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Yogurt does not have to be served this way to be healthy, but I bet many of your friends and relatives would be amazed and much more likely to pass on the cream cake or tiramisu if the option was an appetizing dessert like that.

In a world where being vegan is "the new sexy" and eating animal products "the new smoking", dairy has lost much of its former appeal. I mean, we all remember how the literal "glass of milk" has been marketed as a daily health booster, right? Well, times have changed and that despite the fact that an impartial review of the evidence suggests more benefits than downsides to dairy consumption. Specifically fermented dairy, first and foremost yogurt, but also cheese can, and in the case of yogurt maybe even should be part of your of your diet. And that's not just because both are an often forgotten, but essential part hailed "Mediterranean diet" (Vasilopoulou. 2013). The same diet of which recent studies say that it's associated w/ a -30% reduced CVD risk (Estruch. 2013).
How's that? Well, cheese may be full of saturated fat and cholesterol. In controlled trials, however, even high fat cheese has - in contrast to butter, for example (Hjerpsted. 2011) - no or even beneficial effects on the total and LDL cholesterol levels of otherwise healthy individuals. In addition, real dairy cheese has been found to have neutral effects on body weight when it is consumed as part of an otherwise healthy diet. Some traditional types of cheese even share the anti-hypertensive effects of yogurt, which is still the real star among the fermented dairy products. A star that has been shown to prevent weight gain, reduce cholesterol and more meaningful makers of heart disease risk, to improve glycemia, and to prevent the development and/or progression of type II diabetes in both experimental and observational studies (Tholstrup. 2006; Nestel. 2008; Mozaffarian. 2011, Tapsell. 2015).

Figure 1: A study comparing the effects of getting 13% of one's total daily fat intake from cheese vs. butter on the blood lipids in healthy men and women shows increases in TC and LDL only with butter (Hjerpsted. 2013). In contrast to the total and LDL cholesterol levels, the total / HDL cholesterol ratio wasn't affected sign. by butter though. You can thus expect both forms of high fat dairy having negligible cholesterol mediated effects on the heart health of healthy indiv.

In short, the existing scientific evidence leaves little doubt that yogurt is, maybe next to whey (learn why), the star among the dairy based health foods. Part of its beneficial effects are probably mediated by its ability to improve integrity of our digestive tracts and thus to prevent the influx of pro-inflammatory, obesogenic, and pro-atherogenic endotoxins into the bloodstream. With it being available for almost 10,000 years, yogurt is thus the first and oldest "functional food" to act on the recently discovered link between "leaky gut", obesity and cardiovascular disease (Lam. 2011).

Figure 2: Proposed mechanisms by which yogurt consumption exerts beneficial health effects (Marette. 2015)

Some scientists like Marette & Picard-Deland even go so far as to argue that an early introduction of yoghurt into the diets of children is vital to establish a microbial community that supports long-term health. And while Taspell et al. are right to highlight that "[m]ore research is needed" (Tapsell. 2015). There's little doubt that "yogurt can deliver essential nutrients with high bioavailability and relatively low energy density" (ibid).
The fact pertinent trials still show ambiguous results, when it comes to the effects of yogurt on body weight and composition (Chen. 2012) is mostly a results of the study designs which usually require subjects to simply increase their intake of dairy products, in general, or yogurt, in particular. As Taspell (2015) points out in a recent review this is a problem "if the energy content of the diet is not managed, particularly with high-fat varieties and with added ingredients such as sugar" (ibid). If it is managed, as in habitual consumers, though, high(er) yogurt intakes have been shown to be associated...

• Prevalent Nutrient Deficiencies in the US: More Than 40% are Vitamin A, C, D & E, Calcium or Magnesium Deficient and >90% Don't Get Enough Choline, Fiber & Potassium | read more

  with higher scores for the Dietary Guidelines Adherence Index (DGAI) and higher intakes of key micronutrients, as well as significantly higher potassium and fiber intakes - two nutrients the average Westerner usually doesn't get enough of (Wang. 2013)
• with reduced weight gain in a large US cohort study that tracked the food intake and weight development of 22 557 men and 98 320 women for four years; with R = -0.89 the correlation is similar to the one for the recommended amount of physical activity vs. being sedentary and thus nothing you should ignore as being practically irrelevant
• with reduced inflammation as measured by C-reactive protein, IL-6 and TNF-a in the ATTICA study that involved 3042 healthy Greek adults for whom only 8 servings of dairy products, in general (full fat and low fat!), were linked with already significant reductions in inflammation; since a greater proportion of the cohort reported consumption of fermented dairy foods such as feta cheese (93%), hard yellow cheese (92%) and low-fat yogurt (50%) compared to low-fat milk (46%), we can yet safely assume that many of these anti-inflammatory benefits were actually due to fermented dairy products
• with reduced type II diabetes risk (-12% or both yogurt and cheese) in the European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct Study (Sluijs. 2012);
  

  Table 1: HRs for risk of type 2 diabetes associated with the substitution of yoghurt (137 ga) for snacks and desserts: EPIC-Norfolk study (n=4,127 | O'Connor. 2014)

  with 28% reduced diabetes risk the results of the EPIC-Norfolk cohort study in the UK were even more impressive (O’Connor. 2014); as you can see in Table 1 the results of this study do yet also underline that the benefits will occur only if yogurt replaces other, less healthier ingredients of ones diet.

References:

• Asemi, Zatollah, et al. "Effects of daily consumption of probiotic yoghurt on inflammatory factors in pregnant women: a randomized controlled trial." Pakistan journal of biological sciences: PJBS 14.8 (2011): 476-482.
• 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 LeBlanc, Alejandra de Moreno, and Gabriela Perdigón. "Yogurt feeding inhibits promotion and progression of experimental colorectal cancer." American Journal of Case Reports 10.4 (2004): BR96-BR104.
• Douglas, Steve M., et al. "Low, moderate, or high protein yogurt snacks on appetite control and subsequent eating in healthy women." Appetite 60 (2013): 117-122.
• Elwood, Peter C., et al. "The consumption of milk and dairy foods and the incidence of vascular disease and diabetes: an overview of the evidence." Lipids 45.10 (2010): 925-939.
• Estruch, Ramón, et al. "Primary prevention of cardiovascular disease with a Mediterranean diet." New England Journal of Medicine 368.14 (2013): 1279-1290.
• Fisberg, Mauro, and Rachel Machado. "History of yogurt and current patterns of consumption." Nutrition reviews 73.suppl 1 (2015): 4-7.
• Hjerpsted, Julie, Eva Leedo, and Tine Tholstrup. "Cheese intake in large amounts lowers LDL-cholesterol concentrations compared with butter intake of equal fat content." The American journal of clinical nutrition 94.6 (2011): 1479-1484.
• Lam, Yan Y., et al. "Role of the gut in visceral fat inflammation and metabolic disorders." Obesity 19.11 (2011): 2113-2120.
• Lithell, H., and B. Zethelius. "Glucose Tolerance and Cardiovascular Mortality." Arch. Intern. Med. 161 (2001): 397.
• Marette, André, and Eliane Picard-Deland. "Yogurt consumption and impact on health: focus on children and cardiometabolic risk." The American journal of clinical nutrition 99.5 (2014): 1243S-1247S.
• Moreno, Aznar LA, et al. "[Scientific evidence about the role of yogurt and other fermented milks in the healthy diet for the Spanish population]." Nutricion hospitalaria 28.6 (2012): 2039-2089.
• Mozaffarian, Dariush, et al. "Changes in diet and lifestyle and long-term weight gain in women and men." New England Journal of Medicine 364.25 (2011): 2392-2404.
• Nestel, Paul J. "Effects of dairy fats within different foods on plasma lipids." Journal of the American College of Nutrition 27.6 (2008): 735S-740S.
• Nestel, Paul J., et al. "Effects of low-fat or full-fat fermented and non-fermented dairy foods on selected cardiovascular biomarkers in overweight adults." British Journal of Nutrition 110.12 (2013): 2242-2249.
• Neyestani, Tirang R., et al. "Improvement of vitamin D status via daily intake of fortified yogurt drink either with or without extra calcium ameliorates systemic inflammatory biomarkers, including adipokines, in the subjects with type 2 diabetes." The Journal of Clinical Endocrinology & Metabolism 97.6 (2012): 2005-2011.
• Nikooyeh, Bahareh, et al. "Daily consumption of vitamin D–or vitamin D+ calcium–fortified yogurt drink improved glycemic control in patients with type 2 diabetes: a randomized clinical trial." The American journal of clinical nutrition 93.4 (2011): 764-771.
• O’Connor, Laura M., et al. "Dietary dairy product intake and incident type 2 diabetes: a prospective study using dietary data from a 7-day food diary." Diabetologia 57.5 (2014): 909-917.
• Ortinau, Laura C., et al. "The effects of increased dietary protein yogurt snack in the afternoon on appetite control and eating initiation in healthy women." Nutr J 12.71 (2013): 10-1186.
• Panagiotakos, Demosthenes B., et al. "Dairy products consumption is associated with decreased levels of inflammatory markers related to cardiovascular disease in apparently healthy adults: the ATTICA study." Journal of the American College of Nutrition 29.4 (2010): 357-364.
• Sluijs, Ivonne, et al. "The amount and type of dairy product intake and incident type 2 diabetes: results from the EPIC-InterAct Study." The American journal of clinical nutrition 96.2 (2012): 382-390.
• Struijk, E. A., et al. "Dairy product intake in relation to glucose regulation indices and risk of type 2 diabetes." Nutrition, Metabolism and Cardiovascular Diseases 23.9 (2013): 822-828.
• Tapsell, Linda C. "Fermented dairy food and CVD risk." British Journal of Nutrition 113.S2 (2015): S131-S135. 
• Tholstrup, Tine. "Dairy products and cardiovascular disease." Current opinion in lipidology 17.1 (2006): 1-10.
• Vasilopoulou, Effie, Vardis Dilis, and Antonia Trichopoulou. "Nutrition claims: a potentially important tool for the endorsement of Greek Mediterranean traditional foods." Mediterranean Journal of Nutrition and Metabolism 6.2 (2013): 105-111.
• Wang, Huifen, et al. "Yogurt consumption is associated with better diet quality and metabolic profile in American men and women." Nutrition Research 33.1 (2013): 18-26.
• Zemel, Michael B., et al. "Calcium and dairy acceleration of weight and fat loss during energy restriction in obese adults." Obesity research 12.4 (2004): 582-590.

This is what it's all about. Real food does not come in form of "macros". It comes in form of complex food matrices that determine its effect on one's health - including one's glycemic health.

You will probably remember that I have touched on a specific aspect of the effects of and interactions between different macronutrients in what scientists often refer to as "food matrices" on the glycemic response to standardized glucose loads in previous articles like the famous "True or False?" article that dealt with the question: "Will Adding Fat to A Carby Meal Lower the Insulin Response?" (read it).

You don't remember this or any of the other articles? Well, in that case, I probably have to tell you again that the mere fact that the postprandial glucose are lower does not mean that a certain food or combination of certain macronutrients would increase your insulin sensitivity (adding fat to a high carbohydrate meal certainly doesn't do that, believe me).
While this is possible for certain supplements like berberine and other AMPK activators, it is mandatory that we differentiate the following three cases:

1. Reduced postprandial blood glucose levels in response to an increase in insulin sensitivity as it is triggered by exercise or AMPK activators,
2. Reduced postprandial blood glucose levels in response to increased insulin levels as they occur with the co-ingestion with whey protein and
3. Reduced postprandial blood glucose levels in response to increased insulin levels and a decreased rate of absorption of glucose as it is the case if you add fat to carbohydrates.

That was too fast? Too complicated? Or both? Never mind. The discussion of two recent articles from the Lund University and the Yong Loo Lin School of Medicine (see blue box) will hopefully help you understand the difference - I promise ;-)

Let's take a look at study design, results and implications

In their study, Wathik Alsalim and his colleagues from the Lund University in Sweden and the Consiglio Nazionale delle Ricerche in Italy investigated the integrative impact of macronutrients on postprandial glycemia, β-cell function, glucagon and incretin hormones in man. The subjects were male and female Caucasian subjects, aged 30-70 years and BMI 20-35 kg/m², without diabetes (normal fasting glucose and normal HbA1c) or with T2D without any pharmacological glucose-lowering therapy and HbA1c <60 mmol/mol (<7.8%).

"Exclusion criteria were liver disease, diabetic nephropathy, proliferative diabetic retinopathy, pregnancy or breast feeding, treatment with oral antidiabetic or insulin, previous myocardial infarction, coronary heart disease or angina pectoris, previous surgery on the gastrointestinal tract, larger surgical intervention the last 12 weeks or treatment with oral steroids or thiazide diuretics" (Alsalim. 2015).

Participants were studied at the Lund University's Clinical Research Center on four occasions in a randomized cross-over design, separated by at least four and maximally eight weeks. After overnight-fast (no food after 10pm), subjects were provided with antecubital vein catheter. After two baseline samples at 5, and 2 mins, they ingested in randomized order either one of the macronutrients alone

• glucose - 330kcal = 83g; Skåne University Hospital Pharmacy, Lund, Sweden,
• protein mixture - 110kcal = 30g; ISO WHEY protein consisting of milk and egg protein
• fat emulsion - 110kcal = 24ml; 50% long-chain triglycerides and 50% water;

The response to the individual macros was then compared to the ingestion of a 550kcal meal containing 330kcal (60%) from glucose, 110kcal (20%) from protein and 110kcal (20%) fat - a proportion of which the scientists say that it "was selected to represent a common meal with 60% carbohydrate, 20% protein and 20% fat" (Alsalim. 2015).

Figure 1: To allow for maximal control, the "meal" (macro composition on the right) was a shake (Alsalim. 2015).

Water was ingested at the same time of each load to standardize the ingested volume to 400ml; all ingestions were consumed within 5 min. Blood samples were taken throughout a 300min period after each challenge test.
Now, guess what? Yes, yes, and no ... the glucose meal was not the most insulinogenic one. Accordingly, we have to be careful not to mistake the scientists' conclusion that "[a]dding protein and fat macronutrients to glucose in a mixed meal diminishes glucose" (Alsalim. 2015) as evidence that fat and protein will reduce the potential obesogenic effect of carbohydrates. After all, the data in Figure 2 leaves no doubt that we are not talking about effect (a) from our list at the beginning of the article, i.e. a reduction in glucose excursions in response to "an increase in insulin sensitivity as it is triggered by exercise" (see introduction).

Figure 2: Glucose and insulin response as well as corresponding insulinogenic index and insulin clearance of the individual macros and the mixed meal - all data expressed relative to the values of 110kcal of glucose (Alsalim. 2015).

Rather than that, the reduced glucose AUC was a result of (c), i.e. an increase in insulin levels due to increased insulin production, as well as a decreased clearance of insulin and a decreased rate of absorption of glucose (-16%, -52%, -59% and -70% reduced glucose influx through the portal vein at 30, 45, 60 and 90 min after the meal) - and with the increased insulin levels you will also run an increased "risk" of fat storage (whether you gain weight will still depend on your overall energy intake not your insulin levels, though).

Figure 3: Insulin is not always the bad guy. A 2004 study by Hallschmid, et al. shows that it's centrally mediated effects in the brain can actually help men (but not women) lose weight effortlessly, when they administer it cyclically (only chronically elevated insulin levels are truly problematic) intranasally.

At this point, it may be necessary to point out that the increase in insulin in response to the co-ingestion of protein and fat does not imply that guzzling glucose on its own would be healthier than eating a mixed meal. In conjunction with the increases in the important (fat burning) satiety hormone GLP1, which were observed only in the diabetic subjects, though, these changes are yet far more beneficial for the average type II diabetic than they are for the lean athlete, who doesn't need the extra-insulin to maintain normal blood glucose levels and may even consider them an obstacle on his / her way to single-digit body fat levels.
References:

• Alsalim et al. "Mixed meal diminishes glucose excursion compared to glucose by several adaptive mechanisms in man." Diabetes, Obesity and Metabolism (2015): Accepted article.
• Collier G, O'Dea K. The effect of coingestion of fat on the glucose, insulin, and gastric inhibitory polypeptide responses to carbohydrate and protein. Am J Clin Nutr. 1983 Jun;37(6):941-4.
• Hallschmid, Manfred, et al. "Intranasal insulin reduces body fat in men but not in women." Diabetes 53.11 (2004): 3024-3029.
• Kaur B, Ranawana V, Teh AL, Henry CJ. "The Glycemic Potential of White and Red Rice Affected by Oil Type and Time of Addition." J Food Sci. (2015).
• Robertson, R. Paul, et al. "Glucose toxicity in β-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection." Diabetes 52.3 (2003): 581-587.
• Steen, Eric, et al. "Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer's disease-is this type 3 diabetes?." Journal of Alzheimer's disease 7.1 (2005): 63-80.

No acute changes in blood glucose, but extreme changes in insulin levels. How can this trigger a reduction in glycated albumin - How's that possible?

You've read about gamma aminobutyric acid (GABA) at the waredownloadsoft before. While most people think of it mainly as a calming agent, though, waredownloadsoft readers know that it has the remarkable ability to heal the insulin producing β-cell in rodents by stimulating their replication, protecting them against apoptosis, and attenuating insulitis (Soltani. 2011; Tian. 2013; Prud'homme. 2014; Purwana. 2014). And while these favorable effects were first observed in mice, researchers are quite sure that they are valid in humans, too- that's also because said effects have been confirmed only recently by Tian et al. (2014) and Purwana et al. (2014) in vitro as well as in xenotransplanted human islets.
If you know that, the observations researchers from the Fudan University in Shanghai report in their latest study probably won't come as a surprise. In their investigation into the  pharmacokinetics and pharmacodynamics of GABA in healthy volunteers, the researchers found that the chronic provision of 2g of GABA three times per day triggers a highly significant decrease in glycated albumin (GA) levels, the intermediate measure of blood glucose control (in-between acute blood glucose measurements and HbA1c | Roohk. 2008), within only 7 days.

Figure 1: Acute glucose (top) and insulin (bottom) response after single and repeated administration of 2g of GABA (left). Chronic effects of repeated dose-administration of GABA on glycated albumin (right | Li. 2015).

If you scrutinize the data in Figure 1, though, there are a few questions we still need to find answers to. Obviously, the acute administration of GABA (Figure 1, left) lead to significant increases in insulin - both, under either fasting (1.6-fold, single dose; 2.0-fold, repeated dose; p < 0.01) or fed conditions (1.4-fold, single dose; 1.6-fold, repeated dose; p < 0.01).
Usually, this 1.4-fold or 1.6-fold increase in insulin should trigger a significant (at least transient) decrease in blood glucose. Since the latter wasn't the case in either the fasted or the fed tests the scientists conducted on the twelve subjects, who participated in the open-labeled, three-period trial, it appears more than counter-intuitive that the chronic administration of GABA which does not accumulate in the body and was found to be almost completely absorbed in 60 minutes and to have a half-life of 5h still lead to an GA decrease of approximately 11-12%.

Now this obviously confirms that GABA, due to its ability to increase islet hormonal secretion, has potential therapeutic benefits for diabetes, what the study does not tell us, though, is whether the lack of immediate effects on blood glucose levels can, as the scientists suspect, "in part be attributed to GABA-induced counter regulatory mechanisms, especially elevated glucagon" (Li. 2015) which rose so that the insulin-to-glucagon ratio remained unchanged. Yet while the latter could explain why the subjects did not become hypoglycemic in the face of increased insulin levels, the lack of certainty with respect to the underlying mechanisms makes the study results difficult to interpret.
References:

• Li, Junfeng, et al. "Study of GABA in Healthy Volunteers: Pharmacokinetics and Pharmacodynamics." Frontiers in Pharmacology 6 (2015): 260.
• Prud’homme, Gérald J., et al. "GABA protects human islet cells against the deleterious effects of immunosuppressive drugs and exerts immunoinhibitory effects alone." Transplantation 96.7 (2013): 616-623.
• Prud’homme, Gérald J., et al. "GABA protects pancreatic beta cells against apoptosis by increasing SIRT1 expression and activity." Biochemical and biophysical research communications 452.3 (2014): 649-654.
• Purwana, Indri, et al. "GABA promotes human β-cell proliferation and modulates glucose homeostasis." Diabetes 63.12 (2014): 4197-4205.
• Roohk, H. Vernon, and Asad R. Zaidi. "A review of glycated albumin as an intermediate glycation index for controlling diabetes." Journal of diabetes science and technology 2.6 (2008): 1114-1121.
• Soltani, Nepton, et al. "GABA exerts protective and regenerative effects on islet beta cells and reverses diabetes." Proceedings of the National Academy of Sciences 108.28 (2011): 11692-11697.
• Tian, Jide, et al. "γ-Aminobutyric acid inhibits T cell autoimmunity and the development of inflammatory responses in a mouse type 1 diabetes model." The Journal of Immunology 173.8 (2004): 5298-5304.
• Tian, Jide, et al. "Oral GABA treatment downregulates inflammatory responses in a mouse model of rheumatoid arthritis." Autoimmunity 44.6 (2011): 465-470.
• Tian, Jide, et al. "γ-Aminobutyric acid regulates both the survival and replication of human β-cells." diabetes 62.11 (2013): 3760-3765.
• Tian, Jide, et al. "Combined Therapy With GABA and Proinsulin/Alum Acts Synergistically to Restore Long-term Normoglycemia by Modulating T-Cell Autoimmunity and Promoting β-Cell Replication in Newly Diabetic NOD Mice." Diabetes 63.9 (2014): 3128-3134.