Seabuckthorn Leaves Increase PPAR-Alpha & PPAR-Gamma Expression, Keep the Liver Fat Free and Fatty Oxidation Up. Plus: PPARs - High or Low? How Are They Supposed to Be?

This time, the magic is in the leaves, not the fruits or kernels. And it's dose dependent. With an almost linear increase from 500-1,000mg/kg

Honestly, I don't think that it is coincidence that many of the most promising medical plants are shrubs that live on barren soil, like sand dunes and cliffs and are full of thorns as well as innate polyphenolic defense mechanisms. Whatever the "evolutionary" basis may be, if we go by the beneficial metabolic effects, researchers from the Department of Food Science and Human Nutrition at the Chonbuk National University in the Republic of Korea, it appears worth going through all the traditional used folk medicine across the world and identify which of them work, how they work and whether they may already have what it takes to get rid of one or the other of the typical Western diseases.

In the case of the ethanolic extract of seabuckthorn (Hippophae rhamnoides L) Pichiah et al. used in their most recent experiment, this would be ameliorative effects on weight gain through down-regulation of adipogenic and lipogenic gene expression.

Less weight gain more fatty acid turnover, better glucose management and leptin sensitivity

The ameliorative effects on the detoriation of glucose metabolism, the reduced but still significant weight gain of the 60% fat diet (additional fat 100% from lard) and the profound overexpression of leptin, which is indicative of the fact that the mice developed full-blown leptin resistance within the 13-weeks of HFD administration, were all ameliorated to a greater degree in the high dose seabuckthorn leaf extract group (human equivalent  ~6.5g/day).

Figure 1: Effect of the different diets on weight gain, visceral fat weight, feed intake and energy intake (left; data expressed relative to control diet); effects on blood sugar (AUC in glucose tolerance test) and leptin (Pichiah. 2012)

The differences between high and low dose supplementation of the extract which had been prepared by

"[...] by soaking the dried, powdered leaves in 70% ethanol for 7 days at room temperature. Then the extract was concentrated by evaporating ethanol using a rotary vacuum evaporator (N-N Series, EYELA, Tokyo, JAPAN) set at 60°C and 100 hPa" (Pichiah. 2012)

were even more pronounced, when we compare the effects on fatty acid oxidation (CPT-1), the PPAR-alpha and -gamma values.

Figure 2: Carnitine palmitoyltransferase I (CPT1), PPAR-alpha & -gamma activity and triglyceride & cholesterol content in the liver (left; expressed relative to rodents on normal chow). Histology of liver sections at 200x magnification for the different diets (Pichiah. 2012)

What's yet most striking is however that the liver - the organ that's so heavily involved in the etiology of insulin resistance - was virtually "fat-free" in the rodents who received the 1,000mg/day dose. The total triglyceride and cholesterol content was even lower than in the mice on the normal diet and the overall darker staining in the slices on the right of figure 2 is only further evidence of the beneficial effects the seabuckthorn extract had on the liver histology.

The effects of a 5% conjugated linoleic acid diet do actually resemble that of lipodystrophy, i.e. pathological fat loss and inability to store body fat. Strange, no? Well that's PPAR-gamma (read more).

PPAR-gamma? Wasn't that what you actually wanted to avoid? In a way this is right, since PPAR-gamma and even alpha are somewhat Janus-faced molecules (overview for PPAR-alpha). As beneficial as their expression in the liver may be, both inhibit the oxidation of glucose. PPAR-gamma is also involved in the maturation process from pre-adipocytes to mature adipocytes, increases lipogenesis in white adipose tissues, decreases the cell surface fatty acid transporter on muscle cells and increases glucose uptake in adipocytes (exclusively). All that is healthier than fat clogging your liver, but it's not exactly something that will make you leaner if you are work out and consume a junk-free diet.

In fact, the PPAR-gamma suppressing effects of the trans-10, cis-12 isomer of conjugated linoleic acid (CLA; cf. Kennedy. 2008) are actually what what produces such profound effects, as they were observed in the study I discussed on July 22, 2012 (see link beneath the image of the mice).

TTA and fish oil are potent antagonists of liver PPAR expression. With the uncoupling and anti-inflammatory effects of TTA being the key to unleash & maintain fat-burning (read more).

Bottom line: It appears as if the liver is - once again - emerging as a central player in "sick obesity", meaning being fat and sick and not just fat. Which reminds me of yesterday's post on Gluten and the development of metabolic disease, where fatness is no criteria, at all. The expression of the "liver cleansing" PPAR-gamma enzymes on the other hand was.

This in turn reminds me of the effects of fish oil and TTA (a pan PPAR-activator), which - despite their questionable use as a long-term intervention can in fact stimulate intra-hepatic fatty acid oxidation to levels which are so high that oxidation rates in and out of itself could bring about some problems.

Other nutritional factors you should take into account are choline (a deficiency will actually cause fatty liver disease; read more about choline) or taurine. And on the endocrine side of things you want to keep an eye on optimal DHEA levels (read more about its effects on PPAR-gamma), thyroid hormones, testosterone and estrogen (Nemoto. 2000).

References

• Kennedy A, Chung S, LaPoint K, Fabiyi O, McIntosh MK. Trans-10, cis-12 conjugated linoleic acid antagonizes ligand-dependent PPARgamma activity in primary cultures of human adipocytes. J Nutr. 2008 Mar;138(3):455-61.
• Nemoto Y, Toda K, Ono M, Fujikawa-Adachi K, Saibara T, Onishi S, Enzan H, Okada T, Shizuta Y. Altered expression of fatty acid-metabolizing enzymes in aromatase-deficient mice. J Clin Invest. 2000 Jun;105(12):1819-25.
• Pichiah PB, Moon HJ, Park JE, Moon YJ, Cha YS. Ethanolic extract of seabuckthorn (Hippophae rhamnoides L) prevents high-fat diet-induced obesity in mice through down-regulation of adipogenic and lipogenic gene expression. Nutr Res. 2012 Nov;32(11):856-64.

Beyond Celiac: Study Sheds New Light on Obesogenic Effects of Gluten - Are PPARs & Bacteria Both Involved?

Cornflakes peanut butter cookies - guaranteed not gluten free ;-)

With Christmas Eve being over, and grandma's cookies, Christmas stollen, and all sorts of other stuff from the bakery in front of you (literally), Christmas Day may actually prove to be a way more "dangerous" than Christmas Eve - not just because of the total amount of calories, but also because of the low satiety effect of these sweet treats.

A recent paper by scientists from the Universidade Federal de Minas Gerais in Belo Horizonte in Brazil does now point to another reason you better give those bakery products a wide berth - not just, but especially with the energy overshoot on Christmas day: Gluten!

Study confirms for the first time what scientists and laymen alike have been speculating about

In what the scientists claim is the first well-controlled study of the effects of gluten intake on metabolic health in a non-celiac, but Western-style diet scenario, Fabíola Lacerda Pires Soares and her colleagues put two groups of C57BL/6 mice on identical, iso-caloric high fat (hypercaloric) diets that differed only in terms of the amount of gluten that was added to the chow (0% gluten vs. 4.5% gluten).

Interestingly, the gluten diet did not influence any of the usual suspects, like food intake, total fat-free mass, fecal lipids excretion, blood lipid profile, blood total protein and ectopic (liver and muscle) lipid concentration (if you look closely you will realize that the gluten-free group actually had higher TRIGs, although the difference did not reach statistical significance).

Figure 1: Usual suspects and closer look at the effects 8 weeks gluten supplemented vs. gluten-free diets had on serum markers of metabolic syndrome and visceral fat parameters (Soares. 2012)

The data in figure 1 (right) does yet also show that the gluten content of the diet did nevertheless have a significant impact on the total body mass, visceral fat mass, lipid content and most importantly the adipocyte size.

Figure 2: Absolute adipokine levels (left) and fasting glucose and insulin levels, as well as Homa-IR (Soares. 2012)

Add to that the blunted expression of the anti-inflammatory and anti-diabetic fat hormone adiponectin and the increased the >5x higher expression of leptin (figure 2). And mix that with the reduced expression of PPAR-alpha and gamma of which Soares et al. argue that they may well be the key factor in the detrimental modulatory effect the addition of gluten had on the visceral fat structure and the lowered expression of the fat liberating enzymes LPL and and HSL, as well as reduced levels of the fat burning proteins ACC and CPT-1 (figure 3).

Figure 3: PPAR-alpha, -gamma, LPL, HSL, ACC and CPT-1 expression compared to rodents on regular chow (left); crown like structures in stained slices from visceral fat, inflammatory markers TNF-alpha and IL-6 (Soares. 2012)

So, even if the initially mentioned blood markers (aka the usual suspects) would suggest that both the gluten-consuming and gluten-free rodents were similarly bad off, the profound difference in inflammatory markers within the adipose tissue and the presence of comparatively many necrotic and inflammatory adipocytes in the crown like structures stand in line with increases in HOMA-IR, fasting glucose and insulin and an already compromised glucose clearance which are well-known harbingers of the metabolic syndrome.

These observations do not simply shed a whole new light on a hitherto largely ignored contributer to the etiology of the metabolic syndrome, they do also show that one of the reasons it has not been identified before is an over-reliance on BMI, total fat mass and serum lipids in the early stages of diabesity.

Reardless of whether the gut microbiome is part of the mechanism by which gluten predisposes the development of metabolic syndrome. Eating more inulin- and beta-glucan rich foods like Jerusalem artichokes, agave, bananas, onion, steel cut oats, wild yams, yacon, etc. certainly won't hurt your efforts to get lean, stay lean and leave the role of the obese diabetic to the other (read more)

Bottom line: The study at hand provides a good reason to limit your intake of "healthy whole grains" and other gluten containing foods, regardless of whether you suffer from celiac or not. Whether the established detrimental effects of gluten on the integrity of the intestinal wall and the increased leakage of bacterially produced endotoxins from the highly unfavorably changes in the gut microbiome in response to the high fat diets (Hildebrandt. 2009) are part of, or even the primary cause of these observations still has to be elucidated. The same goes for strategies to counter the translocation of the endotoxins across the gut lining (cf. "Shedding some light on the leaky gut") and the dose response relationship between the total amount of gluten in your diet and its effects on your metabolism. With 7% of pure gluten, it goes without saying that you would basically have to live of wheat in order to get to anywhere similar amounts of gluten in the diet... that said: Is it possible that the effects occur only in the presence of the high fat diet? After all, this alone has been shown to favor a pro-inflammatory gut microbiome.

You see there are enough questions to be answered in 2013 and the SuppVersity is going to be the place you will read the respective answers first ;-)

References:

• Hildebrandt MA, Hoffmann C, Sherrill-Mix SA, Keilbaugh SA, Hamady M, Chen YY, Knight R, Ahima RS, Bushman F, Wu GD. High-fat diet determines the composition of the murine gut microbiome independently of obesity. Gastroenterology. 2009 Nov;137(5):1716-24.e1-2.
• Soares FL, de Oliveira Matoso R, Teixeira LG, Menezes Z, Pereira SS, Alves AC, Batista NV, de Faria AM, Cara DC, Ferreira AV, Alvarez-Leite JI. Gluten-free diet reduces adiposity, inflammation and insulin resistance associated with the induction of PPAR-alpha and PPAR-gamma expression. J Nutr Biochem. 2012 Dec 17.

Santa is Coming to Town and You Better Beware of His Gifts: Fat Gain, Muscle Loss and Increased Mortality Rates.

Image 1: The "modern" image of the Coke-drinking Santa. Do you really believe he is one of the good guys?

Finally, December 24th is there! The day we have all been waiting for, to get together with friends and relatives and wait for the portly, joyous, white-bearded man in the red coat to deliver "his" gifts. Interestingly enough, the word "gift" in German designates "poison" and while those of you who have been following the SuppVersity news earlier this week may now be speculating that this could in one way or another be related to the millions of iPhones Santa is going to be dropping down the chimneys in the night to come (cf. Mobile Contraception), it seems unlikely that the electromagnetic radiation from the gadgetry could explain the statistically significant +4.65% increase in cardiac and a + 4.99% increase in non-cardiac deaths during the holiday season. After all, the data based on which David P. Phillips, Jason R. Jarvinen, Ian S. Abramson, and Rosalie R. Phillips conclude that "the Christmas/New Year’s holidays are a risk factor for cardiac and noncardiac mortality" is from the pre-iPhone era (Phillips. 2004).

Is Santa not the good guy, the Coca Cola ads made us believe?

So, if its not the radiation, what else could it be? Could it be Santa Claus himself? Is he haunting us, just as his robotic counterfeit in the distant future of the year 2999, where an evil Santa robot is after the blood of the protagonists of Matt Groening's and David X. Cohens TV series Futurama? Or is it a result of the consumption of too many of the Coca Cola bottles Santa is supposed to have in his bag?

Image 2: One really has to marvel at how the soft drink producers dissolve the enormous amount of sugar on the right in the small amount of dark brew on the left.

Did you know that the Coca Cola company alone sells 1.6billion (!) servings of Coke per day? With 27g of sugar per serving, this equals 43,000 metric tons of pure sugar. The average American, who consumes an average of 150 to 170 pounds of sugar each year, would have to live into his/her 558th year of age to eat or drink her way through this sugar mountain. And while I have no doubt that there actually are people out there who would do that withing 100 years, I am not quite sure which of the ailments of our sweet convenience society would strike him / her first and put a spoke in the sweet-o-holic's plans: diabetes, cancer, heart failure or stroke? What would you say?

Phillipps et al. who report in a follow-up study based on the same dataset from the holiday periods between July 1, 1973, and June 30, 2001 that there was an "excess of 42,325 deaths from natural causes above and beyond the normal winter increase" (Phillips. 2010), exclude the possibility that the increased mortality rate was simply a result of the bad weather conditions and related respiratory diseases:

Respiratory diseases. Respiratory diseases increase during winter, and patients weakened by respiratory diseases can die from cardiac diseases. The respiratory hypothesis is undermined by 2 considerations: (1) People dying from cardiac diseases with respiratory disease listed as a secondary cause of death produce a smaller holiday peak than do people dying from cardiac diseases alone: 3.51% versus 3.77%. (2) Interaction between cardiac and respiratory diseases cannot easily explain the twin mortality spikes on Christmas and New Year’s.

So, in view of the latest headlines related to "holiday weight gain" here at the SuppVersity and elsewhere on the web, the next best plausible explanation (which would in fact come back to the "Coca Cola < > Santa Connection" ;-) would be gluttony, right?

Holiday weight gain: Distinguishing fact from fiction

Before we jump to any premature conclusions, here, let's initially have a closer look at how much body weight Santa actually has in his bag for you.I mean, the perceived weight gain is enormous, right? Well, science is however not about perceptions and feelings and it should thusly not really surprise you that, according to a US study which was published in the prestigious New England Journal of Medicine (Yanowski. 2000), the "average" American (in this study represented by 195 US adults with a mean age of 39 +/-12 years) gains no more than 0.37kg, or, expressed in terms of the mean weight of the study participants, 0.5% during the holiday period from from mid-November to early or mid-January.

Figure 1: Percentage of normal weight, overweight and obese subjects with "major weight gain", as defined in absolute or relative terms (data adapted from Yanowski. 2000)

And while the average weight gain hardly is something to speak of, there are two other particularly intriguing findings of this study I do want to draw your attention to. The first one relates to the the data in figure 1. As you can see, the number of overweight subjects among those study participants with major weight gain (as defined as >3% of the initial weight) is particularly high. While only 7.9% of the normal-weight (American normal weight ;-) subjects gained more than 3% of their initial body weight 11.1% of the already overweight subjects did. Interestingly, the number of obese subjects was slightly smaller (7.5%). The latter is yet a physical necessity as there simply is a phyiscal limit to the amount of weight you can gain in a given period of time and 3% for a person with BMI>30 is obviously way more than 3% for someone who is only "overweight" (25 < BMI < 30).

The real problem is: The weight does not magically disappear

The real culprit is however that the weight people gain during last weeks of the year "is not reversed during
the spring and summer months", so that he researchers' concern that

[t]he 0.48-kg weight gain of the subjects in this study between September or October and February or March might not appear to be  clinically important and could easily go unnoticed by both the subjects and health care providers [and that] the cumulative effects of yearly weight gain during the fall and winter are likely to contribute to the substantial increase in body weight that frequently occurs during adulthood.

A 2006 by Hull may not only provide a hypothetical explanation for the non-reversibility of the (minor) weight gain (Hull. 2006), it also provides some insights into the true fallacy of "holiday weight gain": The minor increase in total body weight goes at the expense of concomittant increases in body fat and reductions in lean tissue mass.

Figure 2: Relative changes in anthroprometric measures over the holiday season; left axis - overweight / normal weight, right axis + figures - all (data adapted from Hull. 2006)

In the 82 college students from the Hull study, this fat promoting, muscle reducing "recompositioning" effect of the holiday season (Thanksgiving to New Year) was even so pronounced that the study participants actually lost -0.1kg of their total body weight. This was unfortunately a direct result of a +0.8 increase in fat mass and a -0.4kg decrease in lean mass. And what's more, the effect on fat mass was again more pronounced in those subjects, who were already obese.

Beyond candy, coke & co: Five additional reasons why Christmas is potentially deadly

In spite of the fact that these highly unfavorable changes in body composition are certainly not beneficial for anyone's overall health, it stands out of question that their effects would be cumulative and can thusly hardly explain the empirically validated increased mortality risk during the holiday season. In a 2004 comment on the aforementioned paper by Phillips et. al., Robert A. Kloner thusly proposes five additional hypotheses which could explain the potentially fatal side effects of the holiday season (Kloner. 2004):

Image 3: If you do not want to be treated by "beginners" and unexperienced hospital personnel you'd better not get sick over the holidays; and in case you do, please make sure to "postpone your death" in order not to ruin everyone's holidays ;-)

1. Inappropriate delay in seeking medical attention - best way out: don't wait until all the presents have been wrapped out, when aunt Mary chokes over her food
2. Reduced levels of healthcare staffing or fewer staff members who are familiar with individual patients during holiday on-call schedules - best way out: better avoid getting sick in the first place if you do not want to be treated by the SCRUBS staff
3. Increased emotional stress - just ignore your nephew when he starts crying because he did not get the Nintendo Wii he wrote on his wish list
4. Decreased our of daylight - make sure to get as much of the little light there is during prolonged walks with the whole family (may also help cool down any raised tempers ;-)
5. "Postponement of death" - tell your 127 year old uncle that he has been waiting so long now that it would be very inappropriate to die now and ruin everyones' Christmas celebrations

Well, I guess, now that you know about all the terrible things that could happen and the best ways to avoid them, it is about time to wish you, your family, friends and loved ones a happy (death-free) holiday season! And in case you need a break from the festivities, there is no Christmas break, here it at the SuppVersity ;-)

Beyond Warding Off Holiday Weight Gain: 250-1000mg of Freeze-Dried Ginger Reduce Visceral Fat Even When Rodents Are Fed an Obesogenic "High Fat" Diet.

Image 1: If ginger works only half as good in humans as it does in rodents, you can drink your way to a leaner and healthier you with Alisa Profumo's delicious low-carb "Healthy REAL Ginger Ale".

Zingiber officinale, or, in plain English, Ginger, is unquestionably one of the most remarkable plant rhizomes that is known to mankind. It has been used in various cultures for treating common colds or fever, to aid digestion, treat stomach upset, diarrhoea or nausea, to alleviate rheumatic disorders, gastrointestinal complications and dizziness, and, as of late, it has received quite some attention as a possible adjuvant to treatment modalities of cancer (Peirara. 2011). In a pretty recent study, the administration of 500 mg/kg zinigiber officinale to streptozotocin-induced diabetic rats (cf. related study in CLnA, the Omega-3 Variety of CLA), was able to partly restore the deteriorated glucose metabolism (Abdulrazaq. 2011), and a 2010 study was able to show that 6-Dehydrogingerdione, an active constituent of dietary ginger stopped the growth of breast cancer cells in the petri dish. "That is all very well", you may now be thinking, "but what does that all have to do with warding off the holiday weight gain?" Well, the answer lies in the results of a very recent study, which have just been published in the International Journal of Pharmacology (Malik. 2011).

Ginger reverses diet-induced visceral obesity and restores blood lipids to normal

Z.A. Malik and P.L. Sharma, two researchers from the Department of Pharmacology at the ISF College of Pharmacy in Moga, India, investigated whether the administration of 0.25-1g/kg body weight of dietary ginger (freeze dried powder that was made from fresh ginger juice; human equivalent would be 40-160mg/kg) would have any beneficial effect on the high-fat diet induced deteriorations in body composition, energy, lipid and glucose metabolism of male Wistar rats. For eight weeks, the scientists fed the rodents a diet that consisted of 33% normal rat chow, 33% Nestlé milk powder, 7% sucrose, and 27% tap water.

Figure 1: This is probably the lowest fat "high fat diet", I've seen in some time (data adapted from Malik. 2011) - ridiculous, but hey, if the diet had really been "high fat", who knows if the rodents would have gotten obese, anyway ;-)

If you take a look a the macronutrient breakdown of the "high fat" and the "normal diet" in figure 1, it is quite obvious that the former is - if anything - higher in fat than the latter, but by no means what any sane individual would consider a "high fat diet" (I really have to check myself not to start ranting against the "high fat diet induced whatever" in rodent models, again ;-) But be that as it may, ... the data in figure 2 shows that the milk powder and the sucrose were obviously enough to really fatten the rats up, profoundly:

Figure 2: Relative increases in body weight (BW), white adipose tissue weight (WAT), visceral fat weight and brown fat in rats on the "high fat diet" (data adapted from Malik. 2011).

With a whopping +417% increase in the total white adipose tissue weight, the poor rodents became profoundly obese. Their visceral fat depots (mesenteric, epididymal  and retroperitoneal) more than doubled (on average +150%), whereas the weight of their metabolically active brown adipose tissue increased by "only" 107%.

Figure 3: Relative changes in body weight (BW), white adipose tissue weight (WAT), visceral fat weight and brown fat in rats on the "high fat diet" who were supplemented with 250, 500 or 1000mg/kg ginger (data adapted from Malik. 2011).

The addition of 250mg/kg, 500mg/kg and 1g/kg body weight of the freeze-dried ginger juice (now obviously in powdered form) to the chow dose-dependently ameliorated the weight gain and reduced the weight of both the visceral, as well as the brown fat to level that were below those of the rats on the "normal" diet (cf. figure 3). Intriguingly, the "low" dose of 250mg/kg body weight turns out to be the most effective one, when it comes to the reduction of the epididymal, retroperitoneal and mesenteric visceral fat pads.

Figure 4: Relative changes in triglycerides (TG), total cholesterol (TC), HDL and total cholesterol to HDL radio in rats on the "high fat diet" and rats who were fed the HFD with 250, 500 or 1000mg/kg ginger (data adapted from Malik. 2011).

The addition of ginger to the diet also kept the blood lipids in check (cf. figure 4) and normalized the glucose response to an oral blood glucose tolerance test in the "high-fat" fed rodents. Other than the scientists had speculated, it had no effect on energy intake and did not increase the fecal fat content. The two markers of hepatic health, AST and ALT, which were measured in the study, remained almost unchanged - in the 250mg group there was even a -17% and -13% reductions in the respective transaminases (I am thusly amazed why the study has the words "anomalies after chronic administration" in its title).

How does it work and how effective is it?

Let's finally have a brief look at a) the potential mechanism by which ginger exhibits its fat-burning magic and b) how effective ginger would be, as compared to other, better known, "tools" to ward off weight gain or induce weight loss. To check whether the mechanism of action involves increased beta-oxidation, Malik and Sharmaa mixed an additional 30mg/kg of the beta-blocker propranolol into the high fat, ginger-supplemented diets of the animals - and as you can see in figure 5, the addition of the beta-blocker led to a profound reduction in the ameliorative / fat burning effects of the freeze-dried ginger powder.

Figure 5: Relative increases (vs. control on normal diet) in body weight (BW), white adipose tissue weight (WAT), visceral fat weight and brown fat in rats on the "high fat diet" supplemented with ginger, ginger + propanolol, or sibutramine (data adapted from Malik. 2011).

And as far as its effectiveness is concerned, ginger stands the comparison to the (in-)famous weight-loss drug Sibutramine, of which you will probably have heard that Chinese manufacturers of otherwise ineffective herbal weight-loss remedies like to mix it into their products (obviously without mentioning this banned ingredient on the label).

So, if we assume that these amazing results translate to humans, the addition of a few ginger rhizomes to your holiday diet could be a very effective tweak to ward off unwanted weight gain. And if your plans for 2012 include getting rid of the nasty love-handles you have acquired in the course of the past 12 months, you better get accustomed to the spicy, yet fruity flavor of the rhizomes of this perennial reed-like plant. You could, for example start out by following Alisa Profumo's delicious low-carb "Healthy REAL Ginger Ale in Minutes"-recipe on the Super Human Radio webpage (cf. image 1). And just in case you are too lazy to juice and / or freeze-dry some fresh ginger rhizomes yourself, you may want to consider buying a bag of Carl Lanore's  standardized ginger extract, which is also available on the Super Human Radio website.

CLnA, the "Omega-3 Variety" of CLA from Pomegranate & Co, Has Potent Anti-Obesity Effects and the Potential to Become More Than Just Another Anti-Diabetes Drug.

Image 1: Pomegranate - I loved to eat them even before I realized that their seeds are the #1 dietary source (83%) of punic acid.

While more and more people are beginning to grasp the notion that with (naturally occurring) fats - as with everything else in life - there is no simple "good" and "bad", no clearcut "black" and "white" and no definite "beneficial" and "detrimental". The number of different fatty acids and their respective effects on the human metabolism is so vast that it is pretty hard to keep track of all those varieties of saturated and unsaturated carboxylic acids. I would thusly not be surprised if you simply assumed that the "n" in the headline of this blogpost was a type that had slipped in because poor Dr.Andro is chronically stressed from Christmas shopping... well, while the latter is actually correct, the former is not: CLnA is actually the omega-3 variety of the famous conjugated linoic acid (CLA), which in and out of itself is not a single but a group of 28 different trans- and cis-isomers that occur in our diet mainly in the shape of high and full-fat meat and dairy products.

CLnA - Conjugated Linolenic Acid is not a typo ;-)

Within the last couple of years even the medical establishment has come to realize that the chronic omega-6 (n6: linolic acid) overload in our diet is killing us. The "heart-healthy" PUFAs have now become the more and less heart-healthy PUFAs with the totally healthy *rofl* omega-3s and the not just as healthy omega-6s - both, of course, still totally "essential" and WAY better than saturated fats,... (attention: the afore statements are full or irony! Saturated fats are of course NOT the bad guys. Sorry, David if that lead to confusion)... but I am getting derailed, here. So let's get to the point. What every reasonable person appears to agree on, these days, is that we have to lower the ratio of n6:n3 fatty acids in our diets. Now, I am asking you: Has it ever occured to you that CLA essentially is an omega-6 fatty acid? I mean its conjugated linoleic acid - "linoleic" as in omega 6 = linoleic acid! Probably not, right? The reason for that is yet (hopefully ;-) not that you are dump, but simply that the existence of an omega-3 "variety of CLA", namely conjugated linolenic acid, or short, CLnA, is something about which you will only hear, when you read blogs (such as the SuppVersity ;-), which do not stick to copying, pasting and commenting the stuff the authors have read on one of the major news-portals.

Table 1: CLnA isomer content in natural sources (data adapted from Hennesey. 2011)

From a molecular perspective,  CLnA isomers combine the conjugated double bond system of the classic conjugated linolic acid, you know, with the octadecatrienoic fatty acid (C18:3) structure of omega-3s, i.e. linolenic acid. Interestingly, this make-up confers these fatty acids with a high bio-active potential. Now, while this may sound like one of the frankenfood test-tube results of the gene-technology laboratories of Monsanto, we know at least 10 CLnA isomers which occur naturally in foodstuff or as byproduct of fermention processes (cf. table 1).

Adiposity, hyperlipidemia, cancer - CLnAs could help with all!

Image 2: Even if CLnAs would just prevent obesity, this illustration I borrowed from multiplemyelomalifeexpectancy.tk, shows that not being / getting obese alone would prevent a plethora of related maladies. Such as kidney failure, arthritis, gallbladder disease, infertility, asthma, fatty liver disease, sleep apnoea, depression, heart disease, hyperlipidemia, diabetes,... basically every major ailment the increasingly obese convenience society of the Western hemisphere is suffering from.

Due to their anti-adipogenic (meaning preventing the accumulation of body fat) effects CLnA fatty acids have been investigated as potential candidates for the treatment of the obesity epidemic for quite some time, now (Hennesey. 2011). In a 2002 article that was published in the Journal of Applied Biochemistry and Biotechnology, Nishimura et al. report that CLnA isomers exert apoptotic effects on mouse preadipocyte 3T3-L1 cell - or, in plain English, incubation with CLnA did not only hinder the "pubertal" fat cells from becoming mature adipocytes, it actually killed them. In vivo studies with rodents, such as Arao et al. (2004), where the administration of a diet that was enriched with 1% pomegrenate seed oil lead to a 27% reductin in omental white adipose tissue, were able to confirm the "rodent-real world signficance" of these test-tube results.

Other studies showed a normalization of hyperlipidemia in rodent models of the metabolic syndrome and a hand full of studies have explored the usage of CLnA isomers as cytotoxins in the treatment of cancer. In their concise review of the literature, Hennesey, et al. thusly rightly conclude that with their "potent inflammatory and immune modulating properties", their ability to "reduce the risk of obesity, improve cardiovascular health, and mediate strong anti-carcinogenic activity", the use of CLnA isomers or dietary enrichments could offer treatment strategies for pathologies, which "represent some of the greatest mortality risks to humans in the Western world and have been inextricably linked with diet" (Hennesey. 2011).

Adding diabetes to the list of potential targets for CLnA

For today, we are however going to focus on the most recent result from the research front: The effects of CLnAs on diabetes, or, to be precise, the increases in blood glucose, and decreases in anti-oxidant capacity that go hand in hand with the latter. In a recently published study (Saha. 2011), Siddhartha S. Saha and Mahua Ghosh from the Department of Chemical Technology at the University College of Science and Technology of the University of Calcutta (I don't have to tell you that this is in India, do I?) injected male albino lab rats with 60mg/kg streptozotocin (STZ) - this is a common and well-established method to induce a metabolic state that serves as a model of type II diabetes - and fed them diets that contained either no, or 0.5% of the total fat in the form of alpha-eleostearic acid (from bitter gourd, cf. table 1) or punic acid (which was in this case taken from snake gourd oil, but could as well have been extracted from the eponymous pomegrenate, cf. table 1).

Figure 1: Relative blood glucose levels vs. non-STZ injected control in streptozotocin injected rats over the course of the dietary intervention (data calculated based on Saha. 2011)

As you can see in figure 1, this 100% natural "food additive" had a more than pronounced effect on the +300% (vs. non STZ-injected control) elevated blood glucose levels of the "type-2 diabetic" rodents.

Figure 2: Relative level of lipid peroxidation (left) and total antioxidant capacity (right) levels vs. non-STZ injected control in streptozotocin injected rats after the 28-day dietary intervention (data calculated based on Saha. 2011)

And while the glucose levels were still 150% above those of the healthy control levels, the streptozotocin-induced lipid peroxidation in plasma, pancreas and erythrocytes of the lab animals was ameliorated by the snake gourd oil treatment (remember that is the stuff from pomegranate) and even reversed by the bitter gourd diet. Judged by the standardized FRAP assay, the "diabetic animals" that were fed a diet that contained 0.1% alpha-eleostearic acid (of the total diet, which had 20% fat) even exhibited a 10% greater total antioxidant capacity than the totally healthy control!

Figure 3: Relative expression of inflammatory cytokines, TNF-alpha and interleukin 6 in plasma capacity (right) levels vs. non-STZ injected control in streptozotocin injected rats after the 28-day dietary intervention (data calculated based on Saha. 2011)

Snake gourd oil, on the other hand, exhibited more profound effects on the elevated TNF-alpha, interleukin-6 and NF-kappaB levels of the STZ-treated rodents (cf. figure 2) and thus, at least this is my humble opinion, render punic acid the overall more promising agent with respect to the treatment of all sorts of inflammatory (or related diseases). After all, disturbances in the regulation of the nuclear factor kappa-light-chain-enhancer of activated B cells  (NF-kappaB) and the downstream over-expression of TNF-alpha and IL-6 are hallmark features of allmost all the aforementioned ailments of the increasingly obese western convenience society. This is also why I am quite certain that we are going to hear much more about the CLnAs in the month to come... and I guess, I don't have to tell you that right here, at the SuppVersity, is where you will read about respective studies first!

Minimal Carb Reduction, Maximal Results? Study Compares 60% vs. 40% CHO Diets + 6-Week 25% Energy Reduction

Does "moderate low carb" work? And if so how much of the usual triglyceride and glucose lowering benefits of walking the whole nine yard are you going to miss?

I know that 40% carbs is not what you consider "moderate", but for most of our fellow countrymen and women, cutting back on at least one serving of their beloved pasta and bread is already more than you can ask for if you want a compliance that's beyond 1%. Against that background it is all the more important to know whether even small changes in the overall carbohydrate intake have to offer obviously less pronounced, but still significantly beneficial health benefits to overweight and obese individuals -- small changes like the 20% reduction in carbohydrate intake in the "moderately-restricted carbohydrate diet" (MRCD) arm of the most recent study from the Isfahan University of Medical Sciences in Teheran, Iran (Rajaie. 2014), for example.

1/2 low carb = 100% adherence, but at which costs?

The experiment was conducted by Somayeh Rajaie and colleagues. The results will be published in the January 2014 edition of the peer-reviewed scientific journal Nutrition. Results of which the authors say that they are particularly relevant, because...

"[...e]arlier studies on the management of metabolic syndrome (MetS) have mostly focused on very low carbohydrate diets" whereas long-term adherence to such diets is difficult for apparently healthy people."(Rajaie. 2014)

I can already hear the first people arguing that this was bullshit. What is bullshit, though, is to close your eyes and ignore the real world problems people encounter, when they go from years of sugar, sugar, sugar, sugar and fat to diet that have almost no sugar in them. I mean, come on low carb boys and girls, ask your non-fitness-infected friends about going without pasta and pizza for the rest of their lives. What are these people going to answer? ... You see: long-term adherence to very-low-carb diets is difficult for the average "apparently healthy people", the Iranian scientists are talking about, here ;-)

Figure 1: Number of servings from different food groups (left) and macronutrient composition (right) of the basleine diet of the 39 overweight study participants (Rajaie. 2014)

While it may not be as straight forward as it is with rodent studies, we still have to take into account that the baseline diet could render the significance of the data from a human study similarly questionable as that from rodent studies. Figure 1 does yet tell you that these aforementioned "average apparently healthy" man or woman in Iran eats pretty much the same sh*t as his / her American or European counterparts: a diet that's a "perfect" mixture of fats and sugar that will blow you up much more effectively than a really high carbohydrate + low fat, or a really low carbohydrate + high fat diet.

Apropos "high carbohydrate": The basline carbohydrate intake is actually so "low", that the subjects in the high carbohydrate group of the study at hand had to increase their carbohydrate intake to get it up to the recommended 60% of their total energy intake. By implication, this means that the subjects in the "moderately restricted carbohydrate" group didn't reduce their carbohydrate intake by 20% (as the abstract appears to imply), but only by 10% vs. baseline.

Adding or subtracting 10% carbs - what's better when you're dieting?

Ok, enough of the number games. Basically what I am trying to say was that the effective reduction in carbohydrate intake during the 6-week intervention period is only 10% - not 20%, as the difference between the high carbohydrate and the "moderately restricted" carbohydrate group (MRC) would suggest.

Figure 2: Macronutrient composition of the diets during the 6-week intervention (left) and changes in macrontrient composition (right) expressed relative to baseline (Rajaie. 2014)

As I already pointed out, this implies that the high carbohydrate group effectively increased their relative carbohydrate intake (see Figure 2, right). In contrast to what the increasing number of carbophobs out there would probably have expected, this outrageous increase in carbohydrate intake did not result in weight or fat gain.

Small changes make a difference! But that's small changes in energy, not carbohydrate intake

As the data in Figure 3 goes to show you, both groups lost almost exactly the same amount of body weight (1.72kg HC vs. 1.70kg MRC), they also gained the same ~800g of lean mass and lost 1.3kg of body fat.

Figure 3: Changes in body weight, BMI and body composition after 6 weeks (Rajiae. 2014)

In other words: From a body composition perspective the 20% difference in carbohydrate intake obviously didn't make a difference - and the "trend toward greater reduction in waist" in the MRC group, the authors highlight in their abstract could be mediated by the baseline difference (1 cm larger waists in the MRC group).

A very similar image emerges for the often advertised beneficial effects "real" low carb diets have on the serum triglyceride (TG) levels. In the "moderately restricted carbohydrate" group, they were simply not there. With a p-value of p = 0.07 for the inter-group difference, these changes were even more "random" than the previously cited effects on the waist line. And if the "greater reduction of systolic blood pressure (−8.93 versus −2.97 mm Hg; P = 0.06) and diastolic blood pressure (−12.7 versus −1.77 mm Hg; P = 0.001)" in the MRC group was not simply a result of a (in the long term) not necessarily beneficial reduction in the sympathetic tone is similarly difficult to tell.

Read: " Two Days A Week High Protein, Low Carb Fast Cuts >10% of Body Fat in 4 Months" | more

Bottom line: Hovering around in the "comfort zone" is not going to help you make huge changes. When you run a 25% energy restriction you will lose body weight. As the study at hand shows, even without sacrificing muscle tissue. Whether you do that with a 40% or 60% carbohydrate does not appear to matter for the average overweight individual.

Long story short, if you don't go to the extremes and adhere to a sane energy deficit (>20%, but <35%), it really doesn't matter whether you eat some more carbs or some more fats. And let's be honest, brutally honest: For an increasing part of the ever more obese inhabitants of the Western obesity belt, it would already be a remarkable achievement not to get fatter every day. If these people managed to lose ~1.3kg of pure fat while increasing their lean mass by almost 1kg that would be a major success.

Reference:

• Rajaie, S., Azadbakht, L., Khazaei, M., Sherbafchi, M., & Esmaillzadeh, A. (2014). Moderate replacement of carbohydrates by dietary fats affects features of metabolic syndrome: A randomized crossover clinical trial. Nutrition, 30(1), 61-68.

Appetite Short News: Pavlovian Conditioning at Work in the Obese | Polydextrose as a Satiety Promoter | Parents, Just Like Their Kids, Fall for All the Tricks of the Food Industry

Too lean for Pavlovian Conditioning.

In today's "appetizing" installment of the short news, I have picked three of the latest publications from the scientific journal Appetite, of which I thought that they were newsworthy. In that, I cover the Pavlovian Conditioning of overweight individuals, the benefits of polydextrose on appetite control and the way product labels fool parents and children into buying unhealthy foods.

I have to admit: It's not all practically applicable, but who knows maybe you can use it to smart-ass during the holidays. Or maybe you bake some polydextrose enhanced super-satiating cookies for your family, ha?

More facts for your smart-ass sessions on the holidays ;-)

Bugs Dictate What You Crave

Sweeteners & Your Gut

Foods, Not Ma- cros for the Gut

Lactulose For Gut & Health

Probiotics Don't Cut Body Fat

The Macrobiotic MaPi2.0 Diet

• Hedonic food cue conditioning in the obese: You know the story about Pavlov's dog starting to salivate, when the bell rang that would usually accompany his next feeding?
  
  Well, a recent study confirms that something very similar is at work in obese, but not lean subjects. While the former remain calm and cool to a visual cue that had previously been given alongside some tasty chocolate milk, the latter began to swallow, a reliable sign of increased salivation. As the scientists from the Allaint International University in San Diego say, these "
  

  are the first results to show differential acquisition of Pavlovian conditioned responding in overweight individuals compared to lean individuals" (Meyer. 2014)

  The fact that the conditioning worked was yet not the only significant finding, Meyer et al. made. They also observed that hedonic food stimuli were significantly more effective 'conditioners' in the obese than neutral stimuli.
  
  Practically speaking the observations the researchers from the Allaint International University in San Diego made, may partly explain the difficulties obese individuals who may have been conditioned / conditioned themselves to hedonic food stimuli for their whole lives have when it comes to controlling their energy intake.
• Polydextrose as a satiety promoter: In their meta-analysis of the current literature on the effects of polydextrose on energy intake, researchers from the US and Finland found that...
  
  • polydextrose consumed with a mid-morning snack reduces energy intake (EI) at lunch time.
  • this reduction in EI at lunch time occurs in a dose-dependent manner.
  • but the energy intake during the rest of the day did not show any difference
  Now this probably wouldn't be newsworthy, then, if a a regression model had not been able to confirm a dose-dependent effect on the reduction of daily energy intake.

Added polydextrose reduces the insulin response to milk (Lummela. 2009)

What exactly is polydextrose? Polydextrose is a glucose polymer that is completely soluble in water. As a food additive it offers the texture of sucrose but provides only 25% of the equivalent energy, or 4 kJ/g. It has been approved for use in foods in over 60 nations and is recognized as a dietary fiber in more than 20 countries (FAO/WHO, 2009). Next to the reduced energy content it has another benefits of the fibrous substance is that its addition to foods like milk can reduce the insulinogenic response to this meals significantly - even in healthy individuals (Lummela. 2009).

• More specifically, the meta-analysis was able to show that the dose of polydextrose consumed correlated significantly with the reduction of nergy intake at lunch (−0.67 Polydextrose (g/day) | 80% correlation; P < 0.01), due to which the energy intake was reduced by 1% per 2.86g of polydextrose per day.
  
  As Ibarra et al. point out, the sex-specific results are consistent with results for the whole group - the effect is thus similarly pronounced in both men and women. Accordingly, the meta-analysis "supports the notion that the consumption of polydextrose reduces voluntary energy intake at a subsequent meal" and that "this reduction in energy intake occurs in a dose-dependent manner" (Ibarra. 2014).
• Parents of preschool children make (non-)sense of front-of-package visuals and claims on food - A recent study from the Colorado State University and the University of Illinois at Urbana-Champaign investigated what parents make of the colorful packaging of foods their kids like to buy and found that most of them tend to "accept misleading front-of-package claims when making quick food decisions" (Abrams. 2014).
  
  

  

  Parents fall for unwarranted claims, and misleading images children for cartoons.

  While playful visuals appeal to children, parents associate them with junk food. That does yet not mean that they would not fall for health claims, realistic graphics, and natural claims which make them classify the junkfoods that were investigated in the study at hand as healthier.
  
  Fruit graphics in particular were misunderstood to indicate that the respective foods actually contained fruit, when they were simply meant to communicate flavors, instead. Against that background it's not surprising that the unsettling result of this study in 28 women and 2 men revealed that "[parents may make unhealthy food choices as a result of front-of-package information" (Abrams. 2014).

Intensity is key to reduce the exercise induced increase in appetite | more

Bottom line: I understand very well that for most of you only news item #2 is of practical value. Item #1, on the other hand, is rather a description of the misery than a solution and #3 is something that you as a SuppVersity reader probably knew, already... that being said, simply adding more polydextrose to the foods dumb parents buy for their kids because there are fruits on the packaging is not going to help their kids becoming overweight adults who begin to salivate, whenever they see the right food cues. A long-term solution to the problem would thus have to start with the production of healthier foods by the food industry and the education of the public who would then no longer fall for the unwarranted health claims on the packaging of children and adult food products | Comment on Facebook!

References:

• Abrams, Katie M., Caitlin Evans, and Brittany RL Duff. "Ignorance is bliss: how parents of preschool children make sense of front-of-package visuals and claims on food." Appetite (2014).
• Ibarra, Alvin, et al. "Effects of polydextrose on different levels of energy intake: a systematic review and meta-analysis." Appetite (2014).
• Lummela, Netta, et al. "Effects of a fibre-enriched milk drink on insulin and glucose levels in healthy subjects." Nutrition journal 8.1 (2009): 45.
• Meyer, Monica D., et al. "Pavlovian conditioning to hedonic food cues in overweight and lean individuals." Appetite (2014).

The Fat Truth Behind the Dairy Weight Loss Miracle: MUFA and PUFA Impair, Saturated Fat and Plenty of Micronutrients Drive Full-Fat Dairy-Powered Fat Loss.

Image 1: Kids who drink more milk, tend to be leaner... and that despite (?) the fact that this stuff comes out of an animal and is full of bad cholesterol and fat - outrageous ;-)

Plenty of interesting news, lately, so this one - just like the recently released hypertrophy / hormone correlation study by Stuart Phillips, about which I have been talking in yesterday's installments of the Intermittent Thoughts got somewhat delayed. With the Christmas holidays and the approaching and all those New Year's weight loss resolutions (I would prefer the term "fat loss resolution", though ;-) already on your mind, I do yet think that it is about time to break the news on the "fat" reason for the purported beneficial effects an increased consumption of dairy products during periods of caloric restriction appears to have on weight and more specifically body fat loss (Linn. 2000; Peirara. 2002; Shahar. 2010).

Dairy, calcium or simply the right macronutrient composition?

The scientific results I am going to present are taken from a study that was published in the Journal of Nutrition and Metabolism a few weeks ago (Smilowitz. 2011). In a randomized, placebo-controlled study Jennifer T Smilowitz and her colleagues from the USDA-funded (keep that in mind, when interpreting the results, or rather the scientists interpretation of the latter ;-) Western Human Nutrition Research Center assigned their 62, against the background of the rampant obesity epidemic, only slightly overweight young subjects (mean age: 25y; BMI ~28) to a calorically restricted diet (-500kcal) that was specifically designed to "provide comparable levels of macronutrient and fiber, to approximate the average consumption in the US" (35% fat, 49% carbohydrate, 16% protein and 2-3g fiber), which contained either

• 0-1 servings of dairy, with 500mg dietary calcium (from the whole diet) + placebo,
• no dairy (still 500mg calcium from diet), 900mg of supplemental calcium carbonate, or
• 3 servings of dairy, with 1400mg of dietary calcium (from the whole diet) + placebo

Thusly, the study basically mimicked, what would happen if you told the average American to just keep their usual sedentary life-style (the subjects were instructed not to start to exercise or anything like that) and either just reduce his caloric intake by 500kcal, to do the former and to make sure to have three servings of dairy per day, or to just take an additional "healthy" calcium carbonate supplement.

Eat dairy + whatever you want and lose weight?

Now, interestingly, the subjects were not only free to chose whether they wanted to consume the dairy from low or normal fat cheese, milk and/or yoghurt, they were also relatively free as far as the rest of their dietary choices were concerned so that the detailed analysis of their food-logs allowed for conclusions to be drawn that went beyond the initial scope of the study... but let's take one thing after the other.

Figure 1: Dietary intake (macronutrients in kcal/day) of the subjects before and at the end of the 12-week study period and relative changes in carbohydrate, protein and fat intake (data calculated based on Smilowitz. 2011)

If you take closer look at the analysis of the dietary records the subjects had to keep, you will notice that the minor differences in the dietary prescriptions induced quite profound changes as far as the macronutrient composition of the respective diets was concerned. While the subjects in the non-dairy groups, regardless of whether they received a calcium supplement or placebo, cut back on all the three major macronutrients, the requirement to incorparate three servings of dairy into their meal-plan, alone appeared to suffice to keep the protein intake of the dairy group at a reasonably high level (~72g; which would be 0.96g/kg body weight). The protein intake of the two non-dairy groups, on the other hand dropped to 57g (0.75g/kg) and 54g (0.7g/kg) for the calcium and placebo supplemented groups, respectively.

Figure 2: Changes in body composition and measures of insulin sensitivity after 12-weeks on the high dairy, calcium supplemented or placebo supplemented diets (data calculated based on Smilowitz. 2011)

In view of the facts that the subjects had to stick to the calorically restricted diet for 12 weeks, it should not surprise you that all of them lost a statistically significant amount of body weight (cf. figure 1) and improved their insulin sensitivity (as indicated by reduced insulin levels and HOMA-IR values).What should yet strike your eye are the increased reductions in body fat and waist circumference and the greater increase in lean mass-% in the high dairy group. Now, you will probably assume that this was a result of the higher protein intake, and that may in fact have been the case, as one of my beloved model calculations by which scientists "adjust" their data for whatever they want (usually until the result is in accordance with their hypothesis ;-) revealed that

Dairy product consumption was found to be significantly associated with reduced WC [waist circumference] and %BF [percent body fat], however, these relationships were no longer significant after adjustment [my emphasis ;-] for protein and energy intake and physical activity.

Figure 3: Scatterplot of the partial correlations between reported 12-week mean dietary fat intake expressed as % of total energy and changes in lean body mass (LM) and body fat % (taken directly from Smilowitz. 2011)

Assuming that this "adjustment" yielded valid results it is all the more interesting what a subsequent analysis of the "adjusted" data revealed:

When expressed as a percent of total energy, dietary fat composition was correlated with changes in anthropometrics. Reported MUFA at 12 wk was inversely and positively associated with changes in % LM and % BF, respectively.

Or, in the words of the layman: The greater the relative monounsaturated fatty acid (MUFA) content of the subjects' diets, the more lean mass was lost and the more body fat was retained during the study period (cf. figure 3). Similarly, a higher intake of polyunsaturated fatty acids (PUFA) was associated with lower reductions in waist circumference, and while  the scientists claim that the n3:n6 ratio did not matter, it should make you wonder if it could actually be coincidental that the n6:n3 ratio in the dairy group was 6.6, while the ones in the calcium and placebo groups were 8.7 and 7.9, respectively.

And what about saturated fats? 

Moreover, the USDA scientists mention only "in the small print" that most fundamental (and statistically significant) distinguishing feature of the dairy group, who unquestionably had more favorable weight loss results despite an overall greater caloric intake, was (and I am quoting this from the paper) "a significantly higher intake of SFA [saturated fats] and lower intakes of MUFA and PUFA compared with the calcium supplement and placebo groups". Now, guess where this "bad" saturated fat came from? Well, probably from full-fat dairy! And guess why those "good" MUFAs and PUFAs were missing from the diets of the high dairy group. Well, probably because the subjects ate less "healthy vegetable oils"... ah, and did I already mention that the dairy group also ingested disproportionally (relative to their caloric intake) higher amounts of biotin, vitamin B12, vitamin D and - God forbid! - cholesterol?

Image 2: Even if you like animals, eating their eggs and full-fat dairy products won't hurt them.

So, while the scientists do their best to conceal that all those "bad things", like a high protein intake and nutrient dense real non-processed animal products with their original (saturated) fat, cholesterol and micronutrient content left untouched, are the true driving forces of successful weight loss (and, you bet, also maintenance), I am quite confident that you, as a diligent student of the SuppVersity, would not have needed the doctored... ah, pardon me, ... I obviously meant the well-adjusted results of this study to know that. After all, you are probably just enjoying a rib-eye steak with some delicious melted butter from grass-fed cows, right?