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marylin monroe
Showing posts with label yogurt. Show all posts
Showing posts with label yogurt. Show all posts

Milk, a Glucose Uptake Promoter That's More Than the Sum of Its Parts. Plus: HICA & HMB in Yogurt. How Much EAA in Your Protein? Raw Milk Does not Cure Lactose Intolerance

Milk is one of the few foods that are advertized by celebrities that could actually be good for you (photo from the "Got Milk" campaign)
I hope you are not fed up with milk and dairy, yet, because today's SuppVersity short news have a ton of it. What exactly?

Well, after taking a closer look at the surprisingly high amount of HICA and the comparatively small amount of HMB in yogurt and reviewing the EAA content of six common protein sources, we are going to delve deeper into the latest evidence that shows that milk is much more than the sum of its parts, i.e. milk protein, lactose and fat and conclude on a note on another widely known Internet myth that says that people with lactose intolerance could drink raw milk without a problem.
You can learn more about dairy at the SuppVersity

Dairy Has Branched-Chain Fatty Acids!

Is There Sth. Like a Dairy Weight Loss Miracle?

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

Lactulose For Your Gut & Overall Health

Is There a "Fat Advantage" for Dairy Lovers

Dairy, Diabetes, Estrogen, IGF-1, Cancer & More
  • Figure 1: Amount of HICA & HMB (in µg/L) in commercial whole milk and yogurt (Ehling. 2014)
    Significant amounts of HMB and specifically HICA in yogurt. We all know that yogurt is among the dairy products with the most evidence of significant health benefits. That yogurt could be a decent muscle builder, on the other hand, would be news.

    With ~5 mg of β-hydroxy-β-methylbutyric acid (HMB) and up to 12.5 mg of α-hydroxyisocaproic acid (HICA) yogurt would have what it takes if the values of HMB and HICA Stefan Ehling and Todime M. Reddy measured in regular yogurt were on a per gram, not a per liter basis (Ehling. 2014).
  • How much EAA in my protein? Since I have been repeatedly questioned about the essential amino acid content in whey, milk, soy, and egg protein. I have published Table 1 which originally appeared in a 2010 study by Hulmi et al. on Facebook, already.
    Table 1: Approximate amino acid composition of popular protein powders (Hulmi. 2010)
    For those of you who are missing out on the daily 12+ SuppVersity Facebook News, because they haven't liked www.facebook.com/SuppVersity, yet. I will now publish it again - as a reference source, if you will.
  • Milk a glucose uptake promoter that's more than the sum of its parts. In view of the fact that we have already two dairy related news in today's SuppVersity article, I decided to have another "milky news" in today's SuppVersity short news item. One all the milk-drinkers among the SuppVersity readers will cherish.

    Recently, Shirin Panahi and colleagues from the University of Toronto, the Mount Saint Vincent University and the University of Guelph published the results of a randomized, cross-over study that was conducted to prove / disprove the hypothesis that
    "[T]hat regulation of postprandial glycemia after milk consumption occurs through both insulin and insulin-independent actions due to interactions among its macronutrient components and energy content. The objective was to compare the effects of isovolumetric (500ml) beverages of whole milk (3.25% M.F.), each of its macronutrient components (protein, lactose and fat) and their combination (a simulated milk beverage) on postprandial glycemia, glucoregulatory and gastrointestinal hormones and gastric emptying in healthy young men" (Panahi. 2014).
    In the course of the study, the 12 young, male subjects consumed beverages containing 500 ml of whole milk (3.25% M.F.) (control), a simulated milk beverage based on milk macronutrients or milk protein (16g), lactose (24g) and milk fat (16g) in isolation.
    Table 2: Nutritional composition of the test meals | a Composition of each beverage as provided by
    the manufacturer; b amounts given are per 500ml serving. Paracetamol (1.5g), vanilla extract (1.2ml)
    and sucralose (0.02g) were added to all beverages (Panahi. 2014).
    What the researchers found was that both the whole and simulated milk had similar beneficial effects on blood glucose rise after their "meal" (drink), but as it turned out the simulated milk resulted in a significantly higher (41%) glucagon-like peptide-1 (GLP-1) production and lower (43%) ghrelin areas under the curve (AUC) than whole milk (P=.01 and P=.04, respectively).
    Figure 2: Glucose, insulin, c-peptite, rate of insulin secretion, GLP-1, PYY, CKK
    and ghrelin levels after the test "meals" expressed relative to the sum of the effects
    of the same amount of milk protein, lactose and fat (Panahi. 2014)
    Now, all that would hardly be newsworthy (at least not for regular SuppVersity readers, if the two samples, i.e. both the whole and simulated milk, didn't lower the glucose (P=.0005) levels more than predicted by the sum of AUCs for their components (see Figure 2)!
    "Adjusted for energy content, milks produced lower glucose and hormone responses than predicted from the sum of their components. The effect of protein/kcal on the AUCs was higher than fat/kcal for insulin, C-peptide, insulin secretion rate, GLP-1, CCK and paracetamol (P < .0001), but similar to lactose except for CCK and paracetamol, which were lower. The response in PYY and ghrelin was similar per unit of energy for each macronutrient" (Panahi. 2014).
    In other words: Milk is way more than the sum of it's parts. In that, the "regulation of postprandial glycemia after milk consumption occurs through both insulin and insulin-independent actions due to interactions among its macronutrient components and energy content to achieve lower postprandial glycemia than predicted from the sum of its components" (Panahi. 2014).
If you haven't read it, already, take a look at my rebuttal to the latest assault on milk | read more
Bottom line: Quite the "milky" short news, right? Well, I guess it may be worth topping off all these good news about dairy products with a bad one. The common "Internet wisdom" that raw milk could offset the problems of people with lactose intolerance is a myth.
According to a 2014 paper by Sarah Mummah et al. who tested this myth in 16 adults with self-reported lactose intolerance and lactose malabsorption confirmed by hydrogen (H2) breath testing, "raw milk fail[s] to reduce lactose malabsorption or lactose intolerance symptoms compared with pasteurized milk among adults positive for lactose malabsorption." (Mummah. 2014) The "raw milk can be consumed by anyone" anecdote does thus belong to the realms of scientifically unwarranted die-hard bro-science | Comment on Facebook!
References:
  • Ehling, Stefan, and Todime M. Reddy. "Investigation of the Presence of β-Hydroxy-β-methylbutyric Acid and α-Hydroxyisocaproic Acid in Bovine Whole Milk and Fermented Dairy Products by a Validated Liquid Chromatography–Mass Spectrometry Method." Journal of agricultural and food chemistry 62.7 (2014): 1506-1511.
  • Hulmi, Juha J., Christopher M. Lockwood, and Jeffrey R. Stout. "Review Effect of protein/essential amino acids and resistance training on skeletal muscle hypertrophy: A case for whey protein." (2010).
  • Mummah, Sarah, et al. "Effect of Raw Milk on Lactose Intolerance: A Randomized Controlled Pilot Study." The Annals of Family Medicine 12.2 (2014): 134-141. 
  • Panahi, Shirin, et al. "Mechanism of action of whole milk and its components on glycemic control in healthy young men." The Journal of nutritional biochemistry (2014).

    Fat Advantage: 61% Lower Rates of Metabolic Syndrome in High Fat, 101% Higher Rates in Low Fat Dairy Lovers

    "Got milk" is not the question health conscious supermen and -women should pose. "Got full fat milk, fermented dairy and cheese" is the line to remember (the original image was part of the "Got Milk Campaign")
    While diet fads come and go, the advice the wise (not seldom obese or otherwise sick) experts on the boards and panels of our well-meaning governments is calling "dietary recommendations" is about as resistant to reform as the dreaded MSRA strains are to the antibiotics doctors are throwing at you whenever you sneeze. Against that background the recent trend we are seeing with respect to an increase in the recommended amount of dietary protein does almost amount to a quantum leap; a leap with a significant caveat, however. A fat caveat, so to say:
    "A healthy diet includes [...] lean meats, poultry, fish, beans and fat-free or low-fat dairy products" (NIH. 2012).
    Luckily, you as a SuppVersity reader do not have to rely on the NHI's thwarted interpretations of the latest research they claim to use, when they are "turning discovery into health" (no joke, this is a literal citation from the footer of the NHI website!), but can compare it to my thwarted interpretations of the latest research and cherry picked data ;-)

    Cherry pick of the day: Longitudinal large scale study on dairy intake and metabolic health

     For Today, this means that you get to enjoy the latest results of a large scale observational study from the University of Sydney that's based on datasets from the Blue Mountains Eye Study (BMES) a population-based cohort study of common eye diseases and other health conditions in residents aged 49 years and over in the Blue Mountains area, west of Sydney. A longitudinal study the baseline information was obtained in 1992/1994 from  and complemented by follow-up ten years later.

    The data sets included food frequency questionnaires, as well as anthropometric and biochemical assessments all of which were included in the present analysis of the association betweenn dairy consumption with the ten-year incidence of Metabolic syndrome (MetSyn) and type 2 diabetes. What's so special about this dataset, is that the food questionnaires were actually detailed enough to assess the effects of full- and low-fat dairy, separately - a very important advantage, as a cursory glance at the data in figure 1 reveals.
    Figure 1: Odds ratios (95% confidence intervals) of incident metabolic syndrome according to quartiles of reduced/low fat,
    regular fat and total dairy product intake (data based on Louie. 2012; adjustments for age and sex (basic model), smoking status, physical activity (metabolic equivalents), dietary glycemic load, fibre from vegetables, total energy intake and family history of type 2 diabetes (model 1) and calcium (model 2))
    While the standard analysis for total dairy consumption (figure 1, left) yielded neither conclusive, nor statistically significant results (the p-values for the different models can be found in the upper right corner of the respective graphs). The categorization into low- and high fat dairy and the adjustments for age and sex (basic model), smoking status, physical activity (metabolic equivalents), dietary glycemic load, fibre from vegetables, total energy intake and family history of type 2 diabetes (model 1) and calcium (model 2) yields very clear and, after adjustment for calcium intake, pretty unflattering result the formulators of the afore mentioned "dietary recommendations" will probably file in their already bristling "statistical outliers"-folder:
    • after adjustment for calcium intake subject in quartiles 2 / 3 / 4 of low-fat dairy are 50% / 145% / 101% more likely to be struck by metabolic syndrome, than those in the lowest quartile of low fat dairy intake (p = 0.043), while
    • subjects in the highest quartile of full-fat dairy intake are - depending on the adjustments made -  48% / 59% / 61% less likely (base model / model 1 / model 2) to suffer frommetabolic syndrome, than those in the lowest quartile of high fat dairy intake (p-values:  0.018 / 0.004 / 0.004)
    Yet while the scientists are well aware, that these results stand in stark contrast to the initially cited dietary recommendations, is it not this contrast that surprises them, but rather the fact that a similar significant benefit was not observed for type II diabetes, which is, after all, one of the hallmark features of the rather loosely defined triad of obesity, insulin resistance and cardiovascular disease(s), we usually refer to as 'metabaolic syndrome':
    "Due to its higher saturated fat content, regular fat/high fat dairy products were previously believed to increase the risk of type 2 diabetes as a high saturated fat intake is associated with insulin resistance . However, cohort studies and a meta-analysis now suggest otherwise, with higher regular fat/high fat dairy consumption being considered mostly neutral or protective for type 2 diabetes. The results of the present study are consistent with these findings that higher regular fat dairy consumption may be protective of MetSyn and type 2 diabetes. The potential harmful effects of higher saturated fat from regular fat dairy products may have been offset by the protective components of regular fat dairy such as trans-palmitoleate, a fatty acid nearly unique to ruminant foods. Circulating level of trans-palmitoleate was shown to be significantly associated with reduced risk of type 2 diabetes (Q5 vs Q1: 62% reduced risk, p-trend < 0.001). Moreover, the protective effect of trans-palmitoleate may be exerted via the suppression of hepatic fat synthesis, where the latter was strongly associated with insulin resistance." (Louie. 2012; my emphases)
    In view of these mechanism, it is all the more surprising that the study at hand and many previous studies didn't find any significant correlations between (regular fat) dairy intake and type II diabetes.

    Reduction in metabolic risk, but no effect on type diabetes? Hold on...

    Wolverine could be the only face of the "Got Milk" campaign who does not have to care about potential negative health effects of homogenized milk.
    And upon a cursory read of the latest literature it does in fact seem as if "null findings" like this, were nothing special. Only recently by Sluijs et al. who had analyzed datasets from a nested case-cohort within 8 European countries of the European Prospective Investigation into Cancer and Nutrition Study (n = 340,234; 3.99 million person-years of follow-up) includind a random subcohort (n = 16,835) and incident diabetes cases (n = 12,403; cf. Slujis. 2012):
    "This large prospective study found no association between total dairy product intake and diabetes risk. An inverse association of cheese intake and combined fermented dairy product intake with diabetes is suggested, which merits further study." (Sluijs. 2012)
    If we do yet take a closer look at the actual results the actually not so surprising truth is that there was a statistically significant inverse association with diabetes for cheese (p = 0.01) and fermented dairy (p = 0.02).

    An association that suggests a 12% reduction in diabetes risk in those study participants who consumed the most cheese and fermented dairy (cheese, yogurt, and thick fermented milk)

    And since you all know your real foods, I guess I don't have to tell you that despite the fact that there are low fat varieties of cheese yogurts and other fermented milk products, 90% of them contain way more than the 1.5% let alone 0.1% fat the allegedly healthy low fat "milk" is boasting of. Mere coincidence? I don't think so. Reason to assume that low-fat milk will make you sick? No, but certainly not an argument to avoid the full-fat variety simply because it contains fat (which is the only argument the average dietitian has to favor low- over full-fat dairy products).

    Mutant Milk!? New Research Fuels the Flames on Hushed Up Concerns About Ill Health Effects of Homogenized Milk 
    Ask Dr. Andro: Are Colostrum and Milk Products in General Healthy Muscle Builders, a Waste of Money or Toxic Waste?
    All about milk: Browse past news and articles at the SuppVersity
    ^ Suggested reads
    Additional recent dairy science:Similar beneficial findings for all-cause mortality and fermented dairy (yet inconclusive results for CVD and diabetes) come from the recently published Whitehall II study (4526 subjects,72 % men, mean age 56 years; Soedamah-Muthu. 2012) and for dairy intake during adolescents and diabetes (-38% risk reduction for 2 servings per day or more) from a reanalysis of somewhat questionable data (who remembers exactly how much dairy he had during his adolescence?) from the Nurses' Health Study II cohort that comprises 37,038 women who completed a food-frequency questionnaire about their diet during high school were followed from the time of return of the questionnaire in 1998-2005 (Malik. 2012).


    References:
    • Louie JC, Flood VM, Rangan AM, Burlutsky G, Gill TP, Gopinath B, Mitchell P. Higher regular fat dairy consumption is associated with lower incidence of metabolic syndrome but not type 2 diabetes. Nutr Metab Cardiovasc Dis. 2012 Sep 26. pii: S0939-4753(12)00193-7. 
    • Malik VS, Sun Q, van Dam RM, Rimm EB, Willett WC, Rosner B, Hu FB. Adolescent dairy product consumption and risk of type 2 diabetes in middle-aged women. Am J Clin Nutr. 2011 Sep;94(3):854-61.
    • NIH. Health in the News: Love Your Heart. February 2012. < http://newsinhealth.nih.gov/issue/feb2012/feature1 > retreived Oct 02, 2012.
    • Soedamah-Muthu SS, Masset G, Verberne L, Geleijnse JM, Brunner EJ. Consumption of dairy products and associations with incident diabetes, CHD and mortality in the Whitehall II study. Br J Nutr. 2012 Jun 7:1-9.
    • Sluijs I, Forouhi NG, Beulens JW, van der Schouw YT, Agnoli C, Arriola L, Balkau B, Barricarte A, Boeing H, Bueno-de-Mesquita HB, Clavel-Chapelon F, Crowe FL, de Lauzon-Guillain B, Drogan D, Franks PW, Gavrila D, Gonzalez C, Halkjaer J, Kaaks R, Moskal A, Nilsson P, Overvad K, Palli D, Panico S, Quirós JR, Ricceri F, Rinaldi S, Rolandsson O, Sacerdote C, Sánchez MJ, Slimani N, Spijkerman AM, Teucher B, Tjonneland A, Tormo MJ, Tumino R, van der A DL, Sharp SJ, Langenberg C, Feskens EJ, Riboli E, Wareham NJ; InterAct Consortium. The amount and type of dairy product intake and incident type 2 diabetes: results from the EPIC-InterAct Study. Am J Clin Nutr. 2012 Aug;96(2):382-90.

    Want to Benefit from Plant Sterols? Eat Whole Food or Take Supplements With Meals. Plus: Do You "Benefit" at All?

    This is not a joke by a blogger this is how Unilever advocates to use their Flora pro.active product to consumers, who "want to lower your cholesterol and follow a healthy diet and lifestyle."
    Pharma companies and supplement producers are notorious for picking foods apart and providing you with concentrated extracts of the "active ingredients".

    Aside from the fact that more often then not, the activity of those "active ingredients" is critically dependent on co-factors that are lost during the isolation and extraction processes, scientists from the Division of Gastroenterology-Hepatology at the Department of Internal Medicine of the Maastricht University Medical Center have now been able to show that the mere presence of the bulk in which plant sterols would come in the natural form is critically important to their effects.

    Can you achieve a "healthily"(?) low cholesterol level by guzzling tuckloads of low-fat yogurt drinks!?

    Based on the negative outcomes of previous studies into the benficial effect of "functional" foods or dietary supplements enriched in plant sterols, D. Keszthelyi had hypothesized  that
    "100 mL drink, when consumed before a meal, would empty fast from the stomach and would not sufficiently trigger gallbladder emptying, whereas ingestion with or after the solid meal would enable the necessary physiological changes to aid inhibition of cholesterol absorption" (Keszthelyi. 2013)
    To test this hypothesis the researchers recruited a total of 12 healthy male subjects (age, 25 ± 3 years; BMI, 23 ± 2 kg/m²) who reported the scientists' lab on three separate test days with one-week washout between test days.

    Does the Paleo diet ruin your cholesterol levels as the conclusion to a recently published thesis would indicate (learn more)?
    On each of the days, the participants consumed a Phytosterol (PS) containing yoghurt drink (100 mL, Becel Pro-Activ with PS added as their fatty acid esters (3.2 g, equivalent to 2.0 g PS), either
    • 45 min before (test condition A), 
    • during (test condition B), or
    • 45 min after (test condition C) 
    the consumption of a 500 g macaroni meal (Macaroni Bolognese, Henri, Drunen, The Netherlands) at lunch time (I know not the ideal, but for the average Westerner a realistic test meal). T

    he sequence of the test days had been determined by a random pre-selection prior to the start of the study. During each test day, gastric emptying of the test drink as well as the effect of the test drink on gallbladder volumes were determined (figure 1, left):
    Figure 1: Gastric emptying (left) and gallbladder volume (right) depending on the time of ingestion of a phytosterol containing yogurt drink (Keszthelyi. 2013)
    As the results go to show you the ingestion of the functional food before the meal resulted in the fastest gastric emptying. The ingestion with or after a solid meal, on the other hand, caused a significant contraction of the gallbladder.
    "Accepting the postulate that concurrent presence of PS with dietary and/or biliary cholesterol in the small intestine is an important mechanism for the LDL cholesterol-lowering action (Ostlung. 2004), a significant stimulus leading to gall- bladder contraction with simultaneous delivery of the PS-containing food format from the stomach into the duodenum is required. It is therefore important to ascertain which stimuli are able to elicit this postprandial response to a sufficient and desirable degree." (Keszthelyi. 2013)
    This is actually interesting, because in the end it means that cholesterol clearance, even when it's induced / supported by questionable supplemental phytoestrogens critically depend on fat intake! This in turn would explain why the rodents in the "optimal diabesity diet study" from one of the recent installments of the Short News found elevated cholesterol levels only in the high sugar and high fat + high sugar groups, yet not in the rodents on a high fat diet.One thing to keep in mind, though: The main reason I picked and posted this study is not to pimp the use of phytosterol-spiked imho dys-functional junk food. It's rather to raise your awareness of the importance of the whole nutrient matrix in terms of the effects of the individual agent.

    If you want to do something for your blood lipids, you better eat more eggs than overpriced Frankenfood. The eggs will not only improve your cholesterol particle profile, the regular consumption of whole eggs will also increase HDL's ability to carry lipids out of the macrophages. If these accumulate, they will turn the macrophage into pro-atherogenic foam cells (learn more).
    In how far the isolation is also behind the previously observed side effects of plant sterols and stanols, which are likewise used in functional foods remains questionable, but it is not unlikely that sides such as

    • abortion of pregnancy in animal models (Burckh. 1982)
    • reduced sperm concentrations & testis weights
    • neg. effects on the vascular system (Boberg. 1991)
    • increased intestinal tumor formation (Marttinen. 2013)
    are eventually also a consquence of the absence of important co-factors, when the sterols and stanols are removed from their original food matrix and "transplanted" into yogurts, margarines and all sorts of overly expensive and at best useless Frankenfoods.

    References:

    • Boberg KM, Pettersen KS, Prydz H. Toxicity of sitosterol to human umbilical vein endothelial cells in vitro. Scand J Clin Lab Invest. 1991 Oct;51(6):509-16.
    • Burck PJ, Thakkar AL, Zimmerman RE. Antifertility action of a sterol sulphate in the rabbit. J Reprod Fertil. 1982 Sep;66(1):109-12. 
    • Keszthelyi D, Knol D, Troost FJ, van Avesaat M, Foltz M, Masclee AA. Time of ingestion relative to meal intake determines gastrointestinal responses to a plant sterol-containing yoghurt drink. Eur J Nutr. 2013 Jun;52(4):1417-20.
    • Ostlund RE Jr. Phytosterols and cholesterol metabolism. Curr Opin Lipidol. 2004 Feb;15(1):37-41.

    Do You Have the Gut(s) to Lose 8% Belly Fat in 12 Weeks? Lactobacillus gasseri (LG2055) Can Fix Your Gut Problems

    As a diligent student of the  SuppVersity, you'll obviously know that beer is not the main cause of the eponymous belly (Bobak. 2003). Although..., when when you come to think about it: For every glass of beer you drink, you're probably drinking a glass of probiotic yogurt less ;-)
    You've done everything you could and still feel like a whale? You've been low-carbing, even have made sure you are in ketosis by consuming an only 10% protein diet and still the fat won't disappear? Well, I guess it sounds unfair, if I do now tell you that you YOU JUST DON'T HAVE THE GUTS it takes to get rid of that pouch that blocking the view on your toes, when you are standing.

    Now calm down, I am not talking about not being able to curb your insatiable appetite or skipping 90% of your workouts, here. I am talking about your gut(s), literally! Your digestive tract and it's inhabitants. Those critters which are also at the heart of the soon-to-be-published paper by scientists from the Milk Science Research Institute in Fukoaka, Japan (Kadooka. 2013) - a paper, the results of which I am about to present in the next few paragraphs.

    Probiotic in fermented milk shred visceral fat

    I am not telling you something new, when I say (or write) that scientists have long identified the modulation of the gut microbiome, i.e. the bacterial ecosystem in your intestines, could be the long-sought-for lever to get rid or at least ameliorate the negative effects of the way we live and eat promotes the expansion of the highly inflammatory "stress fat" that fills the room between the organs in your trunk. Most of the hitherto published peer-reviewed research has yet been conducted in rodents. The existing evidence from well-controlled human studies, on the other hand is scarce.

    Suggested read: "Probiotics for Athletes: The Supplemental 10 Billion CFS Leaky Gut Solution for the Fermented Food Refusinek?" (read more)
    One of these studies has been conducted by Kadooka et al. in 2010 (Kadooka. 2010). In the pertinent paper the researchers from the Milk Science Research Institute in Japan reported that the provision of 200g/day of fermented milk containing 10^8 colony-forming units (cfu)/g of Lactobacillus gasseri strain SBT2055 (LG2055) led to significant reductions in visceral fat in male and female subjects with " higher body mass index" (BMI: 24.2-30.7 kg/m²) who had been randomized to the active arm of the study. Now, roughly three years later, are about to publish a follow-up paper with great practical relevance, as it summarizes the results of what Kadooka et al. say is the first human trial that examines the effect of different doses of probiotics on abdominal adiposity.

    "We know that it works, but we don't know how much we need to elicit the desired effects"

    The design of the study at hand is essentially identical with the one in the 2010 trial. It is based ona multi-centre, double-blind, parallel-group RCT with 210 healthy Japanese adults with large visceral fat areas (80.2–187.8 cm²), who were now randomly assigned to three instead of two groups who consumed 200g of fermented milk with either 1,000,000 CFU (1m), 10,000,000 CFU (10m) or just the normal yogurt probiotics (control) per gram for 12 weeks.

    The intention was to determine whether the effect of LG2055, which is by the way a probiotic lactic acid bacterium that originates from the human intestine, would be observed with lower / more realistic dosage regimen as well and whether possible reductions in the effect size would be dose-dependent.
    Figure 1: Reduction in visceral and subcutaneous adipose tissue, as well as waist circumference after 8 and 12 weeks on 1,000,000 CFU/g or 10,000,000 CFU/g yogurt drink; data expressed relative to group baseline (Kadooka. 2013)
    If you take a look at the results, the first thing that strikes the eye in figure 1 is that the lactobacilli did their job and that in both the low and high dose group:
    • Even in the 10x and 100x lower dosages there was a significant reduction in the amount of visceral fat the  33/36 respectively 36/35 men and women in the in the 1 million and 10 million CFU/day groups, respectively.
    • The effect size of both dosages of LG2055 was identical, so that it would not actually matter if you consume just 100g or 1kg of an imaginary commercially available milk drink with 1,000,000 CFU of LG2055 per 100g.
    In view of the >8% reduction in visceral fat mass, it should not come as a surprise that the reduction in waist size was likewise statistically significant - both on its own, as well as in comparison to the control group, What is yet not so obvious and probably somewhat disappoint for you is the fact that the reduction in the ugly, but benign subcutaneous fat was statistically and practically non-significant.

    "Visceral fat loss, only? But what about my thigh fat?"

    Not all probiotics are created equal: As the scientists emphasize in the discussion, the "it is also worth noting that the test FM containing both LG2055 and yogurt cultures reduced abdominal adiposity when compared with the control FM containing yogurt cultures alone, even though the bacterial counts of LG2055 (106 and 107 cfu/g) were lower than those in the yogurt cultures (109 cfu/g)." (Kadooka. 2013) The observed superiority of this particular strain of bacteria stands in line with previous rodent studies and is imho one of the reasons we are seeing so much research in this area. How's that? Well, easy: If you came up with a particularly potent strain and patented that, this would be the literary cash machine.
    If you are no newbie to the SuppVersity you will yet be aware that it is by no means extra-ordinary that "healthy fat burners", which work their weight loss magic mostly by modulating local and/or whole body inflammation, have little or no effects on the amount of subcutaneous body fat.

    If you discarded any statistical shenanigan and simply went by the height of the small bars in the middle of figure 1, you could yet probably argue that it appears as if there was a trend towards greater subcutaneous fat loss in the high(er) dose LG2055 group. If you went a step further and made the unwarranted assumption that you could simply compare the results from the study at hand to those of the aforementioned 2010 study b Kadooka et al. you could support this argument by stating that there was a clear trend here with 1.2%, 2.6% and 3.3% reductions in subcutaneous fat with LG2055 at concentrations of 1, 10 and 100 million CFU per gram of the fermented milk drink.

    In the overall context it is yet important to point out that it is as of yet unknown whether the composition of colonic microbiota has a direct influence on abdominal and/or subcutaneous adipose tissue (Hildebrandt. 2009; Conterno. 2011). Moreover, ...
    "[...] environmental factors, including genetics and age, makes it difficult to discuss the causal relationship between adiposity and intestinal microbiota." (Kadooka. 2013)
    The latter are particularly difficult to access in a study like this, where the subjects maintain their habitual mode of living, including diet, and no strict dietary control is applied. Kadook et al. are thus right to point out that "the relation ship between adiposity and intestinal microbiota" has to be investigated more closely "under a strict diet, together with the latest methodology" (Kadooka. 2013) to finally make some progress in our understandings of the intricate interaction between the human gut microbiome and our metabolism.



    Even the nicest subtenants can become a real problem, when they come over without being asked. Unfortunately, all sorts of gut bacteria (even the "good" ones) have a similarly nasty habit of translocating through a leaky gut wall into parts of your body, where you don't wont them (learn more)!
    Bottom line: In view of the fact that the subjects shed the superfluous body fat in the absence of a reduced energy intake and/or exercise / increases in physical activity, the results are unquestionably impressive. To speak of "probiotic fat burner" would yet still not be warranted. After all, the subjects were all overweight and had an average body fat content of 32%, the baseline diet does - at least by the available data - not look really optimal (protein intakes of 0.8g/kg; macro-composition of 15/57/28% from protein, carbs and fats) and the non-disclosed insulin and HbA1c levels as well as the markers of inflammation will probably have left more than enough room for the "get healthy lose weight" effect.

    Against that background I have my doubts that you can expect anywhere similar effects in lean, let alone athletic individuals. This does yet not negate the general usefulness of probiotics, after all, health is something you take for granted only, when you've never been sick - if you want to avoid that, the incorporation of fermented foods makes sense for everyone from the sedentary slob to the elite level athletes*...

    * Note: I am writing the above although it gives me tummy aches (pun intended). Specifically with respect to the use of high dose probiotic supplements, I am asking myself, whether we really know enough about the potential downstream effects of long-term / high dose supplementation. In that, I am particularly concerned about shifting the balance from an "A"-dominant and unhealthy state in which the attributes "good" and "bad" are all of the sudden reversed and the previously dominant "bad" strain X gets totally replaced by the allegedly "good" strain Y that will then turn out to be just as nasty as X, once its natural arch enemy X is no longer present.

    References:
    • Bobak M, Skodova Z, Marmot M. Beer and obesity: a cross-sectional study. Eur J Clin Nutr. 2003 Oct;57(10):1250-3.
    • Conterno L, Fava F, Viola R, et al. Obesity and the gut microbiota: does up-regulating colonic fermentation pro- tect against obesity and metabolic disease? Genes Nutr. 2011; 6:241–260.
    • Hildebrandt MA, Hoffmann C, Sherrill-Mix SA, et al. High-fat diet determines the composition of the murine gut microbiome independently of obesity. Gastroenterology. 2009; 137:1716–1724.
    • Kadooka Y, Sato M, Imaizumi K, Ogawa A, Ikuyama K, Akai Y, Okano M, Kagoshima M, Tsuchida T. Regulation of abdominal adiposity by probiotics (Lactobacillus gasseri SBT2055) in adults with obese tendencies in a randomized controlled trial. Eur J Clin Nutr. 2010 Jun;64(6):636-43. 
    • Kadooka Y, Sato M, Ogawa A, Miyoshi M, Uenishi H, Ogawa H, Ikuyama K, Kagoshima M, Tsuchida T. Effect of Lactobacillus gasseri SBT2055 in fermented milk on abdominal adiposity in adults in a randomised controlled trial. Br J Nutr. 2013 Apr 25:1-8. [Epub ahead of print]
       

    Probiotics Inhibit Ill-Health Effects of 7-Day Overfeeding in Man - Does This Make Yakult(R) the Perfect Tool in Your Bulking Toolbox or is it Just Another Marketing Gag?

    Keep in mind: We are dealing with an industry sponsored study, here. One, w/ high baseline differences in insulin sensitivity between the groups.
    Investigations into the effects of the intestinal microbiome are popping up all over the place. Unfortunately, many of the studies are conducted in rodents. Whether or not and if to which extent the results transfer to human studies is not sure, though.

    Against that background, the results of a recent study from the Loughborough University are all the more intriguing. Why? Well, the study was conducted in a total of seventeen healthy subjects (fourteen males and three females) and the results of the study suggest that  probiotic supplementation may be useful in the prevention of diet-induced metabolic diseases such as type 2 diabetes.
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    Consumption of probiotic yogurt has already been shown to reduce fasting blood glucose concentrations and glycosylated Hb levels in type 2 diabetic patients (Ejtahed. 2012), but whether or not probiotics can also prevent diet-induced insulin resistance in otherwise healthy subjects is not yet known. Therefore, Hulston et al. tested the hypothesis that 4 weeks of supplementation with probiotics (Lactobacillus casei Shirota (LcS)) would prevent insulin resistance induced by short-term, high-fat, overfeeding in healthy young males and females.
    Table 1: Physical characteristics of the study subjects before and after 7 d of overeating (Hulston. 2015).
    The subjects, seventeen healthy subjects (fourteen males and three females; Table 1), were randomly assigned to one of the following two groups: A control group (n=9, seven males and two females),  and  a probiotic group (n=8, seven males and one female). The probiotic that was used in the present study was LcS (commercially available as the fermented milk drink Yakult Light).
    "Both groups maintained their habitual food intake during the first 3 weeks of the study (days 1–21); however, the probiotic group also consumed 65 ml of Yakult Light twice each day. An oral glucose tolerance test (OGTT) was performed on day 22 for the assessment of baseline insulin sensitivity" (Hulston. 2015).
    After completing the first OGTT, subjects were provided with a high-fat (65 % energy), high-energy (approximately 50 % increase in energy intake) diet for 7 d. The probiotic group continued to consume 65 ml of Yakult Light twice throughout the 7 d overfeeding period. We selected a 4-week LcS supplementation period, as previous experiments have demonstrated that this is sufficient to alter the composition of the gut microbiota in humans.
    Figure 1: Baseline and overfeeding macronutrient intake (left) and insulin sensitivity before and after the 7-day overfeeding period in the 17 healthy, normal-weight sedentary study participants (Hulston. 2015).
    Next to a weight increase which did not differ for the two groups, the researchers found significant changes in fasting plasma glucose concentrations in response to the 7 d of overfeeding protocol, changes that reflect (a) the overall increase in carbohydrate consumption and (b) the decrease in insulin sensitivity which was measured separately in response to the meals and yielded a significant reduction of 27% from albeit high baseline levels in the supplementation group and no significant difference in the probiotic group.

    With a study period of only 7 days, the overfeeding did yet not wreak enough havoc to mess with the fasting serum insulin concentrations, the hallmark feature of beginning diabetes. The latter remained stable in both both groups - more evidence that you can neither get fat, nor diabetic in just a few days (reread my article "Can You Get Fat in Only Three Days?" | here).
    Bulking Done Right: What Can the Latest 100 Day +1,000 Kcal/day Overfeeding Study Tell Us About How Baseline Fitness, Fatness, Hormones & More Affect the Outcome | Learn more about the science of bulking in a previous SuppVersity article 
    So what? They both did gain weight, no? Right, the subjects in both groups gained weight, but only the subjects in the control group showed elevated glucose AUC values (+10%) that were indicative of a 27% whole-body insulin sensitivity. The subjects in the probiotic group, on the other hand, were protected from the pro-diabetic insult of the 7-day overfeeding period. Since the baseline insulin sensitivity was significantly higher in the control group, the relative difference should not be overrated, though.

    Practically speaking, this means that the use of a single small 65ml Yakult Light drink during a bulk may postpone the onset of reductions in insulin sensitivity and could thus to avoid unwanted pre-diabetic consequences... well, on the other hand, it is questionable, whether the results would be identical if the overfeeding had been high(er) in protein and complemented with an intense exercise regimen, which is why I would not yet recommend spending money on any of these expensive "functional foods" | Comment on Facebook!
    References:
    • Ejtahed, Hanie S., et al. "Probiotic yogurt improves antioxidant status in type 2 diabetic patients." Nutrition 28.5 (2012): 539-543.
    • Hulston, Carl J., Amelia A. Churnside, and Michelle C. Venables. "Probiotic supplementation prevents high-fat, overfeeding-induced insulin resistance in human subjects." British Journal of Nutrition (2015): 1-7.