Sleep Science Update: New Insights into the Effect of a Lack of Quality Sleep on Glucose Control and Diabesity Risk

Sleep Science Update: New Insights into the Effect of a Lack of Quality Sleep on Glucose Control and Diabesity Risk

diabesity diabetes glucose management health insulin insulin resistance obesity on short notice sleep

Blue light is not the only enemy of sleep, but it's the most prevalent one, today.

Personally, I believe that sleep, "a condition of body and mind which typically recurs for several hours every night, in which the nervous system is inactive, the eyes closed, the postural muscles relaxed, and consciousness practically suspended" (that's what Google's "define"-feature will tell you about sleep), is still an under-appreciated determinant of optimal health and performance.

Evidence to support this assertion comes from a series of studies that were presented at the Winter Meeting of the British Nutrition Society on December 8-9, 2015 - a meeting with the telling title: "Roles of sleep and circadian rhythms in the origin and nutritional management of obesity and metabolic disease" (O'Sullivan. 2015).

Learn more about the health effects of correct / messed up circadian rhythms

Sunlight, Bluelight, Backlight and Your Clock

Sunlight a La Carte: "Hack" Your Rhythm

Breaking the Fast to Synchronize the Clock

Fasting (Re-)Sets the Peripheral Clock

Vitamin A & Caffeine Set the Clock

Pre-Workout Supps Could Ruin Your Sleep

• Circadian disruption in shift workers – the effects of insufficient sleep on dietary and lifestyle behaviours (Nea. 2016) - It will not surprise you that shift workers report more sleep problems compared to the general public. Studies estimate that 10–30 % of shift workers suffer from a circadian rhythm disorder known as “shift work disorder”(Gumenyuk. 2012). With their new quantitative study, a team of young researchers from the Dublin Institute of Technology and the University of Ulster provides some insights into the consequences of this problem.
  
  As the scientists point out, overall, just 34·3 % of the sample was achieving adequate sleep. A number of factors were associated with insufficient sleep – being male (p < 0·001), being 35–54 years of age (p < 0·001), having adult/child dependents (p < 0·001), working in larger organisations (p = 0·045), working in distribution/logistics, manufacturing or construction (p = 0·005), working night shifts (p = 0·042), and working longer shifts (p = 0·002).
  

  

  Factors that increased the subject's risk of not getting adequate sleep (Nea. 2016).

  Furthermore, the scientists observed that insufficient sleep had an effect on the diet of workers. Those who did not achieve adequate sleep were more likely to skip meals on working days and skipped meals significantly more frequently (p = 0·023).

  "Workers with insufficient sleep were also significantly less likely to consume the recommended 5 portions of fruit and vegetables per day (37·5 % vs 43·3 %, p = 0·045) and were less likely to consume the recommended 3 portions of milk/cheese/yoghurt per day (11·6 % vs 8·1 %, p = 0·050). In addition, those with insufficient sleep had higher prevalence of hypertension (10·2 % vs 5·7 %, p = 0·008) and depression/anxiety (7·3 % vs 3·4 %, p = 0·008)" (Nea. 2016)

  Participants were also questioned how they perceived shift work impacts on various aspects of their lives. Compared to those who achieve adequate sleep, those who had insufficient sleep were significantly more likely to report that shift work had a negative effect on their physical health (p < 0·001), mental health (p = 0·003), family life (p = 0·001), social life (p = 0·046), physical activity levels (p = 0·029) and overall quality of life (p = 0·002). Those with insufficient sleep were also significantly more likely to report that shift work increases how much alcohol they drink (p = 0·041).
• Oral glucose tolerance test results are affected by prior sleep duration: a randomised control crossover trial of normoglycaemic adults (Ellison. 2016) - As Ellison et al. rightly point out, "[o]ral glucose tolerance tests (OGTTs) remain the key clinical tool for assessing glucose control and diagnosing diabetes" (Ellison. 2016). In that, they criticize that "[c]urrent guidelines for administering such tests emphasise the importance of a preceding 8 hour fast (often undertaken overnight) but overlook the potential role that preceding sleeping patterns night might play in glucose control the following day" (ibid.). In view of the number of recent observational and experimental studies, which suggest that poor sleep is associated with an increased risk of diabetes, these tests may very well be messed up by a lack of sleep during the previous 8h fast. The aim of the latest study by scientists from the Sound Asleep Laboratory in Leeds was therefore "to explore the effect of early vs. late bedtimes on OGTT results using a cross-over randomised controlled trial" (ibid.).
  
  To this ends, the authors recruited 40 normoglycemic adults who were, after they had been stratification by self-reported pre-existing sleep patterns (as assessed using the Pittsburgh Sleep Quality Index; PSQI), allocated to either a ‘short’ (2·00am-7·00am) then ‘long’ (10·00pm−7·00am), or a ‘long’ then ‘short’ sleep duration, on two consecutive nights.

  "On each occasion, objective measures of sleep were obtained using the ‘SleepMeister’ application on an iPhone 4, with additional subjective assessments of sleep provided by subsequent completion of a version of the PSQI adapted to generate self-reports of sleep during the preceding night (as opposed to the preceding month). On each of the mornings following ‘short’ or ‘long’ sleep, participants again completed the PSQI and underwent a two-hour 75 g oral glucose tolerance test (OGTT), with blood glucose readings taken at 0, +30, +60, +90 and +120 minutes thereafter using finger-prick tests. Data were analysed using STATA v12. Ethical approval was granted by the University of Leeds REC (Ref:HSLTLM12075)" (Ellison. 2016).

  As it was to be expected, both the ‘SleepMeister’ application and the PSQI recorded significantly later bedtimes (SleepMeister: −19·9; 95 %CI: −20·1,−19·7; PSQI: −19·9; 95 %CI: −20·1,−19·7) and significantly shorter sleep durations (decimal hours: ‘SleepMeister’: −3·8;95 %CI: −4·3,−3·4; PSQI: −3·4; 95 %CI: −3·9,−2·9) following a 2am (vs.10pm) bedtime (i.e. ‘short’ and ‘long’ sleep duration, respectively) - a fact, the scientists consider evidence "that levels of compliance were high" (ibid.).
  
  In spite of that, there was no significant effect of sleep duration on fasting blood glucose levels prior to the OGTT after adjustment for sleep duration sequence (i.e. ‘short’ then ‘long’ vs. ‘long’ then ‘short’) and a modest imbalance in gender between the two intervention sequence group.
  

  

  Figure 2: Normal response (=expected response in OGGT, not the actual response of the subjects, because the absolute values are not disclosed in the abstract and an FT is not yet available) vs. calculated response as a consquence of insufficient sleep (normal + difference, rel. difference above bars | Ellison. 2016).

  What did differ, though, were the glucose levels recorded after the ingestion of 75 g glucose, which were consistently higher following a ‘short’ as opposed to a ‘long’ sleep duration, as well as the levels recorded at +60 and +90 minutes, which were likewise significantly higher by 1·18 mmol/l (95 %CI: 0·43,1·92; p = 0·003) and 0·55 mmol/l (95 %CI: 0·05,1·06; p = 0·032), respectively. These results, the scientists say, "indicate that short sleep duration the night before results in an immediate elevation in blood glucose levels the following morning in normoglycaemic adults" (ibid.). That this is a problem, should be obvious, after all it may falsely classify healthy individuals as pre-diabetics. Therefore, "further standardisation of pre-OGTT sleep duration, similar to that for an overnight fast," (ibid.) appears warranted.
• Less Sleep Duration and Poor Sleep Quality Lead to Obesity (Parvaneh. 2016) - In a recent cross-sectional study that was carried out to investigate the association of sleep deprivation and sleep quality with obesity, Malaysian scientists analyzed data from 225 Iranian adults (109 males and 116 females) aged 20–55 years.

  "Heart Questionnaire (SHHQ), International Physical Activity Questionnaire (IPAQ) and a 24-hour dietary recall were interview-administered to evaluate sleep pattern, physical activity and dietary intake of the subjects. Besides, anthropometric also were measured, then subjects were categorized into normal weight and over-weight/obese based on WHO (2000). Sleep duration and sleep quality were assessed based on 2 groups of normal weight and overweight/obese" (Parvaneh. 2016).

  The scientists' analysis of the data revealed that overweight/obese individuals have significantly shorter sleep duration (5·37 ± 1·1 hours) as compared to normal weight subjects (6·54 ± 1·06 hours).
  

  

  Figure 3: Overweight / obesity is linked to sign. sleep problems (Parvaneh. 2016).

  Sleep duration was yet not the parameter the scientists from the National University of Malaysia identified as a major risk factor for obesity - that was a poor sleep quality, which was associated with a 100% increased risk for being overweight or obese (OR: 2·0, 95 % CI: 1·18–3·37, p < 0·05). As a conclusion, the scientists state that "lower sleep quality and sleep duration increase the risk of being overweight and obese" and demand: "[S]trategies for the management of obesity should incorporate consideration on sleeping pattern" (Parvaneh. 2016). These strategies, by the way, may also help people keep their triglyceride levels in check. After all, another study that was presented at the same meeting of the Nutrition Society suggests that a high sleep efficiency shows a strong and negative correlation with triglycrides and another important marker of heart disease risk, the total cholesterol to HDL ratio (Al Khatib. 2016).
• Is insulin resistance associated with light at night in healthy sleep deprived individuals? (AlBreiki. 2016) - The simple answer to this question is "Yes!". The more complex one is that a recent study that was designed to investigate the impact of light and/or endogenous melatonin on plasma hormones and metabolites prior to and after a set meal in healthy sleep deprived subjects found that bright blunts the release of melatonin and the effects of insulin on glucose disposal.
  
  In the study, seventeen healthy participants, 8 females (22·2 years (SD 2·59) BMI 23·62 kg/m2 (SD 2·3)) 9 males (22·8 years (SD 3·5) BMI 23·8 kg/m2 (SD 2·06)) were randomised to a two way cross over design protocol; dim light condition (<5lux) and bright light condition (>500lux), separated by at least seven days.

  

  Melatonin promotes female weight loss - Suggested Read: "Trying to Lose Fat & Get "Toned"? Taking 1-3 mg Melatonin Helps Women Lose 7% Body Fat, Gain 3.5% Lean Mass".

  "Each session started at 18:00 h and finished at 06:00 h the next day. All participants were sleep deprived and semi-recumbent throughout the session. An isocalorific breakfast was consumed at 08:00 h and lunch was timed to be 10 hours before the evening meal. Each participant consumed an evening meal (1066 Kcal, 38 g protein, 104 g CHO, 54 g fat, 7 g fibre) at an individualised time based on estimated melatonin onset. Plasma and saliva samples were collected at specific time intervals to assess glucose, insulin and melatonin levels" (AlBreiki. 2016).

  As previously stated, the bright light reduced the salivary levels of melatonin significantly (p = 0·005). What is more relevant to the research question, however is that it also increased the postprandial glucose and insulin levels significantly compared to dim lights (p = 0·02, p = 0·001) respectively.
  
  

  

  Figure 3: Effect of light intensity on melatonin levels and glucose response of 8 female and 9 male normal-weight normoglycemic subjects to standardized meal consumed at night (AlBreiki. 2016).

  For the scientists this result is not exactly surprising. They had expected that the melatonin release would be suppressed due to the light intensity; that the increase in insulin was not able to compensate for the light-induced increased glucose resistance, however, shows that the ill effects of a  'night-shift-esque' bright light exposure at night on glucose metabolism are more severe than previously thought.

Redeem your sleep dept, now!

Bottom line: Along with studies highlighting the importance of sufficient hours of quality sleep on glucose control in pregnancy (Alghamdi. 2016; Alnaja. 2016) and the "largest study to-date to demonstrate a strong inverse association between late-onset diabetes and poor sleep, even after adjustment for potential confounding factors" (Alfazaw. 2016), the previously discussed studies highlight that sleep hygiene' is as important for your health as "clean eating" (whatever that maybe) and a sufficient amount of light and intense physical activity | Comment on Facebook!

References:

• AlBreiki, et al. "Is insulin resistance associated with light at night in healthy sleep deprived individuals?" Proceedings of the Nutrition Society, 75 (2016). 
• Alfazaw, et al. "Variation in sleep is associated with diagnosis of late-onset diabetes: a cross-sectional analysis of self-reported data from the first wave of ‘Understanding Society’ (the UK Household Longitudinal Study)." Proceedings of the Nutrition Society, 75 (2016). 
• Alghamdi, et al. "Short sleep duration is associated with an increased risk of gestational diabetes: Systematic review and meta-analysis." Proceedings of the Nutrition Society, 75 (2016). 
• Alnaja, et al. "Relationship between sleep quality, sleep duration and glucose control in pregnant women with gestational diabetes." Proceedings of the Nutrition Society, 75 (2016). 
• Al Khatib, et al. "The Sleep-E Study: An on-going cross-sectional study investigating associations of sleep quality and cardio-metabolic risk factors." Proceedings of the Nutrition Society, 75 (2016). 
• DeFronzo, Ralph A. "The triumvirate: β-cell, muscle, liver. A collusion responsible for NIDDM." Diabetes 37.6 (1988): 667-687.
• Ellison, et al. "Oral glucose tolerance test results are affected by prior sleep duration: a randomised control crossover trial of normoglycaemic adults." Proceedings of the Nutrition Society, 75 (2016). 
• Gumenyuk, Valentina, Thomas Roth, and Christopher L. Drake. "Circadian phase, sleepiness, and light exposure assessment in night workers with and without shift work disorder." Chronobiology international 29.7 (2012): 928-936.
• Nea et al. "Circadian disruption in shift workers – the effects of insufficient sleep on dietary and lifestyle behaviours." Proceedings of the Nutrition Society, 75 (2016). 
• O’Sullivan (ed.). "Roles of sleep and circadian rhythms in the origin and nutritional management of obesity and metabolic disease." Proceedings of the Nutrition Society. Volume 75 / Issue OCE1 - Winter Meeting, 8–9 December 2015. Published January 2016: E1-E42.
• Parvaneh, et al. "Less Sleep Duration and Poor Sleep Quality Lead to Obesity." Proceedings of the Nutrition Society, 75 (2016). 
• Peschke, Elmar. "Melatonin, endocrine pancreas and diabetes." Journal of pineal research 44.1 (2008): 26-40.

If You Want to Lose Weight and Stave it Off, You'd Better Not Drink Water Instead of Artificially Sweetened Beverages

If You Want to Lose Weight and Stave it Off, You'd Better Not Drink Water Instead of Artificially Sweetened Beverages

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Meanwhile, even many of those who are against the use of sweeteners admit that drinking diet coke is less of an obstacle to weight loss than regular coke. That it could, as the study at hand clearly indicates, even promote weight loss compared to water is controversial, though.

It is one of the die-hard rumors in the fitness industry: Artificial sweeteners will stall your weight / fat loss and have your weight jojo back up, when you stop dieting. As a SuppVersity reader you know that this claim is not supported by science. For the first part, controlled trials like the 2014 study by Sørensen et al. actually show that the exact opposite is the case, i.e. that the consumption of artificially sweetened beverages promotes, not hinders weight loss.

Skeptics, however, will say that "in a caloric deficit, and in comparison to regular beverages", which was the scenario in the Sørensen study,  "everything will work" - a valid argument, I have to admit. After all, the alleged insulinogenic effects said people ascribe to non-nutritive sweeteners would be more harmful during phases of attempted weight maintenance; phases as they've been investigated in a recent follow up to a previous study by Peters et al. (2015).

You can learn more about sweeteners at the SuppVersity

Aspartame & Your Microbiome - Not a Problem?

Will Artificial Sweeteners Spike Insulin?

Sweeteners & the Gut Microbiome Each is Diff.

Chronic Sweeten-er Intake Won't Effect Microbiome

Stevia, the Healthy Sweetener?

Sweeteners In- crease Sweet- ness Threshold

To be more precise, Peters' study was a year-long trial designed to compare the effects of beverages sweetened with non-nutritive sweeteners (NNS) to water as part of a behavioral weight management program consisting of 12 weeks of active weight loss (results previously published in Peters et al. 2014) and 40 weeks of weight maintenance (results now published in Peters, et al. 2016).

Figure 1: Weight and waist loss during the initial 12-week weight loss phase of the study (Peters. 2014).

As previously discussed in the SuppVersity News on Facebook, the results from the 12-week weight
loss phase of this trial were in line with those of the previously cited study by Sørensen et al. (2014) - with the important difference, however, that Sørensen et al. compared non-nutritive sweeteners (NNS) to sugar-sweetened beverages, while Peters et al. found that the NNS group experienced greater weight loss during the 12 weeks of active weight loss, as well as more pronounced reductions in waist circumference, blood pressure, cholesterol, LDL, and triglycerides, even if the control group consumed plain water group (Peters. 2014 | see Figure 1 for weight and waist data).

Figure 2: Consuming NNSs decreased the hunger of the subjects during the 12-week weight loss phase (Peters. 2014).

Mechanistically, the observed benefits may be explained by the opposing effects the consumption of NNS sweetened beverages and water had on the subjects' appetite: Unlike the group that kept consuming artificially sweetened beverages and experienced a significant reduction in hunger scores even while dieting, the ones who were allowed to consume only water reported significantly increased levels of hunger on the 0-100 pts hunger scale Peters et al. used (see Figure 2).

Saccharin may be the unhealthy exception to the "inert sweetener" rule.

What about the effects on the microbiome? You may have heard it on BBC's "Trust me I am a doctor": saccharin appears to mess with the gut microbiome in some of us to a degree that affects our blood glucose levels. That's at least what the TV-crews mini-study shows; and in fact, as a SuppVersity reader you know that the grand daddy of artificial sweeteners (that is by the way no longer used in many products) appears to actually exert the negative effects some people ascribe to every form of sweetener. Speaking of other forms. The TV team was also able to show that stevia, which has been shown to affect the microbiome, as well (learn more), does not affect fasting glucose levels.

In the follow up paper, Peters et al. (2015) now report that the 158 male and female subjects in the NNS group did also have an easier time maintaining their weight loss than their 150 peers in the water only group (see Figure 3); a result of which the scientists say that it was neither due to differences in physical activity / sedentary time or caffeine intake, which were (within the usual statistical margins) identical in both groups.

Figure 3: Body weight (in kg) after 52-week (weight maintenance phase | left) and percent body weight regained during the weight maintenance phase (grey = water; black = NNS | right; Peters. 2015).

While Peters et al. (2015) rightly point out that "it is not possible from the present data to explain why the NNS group lost more weight than the water group despite receiving identical weight loss instruction and beverage interventions that both contained zero calories", they are right to conclude that their findings ...

"[...] are important as there continues to be uncertainty about the benefit of NNS for weight management based largely on observational studies showing associations between NNS consumption, obesity and weight gain." (Peters. 2015).

This is particularly true in view of the fact that the data clearly opposes the often voiced claim that NNS promote obesity by interfering with normal mechanisms of energy balance.

Sponsorship? Yes, the study was funded by the American Beverage Association, but (a) the American Beverage Association was not involved in the design, conduct, interpretation, or manuscript preparation of this study and a third-party organization was hired at the PIs’ request to audit data at both clinical sites to check for the accuracy and integrity of the data. Since the latter are furthermore not really open to intepretation, the "sponsorship argument" is a weak one when it comes to defending the initially defined weight loss myth. In addition, it must be said that it is unrealistic to assume that you could do a 1-year study with more than 300 subjects without external funding - especially, if the research question is not on the TOP-list of the government.

This claim, however, is - as far as experimental evidence is concerned - based exclusively on animal studies; studies that conflict with both, the study at hand and the few other published long-term human trials that evaluated NNS for weight loss (Blackburn. 1997; Tate. 2012):

Figure 4: Tate et al. observed that drinking diet beverages (DB) promotes weight loss over water (WA) or paying more attention (attention control | AC) to what you eat (Tate. 2012).

• In a prospective randomized trial, Blackburn et al. found that people with obesity in a weight loss program using NNS food and beverage products lost more weight and maintained a greater weight loss over 2 years compared to subjects not using NNS (Blackburn. 1997). 
• Tate et al. (2012) conducted a 6-month randomized trial in people with obesity and found greater weight loss over 6 months and a greater likelihood of achieving a 5% weight loss in participants drinking beverages with NNS compared with participants in an attention control group. There was no difference in the likelihood of achieving a 5% weight loss between participants in the water group versus the control or between the water group versus the NNS group.

And if we take a look at the totality of research, it becomes obvious that even observational data, some of which is often used to support the claim that artificial / non-nutritive sweeteners were among the driving motors of the obesity pandemic, indicate that artificially sweetened beverages and foods are valuable weight loss tools (Phelan. 2009). Among those of the subjects listed in the National Weight Control Registry who maintained a weight loss of at least 30 pounds for at least 1 year, for example, the vast majority of 78% says that artificially sweetened products has helped them tremendously to achieve and maintain their weight loss (Catenacci. 2014).

Artificial Sweetened Foods Promote, Not Hinder Fat(!) Loss. 1.2kg Body Fat in 70 Days By Eating Artificially Sweetened Products. Lower Hunger, Higher Fat Oxidation | more

So what's the verdict? Reliable experimental evidence for the alleged obesogenic effects of artificially or, more generally, non-nutritively sweetened beverages in humans does not exist. The number of studies showing that it supports short- and long-term weight loss and weight maintenance, on the other hand, is ever increasing.

This does not mean, though, that individual differences may make you more susceptible to overeat when you consume artificially sweetened beverages while dieting. For the average dieter, however, the 2014 study by Peters et al.  and its follow-up show that the opposite is the case. It is thus only logical that the majority of 78% of the successful weight maintainers in Catenacci's observational study from 2014 say "that they helped them control or reduce their total food or calorie intake" | Comment on Facebook!

References:

• Blackburn, George L., et al. "The effect of aspartame as part of a multidisciplinary weight-control program on short-and long-term control of body weight." The American journal of clinical nutrition 65.2 (1997): 409-418.
• Catenacci, Victoria A., et al. "Low/No calorie sweetened beverage consumption in the National Weight Control Registry." Obesity 22.10 (2014): 2244-2251.
• Peters, John C., et al. "The effects of water and non‐nutritive sweetened beverages on weight loss during a 12‐week weight loss treatment program." Obesity 22.6 (2014): 1415-1421.
• Phelan, Suzanne, et al. "Use of artificial sweeteners and fat-modified foods in weight loss maintainers and always-normal weight individuals." International Journal of Obesity 33.10 (2009): 1183-1190.
• Sørensen, Lone B., et al. "Sucrose compared with artificial sweeteners: a clinical intervention study of effects on energy intake, appetite, and energy expenditure after 10 wk of supplementation in overweight subjects." The American journal of clinical nutrition (2014): ajcn-081554.
• Tate, Deborah F., et al. "Replacing caloric beverages with water or diet beverages for weight loss in adults: main results of the Choose Healthy Options Consciously Everyday (CHOICE) randomized clinical trial." The American journal of clinical nutrition 95.3 (2012): 555-563.

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

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

diet induced thermogenesis eating frequency food frequency lose fat meal frequency thermogenesis

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).

You can learn more about meal frequency at the SuppVersity

Grazin' Bad For the Obese!

Breakfast Keeps You Lean?!

Frequent Protein Consumption

Myth: Few Meals More Bodyfat

8 Meals = Stable, But High Insulin

Int. Fasting & Exercise

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.

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...

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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

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

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.

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

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

fasting hunger lose fat satiety satiety hormones starvation

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

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

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

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

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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.