Dairy and (Pre-)Diabetes - Re-Evaluated: It's Complicated -- Generally Protective Effects, Though (Risk Reduction ~40%)

If you lump all forms of dairy together into the "total dairy" category, US citizens have a ~40% reduced risk of prediabetes when they consume more than 14 servings of dairy per week. And that's by no means the only novel insight from a recent study by USDA researchers...

When women tell you "it's complicated" that's usually a sign you're in trouble. When scientists tell you "it's complicated", it's usually a smart version of telling you: "We don't know nothing, bro..." With that being said, I didn't find the line "it's complicated" in the latest paper by scientists from the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (Hruby 2017) and still I cannot shake the feeling that... you guessed it: "It's complicated" ;-)

Yet even though it is obviously "complicated", the US dietary guidelines have consistently recommended 2–3 servings dairy/d for adolescents and adults (Office of Disease Prevention). It is thus no wonder that many individuals may perceive dairy products as health foods.... low fat that is; after all, we've been told that fat makes you fat for decades.

You can learn more about dairy at the SuppVersity

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Is There Sth. Like a Dairy Weight Loss Miracle?

There is Good A2 and Bad A1 Dairy, True or False?

Cheese is a Heart + Metabolic Health Food

Milk Kills, PR Says + Perverts the Facts

Milk / Dairy & Exercise - A Perfect Match?

Have we been duped for decades? Not really, dairy products may be, as Hruby et al. point out, an important source of protein and several shortfall nutrients (nutrients that may be under-consumed relative to the Dietary Reference Intakes), including calcium, magnesium, potassium, and vitamin D.

In spite of that, the evidence in favor / against the anti-diabetic effects of dairy are... yeah, you heart it already "complicated". As the Tufts researchers point out in the introduction to their recently published paper "The Journal of Nutrition", existing observational evidence suggests a generally small, equivocal, or U-shaped relation between total dairy or specific dairy product consumption and the risk of T2D and related factors. What has been largely ignored, hitherto, is whether dairy is also associated with the incidence of impaired glucose or hyperglycemic stages preceding T2D. Reason enough to do yet another study to... make things more complicated ;-)

"Therefore, the primary aim of this study was to investigate the relations between consumption of dairy and milk-based products and the long-term risk of prediabetes among initially healthy individuals, and the risk of T2D among individuals with prediabetes in a cohort of middle-aged adults, the Framingham Heart Study Offspring Cohort. As a secondary aim, we examined the effect modification of dairy intake and risk of T2D by baseline glycemic status in the combined study population. We hypothesize that associations with incident outcomes differ by dairy product and type, and that these associations may further differ in initially healthy compared with unhealthy participants" (Hruby 2017).

The data stems from The National Heart, Lung, and Blood Institute's Framingham Heart Study Offspring Cohort, a community-based longitudinal study of cardiovascular disease that began in 1971. The scientists used data from the fifth examination cycle (1991–1995) to the eighth exam (2005-2008) of the Offspring Cohort, in which 3799  participants underwent a standard medical examination consisting of laboratory and anthropometric as well as dietary intake assessments and here's what they found:

(Pre-)Diabetes is RAMPANT - 48 in 100 people affected!

Initially, 1867 participants were free of prediabetes, of these almost every second participant, i.e. 902 (48%), developed prediabetes. Only 21% of these developed full-blown T2DM, though.

Figure 1:Diabetes is the world's eighth biggest killer, accounting for some 1.5 million deaths each year. A major new World Health Organization report has now revealed that the number of cases around the world has nearly quadrupled to 422 million in 2014 from 108 million in 1980. The Eastern-Mediterranean region had the biggest increase in cases. Diabetes now affects one in 11 adults w/ high blood sugar levels linked to 3.8 million deaths per year. (statista.com)

Against that background, it's no wonder that the diabetes rates worldwide keep exploding, as you can see in Figure 1 from one of my favorite websites, i.e. statista.com, which also tells you that the T2DM drug market is going to be worth 42.2 billion(!) $US in 2020 ... and here's the shocker $38.8 billion will be paid by the US, alone (learn more)!

Cheese, cream,  butter are not associated w/ pre-diabetes, protect against full-blown T2DM

While cheese, cream, and butter are still cognitively linked to metabolic problems in many mainstream articles, neither cheese nor cream and butter was associated with prediabetes in the study at hand. In fact, when the scientists looked at those 21% of pre-diabetics that transitioned into full-blown T2DM, the intake of high-fat dairy and cheese products (not sign. for cream and butter, alone | p = 0.18 for the fully adjusted model - for adjustments see caption of Figure 2) protected people from losing the last insulin sensitivity they'd left.

Figure 2: Differential risk (vs. 0 intake) of becoming a diabetic with high intakes of cream and butter, cheese (was evaluated only for 1-4 and ≥4) and total high-fat dairy intake; data fully adjusted for r age, sex, and energy intake, family history of diabetes, smoking, dyslipidemia, hypertension, other dietary characteristics, BMI, and weight change (Hruby 2017).

In other words, the study at hand is yet another study (of the more recent ones) showing a dose-response, inverse associations with incident T2D, with 70% and 63% lower risk, respectively, of incident T2D between the highest and lowest intake categories (≥14 compared with <1 serving/wk for high-fat dairy, ≥4 compared with <1 serving/wk for cheese).

Dairy is generally protective

Overall, it can be said that The subjects' total dairy intake - for both, low-fat, and high-fat dairy - was associated with a 39%, 32%, and 25% lower risk of incident prediabetes, respectively, in the highest compared with the lowest intakes (≥14 compared with <4 servings/wk).

Figure 3: Differential risk (vs. zero intake) of prediabetes with high intakes of total dairy (could not be evaluated for <4) and total high-fat and low-fat dairy intake; data fully adjusted for r age, sex, and energy intake, family history of diabetes, smoking, dyslipidemia, hypertension, other dietary characteristics, BMI, and weight change (Hruby 2017).

As you can see in Figure 2 total dairy, high-fat dairy and low-fat dairy show the same trend: the more you eat, the less likely you're to develop problems with your glucose management.

Cheese is actually a healthy food! In case you still have your doubts that real cheese (the one made from dairy instead of vegetable fat and E-numbers) is a healthy food, (re-)read my article "Cheese & Your Health: CVD, Cancer & Metabolic Syndrome - Cheesy Science or Scientific Revelation? A Brief Review" from July 2016, here. These trends, however, are not all of the same significance; with p = 0.002, the chance that the association the scientists observed for total dairy is 15x less likely to be random than the one for either high-fat or low-fat dairy - while this may be a logical consequence of the size of the dataset, it could also be interpreted as further evidence that the type of dairy doesn't really matter.

Yogurt doesn't have its super rep for nothing 

In fact, the differential analysis for milk products from Hruby et al. supports the notion that yogurt is particularly (pre-)diabetes-protective, but total, low-fat and skim milk, and whole-milk are associated with significantly reduced risks of prediabetes, as well.

Figure 4: Differential risk (vs. zero intake for skim milk+yogurt) of prediabetes with moderate intake of total milk, skim milk and yogurt; whole milk intake left out because there was only one intake category; for adj. see Figure 2 & 2 (Hruby 2017).

In that, it should be noted, however, that these risk reductions do not increase linearly; this means, it's not "the more the better". Rather than that, a moderate intake of all four was associated with the greatest relative risk reduction, namely -30% for total milk, -17% for skim milk, -16% for whole milk and -24% for yogurt.  In that, I find it quite telling that the overall intake of whole milk in the US (or, rather, in this cohort) is so low that the scientists could compare data of subjects consuming zero to one vs. those consuming more than one serving per week, only. The anti-fat scare obviously continues to have an effect.

What do previous studies show?

If you take a look at the most recent reviews/meta-analysis, overall decreases in diabetes risk (Gijsbers 2016, esp. yogurt (-14% w/80g/d); Khoramdad 2017 (-8-12% for total dairy); Guo 2017 (-15% all dairy; also -27% for metabolic disease)), reduced CVD and stroke risk (Alexander 2016; de Goede for milk (-7% per 200g); Pimpin 2016 for butter) are the norm, not the exception. The study at hand should thus be understood as part of the accumulating evidence in favor of dairy products for metabolic disease and its unhealthy consequences on the heart.

Don't expect dairy magic, though: In spite of their beneficial effects on health, dairy products cannot override your energy intake. In fact, studies show that dairy promotes weight loss, only, when it's consumed with a calorically reduced diet (Chen 2012).

Where are the experimental trials? Good question: compared to the unlimited number of observational studies, reviews and meta-analyses, there are only very few intervention studies. This wouldn't be the SuppVersity, though, if we didn't, at least, take a peek at the underlying mechanisms and you know that you won't get to those with epidemiological guesswork.

"Emerging evidence indicates that dairy components that alter mitochondrial function (e.g., leucine actions on silent information regulator transcript 1 (SIRT1)-associated pathways), promote gut microbial population shifts, or influence inflammation and cardiovascular function (e.g., Ca-regulated peptides calcitonin gene-related peptide [CGRP] or calcitonin) should be considered as possible mechanistic factors linking dairy intake with lower risk for T2D" (my emphasis in Hirahatake 2014). 

Furthermore, there's the obvious: the potential to increase muscle mass and thus the ability to burn and store glucose that comes with the high BCAA content of dairy proteins (also prevents sarcopenia | McGregor 2013). What relatively few people know, though, is that dairy also contains functional, bioactive peptides, i.e. amino acid chains that activate or block certain receptors in your body:

"Whey protein and casein both contain the bioactive peptides lactokinins or caseinkinins respectively. In-vitro experiments indicate these peptides can inhibit ACE activity. ACE is a rate limiting enzyme in the conversion of angiotensin I to angiotensin II responsible for vasoconstriction. Therefore, lactokinins or caseinkinins both have potential to lower blood pressure. Vascular reactivity is important for glucose disposal and regulation of blood flow, but is impaired in patients with metabolic syndrome due to decreased insulin-stimulated vasodilation via the eNOS pathway and suppressed NO production in the vascular endothelium" (McGregor 2013). 

Now you may say that this is not about diabetes... however, ACE inhibitors will improve your glucose metabolism - in fact so much so that diabetics end up in the emergency room with hypoglycemia (Morris 1997).

Figure 5: The renin-angiotensin system controls much more than just your blood pressure (Henriksen 2007).

In addition to that, dairy protein-derived peptides may also contribute to the insulinotropic effect via dipeptidyl peptidase-4 (DPP-4) inhibitory activity (Bjørnshave 2014).

Another, but IMHO overrated contributor to dairy's health effect is the CLA content of dairy. In particular with respect to diabetes, the focus of this SuppVersity article, CLA is yet rather problematic.  That's in contrast to dairy's effects on the "satiety" or rather incretin hormones glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP), of which we know from various studies that they help maintain glucose homeostasis, in part by enhancing pancreatic beta-cell responsiveness to glucose (Freeman 2009).

As much as 25% of the postprandial insulin response has been suggested to be attributable to the effects of incretins and dairy is a rockstar, when it comes to their release.

As Hirahatake et al. point out, "[v]arious lines of evidence indicate that GLP-1 production by small intestinal and colonic L-cells is influenced by specific nutrients, and may respond to foods that provide a substrate for certain species of colonic microbiota". Next to dairy, you'll also find prebiotic fibers and resistant starches on the list of GLP1 promoters. This points towards the last, but not least important factor that may contribute to the glucose-normalizing prowess of dairy: the microbiome; and I guess I don't have to tell you that some dairy products have the potential to alter gut microbiota through probiotic effects of live cultures used during fermentation, and others may do so through the prebiotic effects of dairy oligosaccharides (Faye 2012).

Prevalence of lactose intolerance.

Bottom line: Eat your dairy and thrive. While the study at hand shows decently convincing beneficial effects of including dairy products in your diet, I wouldn't call dairy a "must have" of every diet. In spite of the scientists' efforts to adjust for other dietary characteristics, including intake of coffee, nuts, fruits, vegetables, meats, alcohol, fish, the glycemic index, etc. eating dairy will (almost) necessarily also reduce your intake of other foods. Foods that are usually not so healthy.

If you feel that cannot handle dairy in general or certain dairy products (e.g. those that are high in lactose), don't force yourself to eat it. Chances are you would only see pro-inflammatory effects that will increase your risk of prediabetes, and, potentially, type I diabetes (Harrison 1999) | Comment!

References:

• Alexander, Dominik D., et al. "Dairy consumption and CVD: a systematic review and meta-analysis." British Journal of Nutrition 115.4 (2016): 737-750.
• Bjørnshave, Ann, and Kjeld Hermansen. "Effects of dairy protein and fat on the metabolic syndrome and type 2 diabetes." The review of diabetic studies: RDS 11.2 (2014): 153.
• Chen, Mu, et al. "Effects of dairy intake on body weight and fat: a meta-analysis of randomized controlled trials." The American journal of clinical nutrition 96.4 (2012): 735-747.
• de Goede, Janette, et al. "Dairy consumption and risk of stroke: a systematic review and updated dose–response meta‐analysis of prospective cohort studies." Journal of the American Heart Association 5.5 (2016): e002787.
• Faye, Tamburello, et al. "Survival of lactic acid bacteria from fermented milks in an in vitro digestion model exploiting sequential incubation in human gastric and duodenum juice." Journal of dairy science 95.2 (2012): 558-566.
• Freeman, Jeffrey S. "Role of the incretin pathway in the pathogenesis of type 2 diabetes mellitus." Cleveland Clinic journal of medicine 76 (2009): S12-9.
• Guo, Jing, et al. "Milk and dairy consumption and risk of cardiovascular diseases and all-cause mortality: dose–response meta-analysis of prospective cohort studies." (2017): 1-19.
• Harrison, Leonard C., and Margo C. Honeyman. "Cow's milk and type 1 diabetes: the real debate is about mucosal immune function." Diabetes 48.8 (1999): 1501-1507.
• Henriksen, Erik J. "Improvement of insulin sensitivity by antagonism of the renin-angiotensin system." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293.3 (2007): R974-R980.
• Hirahatake, Kristin M., et al. "Associations between dairy foods, diabetes, and metabolic health: potential mechanisms and future directions." Metabolism 63.5 (2014): 618-627.
• Hruby, Adela, et al. "Associations of Dairy Intake with Incident Prediabetes or Diabetes in Middle-Aged Adults Vary by Both Dairy Type and Glycemic Status." J.Nutr. First published August 2, 2017, doi: 10.3945/ jn.117.253401
• Khoramdad, Malihe, et al. "Dairy Products Consumption and Risk of Type 2 Diabetes: A Systematic Review and Meta-Analysis of Prospective Cohort Studies." diabetes 12 (2017): 13.
• McGregor, Robin A., and Sally D. Poppitt. "Milk protein for improved metabolic health: a review of the evidence." Nutrition & metabolism 10.1 (2013): 46.
• Office of Disease Prevention and Health Promotion, U.S. Department of Health and Human Services. 1990 Dietary guidelines [Internet]. 1990. [cited 12 Sep 2016]. Available from: https://health.gov/dietaryguidelines/1990.asp
• Office of Disease Prevention and Health Promotion, U.S. Department of Health and Human Services. Dietary guidelines for Americans 2015–2020 [Internet]. 8th ed. 2015. [cited 2016 Jan 7]. Available from: http:// health.gov/dietaryguidelines/2015/guidelines/.
• Pimpin, Laura, et al. "Is butter back? A systematic review and meta-analysis of butter consumption and risk of cardiovascular disease, diabetes, and total mortality." PLoS One 11.6 (2016): e0158118.
• Zivkovic, Angela M., and Daniela Barile. "Bovine milk as a source of functional oligosaccharides for improving human health." Advances in Nutrition: An International Review Journal 2.3 (2011): 284-289.

Low Carb Diets and Physical Performance - Recent Studies Show Performance Decrements in Average Joes + Athletes

If the above are the ingredients you are using when you prepare your meals, your diet is almost certainly not a low carbohy-drate high fat, but a low carbohydrate high protein diet. Please mind the difference and don't brag in the comments about how great you feel on your "keto diet"!

If you are an avid follower of the SuppVersity News on Facebook (revisit the post), you will remember Louise M. Burke's late 2016 paper which showed that a low carbohydrate, high fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkers" (Burke 2016).

Accordingly, Jørn Wulff Helge from the Center of Healthy Aging in Copenhagen, Denmark, wrote in his recent perspective article in The Journal of Physiology that "in elite athletes training and performing at intensities similar to elite sports competition, keto-adaptation is not the optimal dietary choice" (Helge 2017).

You know, high-protein diets are safer than people say, but there are things to remember...

Practical Protein Oxidation 101

5x More Than the FDA Allows!

More Protein ≠ More Satiety

Protein Oxidation = Health Threat

Protein Timing DOES Matter!

Keto for Superior Weight Loss?

Complementary results for less trained individuals has now been published by Urbain et al. (2017) in the peer-reviewed journal Nutrition & Metabolism - a paper in which the authors report an, albeit "mildly negative", impact of a 6-week non-energy-restricted ketogenic diet on physical performance (endurance capacity, peak power, and faster exhaustion)" (Urban 2017).

Can these observations be surprising? No, they can't. After all, even the most dedicated keto-proponents, like Stephen Phinney acknowledge that "[i]mpaired physical performance is a common but not obligate result of a low carbohydrate diet" (Phinney 2004) - whether and to which extent the effects that were observed in the previously cited studies could have been fixed, as Phinney suggests using his notorious references to "traditional Inuit culture" by "optimized sodium and potassium nutriture, and constraint of protein to 15–25 % of daily energy expenditure" will be discussed in the bottom line of this article. First, however, let's take a look at the methodology and results sections of the Burke and Urban papers.

Low carbohydrate + high-fat diet impairs walking performance and adaptation

Let's address one of the often heard criticisms of this study right away: the subjects didn't eat enough... true! During the three weeks of intensified training, the dietary intake was limited to 40kcal/kg and thus roughly 2400kcal/day, not increased to compensate adequately for the increased energy requirements due to high volume race walking, resistance training and cross-training (running, cycling or swimming | for details see Table 1).

Table 1: Overview of weekly training-diet intervention involving high carbohydrate (CHO) availability (HCHO), periodized CHO availability (PCHO) or low CHO high fat (LCHF) diets in elite race walkers (n = 29 | Burke 2016).

Accordingly, the subjects were in a slight but significant caloric deficit of ~400-450kcal of which Burke et al. expected that it would trigger a 1-1.5kg fat loss over the course of the 21-day study period.

Figure 1: Graphical overview of the study design (I added extra info on the diet | Burke 2016).

You can see all the details about the training and dieting regimens that included both, a high CHO, a cyclical / periodized CHO and the classic Volek / Phinney style ketogenic (Volek & Phinney 2012) diet in Figure 1 (please understand that the LAB, FIELD and LAB test were repeated before and after the training weeks which may be easily overlooked at the bottom of the illustration | see Table 1, too).

Figure 2: Pie charts of the relative contribution of fat, protein, and carbohydrates to the total nutrient intake of 40kcal/kg body weight (~2400kcal/d) the subjects received over the course of the 3-week study period (calc. based on Burke 2016).

To spare you reading all the small print in Figure 1, I also plotted the macronutrient ratios as pie charts in Figure 2. In that, I used the average energy intake as a basis to calculate the 8% CHO intake in the "keto" (LCHF) group as a maximal contribution of carbohydrates to their diet based on the upper intake limit of 50g of carbohydrates per day (the actual contribution of carbohydrates to the total energy intake may thus have been <8% of the total energy on many days). With so little carbs in the LCHF group, it is not surprising that

• the ketogenic low-carbohydrate, high fat (LCHF) diet markedly increases rates of whole-body fat oxidation during exercise in race walkers over a range of exercise intensities.

In view of this increase in peak aerobic capacity, it will be either surprising or re-affirming, depending on whether you're a keto-advocate or -skeptic, that the low carbohydrate and high-fat diet... 

• significantly reduced the subjects' running economy (increased oxygen demand for a given speed) at velocities, and thus 
• translated to real-life race performance decrements in the elite race walkers.

Worth mentioning and actually something to consider for those of you who want the best of both worlds is that the periodized high carbohydrate intervention did not trigger a similar performance impairment in the highly trained subjects of Burke's latest low-carb study.

Ketogenic diet without energy restriction impairs exercise performance in healthy adults

The latest contribution to the accumulating evidence that a high-fat, low carbohydrate diet may, irrespective of any weight loss or health benefits it may have or not have, be not the ideal choice for athletes and wanna-be athletes comes from the University of Freiburg in Germany, where Urbain et al. found the previously cited "mildly negative impact from this 6-week non-energy-restricted KD on physical performance (endurance capacity, peak power and faster exhaustion)" (Urbain 2017) in a group of n=42 normal-weight, healthy adults who got less than 10% (< 20–40 g/day) of their daily energy intake from carbohydrates, 75% from fat, and 15–20% from protein over the course of the 6-week study.

The subjects were free to choose the foods they were eating, the overall caloric diet was not restricted, and their adherence to the carbohydrate limit was tested by daily measurements of urinary ketones and keeping 7-day food records.

Figure 3: Changes (% relative pre vs. post change on top of the bars) in body composition, active thyroid hormone and resting energy expenditure from pre vs. post 6-week high-fat, low carbohydrate dieting in healthy subjects (Urbain 2017).

As you can see in Figure 3, the subjects lost a significant amount of lean and fat mass over the course of the intervention. That's surprising, since the subjects'...

• resting energy expenditure (REE) dropped by 6%, from 1523 kcal/day to 1430 kcal/day (free active thyroid hormone concentrations, i.e. fT3, which declined by 13%) while 
• mean daily caloric intake during the study did not change from the previous habitual diet (PRE 2321 ± 551 kcal/day, POST 2224 ± 584 kcal/day; P = 0.186). 

Whether or to which extent the weight loss was a side effect of ketosis is difficult to tell. What is certain, however, is that the subjects' adherence was, with 7.7% of the energy coming from carbohydrate and confirmed ketosis in 97% of the tests, excellent.

"But eating a ketogenic diet will make you lose weight and improve your health..." While that is something you can read abou everywhere on the internet. The contemporary evidence is everything but clear. Yes, in the obese and diabetic, there's evidence that a ketogenic diet will produce both weight loss and improvements in metabolic health. Whether or not it does this more successfully than other sane diets (i.e. not the one recommended by the American Diabetes Association), such as a Mediterranian or a high(er) protein moderate fat and carbohydrate diet, is yet questionable - even in obese and diabetic subjects.

Changes in markers of metabolic health in the Urbain study. As in comparable studies, lipids increased, glucose and the related trigs decreased - all within normal levels.

The studies at hand, which dealt with healthy and normal-weight subjects, don't support the often heard of clear superiority of ketogenic dieting, either. And that's for both: Body composition, where the Burke study didn't find inter-group differences in weight loss (and did not assess body composition) and the Urbain observed a weight loss that could be due to a reduced energy intake in the early weeks, when many subjects reported side effects, but did not lead to an improvement in body composition. As well as the subjects' metabolic, which wasn't even tested in Burke et al. and about which we cannot make a definitive statement based on the ambiguous results of the Urbain study, where the blood lipids worsened (LDL and total cholesterol went up, HDL stayed the same) the glucose and insulin levels decreased - both within healthy limits, though).

By no way excellent, however, were the results of the repeated exercise tests. While the subject obviously ate enough and also kept their habitual physical activity levels, the subjects' ...

• VO2peak, the study's primary endpoint, decreased significantly from 2.55 ± 0.68 l/min to 2.49 ± 0.69 l/min (P = 0.023) by 2.4%, 
• peak power Pmax decreased significantly from 241 ± 57 W to 231 ± 57 W by 4.1%, 
• rating of perceived exertion increased slightly from 17 (13–19) to 18 (14–19) (P = 0.052)

The participants' ventilatory threshold, their maximal heart rate and even the relative VO2peak (=VO2peak divided by body weight) were not affected by the KD intervention. Especially the latter observation is interesting. After all, it raises the question whether the statistically "large" effect size on the VO2 peak (d = 0.088) is practically relevant (and highlights the need to understand the underyling cause of the weight loss).

Figure 4: Relative pre- vs. post changes (%) in Spiroergometry, EKG and Borg scale (Urbain 2017).

In their own conclusion, the scientists point out that their results only partly conflict with previous studies. While both, Phinney et al. (1983) and Klement et al. (2013) found that the aerobic capacity was not compromised by a ketogenic diet and Zajac et al. (2014) even report a significant relative VO2peak improvement (probably a consequence of the sign. weight loss in the study), the more significant reduction in peak power Urbain et al. observed is in fact consistent with results others have reported (Zajac 2014, Klement 2013). Even in the previously cited studies by Zajac et al. (2014) and Klement et al. the peak performance dropped by 3.3% and 1.5% respectively.

Low(er) Carb Crossfitters May be Missing Out | 11.1% vs. 4% Rep Increase With 6-8g/kg CHO in 12-Min Rohoi Benchmark  - Expect the same for other sports that involve long(er) lasting anaerobic activities | more

Bottom line: If we take the results of both studies, as well as related previous studies into account, it becomes obvious that both training status and type of exercise matter when we talk about the potential negative effects on a subjects' exercise performance.

For endurance exercise in non-athletes, the previously discussed conflicting evidence suggests that the last word has not been spoken yet (the previously mentioned "opti-mized sodium and potassium nutriture" (Volek 2012) could make a difference here, as well). For endurance athletes, on the other hand, the increase in fatty oxidation does not appear to be able to compensate the lack of readily oxidizable glucose. Thus, "in elite athletes training and per-forming at intensities similar to elite sports competition, keto-adaptation is not the optimal choice" (Helge 2017).

The study's main research focuses doesn't allow for conclusive statements about athletes and gymrats whose sports are mostly anaerobic, but in view of the correspondingly higher glycolytic demands of these sports, it's hard to imagine that (again all health and body composition goals aside) a sprinter or cross-fitter would be better off on a low carbohydrate, high fat diet. Whether the often marginal performance decrements outweigh the individual benefits on your well-being and/or body composition is something each of you will have to decide on his/her own | Comment!

References:

• Burke, Louise M., et al. "Low Carbohydrate, High Fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkers." The Journal of Physiology (2016).
• Helge, Jørn Wulff. "A high carbohydrate diet remains the evidence-based choice for elite athletes to optimize performance." The Journal of Physiology (2017).
• Klement, Rainer Johannes, et al. "A pilot case study on the impact of a self-prescribed ketogenic diet on biochemical parameters and running performance in healthy and physically active individuals." Nutr Med 1.1 (2013): 1-27.
• Phinney, Stephen D., et al. "The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation." Metabolism 32.8 (1983): 769-776.
• Phinney, Stephen D. "Ketogenic diets and physical performance." Nutrition & Metabolism 1.1 (2004): 2.
• Volek, Jeff, and Stephen D. Phinney. The Art and Science of Low Carbohydrate Performance: A Revolutionary Program to Extend your Physical and Mental Performance Envelope. Beyond Obesity, 2012.
• Zajac, Adam, et al. "The effects of a ketogenic diet on exercise metabolism and physical performance in off-road cyclists." Nutrients 6.7 (2014): 2493-2508.

Eating 75-100g Fat (M-/PUFA) in the AM Improves Glucose (7-8%), Insulin (40-60%), Trigs (4-16%), GSH & MDA (40-75%)

If we assume that the protein fried eggs with its comparatively low insulinogenicity is not a problem (unlike your whey, for example), avocado and eggs fried in olive oil is the perfect breakfast to replace the liquid test meal used in the study.

There's no debating that increased amounts of free fatty acids in the blood will impair your insulin sensitivity, as they should be there only, when your supply of carbohydrate is running out, AMPK and with it the expression of lypolytic enzymes increase and the triglycerides from your fat stores are broken down into free fatty acids and released into your bloodstream where they can be used by liver, muscle and other organs as an alternative energy source.

Now, the word "alternative" is of paramount importance, here, because you'll find yourself being in (diabetic) trouble if those FFAs pile up on top of high glucose levels. This is what happens with the SAD diet and its high carbohydrate and fat content (and energy!) content.

You can learn more about fat at the SuppVersity

Are Men Fat- & Women Sugar-Cravers?

Fat, not Fructose Cons. Increased in the US

Adding Fats to Carbs Does not Reduce Insulin

The Forgotten Pro-Insulinogenic Effects of SFAs

Margarine Not Butter Incr. EU Waists

Low Fat to Blame for Low Vitamin D Epidemic?

It's a vicious circle: When the levels FFAs are up, insulin sensitivity goes down (after all, with a normal diet you'd have to burn the fat and spare the precious glucose | Bodne. 1997; Koves. 2008). Since there's more and more glucose spilling in over the portal-vein, though, insulin will keep increasing to a point where it does no longer simply impair, but almost block the oxidation of free fatty acids. Now, without insulin working its glucose shuttling magic, however, the cells begin to starve for glucose and... right, more FFAs are being released, the insulin resistance increases, still hardly more glucose is being shuttled into the cells to restore AMP to ATP and the process continues.

What does all of that have to do with eating more MUFAs and PUFAs to control your glycemia? Well, nothing and everything. First- and most importantly, it should remind you that this is not about eating fat with your carbohydrates. That's exactly not what the latest study from the Hospital Clínico Universitario Valencia in Spain would suggest, even though I bet you will have some idiot already have misinterpret the study in this way "for your" online. Rather than that the study was, as the abstract already tells you, conducted to ...

"[...] evaluate the changes in glycemia, insulinemia, and oxidative stress markers during an oral fat load test in nondiabetic subjects with abdominal obesity and to analyze the association between postprandial oxidative stress markers and postprandial glucose and insulin responses" (Martinez-Hervaz. 2016)

This quote also contains another important information you will have people with an agenda forget to mention: the subjects in whom the fats worked their magic were abdominally obese! Later on we will see why this is relevant and why the same rules won't apply to lean individuals, but for the time being let's firstly take a look at the exact characteristics of the N = 40 (total) subjects in the study in Table 1.

Table 1. General characteristics, fasting lipids and lipoproteins, glucose, insulin and HOMA index values in the studied groups (Martinez-Hervas. 2016); ^a control vs abdominal obesity group (p<0.01).

Even though the discriminating feature, i.e. the characteristic the scientists used to find subjects for the two groups was their waist circumference (>102/88 cm for men and women, respectively vs. <102/88 in the control group), it shouldn't surprise you that the scientists have also observed sign. differences in other anthropometric and metabolic markers such as the BMI, the level of triglycerides, blood lipids and postprandial glucose levels after an oral glucose tolerance test (OGTT | see Table 1).

Is it a problem that the male / female ratio differed? That is difficult to tell. We do know that men and women handle nutrients, esp. fat and carbs slightly differently, but I doubt that the difference between an 11/9 ratio in the control group and a 7/13 ratio in the abdominal obesity group will ruin the results of the study at hand. Nevertheless, this should be addressed in future studies.

After initial testing, the subjects from both groups ingested the same commercial liquid preparation of high-fat meal of long chain triglycerides. The product is called SuperCal and must not be confused with a vitamin D + calcium product with the same name that is being sold on the US market. From a previous European study, I've got some extra-information about its composition, namely that

"[...] 125 ml contains 60 g fat, of which 12 g are saturated, 35.35 g are monounsaturated, and 12.75 g are polyunsaturated. Each 100 ml contains <1 g lauric acid, <1 g myristic acid, 4.8 g palmitic acid, 1.4 g stearic acid, 27.7 g oleic acid, 9.6 g linoleic acid, 1.4 g behenic acid, and 0.5 g lignoceric acid" (Fernández‐Real). 

The detailed fatty acid composition of the SFAs, MUFAs and PUFAs emulsion that was administered at a dosage of 50 g fat per m² of body surface (calculate your body surface if you want to know your individual equivalent dose = result of your calculation in m² x 50g g/m²; e.g. 1.78 m² x 50 g/m² = 89 g of fat) at 8:30 after an overnight fast is not mentioned in the Martinez-Hervas study. What the authors of the study at hand tell us, however is that the likewise relevant ratio ω6/ω3 is > 20/1 - similar to the average diet, by the way; a fact that excludes that this is an omega-3 effect we are seeing, here. Similarly, exercise or previous meals, shouldn't have messed with the results, either. After all, in both groups, only water was permitted during the "eating" or rather "drinking" process, and no physical exercise was undertaken before or during the "fasted" fat loading test in the AM.

Figure 1: Overview of the rel. levels of glucose, insulin, HOMA-index, trigs, the GSSG/GSH ratio and MDA, a byproducs of lipid oxidation (Martinez-Heras. 2016); levels expressed relative to control at baseline (T = 0), see explanation below

In order to make the data more accessible (compared to the tabular overview of absolute values in thee FT) for you, I've standardized each of the measurable variables to match 100%. This means that all the fasting bars at T = 0h will be at the 100% mark, because they are what the effects of fat loading are compared to. Let's take a look at two examples:

• 

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

  Insulin: In contrast to what you will see if you co-administer fat and carbohydrates (learn more), the administration of the high MUFA + PUFA fat supplement in the absence of carbohydrates lead to a sign. reduction of the initially 3.8-fold increased insulin levels. Not to normal levels, but at least to 158% (i.e. 1.6-fold elevated) of the fasted value of the lean subjects. Ah, but remember: All that happened with the fat load, alone, and in the absence of CHOs. In the presence of carbs the results would have been much different.
• GSSG/GSH ratio: The effects on the ratio of 'used' glutathione (GSSG) to the amount of the 'fresh' master anti-oxidant (GSH) were quasi the opposite of what the scientists observed for insulin. Here, the abdominally obese group had 2.4x elevated levels to begin with. This tells you that, compared to the normal controls, their anti-oxidant status was a mess. After only 8h, however, their GSSG/GSH ratio had not just declined, it was actually lower than the fasted value of the control group.
  
  And again, likewise similar to the effects on insulin, the control group saw benefits as well, with a 64% decrease in the GSSG/GSH ratio their antioxidant defenses did also benefit from the MUFA + PUFA load in the AM.

For other parameters you will see similar, for many of you probably surprising benefits. Things to keep in mind, though, is that we are talking non diabetic subjects in both groups, even if the abdominally obese subjects had fasting HOMA index values fourth fold higher than controls, higher fasting triglyceridemia and higher fasting oxidative stress markers. If that sounds like you, then the acute ingestion of ~75-120g (depending on your body surface) of fat on empty in the AM, when hyperlipidemia is not that much of an issue, you can benefit from a high MUFA + PUFA fat load as you would find it in an avocado + egg fried in olive oil, for example... or, as the authors of the study at hand have it:

"[O]ur study has demonstrated a significant reduction of postprandial glycemia, insulinemia, c-peptide and oxidative stress markers using an acute oral overload of unsaturated fat. We have found a significant correlation between oxidative stress markers and postprandial lipemia. There is an increase of TG achieving the maximum peak four hours after the beginning of the test. However, although postprandial lipemia has been implicated in the development of insulin resistance and oxidative stress, and despite the increase of TG, there are significant reductions of the HOMA index and oxidative stress markers" (Martinez-Hervas).

Even though you may think otherwise, the authors are also right, when they point out that "[t]he influence of dietary macronutrients in insulin sensitivity is not well known" (ibid.) This is especially true, when we begin mixing proteins, carbohydrates and fats and start to take into consideration that we can have a dozen of types of the three in a single meal.

What about me? I am not abdominally obese, will I benefit, too? If we assume that you deprive yourself of any carbohydrates (and proteins?), you should see the same benefits as the subjects in the control group - those are lower than what we see in the big belly group and may simply be a result of the moderate energy intake (that's < 900kcal before an 8h fast even for many bigger guys), it would appear as if the answer to your rightly asked question would be "Yes, you can benefit, as well." Whether this will also require you to abstain from all, not just insulinogenic dairy proteins, however, will have to be tested in future studies.

It may thus depend on the food-matrix whether the results of previous studies, most of which clearly indicate that saturated fat will increase in fasting and postprandial insulin resistance would have yielded different results if the meals were administered in the absence of carbohydrates, for example - even though, additional evidence traced these effects back to increased levels of saturated fat in the cells' phospholipids that can alter their phyco-chemical properties and decrease the glucose transporters (while MUFA and PUFA have been shown to do the opposite | Borkman. 1993). Martinez et al. who have not actually tested the effect of SFAs in their studies provide additional evidence in their discussion:

Will the additional butter on top of the potatoes reduce the insulin response? You can find the answer to this and the other questions in today's episode of "True or False?" | Learn the answer

"Iggman et al demonstrated in elderly men that palmitic acid, the major saturated fatty acid found in adipose tissue, inversely correlates to insulin sensitivity measured by euglucemic-hyperinsulinemic clamp. However, they also found a positive relation of insulin sensitivity with the content of linoleic acid in adipose tissue (Iggman. 2010). It is in accordance with our results because our commercial liquid preparation of high-fat meal of long chain triglycerides is composed in the majority by linoleic acid (59%). Furthermore, in line with our findings, the replacements of dietary saturated fat by unsaturated fat also improved fasting insulin sensitivity (Vessby. 2001).

Several other studies have demonstrated that unsaturated fat improves fasting and postprandial IR, although the mechanism is largely unknown (Wang. 2015). Moreover the PREDIMED study has recently demonstrated that unsaturated fat can improve fasting insulin sensitivity and prevent the incidence of type 2 diabetes (Salas-Salvadó. 2011).

Another thing the study could not address is the chicken or egg question: After all, you can argue athat the significant reduction in oxidative stress markers the scientists throughout the fat load test could - as a result - have improved the subjects insulin sensitivity, but - at least in theory - it is imaginable that this worked the other way around... by an unknown feedback loop.

Figure 2: Relative in-group reduction in the parameters from Figure 1 from 0h to 8h (Martinez-Hervas); in contrast to the previous figure the one at hand shows the in-group difference, i.e. the change in control at 0 vs 8h, etc.

As you see, there's still lots to be learned about dietary fat out there - including the fact that a "high fat" diet that combines high energy with high fat and high carbohydrate intakes is always detrimental for your health and should no longer be used in studies, unless the goal is to mimic the Western diet (and I beg scientists to then call it what it is, and that's not a "HFD").

Beware of dairy proteins, especially whey, but also casein are highly insolinogenic and may reduce if not reverse the effects of fat loading in the AM on glucose management and inflammation | learn more.

Bottom line: Before you get addicted to the previously suggested avocado + eggs fried in olive oil breakfast, please keep in mind that this is not what the scientists tested. Especially in view of the relatively high protein level in eggs, another study would have to make sure that the latter won't interfere with the benefits... even if that's much less likely for eggs, meat or fish than for the highly insulinogenic dairy proteins.

Furthermore, the study at hand cannot tell us anything about the long-term effects, because it is an acute intervention (not even lasting for 24h, there could have been a rebound at 12h or 24h or with the ingestion of another meal at noon, etc.) that suffers from another methodological problem.

Without a control supplement containing high(er) amounts of saturated fat, the assumption that the results were MUFA + PUFA specific is simply based on the scientists' review of the existing research (see previous elaborations + quotes). And as the scientists add, last- and [f]inally, oxidative stress markers analyzed could be also altered by others players regulating the postprandial state" (Martinez-Hervas. 2016) | Leave a comment, praise or criticism on Facebook!

References:

• Boden, Guenther. "Role of fatty acids in the pathogenesis of insulin resistance and NIDDM." Diabetes 46.1 (1997): 3-10.
• Borkman, Mark, et al. "The relation between insulin sensitivity and the fatty-acid composition of skeletal-muscle phospholipids." New England Journal of Medicine 328.4 (1993): 238-244.
• Fernández‐Real, José M., et al. "Fat overload induces changes in circulating lactoferrin that are associated with postprandial lipemia and oxidative stress in severely obese subjects." Obesity 18.3 (2010): 482-488.
• Iggman, David, et al. "Adipose tissue fatty acids and insulin sensitivity in elderly men." Diabetologia 53.5 (2010): 850-857.
• Koves, Timothy R., et al. "Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance." Cell metabolism 7.1 (2008): 45-56.
• Martinez-Hervas, Sergio, et al. "Unsaturated Oral Fat Load Test Improves Glycemia, Insulinemia and Oxidative Stress Status in Nondiabetic Subjects with Abdominal Obesity." PloS one 11.8 (2016): e0161400.
• Vessby, Bengt, et al. "Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU Study." Diabetologia 44.3 (2001): 312-319.

Baking Bread With ~100g Extra-Fat Reduces the Glycemic Response: Coconut Oil Beats Butter, Grapeseed & Olive Oil

No, adding fat to your bread's dough won't make you lose fat magically.

While fat no longer has the bad rep it still had a decade ago, the notion that baking bread with extra fat could have anti-diabetic effects, because it reduces the glucose peaks and the 2h area under the curve (AUC) is unconventional, to say the least; and thus SuppVersity news-worthy, because it is not broscience, but the result of a recent study.

In said study, the scientists tested (a) the effect of different types of fat / oil on the formation of amylose–lipid complexes (ALC) and, more importantly, (b) the effect of the ALCs on the glycemic response to a standardized amount of bread that was baked with the same amount of different fats / oils.

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The study was an acute, randomised, controlled, single-blinded trial that consisted of five types of bread, each tested on one occasion in a randomised order on separate days, with at least 3 washout days between test visits.

"Participants were recruited through advertisements and personal communications. Inclusion criteria were as follows: (1) males aged between 21 and 50 years, (2) BMI values between 18·0 and 24·9 kg/m2, (3) blood pressure≤120/80 mg/dl and (4) fasting blood glucose≤6·0 mmol/l. People who had metabolic diseases, were on prescribed medication, were smokers, took part in sports at competitive levels or were concurrently participating in other clinical trials were excluded from the study. Females were excluded from the study to prevent differences in menstrual cycles from affecting carbohydrate metabolism" (Lau. 2016).

On the day before a test session, no drinks, caffeine or physical activity were allowed. In addition, a standardised dinner was provided the evening before to reduce potential variations in GR that may arise because of the second meal effect. On the day after, participants had to report to the centre after a 10–12 h fast between 08.00 and 09.00 hours. There, they rested for at least 15 min before starting the test session, before the test meal was consumed "at a comfortable pace within 15 min" (Lau. 2016). Following consumption of test bread, participants were asked to rate their liking of the bread on a 100-mm liking scale. Blood samples (both venous and capillary) were collected at 15, 30, 45, 60, 90, 120, 150 and 180 min after test bread consumption. The same protocol was repeated until the completion of all the five test sessions.

Serving size, energy content and macronutrient composition of the test breads (per serving | Lau. 2016)

How was the bread prepared? This is what the scientists report: "The five types of bread used were as follows: control bread without any added fats (CTR) and breads baked with butter (BTR), coconut oil (COC), grapeseed oil (GRP) or olive oil (OLV). The ingredients used for test breads were as follows: 250 g bread flour (Prima), 125 g potable water, 10 g baker’s yeast (SAF), 40 g sugar (Fairprice) and 6 g salt (Fairprice). These ingredients were mixed at speed 1 for 8 min (Kitchenaid) to form base dough, of which 320 g was weighed and then fat/oil was added.

The fats/oils added were 96 g butter that contained predominantly SFA (Anchor), 87 g coconut oil that was rich in medium-chain TAG (Titi Ecofarm), 80 g grapeseed oil containing predominantly PUFA (Borges) and 76 g olive oil containing predominantly MUFA (Naturel). The amount of fats/oils added was calculated based on the percentage fat as stated on the nutritional panel on the packaging, and was added at 20 %, w/w of dough. Oil was not added into the control bread. The dough mixture was kneaded for a further 12 min, and was then allowed to rest at room temperature for 10 min. Following this, the dough was moulded into serving portions and proofed in the oven (EOB98000; Electrolux) at 40±1°C for 30 min in a fan-assisted mode. Baking was carried out in the same oven at 200°C for 18 min, and bread was allowed to stand for 10 min before being served warm" (Lau. 2016).

The results of the scientists' analysis of the ALC formation in the bread showed that the coconut (COC) and olive oil (OLV) had significantly higher amylose–lipid complex forming ability [reported wrong in the result section of the FT, but correct in the discussion] as compared with butter (BTR) and grapeseed oil (GRP | P<0·05).

Figure 1: Complexing index results for different types of bread. Values are means (n 6), with standard errors represented by vertical bars. a,b Mean values with unlike letters were significantly different (P < 0·05; one-way ANOVA with post hoc Tukey’s test). BTR = butter; COC = coconut oil; GRP = grapeseed oil; OLV = olive oil (Lau. 2016).

Interestingly, the increased ALC levels in the olive oil bread did not produce the same beneficial effects on the glucose response the scientists observed when the subjects consumed the bread that was baked with coconut oil.

Figure 2: (a) Postprandial response curves for change in blood glucose and (b) plasma insulin levels after consumption of 50 g available carbohydrate portion of test bread. Values are means (n 15), with standard errors represented by vertical bars. For glucose response, there were significant time (P < 0·001), bread (P < 0·001) and bread×time interaction effects (P=0·002) when analysed by two-way, repeated-measures ANOVA. For insulin response, two-way, repeated-measures ANOVA showed a significant time effect (P < 0·001) and bread×time interaction effect at near significant levels (P=0·074), but no effect of bread was seen (P=0·195). open circle, Control bread without oil; filled circle, bread with butter; open triangle, bread with coconut oil; filled triangle, bread with grapeseed oil; open square, bread with olive oil (Lau. 2016).

As you can see in Figure 2, all fat-enhanced breads improved the glycemia, but only the grapeseed (closed triangle) and coconut (open triangle) oils also rduced the insulin levels.

Can't I just add the coconut oil on top of the bread? No, you can't, because it has to be in the dough during baking - otherwise the amylose–lipid complexes won't form. What will happen though is that your insulin levels will rise sign. longer (see previous SV article). Edit: Elizabeth Alcott just posted this cool suggestion on Facebook: "Bake low carb coconut flour bread with coconut oil. Reduced calories and glycemic response at the same time." Not a bad idea, for sure.

What is interesting to see, though, is that the glucose AUC, i.e. the total amount of glucose that is released into the blood was still the lowest in those oils / fats with the highest ALC levels: coconut oil and olive oil.

Figure 3: Postprandial glycaemic and insulinaemic responses (AUCs for 180min) after consumption of test bread (Mean values with their standard errors for fifteen healthy young men | Lau. 2016)

As the authors point out in the discussion of the results of their study, their regression analysis "further confirmed that CI [=indicator of ALC formation] was a significant predictor of GR [glucose response], although it only accounted for 13·3 % of the observed variability" (Lau. 2016). Furthermore, the scientists highlight that ...

"[w]hen examined as IAUC, COC showed the greatest attenuation of GR [glucose response] in baked bread. A similar study by Clegg et al. (2012) showed that high-fat pancakes containing MCT had the slowest gastric emptying rate as compared with other fats/oils over a 4-h period. The low GR [glucose response] of COC in this study could be due to a combination of factors. These include delay in gastric emptying rates to MCT having a higher osmolarity (Clegg. 2012) and formation of ALC resulting in resistant starch (Kaur. 2000)" (Lau. 2016).

To assess the physiological significance of these observations, Lau et al. also investigated the surrogate measures of postprandial β-cell function (IGI30 and IGR) and the insulin response which did - in contrast to the glucose response (see Figure 3), not correlate with the ALC content of the breads. Instead, it appeared to be "partially due to rate of appearance of glucose as a result of carbohydrate digestibility" (Lau. 2016).

Will the additional butter on top of the potatoes reduce the insulin response? You can find the answer to this and the other questions in today's episode of "True or False?" | learn more!

So, what's the verdict? Well, adding ~25g of fat to bread increases its energy content significantly. Therefore, it is not clear how advantageous the improvements in glycaemia observed in the study at hand will actually be - after all, calories still count!

With that being said, the scientists' conclusion that "[t]he incorporation of fats during bread baking reduces GR, with the greatest attenuation seen in COC," is a significant result. One that can be partly explained by the reduction in carbohydrate digestibility via ALC formation, but not by any effects on the insulin response to the meal (if you fear insulin, adding fat is thus not going to cut it | learn more).

That the 'coconut advantage' is due to lauric acid and myristic acid in coconut oil is likely, but warrants further investigation; the same goes for the scientists' concluding remark that "[t]he use of simple dietary interventions (addition of functional lipids during cooking of carbohydrate-rich staple foods) may be an effective and practical strategy for improving glycaemic control, and may help in the prevention and management of [...T2DM] and CVD" (Lau. 2016) | Comment!.

References:

• Clegg, Miriam E., et al. "Addition of different fats to a carbohydrate food: Impact on gastric emptying, glycaemic and satiety responses and comparison with in vitro digestion." Food Research International 48.1 (2012): 91-97.
• Kaur, Kulwinder, and Narpinder Singh. "Amylose-lipid complex formation during cooking of rice flour." Food Chemistry 71.4 (2000): 511-517.
• Lau, et al. "Effect of fat type in baked bread on amylose–lipid complex formation and glycaemic response." British Journal of Nutrition, Published online: 22 April 2016.