Cheese & Your Health: CVD, Cancer & Metabolic Syndrome - Cheesy Science or Scientific Revelation? A Brief Review

Cheese & Your Health: CVD, Cancer & Metabolic Syndrome - Cheesy Science or Scientific Revelation? A Brief Review

cheese dairy diet health healthy diet healthy eating lose fat

Cheeses come in all forms and colors.

Cheese is not exactly the first food that comes to mind when we think about "healthy eating". Rightly so? Today's overview of recent cheese studies tries to answer this question.

The article will, among other things, also address the claim that cheese was addictive (see red box) and / or that the consumption of a dairy product with a saturated fat content that is second only to that of butter would harm your cardiovascular and metabolic health.

So, where do we start? Netherlands? Well, even though the Dutch are famous for the many different types of cheese they produce and consume, they are probably not the ones who "invented" it. Rather than that it appears to be certain that the first cheeses were produced 5,000 BC - accidentally.

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Back in the day, humans had not invented pottery and thus stored their foods - including their milk - in animal stomachs, ... stomachs the cuagulating enzyme content of which turned milk into curd during storage (Fox. 1993). The first recorded "production" of cheese, in that case Gorgonzola dates back to the year 897, however (see Table 1).

Table 1: First Recorded Date for some Major Cheese Varieties (Fox. 1993).

Another cheesy fact about the Netherlands is that the Dutch would be the world's #1 cheese producer and consumer. Both is not the case! Rather than that, France holds both the title of the greatest producer (1.3 m tonnes) and consumer (22kg / per capita | Fox. 1993 // relative to their total dairy consumption, the Italians are the kings of cheese w/ up to 28% and 33%  of the dairy intake from cheese of women and men in the province Ragusa | Hjartåker. 2002). It is thus also France, where we will probably find the most significant evidence with regards to the health effects of cheese consumption. The most prominent study investigating this issue comes from the Aarhus University (Zheng. 2015)..

Is cheese the reason for the "French paradox"?

In said study, Zheng et al. used an NMR-based metabolomics approach "to investigate the differentiation between subjects consuming cheese or milk and to elucidate the potential link to an effect on blood cholesterol level" (Zheng. 2015). To this ends, the researchers recruited fifteen healthy young men for a full crossover study during which all subjects consumed three isocaloric diets with similar fat contents that were either (1) high in milk, (2) high in cheese or (3) contained only limited amounts of dairy for 14 days.

Only the fat "Norvegia" gouda has cholesterol-lowering effects in an 8 week RCT (Nilsen. 2015).

Question 1 - Does the type of cheese matter? High fat may matter. Well, "fake cheese" that's made from vegetable oils + tons of additives, as you will find it on most frozen Pizza from the supermarket is obviously not an option, but even among "real" cheeses there appear to be differences in terms of their individual health effects. The results of a 2015 study from Norway, for example, show that only fat gouda (80g/day), yet not fat- and salt-free Gamalost, a traditional form of Norwegian cheese will significantly reduce elevated cholesterol levels in non-medicated men and women over 18 years of age (Nilsen. 2015).

As the data from the scientists urine and feces analyses shows, the cheese diet significantly reduced the urinary citrate, creatine, and creatinine levels and significantly increased the microbiota-related metabolites butyrate, hippurate, and malonate compared to the milk diet. Overall, the study shows...

"[...] that cheese consumption is associated with an increased level of SCFAs in the gut, possibly induced by stimulation of beneficial gut microbiota, as well as an increased extent of lipid excretion with resultant beneficial effects on cholesterol metabolism"(Zheng. 2015 | my emphasis).

In conjunction with the significant reduction of the subjects' TMAO production [Trimethylamine N-oxide has been associated with increased CVD and even cancer risk] of which the authors rightly say that it could "also contribute to potential beneficial effects of cheese intake on the risk of CVD" (Zheng. 2015), the results of this controlled human trial are in stark contrast to the cheese = "high cholesterol" = "bad for your heart" myth that's still so prevalent:

"Overall, this metabolomics study suggests that cheese could be an important piece in the French paradox puzzle. However, further studies are needed to explore the exact metabolic mechanisms linking cheese consumption, stimulation of the gut microflora, and cholesterol metabolism" (Zheng. 2015 | my emphasis)

Just as many other researchers working in this area, Zheng et al. received support for their study from the dairy industry - a factor that is as prevalent in other areas of nutrition research, but interestingly most heavily criticized for dairy (Armstrong. 2005) and, obviously, artificial sweeteners.

Percentages of women reporting a craving for a given food at four different timepoints during their menstrual cycle (Rodin. 1991). 

Question 2 - Is cheese addictive? Prolly not! Even though the whole concept of food addiction is still contested (Rogers. 2000; Corwin. 2009; Albay-rak. 2012; Ziauddeen. 2012; Hebebrand. 2014), the Internet is full of "information" about the addictive nature of cheese. Claims that are not really backed up by science, as the data from Judith Rodin et al.'s study of the food cravings of women during different phases of the menstrual cycle in the Figure (left) shows (Rodin. 1991) - the real world does thus not confirm the relevance of the theor. addictive potential of casomorphines (Freye. 2004).

In general, rather than a role for individual molecules, the existing data appears to suggest "addictive", or rather hyperpalatable foods share common macronutrient compositions that distinguish a dairy queen chocolate ice cream cone with 34 g sugar 10 g fat and 160 mg sodium (+22 extra ingredients) per serving from roasted chicken breast or an apple (Gearhardt. 2011). This does not exclude that you can be "addicted" to cheese, but the same goes for carrots of which Kaplan reported 10 years ago that they got a 49-year-old woman addicted (Kaplan. 1996).

The reasons why I would argue that you can still put faith into the accuracy of the results Zheng et al. present in their paper are: (1) they openly declared the funding, i.e. support by The Danish Council for Strategic Research, Arla Foods, and the Danish Dairy Research Foundation in the project “FIAF - Milk in regulating lipid metabolism and overweight. Uncovering milk’s ability to increase expression and activity of fasting-induced adipose factor” (10-093539) and (2) the supporting evidence from various previous studies:

• Beneficial effect on CVD health - "The majority of prospective studies and meta-analyses examining the relationship between milk and dairy product consumption and risk of CVD show that milk and dairy products, excluding butter, are not associated with detrimental effects on CVD mortality or risk biomarkers that include serum LDL-cholesterol" (Lovegrove. 2016).
  

  

  Figure 1: Unlike 40 g dairy fat from butter, 40g of fat from matured cheddar cheese do not sign. affect the levels of total cholesterol and LDL in a 4 weeks cross-over study in healthy subjects (Nestel. 2005).

  With the latest evidence for this claim coming from an impartial source, namely Iran, where Sadeghi et al. found that higher cheese intakes are are associated with 19% reduced risk of metabolic syndrome and 13% reduced risk of suffering from (too) low HDL-C level, one may still doubt the objectivity of this claim being made at a conference about animal products, but can hardly argue that there was only potentially biased research to support Lovegrove's claim and the conclusions of the latest meta-analysis of its effects on blood lipids (de Goede. 2015):

  "Compared with butter intake, cheese intake (weighted mean difference: 145.0 g/d) reduced low-density lipoprotein cholesterol (LDL-C) by 6.5% (−0.22 mmol/l; 95%CI: −0.29 to −0.14) and high-density lipoprotein cholesterol (HDL-C) by 3.9% (−0.05 mmol/l; 95%CI: −0.09 to −0.02) but had no effect on triglycerides" (de Goede. 2015).

  In addition every regular gouda (and many other classic cheeses) contains peptides that have proven to have anti-hypertensive effects (Saito. 2000) and will thus lower the #1 risk factor for stroke and related cardiovascular problems - including death (Fagard. 2008).
• Reduced breast cancer risk -  A case-control study from the Netherlands suggests that each 60g increase in gouda intake will reduce the breast cancer risk of 25-64 year-old women (analysed according to age groups) with a 34% reduced risk of breast cancer.
  

  

  Figure 2 A high intake of gouda is associated with highly significant reductions in breast cancer risk even after adjusting for familial history, smoking,education, contraceptive use, age at menarche and first full-term pregnancy, parity, body mass index, and geographic area in Dutch women (van't Veer. 1989)

  What is also interesting about the effects plotted in Figure 2 is that a similar beneficial effect was not observed for milk (had no negative effect, either) or similarly low intakes of other fermented dairy (van't Veer).
• Anti-NAFLD and prometabolic effects - At least in comparison to a butter-fat based diet a similarly low fat (20%) likewise AIN76 (that's std. rodent chow) based diet with freeze-dried cheese powder significantly reduced the accumulation of triglyceride and cholesterol in the liver (P = 0.016 and P < 0.001, respectively) of rats who received the cheese or control diet in a 9-week study.
  

  

  Figure 2: Liver triglyceride (a) and total cholesterol (b) concentrations in rats fed control or cheese diet. Mean ± standard error. Asterisks indicate significant differences between groups (Higurashi. 2016)

  Just like the previously reported human studies, the rodent study als found significant increases in HDL and decreases in non-high-density lipoprotein (non-HDL) cholesterol, as well as elevated levels of metabolically healthy serum adiponectin concentration at week 9 in rats fed the cheese diet. To which degree this effect was due to or related to the increase in fat excretion in the feces will have to be determined in future studies. What appears to be clear, though, is that these "results suggest that cheese mediates various beneficial effects for preventing the development of metabolic syndrome by suppressing the accumulation of fat in the liver" (Higurashi. 2016).
• High nutritional value - Cheese is a low carbohydrate food that's packed with high concentration of essential amino acids saturated fats that could be good, not bad for your health (e.g. conjugated linoleic acid and sphingolipids present in cheese may have anti-carcinogenic properties, too), a lot of highly bioavailable calcium with beneficial effects on bone, teeth, blood pressure and weight loss (when combined with low-energy diets). Reason enough for researchers to state that "[c]heese is an important dairy product and an integral part of a healthful diet due to its substantial contribution to human health" (Walther. 2008).

Whether the average young, whites, female knows all the above or whether there's another reason that this part of US society consumes the highest amounts of cheese (Glanz. 1998) is something I cannot tell you. What I can tell you, though, is that the previously presented evidence suggests that weight concerns should not, as they still were in 1998 in the US (Glanz. 1998), be a reason for you not to consume cheese (in controlled amounts). Rather than that you should follow the example of the rich and intelligent of which a more recent study shows that they tend to consume the most cheese in Europe (Sanchez-Villegas. 2003).

A high cheese will also increase the level of the "good lipoproteins" HDL and apo A-I (Thorning. 2015a).

Bottom line: Don't get me wrong. The purpose of today's article is not to promote a "cheese only diet" or to tell you to consume at least X amounts of cheese per day. It is rather meant to critically evaluate the irrational fear that still characterizes the relationship of many health-conscious dieters to (esp. fatty) cheeses.

When consumed in moderation, cheese is not just a highly nutritious food, but can, as a lot of the more recent studies indicate, even have beneficial effects on your cardiovascular and metabolic health that are probably mediated by key nutrients and the beneficial effect cheese will have on your microbiome | Comment!

References:

• Albayrak, Ö., Sebastian Mathias Wölfle, and Johannes Hebebrand. "Does food addiction exist? A phenomenological discussion based on the psychiatric classification of substance-related disorders and addiction." Obesity facts 5.2 (2012): 165-179.
• Corwin, Rebecca L., and Patricia S. Grigson. "Symposium overview—food addiction: fact or fiction?." The Journal of nutrition 139.3 (2009): 617-619.
• de Goede, Janette, et al. "Effect of cheese consumption on blood lipids: a systematic review and meta-analysis of randomized controlled trials." Nutrition reviews 73.5 (2015): 259-275.
• Fagard, Robert H., et al. "Daytime and nighttime blood pressure as predictors of death and cause-specific cardiovascular events in hypertension." Hypertension 51.1 (2008): 55-61.
• Fox, P. F. "Cheese: an overview." Cheese: chemistry, physics and microbiology. Springer US, 1993. 1-36.
• Freye, Enno. "Exorphine (exogene Opioidpeptide) und β-Casomorphine." Opioide in der Medizin. Springer Berlin Heidelberg, 2004. 323-324.
• Gearhardt, Ashley N., et al. "Can food be addictive? Public health and policy implications." Addiction 106.7 (2011): 1208-1212.
• Glanz, Karen, et al. "Why Americans eat what they do: taste, nutrition, cost, convenience, and weight control concerns as influences on food consumption." Journal of the American Dietetic Association 98.10 (1998): 1118-1126.
• Hebebrand, Johannes, et al. "“Eating addiction”, rather than “food addiction”, better captures addictive-like eating behavior." Neuroscience & Biobehavioral Reviews 47 (2014): 295-306.
• Higurashi, Satoshi, et al. "Cheese consumption prevents fat accumulation in the liver and improves serum lipid parameters in rats fed a high-fat diet." Dairy Science & Technology (2016): 1-11.
• Hjartåker, A., et al. "Consumption of dairy products in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: data from 35955 24-hour dietary recalls in 10 European countries." Public health nutrition 5.6b (2002): 1259-1271.
• Lovegrove, Julie A., and Ditte A. Hobbs. "Plenary Lecture 2: Milk and dairy produce and CVD: new perspectives on dairy and cardiovascular health." Proceedings of the Nutrition Society (2016): 1-12.
• Nestel, P. J., A. Chronopulos, and M. Cehun. "Dairy fat in cheese raises LDL cholesterol less than that in butter in mildly hypercholesterolaemic subjects." European journal of clinical nutrition 59.9 (2005): 1059-1063.
• Nilsen, Rita, et al. "Effect of a high intake of cheese on cholesterol and metabolic syndrome: results of a randomized trial." Food & nutrition research 59 (2015).
• Rodin, Judith, et al. "Food cravings in relation to body mass index, restraint and estradiol levels: a repeated measures study in healthy women." Appetite 17.3 (1991): 177-185.
• Rogers, Peter J., and Hendrik J. Smit. "Food craving and food “addiction”: a critical review of the evidence from a biopsychosocial perspective." Pharmacology Biochemistry and Behavior 66.1 (2000): 3-14.
• Saito, T., et al. "Isolation and structural analysis of antihypertensive peptides that exist naturally in Gouda cheese." Journal of Dairy Science 83.7 (2000): 1434-1440.
• Sanchez-Villegas, A., et al. "A systematic review of socioeconomic differences in food habits in Europe: consumption of cheese and milk." European journal of clinical nutrition 57.8 (2003): 917-929.
• Thorning, Tanja K., et al. "Diets with high-fat cheese, high-fat meat, or carbohydrate on cardiovascular risk markers in overweight postmenopausal women: a randomized crossover trial." The American journal of clinical nutrition 102.3 (2015): 573-581.
• Thorning, Tanja K., et al. "Cheddar Cheese Ripening Affects Plasma Nonesterified Fatty Acid and Serum Insulin Concentrations in Growing Pigs." The Journal of nutrition 145.7 (2015b): 1453-1458.
• van't Veer, Pieter, et al. "Consumption of fermented milk products and breast cancer: a case-control study in The Netherlands." Cancer research 49.14 (1989): 4020-4023.
• Zheng, Hong, et al. "Metabolomics investigation to shed light on cheese as a possible piece in the French paradox puzzle." Journal of agricultural and food chemistry 63.10 (2015): 2830-2839.
• Ziauddeen, Hisham, I. Sadaf Farooqi, and Paul C. Fletcher. "Food addiction: is there a baby in the bathwater?." Nature Reviews Neuroscience 13.7 (2012): 514.

10 Days of 'Paleo Life in the Wilderness' Will Strip up to 18 cm off Your Waist and Boost Your Insulin Sensitivity by 53%

10 Days of 'Paleo Life in the Wilderness' Will Strip up to 18 cm off Your Waist and Boost Your Insulin Sensitivity by 53%

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Even though it may have been funny, this is not exactly how the scientists simulated the "paleo lifestyle" in the study at hand. Eventually, however, it came down to eating healthier, being active and even being stressed (within the limits of natural "paleo stress", though).

No, this science website is not going to turn into a paleo blog, ... don't worry. It's mere coincidence that this is the 2nd "paleo" study in 2 weeks that is interesting enough to get its own SuppVersity article devoted to it (last one).

Moreover, said study, which was published in the peer-reviewed scientific journal BioMed Research International, recently (Pruimboom. 2016), doesn't even have the world "paleo" in title of full-text and could still be called "the true paleo" study. It does, after all, revolve around a 10-day mimic of a "hunter-gatherer lifestyle" and its favorable effects on anthropometrics and clinical chemical indices such as the reductions in insulin, triglycerides, HDL, elevated liver health markers and other indices that are usually far from being optimal in the average student, scientist, physician, and other health professionals who participated in the study at hand.

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As the researchers point all, all subjects (n=10, n=32 and n=11) "were interested to experience the impact of ancient lifestyle on their own health and well-being and therefore jointly decided to engage in this study" (Pruimboom). In that, the term "this study" refers to three separate 10-day trips through the Spanish Pyrenees during the summers of 2011 (𝑛 = 10), 2012 (𝑛 = 32), and 2013 (𝑛 = 11), on which ...

"[t]he participants lived outdoors and walked from one watersource to another. Food was provided by the organization and with help of forest-guards from official institutes of the Catalan county. Food intake was planned before the trip, based on the average daily food intake by the traditionally living Hadzabe people in Tanzania. The use of mobile phones or other electronic devices was not allowed" (Pruimboom. 2016)

It is obviously debatable, if "mayonnaise" is a paleo food (not sure if they made it themselves) and how "paleo" the rest of the subjects' diet which may have been designed to mimic the macros, but probably not the foods of the Hadzabe (see Figure 1, tabular overview on the left) actually was.

Figure 1: Exemplary food intake (left) and changes in anthroprometrics (right); stat. sign. w/ p < 0.001 was observed for the median changes, not the minimal and maximal changes, obviously (Pruimboom. 2016).

What is undebatable, though, is the statistical significance and health relevance of the reductions in weight and body fat you can deduce from the sign. reduction in the median subjects' waist circumference.

Mind the statistics: There's a reason why I plotted more than one value in Figure 1. While I cannot tell you the reason why, I can tell you that at least one subject did not see the expected improvements in waist circumference. Possibly, he or she ate too much mayonnaise ;-), ... Why's that relevant? Well, it obviously goes to show you that calories still count. While the median subjects (with the low number of participants the scientists didn't calculate averages) obviously was in a caloric deficit, this one person probably just wasn't caught feasting secretly on the supply.

It should be noted, though, that these changes were certainly not attributable solely to the diet. Rather than that it should be obvious that the significant reduction in body and most certainly belly fat was the consequence of (a) what and how much the subjects ate while (b) experiencing what the Dutch scientists call "ancient stress factors" they were facing during a 10-day trip that revolved around the following four principles:

• Walking and limited manual work- providing the exercise / general physical activity stimulus modern humans lack: There were daily walking trips from waterhole to waterhole, with an average walking distance of about 14 km/day, including altitude differences up to approximately 1,000 m. The participants carried their own backpacks with an average weight of 8 kg. The trip took place in the part of the Pre-Pyrenees with a maximum altitude of 1,900 meters above sea level. In addition, some manual work was done to clean mountain trails as agreed upon with the Catalan Government.
• Intermittent fasting - leaving room to actually experience hunger and all its beneficial hormonal correlates (e.g. AMPK increase => mitochondrial housekeeping, etc.): Participants consumed two meals daily. The first meal was provided by the organization halfway and the second meal prepared on arrival at the camping site. Animals, including ducks, chickens, turkeys, rabbits, and fish, were delivered alive and killed by the participants. Fish were caught with nets in the Noguera river. All foods were prepared on the spot by the participants.
• 100% exposure to the elements - resynchronizing the internal clock: The participants slept outside in sleeping bags on small inflatable mattresses. Outside temperatures varied from 22 to 42∘C during daylight, whereas night temperatures varied from 12 to 21∘C. One group experienced a day of snow in the middle of July, which prompted the organization to provide hotel accommodations for a single night.
• Cyclic water intake - experiencing thirst to benefit from the anti-inflammatory release of oxytocin (Krause. 2011): Bulk (intermittent) drinking behavior was recommended by drinking as much as possible (up to satiety) after reaching a waterhole. The waterholes contained nonchloritized drinking water (Note: I would not suggest using "dehydration" as a means to improve your health; while it may have done this in the study at hand, it's simply stupid - and that's in the literal sense, as you've read in my article "Hydrated or Dumb").

Only in conjunction, with these "stress factors" did the diet do its body fat reducing and, as the data in Figure 2 shows, glucose and blood lipid reducing effects:

Figure 2: Changes in glucose and lipid metabolism over (I repeat) only 10 days; worth mentioning: all but the effect on HDL were statistically highly sign. with p < 0.001 (Pruimboom. 2016).

Effects of which the scientists say that they were the result of acute stress, which promotes release of stress hormones, including adrenaline, noradrenaline, and cortisol, all of which are bad in excess, but will "give rise to recovery from the reigning state of chronic low-grade inflammation and the return to homeostasis" (Pruimboom. 2016), when the stressors are hit the sweet spot of hormesis as it occurred in response to / corollary with the elevation in AST, ALT and hs-CRP of which I've explained previously that all of them can be natural reactions to (especially unaccustomed) physical activity (learn more about ALT, AST and exercise induced inflammation that may be misunderstood as a health problem).

In the study at hand, said "recovery from the reigning state of chronic low-grade inflammation" was characterized by "profound metabolic and immunologic adaptations", of which the scientists highlight that they relate to three classic features of the metabolic syndrome, i.e. body mass, glucose homeostasis, and circulating lipids. The fourth, i.e. blood pressure was - unfortunately - not recorded.

Ad-Libitum Paleo Diet W/ a Handful of Simple Rules Cuts 5-7 kg of Body Fat in 12 Weeks - Plus: Paleo Research Overview | more.

Bottom line: With the metabolic syndrome, also named the insulin resistance syndrome, being "a well-established risk factor for various diseases of affluence, including type 2 diabetes, cardiovascular disease, essential hypertension, polycystic ovary syndrome, nonalcoholic fattyliver disease, certain types of cancer (colon, breast, and pancreas), sleep apnea, and pregnancy complications, such as preeclampsia and gestational diabetes", the scientists are right to highlight in their conclusion that the subjects didn't just feel better subjectively (according to questionnaire), but returned from the "wilderness" in an objectively healthier state.

A state of which the scientists say that it has been promoted by the previously discussed consequences of the four pillars (see list) and related effects, such as the reduction of the postprandial inflammatory response (Holmer-Jensen. 2011; Klop. 2011; Peairs. 2011) and increased protection against pathogens (Fielding. 2000; MacEneaney. 2009) that occurs, when you are physically active before a meal. Even the presence of "cutaneous- and other body surface-directed danger signals" could, as Pruimboom et al. point out have been "hormetic triggers" | Comment!

References:

• Fielding, Roger A., et al. "Effects of prior exercise on eccentric exercise-induced neutrophilia and enzyme release." Medicine and science in sports and exercise 32.2 (2000): 359-364.
• Holmer-Jensen, Jens, et al. "Differential effects of dietary protein sources on postprandial low-grade inflammation after a single high fat meal in obese non-diabetic subjects." Nutrition journal 10.1 (2011): 1.
• Klop, Boudewijn, et al. "Understanding postprandial inflammation and its relationship to lifestyle behaviour and metabolic diseases." International journal of vascular medicine 2012 (2011).
• Krause, Eric G., et al. "Hydration state controls stress responsiveness and social behavior." The Journal of Neuroscience 31.14 (2011): 5470-5476.
• MacEneaney, Owen J., et al. "Effect of prior exercise on postprandial lipemia and markers of inflammation and endothelial activation in normal weight and overweight adolescent boys." European journal of applied physiology 106.5 (2009): 721-729.
• Peairs, Abigail D., Janet W. Rankin, and Yong Woo Lee. "Effects of acute ingestion of different fats on oxidative stress and inflammation in overweight and obese adults." Nutrition journal 10.1 (2011): 1.
• Pruimboom, Leo, et al. "Influence of a 10 days mimic of our ancient lifestyle on anthropometrics and parameters of metabolism and inflammation. The ‘Study of Origin’."

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

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

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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).

Nicotine gums are made for smokers. Smokers are leaner than no-smokers. Chewing nicotine gums helps you lean out... broscience? Logic? Or bullshit? Learn more in this SV Classic!

"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.

Elimination Diet Kickstarts Fatloss in "People Who Cannot Lose Weight" - 16% Body Fat Reduction in 6 Months, But...

Elimination Diet Kickstarts Fatloss in "People Who Cannot Lose Weight" - 16% Body Fat Reduction in 6 Months, But...

allergies diet dieting elimination diet food allergies IgG immune health immune system lose fat

Many of these foods contain supposed allergens and have thus to be eliminated from your diet... is it any wonder that this triggers weight loss? Hardly...

While I have to admit that I am a bit skeptical about the reliability of the results of a recent study from the Sifa University, Faculty of Health Sciences in Turkey, I cannot ignore that Meltem Yaman Onmus, Elif Cakirca Avcu, and Ali Saklamaz claim that "people who cannot lose weight by low-calorie diet can lose weight and fat with elimination diet according to the results of FI [food intolerance] test. FIED [FI elimination diet] is also significantly effective in triglyceride levels" (Onmus. 2016). I know that sounds as if it was taken from the latest unreferenced blogpost on a dubious website, but let's not judge prematurely and instead take a closer look at the design and results of the study.

Unlike elimination diets, fasting must be considered a scientifically proven weight loss trick

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82 patients (24 male, 58 female) were included in the study. The mean age was 42.04±11.81 (18-65 years). All of them were "unable to lose weight", i.e. patients who said of themselves that they couldn’t lose weight by diet programs and who had a positive reaction to at least one nutrient in food intolerance test and a BMI value ≥ 25kg/m² - in other words: the subjects were the average Internet bullet-in board dwellers searching for the "magic key" to weight loss.

This is obviously an important fact, because it increases the significance of the study for said group of subjects. Whether the results are significant for anyone else, though, is questionable, since patients who had no food reaction in food intolerance test were excluded from the study. The same goes for subjects who had chronic diseases like diabetes mellitus, coronary heart disease, renal diseases, etc., or individuals who use(d) weight loss drugs and who had allergy to any drug or food and who overuse medications or have pure menstrual migraine or headache that associated a disorder.

No health benefits from "eliminating" foods: Interestingly, the food intolerance elimination diet failed to do what its proponents say it's actually doing: Improve the subjects health. With the exception of a statistically significant decrease in triglyceride levels, there was no improvement in health markers (fasting blood glucose, A1C, total cholesterol, HDL-cholesterol, LDL-cholesterol, AST, and ALT) the scientists didn't observe in the control group, too.

As you can see in Figure 1, this particular group of subjects saw significant benefits from following a diet that did not allow the subjects to consume any of the foods to which they showed an IgG response in the previously conducted food intolerance test for 6 months. Otherwise, the diets of the elimination diet (ED) and control diet were personalized diets with "identical" (according to the size, weight, physical activity, dietary habits and socioeconomic status) energy content.

Figure 1: Pre- and post-intervention weight, body fat, lean body mass, and waist / hip ratio (x10); * indicates significant inter-group difference, this means that everything, but the effect on lean mass was sign. more pronounced in the ED group.

Against that background it is unquestionably striking that the subjects in the elimination diet group lost 16% body fat, while the control group didn't lose either significant amounts of fat or weight. Now, the obvious question is: "Which foods were eliminated?" Unfortunately, this question is neither answered in the study at hand, nor in previous studies showing that elimination diets reduce also reflux disease, chronic fatigue syndrome, and headaches (Selvin. 2007; Akmal. 2009).

Unlike Onmus et al., Akmal et al. publish-ed a list of allergens their IgG test could supposedly identify. A list eliminated foods is yet missing from study, too.

Why's it a problem that we don't know which foods were eliminated? Actually, the answer to this question should be obvious. Let's assume you're "allergic" to sugar, alcohol and high omega-6 vegetable oils like soybean oil. Would you be surprised if you lost significant amounts of body fat if you dropped all sugary and pro-inflammatory high omega-6 foods and stopped drinking alcohol? I, for my part, wouldn't and I guess you wouldn't and you certainly shouldn't be surprised either.

Accordingly, the study at hand does unfortunately not provide enough information to decide whether it provides convincing evidence of using IgG-tests to guide you when you're designing diets for yourself or your clients. Hopefully future research will do just that | Comment!

References:

• Akmal, Mohammed, Saeed Ahmed Khan, and Abdul Qayyum Khan. "The Effect of the ALCAT Test diet therapy for food sensitivity in patient’s with obesity." Middle East Journal of Family Medicine 7.3 (2009).
• Onmus, Meltem Yaman, Elif Cakirca Avcu, and Ali Saklamaz. "The Effect of Elimination Diet on Weight and Metabolic Parameters of Overweight or Obese Patients Who Have Food Intolerance." Journal of Food and Nutrition Research 4.1 (2016): 1-5.
• Selvin, E., Paynter, N. P., Earlinger T. P. "Nutrition and allergy." Arch Intern Med, 167.1 (2007): 31-39.