Cure! Diabetes With 8 + 24 Week Diet Intervention: 40% Stay Normo-Glycemic After Switching from VLCD to Normal Diet

Cure! Diabetes With 8 + 24 Week Diet Intervention: 40% Stay Normo-Glycemic After Switching from VLCD to Normal Diet

diabesity diabetes diabetes cure health lose fat obesity T2DM very-low-calorie-diet VLCD

If gaining body fat triggers T2DM, is is not surprising that losing it, cures it.

From the SuppVersity Facebook News you will remember that studies have shown that type II diabetes can be send into remission with "nothing" but a very low energy diet (Steven. 2015). The question scientists still had to answer, though, was whether the astonishing improvements in glycemia and overall health could be maintained on an energy-sufficient diet. In a newstudy from the Newcastle University scientists did now try to confirm just that by combining an 8-week dieting phase with a stepped return to isocaloric diet based on a structured, individualized (isocaloric) program of weight maintenance.

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Glucose control, insulin sensitivity, insulin secretion, and hepatic and pancreas fat content were quantified at baseline, after return to isocaloric diet, and after 6 months to permit the primary comparison of change between post–weight loss and 6 months in responders.

Table 1: Fasting anthropometric and metabolic data in responders and nonresponders at baseline, after VLCD and return to isocaloric eating, and after the 6-month weight maintenance period (Steven. 2016).

To qualify as "responder" and thus patient who successfully reversed his diabetes, the subjects, thirty individuals with T2DM who had been suffering from T2DM for either either short- (<4 years) or long (<8 years)-duration, had to achieve a fasting blood glucose <7 mmol/L - and that not just after the initial 6 weeks, but after return to isocaloric diet.

Figure 1: The weight loss speaks in favor of the efficacy of the diet intervention in both groups; filled responders, open circles non-responders (Steven. 2016).

What did the diet look like? The VLCD consisted of a liquid diet formula (43% carbohydrate, 34% protein, and 19.5% fat; 2.6 MJ/day [624 kcal/day]; OPTIFAST; Nestle Nutrition, Croydon, U.K.) taken as three shakes per day. In addition, up to 240 g of nonstarchy vegetables was consumed, making total energy intake 624–700 kcal/day. Participants were encouraged to drink at least 2 L of calorie-free beverages per day and to maintain their habitual level of physical activity. To maximize adherence, one-to-one support was provided weekly by telephone, e-mail, text message, or face-to-face contact (S.S.).

During stepped food reintroduction, shakes were gradually replaced by solid food over 7 days; with one meal replacing a shake every 3 days. Isocaloric intake was determined from resting energy expenditure measured by indirect calorimetry using an open circuit calorimeter (Quark RMR; COSMED, Rome, Italy) and a canopy hood and ended up ~1/3 below their previous obesogenic food intake - no wonder that they got diabetic before at an energy intake that was ~30% above what they'd needed to stay in a healthy body fat range. Physical activity was encouraged, but food behaviors were the priority.

As the average weight loss in Figure 1 tells you, all but one subject that was excluded after the initial 8-week VLCD phase, achieved a highly significant weight loss. What not all subjects achieved, however, was the desired diabetes remission. To be more precise, only 40% of the participants (12 of 30) achieved the targeted fasting glucose <7.0 mmol/L levels (responders) after return to isocaloric eating (to put that in perspective | even RYGB weight loss surgery achieves only 9% remission rates; albeit measured over 14 vs. 4 months | Wood. 2015). Since that's in spite of similar weight loss, the question is: What is it that made the difference between responders and non-responders? The answer is complex and consists of many factors:

• The responders (n = 12 [8 males, 4 females]) had a shorter diabetes duration (3.8 +/- 1.0 vs. 9.8 +/- 1.6 years, P = 0.007) 
• The responders were also younger (52.0 +/- 2.9 vs. 59.9 +/- 2.1 years, P = 0.032) than nonresponders (n = 17 [7 males, 10 females]). 
• Responders were more likely to suffer from diabetes for a short(er) duration (9 of 15 of the short-duration and 3 of 14 of the long-duration groups).
• At baseline, responders had lower fasting glucose(8.9 +/- 0.7 vs. 13.2 6 0.6 mmol/L, P < 0.001) and HbA1c (7.1 +/- 0.3 vs. 8.4 6 0.3% [55 +/- 4 vs. 68 +/- 3 mmol/mol], P = 0.01). 

In addition, the responders had a lower total fat mass than the nonresponders at baseline (P = 0.04) (see Table 1) and didn't try as many (failed) treatment options, such as diet control (five vs. two); metformin only (six vs. four); metformin and sulfo nylurea (one vs. seven); metformin, sulfonylurea, and insulin (zero vs. two); metformin, sulfonylurea, and thiazolidi nedione (zero vs. one); and insulin only (zero vs. one), as the nonresponders did before participating in the study at hand.

Diabetes can be cured by dieting down below your personal fat threshold! A previous study led by Professor Roy Taylor from 2011, who commented on the study at hand in press release stating that "[t]he study also answered the question that people often ask me - if I lose the weight and keep the weight off, will I stay free of diabetes?" and answering his own question as follows: "The simple answer is yes!" In the same press release from the Newcastle University, Taylor highlights that the results of the study at hand "supports our theory of a Personal Fat Threshold. If a person gains more weight than they personally can tolerate, then diabetes is triggered, but if they then lose that amount of weight then they go back to normal" and adds "[t]he bottom line is that if a person really wants to get rid of their Type 2 diabetes, they can lose weight, keep it off and return to normal."

It is important to point out that the study at hand is part of a growing body of evidence showing that people with Type 2 diabetes who successfully lose weight can reverse their condition (Lim. 211; Steven. 2015)- probably because the fat loss correlates with a reduced fat deposition and increased function in / of the pancreas.

Figure 2: While there were no sign. differences in weight loss, there were other antropometric and related differences between the two groups: BMI, body fat %, triglycrides and the insulin resistance of the liver (Stevens. 2016).

And with a larger trial involving 280 free-living patients is already underway, it may only a question of time before people can no longer ignore that type II diabetes, which is triggered by bad lifestyle choices, can be reversed by healthy ones. This can be "tough" as Allan Tutty, 57, from Sunderland, who transformed his health by taking part in the study and is now

"eat[ing] normal foods though [...] less than [he] used to, and enjoy[ing] takeaways and chocolate but not on a regular basis so [he has] maintained my lower weight [and] changed [his life]completely thanks to this research" (Tutty in press release),

says; and still, I am pretty sure that, just like Tutty who says that, "with [his] diabetes in remission, I haven't looked back", those who are able and willing to follow Tutty's example won't look back either.

The elevated liver enzymes observed in the study point, once again, to the liver - Learn how to help your liver manage your glucose metabolism in this SuppVersity Classic.

Dieting is a diabetes cure, but one that does not work for everyone - yet? While it is not clear whether a longer weight-loss phase that would have brought the non-responders to similarly low bodyfat percentages as the responders wouldn't have changed the results, we have to be honest:  losing weight is easy, but eating 30% less than before, because that's all you need w/ your now normal weight is difficult... too difficult for many, probably.

With that being said, it should be obvious that further research is necessary to determine the factors that distinguish responders from non-responders and whether the latter simply failed to pass their "personal fat threshold" as Professor Taylor's remarks suggest | Comment!

References:

• Lim, Ee Lin, et al. "Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol." Diabetologia 54.10 (2011): 2506-2514.
• Steven, S., and R. Taylor. "Restoring normoglycaemia by use of a very low calorie diet in long‐and short‐duration Type 2 diabetes." Diabetic Medicine 32.9 (2015): 1149-1155.
• Steven, et al. "Very-Low-Calorie Diet and 6 Months of Weight Stability in Type 2 Diabetes: Pathophysiologic Changes in Responders and Nonresponders." Diabetes Care (2016) Accepted Article.
• Wood, G. Craig, et al. "Preoperative use of incretins is associated with increased diabetes remission after RYGB surgery among patients taking insulin: A retrospective cohort analysis." Annals of surgery 261.1 (2015): 125-128.

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).

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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.

Is Lard More Fattening Than Hydrogenated Vegetable Oil!? 17% Extra Weight, 32% Extra Fat Gain + Increased Appetite

Is Lard More Fattening Than Hydrogenated Vegetable Oil!? 17% Extra Weight, 32% Extra Fat Gain + Increased Appetite

diabesity fat fats health homa-ir insulin lard obesity oil oils partially hydrogenated fats partially hydrogenized fats QUICKI shortening transfats vegetable oils

Not all fats are created equal and lard and hydrogenated vegetable oils are not on the top-list of "healthy fat choices".

Our perspective on fat has changed significantly over the last decade. While some people still propagate that "fat is bad" and "should be generally avoided", most experts have stopped bashing fat in general and are now focusing on saturated fats. Saturated fats as they occur in lard,.. but wait! If you take a closer look at the fatty acid composition of lard, it turns out that it contains "only" 39.2% saturated, but 45.1% mono- and 11.2% polyunsaturated fats. That's actually not too far off of the average vegetable shortening with a saturated to monounsaturated to polyunsaturated fat ratio of 25.0 / 41.2 / 28.1% (nutritiondata.com)

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In contrast to said even more dreaded partially hydrogenized vegetable fats, which contains a whopping 13.2g of transfats per 100g, lard is yet mostly trans-fat free. That's a good thing, right? After all, high trans-fat intakes have been associated with increased inflammation and cardiovascular disease  (Hu. 1997; Lopez-Garcia. 2005. Now, while experimental evidence confirming negative effects in humans is non-existent, negative effects have also been observed in controlled animal experiments. It is thus more than reasonable to assume that of two of the most commonly used fat sources for cooking, i.e. lard and hydrogenated vegetable-shortenings, the former, the trans-fat free 100% "natural" fat source should be the healthier one.

Figure 1: Fatty acid content (g) of the three test diets (Kubant. 2015)

To check the validity of this hypothesis, scientists from the University of Toronto fed male Wistar rats for 14 weeks diets which contained either (1) high vegetable fat (HVF, 60 kcal% from vegetable shortening) or (2) high lard fat (HLF, 60 kcal% from lard). A group of rats that received the normal-fat chow (NF, 16 kcal% from vegetable shortening) served as control (see Figure 1). Body weight, food intake, adipose tissue mass, serum 25[OH]D3, glucose, insulin and fatty acid composition of diets were the scientists' main outcome data - data that confirm that not everything we take for granted will actually stand the test of science.

Figure 2: Body weight and fat gain over 12 weeks on control (low fat) or high fat diets w/ lard (HLF) or hydrogenated vegetable oils (HVF) as main fat sources (Kubant. 2015).

In contrast to what common sense would dictate, the rodents in the lard group were not leaner and healthier. In fact, the data in Figure 2 tells you that the exact opposite was the case: The rodents on the high lard diet gained significantly more body weight and - more importantly - body fat and did not, as some may now speculate, simply store the extra energy away instead of having it float around in the blood and ruin their insulin sensitivity (see Figure 3).

Figure 3: Markers of glucose metabolism at the end of the study (data expressed relative to control | Kubant. 2015)

So, basically, the scientists, who had even speculated that lard, due to its naturally high vitamin D content "may act to reduce the metabolic consequences associated with obesity, as suggested by other investigators" (Kubant. 2015), had to realize that their prediction was wrong. Whether lard is simply unhealthier or whether the effect was a results of the comparably lower food intake of the vegetable shortening group is difficult to say. What we do know, however, is that the animals who were on the lard diet consumed more calories than the HVF group. That 1g/day of extra food, however, was enough to have the scientists conclude that the rats have a strong preference for the taste of fat sources containing long-chain fatty acids (that is, oleic and linoleic), but by no means enough, to fully explain the significant difference in weight and body fat gain.

The Quest for the Optimal Cooking Oil: Heat Stable, Low PUFA & Cholesterol Free - High MUFA Sunflower / Canola, Olive, Coconut & Avocado Oil Qualify for the TOP5 | Learn more!

So lard is much worse than transfats? I wouldn't dare making a general statement about lard vs. vegetable shortenings based on this study. One thing I would like to remind every saturated animal fat worshipper of, however, is that his beloved "saturated fat sources" like lard are in fact hardly saturated at all. The common lard, the scientists used in the study at hand, for example, has higher amounts of polyunsaturated fatty acids in it than the average vegetable shortening. Its (by the saturated fat lovers dreaded) content of omega-6 fatty acids in the form of linoleic acid, which is currently everybody's favorite scapegoat for being obese, diabetic or whatnot, is even three times higher!

What we must not forget, either, are the divergent results about the fattening effects of transfats from monkey and rodent studies. While the one existing monkey study showed higher levels of intra-abdominal adiposity and insulin resistance in monkeys fed trans fatty acids (TFAs) for 6 years under a controlled feeding regimen (Kavanagh. 2007), a more recent study in rats found that dietary TFAs fed ad libitum (as much as the rodents wanted) did not influence food intake or body fat accumulation (Ochiai. 2013). Now, monkeys are more reliable than rats, right? Well, yes, but if the monkeys are on an energy restricted and the control diet was no lard diet, but rather the "perfect monkey diet", the rodent study with its realistic ad-libitum access to food and a diet composition that was more akin to what people eat these days becomes increasingly attractive. Overall, however, it doesn't really make sense to use any of these studies to speculate about the practical significance Kubant's rodent study has for men. If you asked me, it is not even relevant, anyways, because neither lard nor hydrogenated vegetable oils should be a regular part of your diet | Learn why in a previous SuppVersity Article or tell me what you think on Facebook!

References:

• Hu, Frank B., et al. "Dietary fat intake and the risk of coronary heart disease in women." New England Journal of Medicine 337.21 (1997): 1491-1499.
• Kavanagh, Kylie, et al. "Trans fat diet induces abdominal obesity and changes in insulin sensitivity in monkeys." Obesity 15.7 (2007): 1675-1684.
• Kubant, R., et al. "A comparison of effects of lard and hydrogenated vegetable shortening on the development of high-fat diet-induced obesity in rats." Nutrition & Diabetes 5.12 (2015): e188.
• Lopez-Garcia, Esther, et al. "Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction." The Journal of nutrition 135.3 (2005): 562-566.
• Ochiai, Masaru, et al. "Effects of dietary trans fatty acids on fat accumulation and metabolic rate in rat." Journal of oleo science 62.2 (2013): 57-64.

Cinnamon as Nutrient Partitioner and 1st-Line Treatment for Pre-Diabetes? 5% Decrease in Fasting Glucose per Month in Human Studies, Up to 24% in 40 Days W/ High(er) Doses

Cinnamon as Nutrient Partitioner and 1st-Line Treatment for Pre-Diabetes? 5% Decrease in Fasting Glucose per Month in Human Studies, Up to 24% in 40 Days W/ High(er) Doses

anti-diabetes cassia cinnamon cinnamon Coumarin diabesity diabetes fasting blood sugar glucose management HbA1c health insulin sensitivity lose fat

Yes, that's how real cinnamon look like. It does not grow as powder in plastic boxes on trees as I suspect the members of the generation McBurgerSubway believe ;-)

No, this is not absolutely new. In fact this is just "another" SuppVersity articles on the anti-diabetic effects of cinnamon, but I promise it's going to be the most comprehensive one. One that discusses the currently available evidence from human trials, as well as the things we know and believe to know about how cinnamon acts its anti-diabetic magic qualitatively and quantitatively.

Before I even go into further details, though, I would like to address one of the "cinnamon myths" that says that only the highly expensive Ceylon or Sri Lankan Cinnamon would do the trick, while the commonly sold Cinamon cassia would be useless or even dangerous due to its high (and in fact toxic) coumarin content.

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Interestingly, all human studies have been done with the "cheap toxic stuff from the supermarket". In view of what you are about to learn about its effects on blood glucose later in this article, the first take-home-message from today's article is thus: "Cheap cinnamon cassia will work just fine as a blood glucose management supplement!" Unfortunately, long-term studies the safety of "common cinnamon" with its highly variable coumarin content (0.31 g = harmless to 6.97 g = potentially dangerous per kg raw powder | Wang. 2013 | see Table 1) are non-existent.

Table 1: Content of Coumarin 1, Cinnamyl Alcohol 2, Cinnamaldehyde 3, Cinnamic Acid 4, Eugenol 5, Cinnamyl Acetate 6 in Cinnamomum Species and Commercial Samples (g/kg) | DUL = Detected under limits of quantitation; ND = not detected (Wang. 2013).

The only advise I can give you is thus to rely on supplements with standardized (low to non-detectable) amounts of this potentially carcinogenic substance (Wang. 2014) if you plan to take it regularly for years. Using the next best cinnamon powder from the supermarket next door on the other hand is probably not advisable even though some of the scientists who conducted the studies Arjuna B. Medagama reviewed for his (or her?) latest paper in Nutrition Journal (Medagama. 2015) probably did just that: Buy cinnamon powder from the supermarket next door to test its effects on blood glucose management in 40-days- to 4-months-studies in cinnamon-naive patients with (pre-)diabetes.

If you take a closer look at the data, though, it becomes obvious that some studies used plain cinnamon powder, while others used regular or commercial water-extracts (CinSulin. Anderson).

Effect of 6g of cinnamon on post-prandial blood glucose in healthy subjects (Hlebowicz. 2007). This hefty dose also slowed down gastric emptying and triggered non-significant increases in satiety in 14 healthy subjects after high CHO meals.

What's the optimal dosage? Even though the overview in Figure 1 suggests that "more helps more", Anand, et al. (2010) observed negative effects on the liver of rodents at dosages that would tantamount to ~40g of cinnamon per day. Ok, I assume you already apprehended that this is madness, but in the world of fitness maniacs and mad bodybuilders I thought it would be worth mentioning that even the coumarin free Ceylon cinnamon appears to have ill side effects when it is consumed in extremely high dosages. It would thus appear to be more reasonable to target an intake of 3-6 g of cinnamon with every major meal (it slows down gastric emptying and reduces postprandial blood glucose, therefore it makes sense to take it with a meal | Hlebowicz. 2007, see Figure to the left).

If you scrutinize the results I've plotted for you in Figure 1, you will notice that (a) the improvements in fasting blood glucose were significantly more pronounced than those of the long-term blood sugar maker HbA1c, that (b) the former appear to increase with the dosage that was used (Klan and Mang observed the highest reductions and used the highest amounts of cinnamon powder), and that (c) the reductions in HbA1c take time, i.e. several months and are not guaranteed, even if there are significant reductions in fasting blood glucose (cf. Belvins).

Figure 1: Relative changes in fasting blood glucose and HbA1c levels of pre-diabetic subjects (Medagama. 2015)

On average, the fasting blood glucose levels of the study participants in all studies decreased by 4.7% in four weeks; the HbA1c, on the other hand, by only 1%. Since part of the effects on blood glucose are merely a results of the reduced gastric emptying and will thus affect the peak values, yet not the overall glycemia, it appears logical that the HbA1c reacts slowly to the intervention. As Medagama points out, the effects of cinnamon are yet more far-reaching, so that more pronounced effects on the slow-reacting HbA1c levels can be expected to be seen in the hitherto non-existent long-term (= 1-2 year) studies, because cinnamon will also have ...

• 

  Figure 2: Molecular mechanisms of Cinnamon by which it exerts hypoglycaemic activity. (Medagama. 2015).

  direct effects on the insulin receptor have been observed for Cinnamtannin B1, a proanthocyanidin isolated from the stem bark of Ceylon cinnamon that activates the phosphorylation of the insulin receptor β-subunit on adipocytes as well as other insulin receptors,
• indirect effects on glucose management that are mediated by increased GLP-1 levels, a satiety hormone that decreases the amount of insulin that is necessary to clear glucose from your blood - as Medagama points out, probably by improving glucose transport,
• direct effects on the GLUT-4 glucose uptake receptor, the expression of which is increased by 42.8 % to 73.1 % in brown adipose tissue and muscle by cinnamon in a dose dependent manner,
• indirect effects on insulin sensitivity that are mediated by the effects of cinnamon on the expression of PPAR (α) and PPAR (γ), the increase of which is linked to increased glucose uptake - unfortunately, also in fat cells,
• direct effects on carbohydrate availability that are mediated by the inhibition of the amylase enzyme that is responsible for breaking down complex carbs into simple sugars,
• indirect effects on the endogenous production of glucose in the liver that is inhibited by cinnamon (glucogenesis, i.e. the storage of sugar in the liver, on the other hand, is promoted), and
• indirect effects that are brought about by the reduced rate of gastric emptying that will naturally slow down the absorption of glucose after a meal.

If that was too much for you to remember, I guess the graphical overview Medagama created may serve as a memory aid, when you come back to this article to refresh your knowledge about cinnamon and pre-diabetes. Speaking of which...

Glucose Control Beyond Carb Reduction ➲ Amino Acids, Proteins, Peptides | learn more!

So, what's the verdict about cinnamon and pre-diabetes? As Medagama points out in the conclusion to the previously referenced recently published review, "[b]oth true cinnamon and cassia cinnamon has the potential to lower blood glucose in animal models and humans" (Medagama. 2015). The problem is yet that we do not have reliable long-term safety studies for both, the problematic, potentially coumarin-laden regular cinnamon, as well as the expensive 99% coumarin-free Ceylon cinnamon, which has actually never been tested in human studies (rodent studies suggest that it works at least as well, though).

Addendum: As previously hinted at, there is no evidence from human studies that the "healthier", "true cinnamon" aka Ceylon cinnamon even works. Well, I just noticed that there's a single, rarely cited study in healthy individuals from the Lund University in Sweden that says that Ceylon cinammon has no effect whatsoever on glycemia and thus concludes "The Federal Institute for Risk Assessment in Europe has suggested the replacement of C. cassia by C. zeylanicum or the use of aqueous extracts of C. cassia to lower coumarin exposure. However, the positive effects seen with C. cassia in subjects w/ poor glycaemic control would then be lost." (Wickenberg. 2012)

To recommend regular cinnamon as a standard-supplement, you'd take everyday for years, on the other hand cannot really be recommended - not for pre-diabetics and by no means for healthy, active individuals who have no reason to take supplements with non-muscle specific glucose partitioning effects, anyways. If you want to improve your glucose management folks, work out - a glycogen-depleting strength or HIIT workout, that's the only scientifically proven muscle specific glucose repartitioner | Comment on Facebook!

References:

• Akilen, R., et al. "Glycated haemoglobin and blood pressure‐lowering effect of cinnamon in multi‐ethnic Type 2 diabetic patients in the UK: a randomized, placebo‐controlled, double‐blind clinical trial." Diabetic Medicine 27.10 (2010): 1159-1167.
• Anand, Prachi, et al. "Insulinotropic effect of cinnamaldehyde on transcriptional regulation of pyruvate kinase, phosphoenolpyruvate carboxykinase, and GLUT4 translocation in experimental diabetic rats." Chemico-biological interactions 186.1 (2010): 72-81.
• Anderson, Richard A., et al. "Cinnamon extract lowers glucose, insulin and cholesterol in people with elevated serum glucose." Journal of Traditional and Complementary Medicine (2015).
• Blevins, Steve M., et al. "Effect of cinnamon on glucose and lipid levels in Non–insulin-dependent type 2 diabetes." Diabetes care 30.9 (2007): 2236-2237.
• Crawford, Paul. "Effectiveness of cinnamon for lowering hemoglobin A1C in patients with type 2 diabetes: a randomized, controlled trial." The Journal of the American Board of Family Medicine 22.5 (2009): 507-512.
• Hlebowicz, Joanna, et al. "Effect of cinnamon on postprandial blood glucose, gastric emptying, and satiety in healthy subjects." The American journal of clinical nutrition 85.6 (2007): 1552-1556.
• Khan, Alam, et al. "Cinnamon improves glucose and lipids of people with type 2 diabetes." Diabetes care 26.12 (2003): 3215-3218.
• Mang, B., et al. "Effects of a cinnamon extract on plasma glucose, HbA1c, and serum lipids in diabetes mellitus type 2." European journal of clinical investigation 36.5 (2006): 340-344.
• Suppapitiporn, Suchat, and Nuttapol Kanpaksi. "The effect of cinnamon cassia powder in type 2 diabetes mellitus." Journal of the Medical Association of Thailand= Chotmaihet thangphaet 89 (2006): S200-5.
• Vanschoonbeek, Kristof, et al. "Cinnamon supplementation does not improve glycemic control in postmenopausal type 2 diabetes patients." The Journal of nutrition 136.4 (2006): 977-980.
• Wang, Yan-Hong, et al. "Cassia cinnamon as a source of coumarin in cinnamon-flavored food and food supplements in the United States." Journal of agricultural and food chemistry 61.18 (2013): 4470-4476.
• Wickenberg, Jennie, et al. "Ceylon cinnamon does not affect postprandial plasma glucose or insulin in subjects with impaired glucose tolerance." British journal of nutrition 107.12 (2012): 1845-1849.

Artificial Sweetener Saccharin Increases Weight Gain in Rodent Study Without Increasing Food Intake | Plus: Meta-Analysis of Human Studies Says: "No Reason to Worry!"

Artificial Sweetener Saccharin Increases Weight Gain in Rodent Study Without Increasing Food Intake | Plus: Meta-Analysis of Human Studies Says: "No Reason to Worry!"

artificial sweetener artificial sweeteners diabesity fat gain glucose health insulin leptin lose fat saccharin sweeteners weight gain

Should you freak out about a small increase in body weight in a small-scale rodent study that is attributed to the consumption of saccharin in yogurt?

While epidemiological studies show that the consumption of products containing non-nutritive sweeteners (NNS) is associated with increased adiposity (Colditz. 1990; Fowler. 2008), type 2 diabetes mellitus (T2DM), metabolic syndrome and cardiovascular disease (Dhingra. 2007; Lutsey, Steffen. 2008). A mechanistic link between aspartame, sucralose, stevia & co and weight gain as well as its ill metabolic and cardiovascular consequences in humans is non-existent (learn more).

Rather than weight increases controlled human studies show that the consumption of artificially sweetened foods promote, not hinder the loss of body fat (Sørensen. 2014).

You can learn more about sweeteners at the SuppVersity

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In animal models, though, the results have been more conflicting. While many studies show no effect of artificial sweetener consumption, the latest stud by Kelly Carraro Foletto and colleagues is not the first rodent study to suggest that non-nutritive sweeteners may also interfere in the regulation of compensatory appetite promoting weight gain (Davidson. 2011; Polyák. 2010; Rogers. 1988). This does yet not refute the findings of one of the latest meta-analysis of the effects of low-energy sweetener consumption on energy intake and body weight in man - a meta-analysis published in Nature's prestigious International Journal of Obesity that says...

Figure 1: The forest plots of the practically most relevant data of individual and combined effect sizes for sustained intervention studies comparing the effects on body weight of sweeteners versus sugar (upper panel) and versus water (lower panel) shows that not a single long(er) term study found negative effects - the exact opposite is the case. Even compared to water the use of low-energy sweeteners (artificial or not) lead to measurable, yet not always significant decreases in body weight in human trials (Rogers. 2015).

"that the balance of evidence indicates that use of LES [low or no energy sweeteners] in place of sugar, in children and adults, leads to reduced EI and BW, and possibly also when compared with water" (Rogers. 2015 | my emphasis).

And with respect to the often-cited "evidence" from animal and observational studies, the autors of the meta-analysis submit that...

"[...] the present review of a large and systematically identified body of evidence from human intervention studies, with varying designs, settings and populations (including children and adults, males and females, and lean, overweight and obese groups), provide no support for that view. The question then is whether those hypotheses should be rejected or whether, as seems unlikely, the relevant human intervention studies are consistently flawed in a way that leads, in most cases, to exactly the opposite outcome" (Rogers. 2015)

I do thus want to warn you: Do not overrate the already relatively small amount of extra-weight the rodents in saccharin group of Foletto's recent study gained (see Figure 2, left).

Figure 2: Cumulative weight gain and total cumulative energy intake of (only) 16 male Wistar reds fed diets that were supplemented with either saccharin-sweetened or non-sweetened yogurt added (Foletto. 2015)

In a previous study, Folleto et al. had already observed that saccharin can induce weight gain when compared with sucrose in Wistar rats despite similar total caloric intake. In their latest study they did not try to prove that this effect is independent of the rodents' energy intake and mediated by insulin-resistance and / or modified levels of leptin and PYY in the fasting state.

Was it fat they gained or lean tissue mass? Well, I would like to answer these important questions, but Foletto did not disclose (or not even measure?) this important parameter. The practical relevance and reliability of their results is further reduced due to the small cages (44x34x16 cm individual cages) into which the rodents were confined to reduce their voluntary physical activity during the 14 weeks of the experiment, as well as the exclusion of rats who didn't consume the aspired 70% of the planned 75 kcal in form of yogurt per week (the number of rats who fell into this category is also not disclosed).

To this ends, the researchers randomly assigned 16 male Wistar rats to receive ~78kcal per week from either saccharin-sweetened (0.3% saccharin) yogurt or non- sweetened yogurt (0.5 kcal/g) in addition to chow (2.93 kcal/g) and water ad lib. For 14 weeks, Foletto, et al. measured the total food intake (from yogurt and chow) daily and the weight gain on a weekly basis (the results are plotted in Figure 2). Fasting leptin, glucose, insulin, PYY and HOMA-IR levels were measured only at the end of the 14-week study period, though.

Table 1: In view of the fact that any existing negative effects of dietary sweeteners may well be compound-specific. It is certainly worth noting that saccharin is no longer used in modern sweetener formulations of sodas (Wikipedia. 2015)

In spite of the already reported ~5% increase in cumulative weight gain over 14 weeks (p=0.027), the researchers found no differences in HOMA-IR (=insulin resistance), fasting leptin or PYY levels between groups that could mechanistically explain why the rodents who received saccharin sweetened yogurt gained more weight than their peers who received non-sweetened yogurts.

Measurable weight increases are a common pattern in rodent studies particularly for the (today rarely used) artificial sweetener saccharin. It is thus well possible that any existing negative effects are compound-specific. For aspartame, for example, similar evidence is rare to non-existent.

Bottom line: In the absence of a proven theory about the mechanism that may trigger the increased weight gain and in view of the lack of health-relevant data (no information about the body composition of the rodents) and health-relevant side-effects you would usually see in response to pathologic weight gain (changes in insulin resistance, leptin or PYY), I can only refer you back to the quote from the latest meta-analysis of the effects of low- to no-energy-sweetener intake on food intake and weight gain in humans, which say that "the balance of evidence indicates that use of LES [low or no energy sweeteners] in place of sugar, in children and adults, leads to reduced EI and BW, and possibly also when compared with water" (Rogers. 2015).

Furthermore, more relevant evidence from human clinical trials supports the use of artificially sweetened foods as dieting aids (Sørensen. 2014 | learn more).

Whether that's enough to convince you that the unproven negative effects of saccharin on caloric expenditure or increases in the glucose transport mediated by gut sweet-receptors, of which Foletto et al. speculate that they may explain the results of their study, are relevant enough to avoid non-nutritive sweeteners altogether is now up to you. For me it's not enough... | Comment on Facebook!

References:

• Foletto, Kelly Carraro, et al. "Sweet taste of saccharin induces weight gain without increasing caloric intake, not related to insulin-resistance in Wistar rats." Appetite (2015).
• Rogers, P. J., et al. "Does low-energy sweetener consumption affect energy intake and body weight? A systematic review, including meta-analyses, of the evidence from human and animal studies." International Journal of Obesity (2015).
• 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.