you're lean or fat. It is just one of a bazillion factors that influence your energy balance which in turn controls your weight.

Thermogenesis is (falsely) treated like the holy grail in fat loss supplement ads. When all is said and done, though, even a 100% increase in thermogenesis, which has nothing to do with a 100% increase in total energy expenditure, is usually easily compensated for by increased energy intakes in the average and extraordinary male or female dieter.

Against that background you may be asking yourselves why the latest study from the School of Life Sciences at the University of Nottingham even made the "SuppVersity newsworthy"-cut. Well, the answer can be seen in Figure 1, which tells you that modulating the eating patterns in said randomized crossover trial didn't just affect the extent of postprandial thermogenesis, but also the weight, body fat and, in particular, the 'waist trajectory' of the subjects, 9 obese women (mean ± SD BMI: 33·3 ± 3·1 kg/m²).

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To ascertain whether modulating the regularity of meal pattern over two weeks would affects the thermogenic response to a test meal and anthropometric measurements in obese women, Alhussain et al. had their subjects follow irregular and regular meal patters for 2 weeks, each:

• regular meal pattern - 6 meals/day
• irregular meal pattern -  varying from 3 to 9 meals/day

In that, it is important to note that "[i]n the two intervention periods, identical foods were provided in amounts designed to keep body weight stable" (Alhussain. 2016). For the testing sessions, the participants attended the laboratory after an overnight fast pre and post each intervention period.

"On arrival, measurements were made of body weight, body composition, waist circumference and waist to hip ratio. Resting energy expenditure was then assessed by using indirect calorimetry, fasted and during the 3 h period after consumption of a milkshake, test drink (50 % CHO, 15 % protein and 35 % fat of energy content)" (Alhussain. 2016).

As already hinted at, the scientists observed significant changes in the postprandial thermogenic response and non-significant effects on the subjects body composition.

Figure 1: Changes in markers of body composition during the two 2-week periods (Alhussain. 2016).

More specifically, the regular meal pattern that allowed for weight and body fat stability and even triggered a non-significant decrease in waist circumference. The irregular pattern, on the other hand, produced an albeit statistically non-significant increase in body weight and body fat - a change, of which we can hypothesize that it would reach statistical significance in the weeks to come.

A 2004 study in lean women shows: This is not a "fat-girl thing". TEF of lean women suffers even more (Farshchi. 2004).

This is not a "fat girl-thing"! In case you think 'Well, that's not me, I am lean and for me these results are irrelevant', you may want to take a look at a 2004 study by Farshchi et al. in which the researchers observed a similar effect in perfectly lean women. If you take a look at the figure on the left, I've copied right from the full text of said study, you will even notice that the decline in energy expenditure in the lean women is significantly more pronounced than in the obese women in the study at hand.

In view of the lack of strict dietary control outside of a metabolic ward, it is hard to say whether the effects on body composition (Figure 1) were triggered solely by the decrease in thermogenesis (Figure 2) due to the irregular meal pattern. As I've pointed out in countless previous SuppVersity articles these effects may just as well be caused by increases in food intake, which are never (or at least rarely ;-) 100% accurately reported by subjects of clinical trials.

Figure 2: Postprandial extra energy expenditure due to thermogenesis (kcal/3h) before and after 2-weeks on regular or irregular meal pattern in 9 obese women [mean ± SD BMI: 33·3 ± 3·1 kg/m² | Alhussain. 2016).

Eventually, the lack of dietary control must not necessarily be a disadvantage. After all, there's no strict dietary control in the real world, either. Therefore, any study that tightly controls their subjects food intake will fail to portray a correct picture of its subjects real lives - lives in which the average subject shows a very low adherence to his/her (self-)prescribed diet and will thus (just as it may have been the case in this study) simply eat, when he/she is hungry, even if his/her meal plan tells him/her not to do so - and regular meal patterns certainly help avoiding hunger pangs.

Previous research clearly indicates that it would be a "fat mistake" to believe that a reduced meal frequency on some of the 14 days on the irregular pattern was behind the non-sign. weight and fat gain in this study.

Bottom line: It should be obvious that it would be a mistake to consider the study at hand "convincing evidence" that irregular meal patterns promote weight and, more importantly, fat gain. An effect on thermogenesis, on the other hand, appears to exist - at least in women.

In spite of the paucity of evidence, the way many people in today's society are "always on the run" and hardly able (or willing) to stick to regular meal patterns, it does seem at least "likely" that irregular meal patterns are part of the reason our hectic life-styles lead to ever-increasing obesity rates. How important the impact of regular meal-patterns on our thermogenic response to meals actually is, though, will have to be evaluated in future studies | Comment!

Addendum: No, this is not your average meal timing article. I am not saying you have to eat at a specific time, or you have to eat 6, 3 or 5 meals a day. The one and only thing the study suggests (and this is in line with previous studies on skipping breakfast) that you should eat at the same time (roughly) everyday. The mechanism behind the benefits is probably related to the ability of timed meals to entrain a stable circadian rhythm and optimize the way your body handles the food you consume (e.g. stable insulin and glucose levels => no release of glucocorticoids, etc.).

References:

• Alhussain, et al. "Deleterious effects of irregular meal pattern on dietary thermogenesis in obese women." Proceedings of the Nutrition Society 75 (2016): OCE1, E6.
• Farshchi, H. R., M. A. Taylor, and I. A. Macdonald. "Decreased thermic effect of food after an irregular compared with a regular meal pattern in healthy lean women." International journal of obesity 28.5 (2004): 653-660.

PUFA Increases Postprandial Thermogenesis in Healthy Premenopausal Women & Beyond - 14% Increase Over MUFA & SFA Sounds Huge, But Does it Matter?

Is there something to the good vs. bad fat shenanigan, after all?

Only recently scientists from the Texas Tech University report that a PUFA-rich high-fat meal led to a greater diet-induced thermogenesis in normal-weight premenopausal women compared with SFA- or MUFA-rich high-fat meals.

Reason enough to take a closer look at this and previous studies investigating the diet-induced thermogenic effects of PUFA-, MUFA- and SFA-rich meals and to conduct a reality check wrt to the question whether these differences actually matter - I mean, will you get and stay lean by upping your PUFA intake? Let's take a look!

You can learn more about fat at the SuppVersity

Are Men Fat- & Women Sugar-Cravers?

Fat, not Fructose Cons. Increased in the US

Adding Fats to Carbs Does not Reduce Insulin

The Forgotten Pro-Insulinogenic Effects of SFAs

Margarine Not Butter Incr. EU Waists

Low Fat to Blame for Low Vitamin D Epidemic?

In the initially mentioned study, Hui C. Clevenger, Amanda L. Kozimor, Chad M. Paton and Jamie A. Cooper explored the effect of three HF meals enriched with different fatty acids (MUFAs, PUFAs or SFAs) on metabolism in premenopausal women of normal weight. In that, the metabolic parameters of interest included postprandial energy expenditure (EE), which is then used to calculate DIT, and substrate oxidation, which included respiratory exchange ratio (RER), fat oxidation and carbohydrate (CHO) oxidation.

Based on previous research in men of normal weight, the Texas Tech researchers hypothesized that the diet induced thermogenesis (DIT) and fat oxidation would be the highest after the PUFA- and MUFA-rich meals and lowest after the SFA-rich meal in premenopausal women - a result of which you already know that it was only partly confirmed.

Figure 1: Diet-induced thermogenesis and respiratory exchange rate (higher RER = lower fatty acid oxidation vs. higher CHO oxidation) in the 5h after the test meal (Clevenger. 2014)

The data in Figure 1 does after all tell you that the expected MUFA-induced increase in diet-induced thermogenesis did not occur. PUFAs, on the other hand did the job, Clevenger et al. expected them to do. They increased the DIT by an ostensibly whopping 14% over the DIT the scientists observed in response to the ingestion of the high MUFA and SFA liquid meals that had been prepared with the same base of 8 fl oz (237 ml) of chocolate Ensure(R) with soy lecithin and Nesquik (R, but contained different additional dietary fatty acids added depending on the treatment condition:

• 

  Table 1: Liquid meal nutrient composition
  breakdown (Clevenger. 2014).

  The PUFA-rich meal was ‘base’ plus sunflower oil and flaxseed oil, with 42% of total energy coming from PUFA.
   
• The MUFA-rich meal was ‘base’ plus canola oil and extra virgin olive oil, with 42% of total energy coming from MUFA.
  
  
• Finally, the SFA-rich meal was ‘base’ plus butter, coconut oil and palm oil, with 40% of total energy coming from SFA. 

As the data in Table 1 indicates, the nutrient profiles didn't differ much. The fatty acid composition, on the other hand did, with the SFA meal being the only one with measurable amounts of Butyric, Caprioc, Caprylic, Capric, Lauric, Myristic and Hepatedic acid. Fatty acids of which previous research indicate that they induces an obesity-linked proinflammatory gene expression profile in adipose tissue of subjects at risk of metabolic syndrome (van Dijk. 2009).

High MUFA diets, on the other hand, have been shown to potentiate the effects of weight loss in obese NIDDM patients (Low. 1996). They are the major group of fatty acids in the one oil, everyone appears to agree that it's health (Olive oil). And last but not least, even the allegedly unhealthy omega-6s have been shown in randomized controlled to reduce liver fat and modestly improve metabolic status, without weight loss, when compared to high saturated fat diets (Bjermo. 2012).

All of these effects / this evidence could potentially be more important than the increase postprandial thermogenesis in the study at hand - so the ultimate question is: Does DIT even matter?

Now, does this increase in DIT matter? Westerterpet et al. who found a negative correlation between body fat levels and the diet induced thermogenesis in their 2008 study (Westerterpet al. 2008), certainly believe it matters. If we look at the total extra diet-induced energy expenditure in 5h after the test-meal in the study at hand, on the other hand, I cannot but ask myself, whether those 1.4kcal can actually make a difference.

I am not sure what you think, but considering the fact that you can burn those 1.4 extra calories in less than one minute in the gym, it's hard to believe that the increased thermogenesis alone warrants the layman's conclusion that the study at hand would provide evidence for the superiority ot PUFAs over MUFAs and saturated fats ... what do you think?

References:

• Bjermo, Helena, et al. "Effects of n− 6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial." The American journal of clinical nutrition 95.5 (2012): 1003-1012.
• Clevenger, Hui C., et al. "Acute effect of dietary fatty acid composition on postprandial metabolism in women." Experimental physiology (2014): expphysiol-2013.
• Westerterp, Klaas R., et al. "Dietary fat oxidation as a function of body fat." The American journal of clinical nutrition 87.1 (2008): 132-135.