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

Devil in the Feeding Trough: PGE-Response to "Bad" Red Meat from Grass-Fed Cattle Could Prevent not Cause Cancer, Stroke and a Whole Host of Autoimmune Diseases.

Image 1: You do not need to hunt your red meat like a paleolithic human being, just make sure it comes from grass-fed animals and you will have a "health food" that modulate the your prostaglandin response to inflammatory assaults and thusly reduce your risk of cancer, stroke and autoimmune disesases in a way no fat-free chicken breast will ever do.
I have had this in the news before, in the context of the purported health benefits of CLA, with respect to the modulation of the n3/n6 ratio in your diet and in various other context, you heard me saying, or, I should say, read me writing that rather than popping tons of fish oil caps, you should rather focus on decreasing your overall omega-6 intake by making healthy food choices at the supermarket. In this regard, choosing grass-fed over commercially raised beef (and other meat) products could turn out to be one of the most far-reaching choices you can make. While that alone will help you to concomitantly reduce the n-6 overload, as well as the overall PUFA-burden that is so characteristic of the "Western diet", a recent study shows that eating red meat, even instead of the "healthy" white fat-free chicken breasts, everyone is pounding these days, could actually have profoundly beneficial effects on your (auto-)immune health, protect you from cardivascular disease and (this is important for the ladies) get your menstrual periods and related issues back in order.

How grass-fed beef can help and why it outperforms bison, elk and chicken

In their study, the results of which were published in issue 31 of the journal Nutrition Research, K. Shane Broughton, Daniel C. Rule and Eldon Handrich did what scientists have been doing for decades now. They took mice (your usual carnivorous animal) and put them on one of those grain-based diets that was then enriched with "bad" red meat to make the animals sick. Well, ... while the design was in fact the same, the good news is that the intention was by way of exception not to show "prove" (as if mainstream dietary advice would be interested in "proof", anyway) how bad those nasty red meats are, but to evaluate whether the
[...] consumption of meat from range-fed bison vs range-fed and grain-finished cattle and grain-finished bison would lead to reductions in PGE-2 [prostaglandin E2] release without altering PGI-2 [prostacyclin] release after an infl ammatory stimulus in a mouse model.
Or put simply, the scienists wanted to check whether there was any truth to the superiority of bison compared to the "bad" red meat, when it comes to balancing out the ratio of PGE-2 and PGI-2.
Image 2: Bayer probably won't like it if everyone would start eating grass-fed beef. After all, that would probably reduce the sales of their COX-inhibitor Aspirin protect.
For those of you wondering about a) what those prostaglandins are and / or b) why you would want to modulate their ratio and not eradicate them completely, here is is brief rundown on one of my favorite topics, the Yin&Yang of life and, on a related note, the fallacy of common black-or-white thinking. As with almost everything there are also two sides (in fact there are many more ;-) to the inflammatory coin and PGE-2 and PGI-2, two acronyms that differ by only a single letter, are situated on those opposing sides. If they are expressed at the right ratio, everything is fine. The (relative) over-expression of PGE-2 that is commonly observed in people following the "Western diet", on the other hand, is associated with a host of pathologies, such as elevated risk for color ectal cancer, suppression of ovulation, and increased problems with rheumatoid arthritis and headaches. (Relative) underexperssion of PGI-2, the other hallmark result of the "food" people are poisoning themselves with on a daily basis, in turn, increases the risk of thrombosis and stroke. If any of that does ring a bell, but you do not know which one, you may want to check out the label of your Aspirin tablets - as a cyclooxygenase inhibitor Aspirin also blocks the production of PGE-2... but before you do now pop another of those tabs, I suggest you read on and learn that by paying a few extra bucks for "real meat", you will probably never have to take your daily dose of Aspirin protect.
And while the scientists were right, grass-fed bison is in fact better than grain-fed beef, a closer analysis of their results will show that the often-heard and widely believed statement that "bison is the best form of red meat you can possibly find" is nothing but another of the 1001 dietary fairy-tales of the bloggosphere.
Figure 1: Fatty acid content of the diet (in g per 100g of the whole chow) - saturated, mono- and polyunsaturated fatty acids (n3, n6), left; CLA content, right (data adapted from Broughton. 2011)
But let's first take a look at the experimental diets, the male CD-1 mice were fed for 14 days. What is interesting about these, is that, due to the inclusion of standard rodent chow, the differences in fatty acid composition between the grass-fed vs. corn-fed bison and beef diets and the diets that were based on (wild-type) elk and commercial chicken breast meat were actually not very pronounced (cf. figure 1). And while the inclusion of corn oil in every diet may sound blasphemic in the ears of the hard-core anti-grain croud (I know you are out there ;-), the addition of grass-fed meat to an otherwise standardized (and probably suboptimal) diet is actually a strength of the study. Thusly, the study does reflect pretty well, what could happen, if the average Joe or Jane did nothing else, but replace the corn-fed meat in his/her diet with meat from range-fed animals - and wouldn't you agree that this is a much more realistic scenario than living on nothing but grass-fed beef or bison?
Figure 2: Modulatory effect of 2 weeks on prostaglandin expression of mice after two weeks on diets enriched with range-fed, or feedlot fed meat of different sources (data adapted from adapted from Broughton. 2011)
And, if we focus solely on the PGE-2 to PGI-2 ratio (you can read up on its importance in the red box above), it is obvious that a small dietary change from grain- to grass-fed meets could actually have pretty profound effects on your (auto-)immune health. The data also shows that the "healthy" lean chicken breast your nutritionist has probably told you to eat actually should not be your first choice, when it comes to establishing a healthier prostaglandin milieu - and if you don't believe me, maybe you want to trust Broughton et al.'s judgement:
[...] chicken is promoted for its health benefits, yet in our study, it was no better for possible prevention of PGE 2-associated immune pathophysiology. Furthermore, chicken would not be as beneficial as grain-fed beef and elk consumption in reducing thrombos is and stroke potential.
So, while eating (commercially raised) chicken won't harm you, it will not help you steer your inflammatory response into either the PGE or the PGI direction. Broughton, Rule and Handrich are thusly right, when they conclude that
Based on results of the present study, consumption of any of the range-fed meat sources examined would be better at reducing the possibility of immune-related pathophysiologies than meat from grain-fed cattle. [...] Although range-fed beef and bison consumption would be equivalent for their immune-based role, consumption of range-fed beef would be better for the prevention of thrombosis and stroke.
Now, isn't that surprising? Chicken not the best thing you can eat? The "healthy alternative to beef" that has been pimped in the mass media lately only on par with plain beef and superior as far as reduction in the risk of stroke and thrombosis are concerned? Could it really be possible that the "bad red meat" is not so bad, after all? Is there the remote possibility that it's not red meat per se, but sick meat, or I should say the meat of animals we have been making sick by feeding them the same "healthy whole grains" with which we have been poisoning... ah, I mean nurturing *rofl* ourselves over all these years that is giving us migraines, arthritic joints, cancer, strokes and a whole host of nasty autoimmune diseases? I guess, I will leave it up to you to find and answer to that question ... and I am confident that you are smart to one and one, or rather grain-fed meat and (auto-)immune disease together ;-)

Chicken, Rice, Veggies & Oil and How Their Effects on Your Insulin & Glucose Levels Are 50% Off Those You'd Expect Based on the Calculated Glycemic Index of This Meal

The power of GI calculations is limited and even with meals as simple as the one in the picture, the calculated glycemic index can be ~50% off!
As a SuppVersity reader you've repeatedly read about macronutrient interactions, such as the insulin boosting effects of whey protein or dietary fat, studies that investigate the effects of the individual ingredients of a complete meal on the glycemic response healthy men and women, however, are scarce. Against that background the results of a recent study from the Clinical Nutrition Research Centre at the Singapore Institute for Clinical Sciences are of particular interest. After all, the Lijun Sun et al. (2014) determined the effect of co-ingesting a high-protein food (breast chicken), a fat (ground nut oil), a leafy vegetable or all three on the glycaemic and insulinaemic responses of white rice in healthy adults and did thus produce results that could be practically relevant for all of us - more relevant than inaccurately calculated GIs.
Use sugar alternatives if you want to improve your blood glucose!

Unsatiating Truth About Sweeteners?

Will Artificial Sweeteners Spike Insulin?

Sweeteners & the Gut Microbiome Each is Diff.

Sweeter Than Your Tongue Allows!

Stevia, Much More Than Sweet?

Artif. Sweetened Foods Good, Not Bad for Fat Loss.
Before we get to the study results, though, let's briefly recap what the researchers actually did: Sun et al. recruited twelve healthy participants (six female and six male) by means of advertisements, flyers and personal communications.
"Before inclusion into the study, potential participants were briefed on all aspects of the experiment and were given the opportunity to ask questions. Following the securing of consent, a health assessment was performed which included anthropometric measurements and a health questionnaire (giving details of food allergies/intolerance, metabolic diseases, special dietary needs and smoking habits). Those who fulfilled all the inclusion criteria [body mass index 18.5–24.99 kg/m2; blood pressure (BP)—systolic BP between 110 and 120 mmHg and diastolic BP between 75 and 85 mmHg; age 21–50 years; fasting blood glucose, 4–6 mmol/L; not on prescription medication, non-smoking; no genetic or metabolic diseases) were enrolled into the study." (Sun. 2014)
In addition, the amount of regular physical activity was quantified and subjects who were partaking in competitive sports and endurance events were excluded. Eventually, the scientists ended up with a group of normal-weight men and women at the age of 21–34 years.
Table 1: Composition of the test meals, ACHO = available carbohydrates.
Nutritional data were obtained from the manufacturers (Sun. 2014).
The subjects visited the laboratory 5 times (plus a baseline testing with a glucose solution). On each of these testing sessions, which were separated by at least one week, the subjects arrived at the laboratory between 7:30 and 8:30 after an overnight fast and received one of the five test meals from Table 1, which contained 194 g white of plain white rice,  254 g of white rice with fat, 294 g of plain white rice with chicken breast, 314g of white rice with vegetable and 474g of white rice with fat, chicken and vegetable, respectively.
Ground nut oil? I guess most of you will know the oil that was used in the study at hand as "peanut oil" and it is - as you will probably know, as well - not exactly high in "holy" omega-3 fatty acids. Rather than that, peanut oil contains oleic acid (46.8% as olein), linoleic acid (33.4% as linolein), and palmitic acid (10.0% as palmitin), as well as small amounts of stearic acid, arachidic acid, arachidonic acid, behenic acid, lignoceric acid, but not a singly milligram of omega-3s.
The test or reference food was then given to consume within 15 min. Further blood samples for glucose and insulin analysis were taken for the subsequent 180 min (every 15 min in the first hour and every 30 min for the subsequent hours) - a procedure that yielded the following results.
Figure 1: Glucose levels expressed relative to the ingestion of 250g of glucose (Sun. 2014)
The values in Figure 1 are expressed relative to the glucose response to 250g of pure glucose, of which a brief glimpse at the data tells you that they produce higher peak and incremental area under the curve (iAUC, a measure for the glycemia over the whole testing period) levels than any of the meals. Statistical significant differences were yet observed only for rice with chicken breast, rice with vegetable, and rice with fat, chicken and vegetable - yet not for the plain rice and the rice + fat meal (the latter was to be expected based on the discussion in my previously referenced article "True or False? Adding Fat to A Carby Meal Lowers Insulin Response" | read more).

Significant differences for the insulin response were observed for the white rice + chicken meal, where the insulin response was significantly higher compared to the white rice only (+22%), as well as the rice with + vegetable meal, where the insulin response was significantly lower compared to the white rice only condition (-16%).

The combination of foods determines the GI of the meal

Based on the classic equation that's usually used to determine the glycemic index of a meal (Hätönen. 2011), Sun et al. calculated the predicted glycemic of the five test meals and compared it to the actual glycemic index (GI) that was calculated based on the measured glucose and insulin response of the subjects.
Figure 2: Predicted and measured glycemic index as well as measured insulinemic index of the meals (Sun. 2014)
As you can see in Figure 2, the comparison yields an unsurprising result. As it's usually the case, when simple equations are used to predict physiological effects, the real GI values were significantly different from the calculated ones and  - significantly lower, that is. Accordingly, the meal with the least impact on postprandial glycemia and a comparatively low insulinemic effect is the one containing rice, fat, chicken and veggies - in other words, the complete meal. 
Suggested Read: "Get Your Protein, Veggies & Fruits and Get Them Regularly: High(er) Meal Frequency (6 à Day) + High(er) Protein Diet Support Weight & Fat Loss on a Diet." | read more
Bottom line: While the importance of the glycemic index (GI) has long been totally overrated, there is accumulating evidence that high postprandial glucose levels are a significant contributor to increases in cardiovascular disease risk even in healthy individuals (Einarson. 2011; Mah. 2011). Against that background the results of this recent trial support my previous recommendation to consume balanced meals containing protein, fat and carbohydrates, instead of no-fat or no-carb meals.

In contrast to what the "paleo hypothesis" and the notion that our ancestors would not have collected some berries or boiled some rice to have it alongside the chicken they just caught would say, the contemporary scientific evidence indicates that we are well equipped to handle complex meals, as long as they don't contain exorbitant amounts of fat and carbohydrates.

One thing we should not forget, though, is that the 50% discrepancy between the calculated and real glycemic index of the "complex" test meal (four ingredients is not exactly "complex", actually) suggests that one of the reasons that many of the previous studies failed to detect a meaningful association between the (obviously calculated) GI of an individuals diet and his / her cardiovascular or diabetes risk may be that the data the scientists used was similarly inaccurate as the predicted glycemic indices of the test meal in the study at hand | Comment on Facebook!
References:
  • Hätönen, Katja A., et al. "Protein and fat modify the glycaemic and insulinaemic responses to a mashed potato-based meal." British Journal of Nutrition 106.02 (2011): 248-253.
  • Mah, Eunice, et al. "Postprandial hyperglycemia impairs vascular endothelial function in healthy men by inducing lipid peroxidation and increasing asymmetric dimethylarginine: arginine." The Journal of nutrition 141.11 (2011): 1961-1968. 
  • Sun, Lijuan, et al. "Effect of chicken, fat and vegetable on glycaemia and insulinaemia to a white rice-based meal in healthy adults." European journal of nutrition (2014): 1-8.
  • Wolever, T. M. S. "Is glycaemic index (GI) a valid measure of carbohydrate quality&quest." European journal of clinical nutrition 67.5 (2013): 522-531.

Underestimated Vitamin D Sources: Especially Eggs, But Also Chicken, Pork, Fish & Dairy Contain an Overlooked, Physiologically Relevant Amount of Ready-Made 25OHD

What do you need for a high 25OHD picnic on day at the beach? Eggs!
Regular SuppVersity readers know: The slowly abating vitamin D hype is driving me up the walls. Whenever you search a database for recent articles with the word "vitamin" in it, you are flooded with papers on vitamin D - many of them simplistic adulations without any new data or information. Others are totally irrelevant experiments on cell lines or non-significant epidemiological analyses, where no one can tell you whether the low vitamin D levels are mechanistically or corollarily involved in whatever the scientists are trying to tell you vitamin D was beneficial for.

Among all this mess, you can still find a handful of interesting papers. You just have to look close enough to spot gems such as a review by Ovesen, Brot and Jakobsen (2013).

Are Eggs the Best Dietary Vitamin D Source We Have?

"Eggs? The best vitamin D source?" I don't have the hubris to say that eggs are the absolute #1, but considering the fact that eggs are the #1 source of "actual", preformed 25OHD, aka 25-hydroxyvitamin D*, in our diets, you are probably going to agree that eggs may well be the most underrated source of vitamin D in our diet (25OHD is what doctors and scientists will measure in your blood stream; most essays measure total 25OHD, so I will not differntiate the different forms here).
Preformed vitamin D? Isn't that dangerous? No, quite the opposite: Pharmacologic doses of 25OHD do not change or may even decrease plasma levels of 1,25(OH)D, aka calcitriol, which can potential cause calcification (Trummel. 1669; Heaney. 1997). When you are D-ficient, though, your body will retain the 25OH. This is particularly interesting for people with intestinal malabsorption, for whom 'regular' vitamin D supplements, i.e. vitamin D3, aka cholecalciferol, or vitamin D2, aka ergocalciferol, don't work (Francis. 1983)
When it comes to vitamin D, eggs, fish, dairy, meat and offal are quite unique. All of them contain "vitamin D" in the still-to-be-converted D3 form you all know. What only few people know is that they also contain the celebrated vitamin D metabolite 25-hydroxyvitamin D (25OHD). This is not only the form your doctor will measure, when you ask for a "vitamin D test", it's also the "vitamin D" that has been linked to all sorts of health benefits in the aforementioned epidemiological studies.

If you want to increase or maintain your 25OHD levels, it is obviously an advantage if you don't have to rely on your body to transform the dietary D2 + D3 into 25OHD. It is even better though, if the efficacy of this "supplement" (as of now I have not seen 25OHD in caps, so you better stick to eggs) has a higher bioavailability than its non-polar precursor, vitamin D3, which is absorbed mainly into the lymph (Thompson. 1966; Blomstrand. 1967).
"[T]he more polar metabolite 25OHD at physiological concentrations is also absorbed directly, and more rapidly and efficiently, from the proximal jejunum into the portal vein independent of fat absorption. These findings are consistent with results from clinical studies, which have found better absorption of 25OHD versus vitamin D in patients with fat malabsorption. Also, in healthy subjects and in patients with bone disease  25OHD is absorbed better and faster than vitamin D." (Ovesen. 2013)
I would hope that you are by now at least considering to eat an egg instead of popping dozens of vitamin pills. For those who still need actual data before they subscribe to the egg-ological approac to vitamin D 'supplementation', I have compiled a couple of figures in Table 1:
Table 1. 25OHD content (µg/100g) of chicken & egg, pork, beef, fish, dairy (various sources; cf. Oveson. 2013)
With respect to fish it's worth mentioning that the exact concentrations vary from species to species. Moreover  25OHD content of fish is distributed relatively evenly in muscle, fat and organ mass of the fish - much in contrast to vitamin D3, by the way, which is contained mostly in the organs, specifically the liver. For the average human being this means that he or she will actually get his / her share of 25OHD with every serving of fish. For vitamin D3 that's clearly not the case, because few of us actually eat cod liver on a regular base.

The sentence "You Eat What You Feed" is not new to SuppVersity regulars - it's also the title of an older article discussing how you can use food additives to increase the Omega-3 content of your steaks, milk and other animal products | read more
Another thing we should not forget is the influence of the diet. As you as a SuppVersity reader know, it's very difficult to predict the exact amount of almost every nutrient you will get from the products you buy at the super market, in this day and age of food supplements and synthetic chow (see "You Eat What You Feed: How Much Omega-3s Can You Possibly Pack into a Single Steak? The Impressive Effects of a "Grass(+)" Diet on Raw Meat & Meat Products" | read more).

If you ate the bacon of the pigs in the Thompson study from the late 1960s, for example, you would get a whoppy dose of 0.7–2.0µg 25OHD per 100g and thus max. 10x more than from regular bacon. Why? Easy: The sows were on a(n extremly) high vitamin D diets (total D-intake was 2–3mg/day for 2-3 weeks; Thompson. 1966).
What's the "minimal" vitamin D level: If we take the most recent study by Tepper as our guide, you need much less vitamin D to keep your heart disease risk, or rather the markers that have been associated with the latter in check.
In their study, the scientists measured the vitamin D levels of 400 healthy men (age 25-65 years) and identified their relationship to fasting plasma insulin (FPI), fasting plasma glucose (FPG), triglycerides (TG), high sensitive C-Reactive Protein (hs-CRP), blood pressure and triglycerides and found that (a) vitamin D status is related to cardiometabolic indicators in healthy men and that (b) their data would suggest that 11−14 ng/ml should be defined as the minimal vitamin D threshold. So, if you are below that mark you are in for trouble and supplementation actually necessary.
Egg yolks instead of pills? The question, whether you can trash your vitamin D3 (or D2) supplements, as long as you make sure you get your daily dose of egg yolks (the 25OHD is in the yolk, not the egg white!), is difficult to answer. The 'potency' of oral 25OHD is estimated to be 1.5-5x higher than the one of 'regular vitamin D3' the form of 'D' you will find it in the majority of OTC supplements. Since we don't even know how much D3 a given individual actually needs the best thing you can do is to get tested, even if the estimated equivalent values and bioactivity were accurate.

The optimal dietary / supplemental intake is not the only thing that's still highly debated, though. The "optimal" serum levels are similarly dubious. While there appears to be a consensus that you would be ill advised not to take action, when your 25OHD levels come back in the deficiency zone from 30ng/ml-0ng/ml, the answer to the question whether it makes sense to opt for the 'magic' 80ng/ml depends on the expert you ask.

In view of the emerging importance of free vs. total vitamin D, the 25OHD number (=total) on your blood test may soon be deemed completely irrelevant, anyways. There are after all numerous recent studies that support the hypothesis that free 25OHD and not total 25OHD is, where the magic happens. In fact, I have only recently covered two of them in the SuppVersity Facebook news. News-item (1) deals with vitamin D binding and insulin resistance (read more) and news-item (2) addresses the correlation between the free vitamin D and lipid levels in the blood.

References: 
  • Blomstrand R, Forsgren L: Intestinal adsorption and esterification of vitamin D31,2-3H in man. Acta Chem Scand 1967;21:1662–1663. 
  • Francis RM, Peacock  M, Storer JH, Davies AEJ, Brown WB, Nordin BEC: Calcium malabsorption in the elderly: The effect of treatment with  oral  25-hydroxyvitamin  D3.  Eur  J  Clin Invest 1983;13:391–396. 
  • Heaney RP, Barger-Lux MJ, Dowell MS, Chen TC, Holick MF: Calcium absorptive effects of vitamin D and its major metabolites. J Clin Endocrinol Metab 1997;82:4111–4116. 
  • Ovesen L, Brot C, Jakobsen J. Food contents and biological activity of 25-hydroxyvitamin D: a vitamin D metabolite to be reckoned with? Ann Nutr Metab. 2003;47(3-4):107-13. Review. 
  • Thompson GR, Lewis B, Booth CC: Absorption of vitamin D3-3H in control subjects and patients with intestinal malabsorption. J Clin Invest 1966;45:94–102. 
  • Trummel CL, Raisz LG, Blunt JW, DeLuca HF: 25-Hydroxycholecalciferol: Stimulation of bone resorption in tissue culture. Science 1969; 163:1450–1451. 

Meat Science: To Cook or Not to Cook? The Raw Truth About Antioxidants in Raw and Cooked Meat and Fish.

Image 1: Now, that we know that meat is not
bad for you. Let's get to the meat of the matter:
Is raw meat better than cooked meat?
"Eat Raw!" If its referring to peppers, tomatoes and salads, even the Vegan lobby won't disagree with this slogan, yet when it comes to eating raw meat, dairy and eggs, hell breaks lose. "Don't do that you will kill yourself!" is what you will hear even from respected scientists. Strangely, I am eating raw eggs and other raw stuff on a daily basis without noticing any detrimental health effects whatsoever. All bacteria-hysteria aside (this would be the topic for a whole new blogpost, cf. red info-box at the bottom), the idea that meat has to be cooked before it is eaten is actually counterintuitive. I do not want to bring up the "Look at the lion, does he cook his pray before savoring on his bloody prey?"-debate, but didn't you ever ask yourself, why the same people who are scared of a medium steak, order their veggies steamed, or even raw (again see red info box at the bottom of the page), so that the antioxidants in them do not get damaged by the heat. Assuming that these people are aware that raw meat is full of healthy antioxidants (I assume many or them are not, though), common wisdom about the effects of heat on anti-oxidants tells us that they should be eating all our foods raw. As it turns out, though, even that may not be the optimal strategy to boost your antioxidant defenses...

A recently published study by Serpen et al. (Serpen. 2011) showed that the total antioxidant capacity (TAC) of meat and fish actually peaked after brief (<5 min) heating at 180°C - intriguing, no?

The Turkish scientists had bought four samples of your favorite meats and fish - chicken (breast), pork (tenderloin), beef (tenderloin) and fish (Sea bream, fillet) - at a local market, determined the proximate composition (cf. fig 1) of the samples and cut identical cylindrical (5x2cm) slices from the samples.
Figure 1: Composition of raw meat extracts (data adapted from Serpen. 2011)
In the next step, Serpen and his colleagues determined the total antioxidant value of raw and thermally treated meat / fish samples using a process that is called the QUENCHER method. The method was described by the same authors in a previous paper (Gökmen. 2009) and has already become a widely used and generally accepted way of determining the total antioxidant content of foodstuff.
Figure 2: Total antioxidant capacity (calculated average from ADPS and DPPH probes) of meat and fish samples after 0, 5, 10, 15 and 20 minutes of heating at 180°C (data calculated based on Serpen. 2011)
As can be seen in figure 2, where I plotted the mean total antioxidant values of the meat / fish samples as measured by ABTS and DPPH challenges, heating at 180°C does not - as common wisdom would have it - lead to a linear or even exponential decline of the antioxidant capacity of raw meats and fish. The total anti-oxidant capacity rather peaks at around 5 minutes, decreases thereafter, just to rise again at about 20 min. According to the scientists, the highly non-linear effects of heating on the antioxidant value of various meats and the observable variety in heat responses among the different samples can be explained by the interaction of the following processes
  1. denaturation and exposure of reactive sites of proteins; 
  2. thermoxidation and degradation of endogenous antioxidants; 
  3. formation of antioxidant MRPs (Maillard Reaction Products)
While some antioxidants are destroyed in the course of the heating process, others are created. This interplay appears to be most pronounced in the case of chicken (breast) and is the least obvious in fish (Sea bream fillet). Yet, despite the fact that short-fried <5 min meat and fish appears to be the best choice in terms of its overall antioxidant properties, specific anti-oxidants, amino acids and proteins, such as L-cysteine could get damaged even in the course of very brief heating processes. Furthermore it should be mentioned that other than a chef would do it, the scientists removed their probes from the oven and cooled them down immediately, in order to stop the continuing chemical processes. To see the same results as the scientists did for their 5min-steak, you would thus have to fry it for no more than let's say 2 minutes (this is just a very rough estimation) to make up for the ongoing reactions that won't stop if you do not shock-freeze your food before you eat it.
Note for the non-Europeans: Just in case you did not see it on CNN - the EHEC bacteria that killed people in Germany and all over Europe did not come from raw meats, but from sprouts. And it was the prejudice that raw meat, dairy and eggs were the worst (if not only) offenders, when it comes to food poisoning, that significantly hindered the investigations into the roots of an infection that has killed 37 people (according to Bild.de, 07-02-2011) in Germany, alone, when the first patients were hospitalized a few weeks ago.
Bottom line: While heating is obviously less detrimental to the overall antioxidant capacity of meat and fish, as some raw food eaters (and interestingly even the steam cooker faction) would have it, it remains questionable how you can reproduce the optimal fyring time of 5 minutes without immediately deep freezing your meat in a way, which would not leave you with your a steak that would be at least pretty rare. In turn, this means that a steak without a few drips of blood will not provide an optimal level of total antioxidants (TAC). Now, its up to you to decide whether a 2.3% decrease in mean TAC values are worth eating your steak rare - I would say no, but I don not love my steak rare, anyways, but I also read Sean Casey's formidable article on AGE formation, so if you cannot get over your socialized aversion against raw meat, dairy and eggs for what it does contain, i.e. antioxidants, then maybe for what it does not contain, which is advanced glycation end-products ;-)

Switch From Chicken to Lamb to Rid Yourself of Belly Fat, Reduce Your Triglyceride and Basal Insulin Levels

If you consider this, i.e. you suprailaic body fat (here measured by a caliper, just as it was done in the study at hand), ditching the chicken for some lamb, may be one of the myriad factors that could help you "solve" the problem.
Chicken, rice and broccoli. That is still the dietary paradigm, most people have on their minds, when average Joes and Janes are talking (often with some disdain) about what "healthy eating must look like".

Now, a recent study from GENUD, the "Growth, Exercise, Nutrition and Development" Research Group at the Universidad de Zaragoza in Spain (Graffe. 2013) suggests that at least item #1 on that list, namely chicken, would have been better replaced with a protein source of which I suspect even most of you won't be consuming on a regular base: Lamb!

That a proper sleep hygiene is of utmost important for your health and body composition is something you, as a SuppVersity veteran will be highly familiar with (if you are a newbie read yourself smart, here).

"Switch out the light and dish up the lamb, bro!"

That the second part of the jovial imperative in the above headline could be another factor to take into consideration, on the other hand, is true news (even for me) and should - with only one study backing it up - be considered more of an empirically grounded hypothesis than a "100% certain scientific result".

Table 1: Cooking methods for both lamb and chicken (Graffe. 2013)
Nevertheless, the observations, María Isabel Mesana Graffe and her colleagues made, when they put a group of healthy 16-26-year old "men" and "women" (I know, when I was sixteen, I thought I was a man, too - little did I know ;-) from Teruel and Zaragoza on an 8-week dietary regimen containing either...
  • 150 grams of chicken, three times per week, or
  • 150 grams of boneless lamb, three times per week,
... are quite intriguing. The participants received their otherwise (roughly) identical diets in in their local university accomodation halls:
"To ensure harmonisation, product-rich diets were served during lunch time and with each chef of the designated university accommodation halls were given instructions on the cooking methods." (Graffe. 2013; cooking methods, see table on the right)
The whole study design was in fact pretty straight forward and resembles an ideal world, where the citizens obey to dietary recommendations like "eat at least three meals with 150g of lamb per week" as if their lives depended on it (is it ironic or just sad that it actually does depend on the pathetic advice people are given?).

After an initial visit at which the medical history of all participants was assessed, a first blood draw, as well as anthropometric, blood pressure and heart rate measures were undertaken. After an 8-week period, all subjects came in for a second visit and the second testing session and crossed over to the other other group, i.e. subjects who had been consuming chicken for the first 8-weeks were then assigned to eat lamb and vice versa.

2x 8 weeks + an intermediate 5-week washout later...

Thus, after 8 weeks on diet A, a 5-week washout and another 8-weeks on diet B, all subjects had been consuming one or the other diet for 8 weeks, when they eventually arrived for the third and last assessment of their cardiovascular risk markers, body composition, blood pressure and heart rate.
Figure 1: Changes in skinfold thickness (before vs. after) and corresponding arm, hip and waist circumferences in the participants after 8 weeks on the "chicken" vs. "lamb diets" (Graffe. 2013)
As I know that "looking good naked" is much sexier (in the literal, as well as the figurative sense), than being healthy, we'll take a look at the anthropometric data, first (see figure 1). It probably doesn't take much explaining on my side. The general trends speak for themselves and I guess, you won't complain that it is in the change of the amount of fat that's covering the abs, where the scientists observed the only significant inter-group differences - do you?
Figure 2: Changes in blood lipids cardiovascular parameters, glucose and insulin levels during the 8-week chicken / lamb diet phases; only non-pastel bars are statistically significant  (Graffe. 2013)
With the fat mass differences being most significant in the abdominal area, it is also no surprise that the major changes among the cardiovascular risk parameters were (a) reduced triglyceride levels and (b) improved insulin levels - exactly those parameters that are usually most closely related to abdominal obesity and "all things metabolic syndrome".

Not chicken or lamb, "chicken or egg" - that's the question!

These observation do obviously rise the usual SuppVersity question: "What's the mechanism, here?" What is certain is that the beneficial effects on abdominal fat, trigs and insulin are not due to the clenbuterol residues in chicken (up to 224ng/g; cf.Malucelli. 1994) cyclists love to use as an excuse, when they have once again been busted for the abuse of beta-agonists. Why? Well than eating chicken should help not hinder leaning out. Could it be the remnants of antibiotics in the chicken meat, as proposed by eg. Nicholson et al. (2005)? Or is it simply the bad arachidonic acid chicken common wisdom will tell you that it was so high in chicken meat?
Figure 3: Fatty acid composition of beef, lamb, pork, chicken, duck and turkey in % of total lipids (left) and arachidonic acid content in mg/100g (Li. 1998)
If you peek at the data in figure 3, which is obviously not based on the dietary intake of the subjects in the study at hand, but displays the general fatty acid composition of various meats, including lamb and chicken (both marked with grey boxes) as they were reported by Li et al. in 1998, it would appear as if "everybody's favorite devil", the essential omega-6 fatty acid arachidonic acid can hardly be blamed for the superiority of lamb - after all there is about the same amount of it in lamb as there is in chicken (for Ducks and dark poultry things are different!)

Did you know that lamb is the #1 dietary source of CLA?

Lamb contains 5.6 mg/g CLA, whereas beef and veal contain only 2.9–4.3 mg/g and 2.7 mg/g, respectively.

Non-ruminant meats such as chicken and pork, contain 0.9 mg/g and 0.6 mg/g, respectively (Mulvihill. 2001).

Eggs contain no CLA, at all - unless the chicken are fed with CLA enriched diets and the yolk between 3mg and 14-32mg/100g total fat (Jones. 2000; Raes. 2002).

Whether the CLA is at the heart of the effects in the study at hand is yet questionable, after all one of the side effects is insulin resistance and that's the opposite of what the sign. decrease in insulin would suggest.
What could be a culprit, though is the overall higher n-6/n-3 ratio of chicken. There is no debating that there is a statistically significant difference between chicken with 9.73g of omega-6 fatty acids per omega-3 vs. lamb in which every omega-6 fatty acid is "appropriately (?) buffered" with 0.57g of omega-3s (the corresponding n3/n6 ratios are 1.59, 1.78, 13.92, 9.73, 10.82 and 10.53 for beef, lamb, pork, chicken, duck and turkey, respectively; data based on Li. 1998).

But is it really that easy? The n3/n6 ratio - again!? I 'd say no. Also, or rather particularly in view of the relatively lose dietary control... I mean, if you have to eat chicken at least three times a week in the canteen, you are certainly more likely to grab a burger with "red meat" (or whatever it is they put in-between the patties) on the weekends or in the evening.

This and other confounding factors would obviously negate neither the previously mentioned n3/n6 ratio hypothesis, nor the scientists' very own hypothetical explanation that the "the presence of unsaturated fats [...], such as oleic acid and conjugated linoleic acid" which are naturally high in ruminant meat (see infobox on the right), can have figured here, as well. It should however remind you that there is, if anything, only one single reason that "we are fat" and that's the way "experts" base their advice on observations like these, cherry pick those they like and discard the ones they don't like until the various net result - call it the "XY diet" or the "dietary guidelines" - confuse the hell out of the poor average Janes and Joes who are looking up to those "experts" to rescue them before the obesity pandemic carries them off just like the 35.7% of the US adults who are already obese (the latest data is still based on figures from 2009-10; cf. Ogden. 2012)



If you work anyway similar to a male rodent, 4g/day Tongkat Ali, could help with the abs, your testosterone levels and "other issues", as well (learn more)
Bottom line: My personal take away message from the study at hand is not "never eat chicken again" or "eat lamb everyday", but rather: "Don't forget about how lucky we are that we have so many foods to chose from." So don't get stuck on only one of them - and that regardless of what common wisdom, recognized or unrecognized experts or individual studies may suggest would be "best" for the way you look and feel!

There is no magic bullet and no singular reason that "we" are fat and I am 100% sure that eating chicken instead of lamb is the smallest obstacle standing between your and a shredded set of abs.

 References:
    • Jones S, Ma DW, Robinson FE, Field CJ, Clandinin MT. Isomers of conjugated linoleic acid (CLA) are incorporated into egg yolk lipids by CLA-fed laying hens. J Nutr. 2000 Aug;130(8):2002-5.
    • Li D, Ng A, Mann NJ, Sinclair AJ. Contribution of meat fat to dietary arachidonic acid. Lipids. 1998 Apr;33(4):437-40.
    • Malucelli A, Ellendorff F, Meyer HH. Tissue distribution and residues of clenbuterol, salbutamol, and terbutaline in tissues of treated broiler chickens. J Anim Sci. 1994 Jun;72(6):1555-60.
    • Mulvihill, B. Ruminant meat as a source of conjugated linoleic acid (CLA). Nutrition Bulletin. 2001; 26: 295–299. 
    • Ogden CL et al. Prevalence of Obesity in the United States, 2009–2010. NCHS Data Brief No. 82 January 2012.
    • Nicholson JK, Holmes E, Wilson ID. Gut microorganisms, mammalian metabolism and personalized health care. Nat Rev Microbiol. 2005; 3:431–438.
    • Raes K, Huyghebaert G, De Smet S, Nollet L, Arnouts S, Demeyer D. The deposition of conjugated linoleic acids in eggs of laying hens fed diets varying in fat level and fatty acid profile. J Nutr. 2002 Feb;132(2):182-9.

    The Meaty Gritty on the Red Meat Debate: A Comprehensive Rebuttal of the Constant Assault On My Beloved Steaks

    Image 1: Even if you find this disgusting, I would like to invite you at least read what the outspoken carnivor in me has to tell you.
    It appears to be an endless debate: Can you eat meat? May you eat meat? And even should you eat meat? I already mentioned in my post on the "Chinese meat supplement" study from last week that many of the accepted "truths" about real, unprocesed red meat are about as "true" as the hilarious statement that "going to the hospital causes pre-mature death"... After reading my friend Carl Lanore's luckily very reasonable and not overtly "ranting" blogpost on "What to say to a Vegan", a few days ago, I decided to sum up some of the research to scrutinize, which of the objections against and arguments for eating meat are actually rooted in science (I mean, my life as a meat eater could depend on it, right? ;-).

    Pork rules, but is that a good thing?

    If we take a look at the actual meat consumption in what is usully called the "developed world" (this is us), we find that pork is the most widely consumed form of red meat (>50% in developed countries; FAO. 2009)  - what's more, pork is rarely consumed "intact", in the form of a whole cut of meat, but more often as processed meat like sausages etc. Overall, the average available amount of red meat (pork, beef and veal, sheep) people in the developed world consume on a daily basis is ~110g, which is well within the "save limit" of as defined by the dietary recommendations in the respective countries.
    Figure 1: Relative contribution of beef (total and lean) to individual nutrient consumption in the American diet (adapted from Zanovec. 2010)
    In fact, a 2010 dietary analysis by Zanovec et al. suggests that with an average beef intake of 49.3g/day US adults eat way less than the recommended 142-198g of meat per day (at least if we count beef alone; Zanovec. 2010). In this context it is also worth mentioning that:

    "Lean beef contributes significant amount of key nutrients to the US diet"

    This statement, by the way, is taken directly from the title of Zanovec's analysis of data from the National Health and Nutrition Examination Survey (NHANES. 1999-2004). The years of dietary recommendations asking the public to avoid red meats, because their high saturated fat content would clog their arteries have obviously made a profound impact on people's perception of meat as a "dietary treat" that is about as unhealthy, if not worse, than their beloved potato chips, twinkies and dingdongs and that despite increasing evidence that saturated fat is not associated with an increased risk of heart disease, but showed a statistically non-significant association with reduced risk of stroke (-19%, p = 0.11; Siri-Tarino. 2010).

    The dietary advice people are given does "not reflect available scientific literature"

    In a relatively recent "review of the reviews" the purported experts on respective dietary advisory boards conduct,  Robert Hoenselaar a researcher from the Department of Nutrition and Dietetics at the High School of Arnheim and Nijmegen in the Netherlands concludes that
    [t]he results and conclusions about saturated fat intake in relation to CVD, from leading advisory committees, do not reflect the available scientific literature."
    and criticizes the policymakers (if applicable to a certain organization, I will name the latter in brackets after each statement) for
    • advising people to replace saturated with polyunsaturated fats in their diets based on two non-randomized trials (EFSA)
    • mentioning the existing evidence that saturated fat intake increases HDL cholesterol, but ignoring the conclusive evidence that increased HDL levels are associated with a lower CVD risk (IOM, EFSA)
    • not taking into account data from existing prospective studies examining the direct relation between saturated fat intake and CVD (USDA, IOM, EFSA) and instead including their "own randomly selected data on this subject" in their reports
    • ignoring their own previous results (USDA), which suggest that replacing saturated fats by carbohydrates or monounsaturated fats decreases the CHD risk and the mere fact that in the studies Hoenselar analyzed, none of the authors concluded that "changes in saturated fat intake would change the risk of CVD, regardless of the study design and the endpoint"
    • not discussing other modifiable dietary risk factors, which often go hand in hand with an increased meat consumption such as higher intakes of industrial trans fatty acids, a overtly high salt intake or a carbohydrate-laden high GI diet.
    Any probably inevitable selection biases aside, it is also interesting that papers such as the one by Li et al., which found no increase in cholesterol (in fact a reduction in LDL) or thrombotic risk factors from the consumption of lean red meat (grass- and grain-fed) in their 2005 review of 54 pertinent studies (Li. 2005), do not appear in the extensive lists of literature the members on respective advisory boards attach to their well-worded reviews.

    RCTs confirm independent reviews of the literature and well-conducted epidemiological studies

    Moreover, most recent randomized controlled trials, such as Roussell et al. support the notion that the inclusion of lean red meats (153g/day) in a "heart healthy" DASH-like diet does not diminish its favorable effects on markers of cardiovascular disease (Roussell. 2012), but...
    [...] in conjunction with the beneficial effects on apolipoprotein CVD risk factors after consumption of the BOLD and BOLD+ [BOLD 133g; BOLD+ 153g/day of lean beef, cf. DASH <28g/day] diets, which were greater with the BOLD+ diet, provide support for including lean beef in a heart-healthy dietary pattern.
    Eating a small steak every day is thusly - according to the results from the latest randomized controlled trials more beneficial for your heart (and probably overall health, e.g. "Heal Your Thyroid by Eating More Beef") than avoiding red meat like a plague.

    Don't freak out over real meat, or your blood pressure will raise; yet not from the meat!

    The list of studies showing no association to another often touted "meat-related" cardiovascular risk factor, high blood pressure (the "silent killer"), is extensive, and even the 2010 U.S. Dietary Guidelines Advisory Committee recently concluded that there is
    [...] no clear association between intake of animal protein products and blood pressure in prospective cohort studies.

    In randomized controlled trials, as those by Hodgson et al. and Nowson et al,. the addition of red meat to a diet that was "otherwise considered heart healthy" lead to modest reductions (not increases!) in blood pressure (Hodgson. 2006; Nowson. 2009). It is thusly no wonder that in a forerunner study to the aforementioned Roussell trial a sixfold increase in real red meat intake (from DASH to BOLD, cf. above) did not lead to any statistically significant elevations in blood pressure. What is quite interesting in this context is that, at least in the Nowson trial, the dietary restriction of sodium basically precluded the intake of "regular" processed "meats" (I personally would not call them such, but scientists and most people consider sausages & co "meat").

    Meat does not make you fat! It can make you lean - not skinny, though...

    Another commonly touted myth that is widely accepted - especially among female mainstream dieters - is that meat will make you fat (or if not fat, then at least "bulky"). That this is not the case and chicken and fish are not per se better protein sources when you are dieting for weight loss has been shown in randomized controlled trials (Leslie. 2002; Campbell. 2010) - particularly in women, by the way. This should also remind the "regulars" among you (i.e. all of you who follow my advice to get their daily dose of SuppVersity news in order to stay sane and prolong their lives ;-) of a previous blogpost of mine, in which I discussed the results of a study by Petzke et al. from September 2011, which found increases in lean mass in weight stable women who were advised to include additional lean pork (=red meat ;-) in their diets. I have written about similar results in an obviously tighter controlled rodent study, little less than a week or two, ago.

    Image 2: If you put any faith in prospective studies, you should make sure that your grand parents do not follow this selfish advise.
    A 14-year prospective follow-up study of older adults by Gilsing et al. did even identify the men in the highest quintile of beef consumption (>40g/day, which is hilarious and just goes to show you why old people get sick and fragile, by the way) as those with the lowest increase in BMI (Gilsing. 2012). However (and moreover), at the end of the 14 year follow up, ...
    [...], a significantly higher increase in BMI was associated with higher intakes of pork in women (BMI change highest vs. lowest quintile: 0.47 kg/m²) and chicken in both sexes (BMI change highest vs. lowest category in both men and women: 0.36 kg/m²).
    To stay away from unprocessed red meats, and beef, in particular, in order to lose weight or maintain a healthy body weight, is thusly not only unnecessary, but probably even counter-indicated. Also, because red meat is one of the richest sources of protein, iron, zinc, vitamin A and other vital nutrients, all of which could be scarce on voluntary (young dieters) or involuntary (loss of appetite in the elderly) calorie reduced diets.

    "Fine, but you will die from cancer, when you eat too much meat"

    When the CVD and obesity debate are settled, the meat opponents usually feel that it's now time to play what they believe is their ultimate trump: The red meat "causes" cancer argument - an argument on the validity of which McNeill et al. state (McNeill. 2012):
    Disentangling the independent effects of individual foods, such as red meat, in cancer etiology is a substantial challenge (Magalhaes et al., 2012). Although many epidemiologic studies have observed positive associations between red/processed meat intake or associated dietary patterns and various cancers and thus concluded that these convincingly increase cancer risk, these associations have generally been weak in magnitude and/or the large majority of associations have not been statistically significant (Chan et al., 2011; Alexander et al., 2010; Alexander et al., 2010b; Alexander et al., 2009b).  Not surprisingly, analyses of data from large prospective studies have found little or no association between fresh red meat consumption and colorectal cancer risk.
    Image 3: Linda van Horn is a chair on the 2010 US Dietary Guidelines Advisory Commitee that is going back on its previous advice against all things meat.
    As in the case of increased blood pressure, the 2010 US Dietary Guidelines Advisory Committee (DGAC) is thusly backpedaling on previous statements and recommendations and ascertains that the existing scientific evidence shows "no consistent findings on type of meat or meat product and colorectal cancer" and even recommends that
    Americans may choose animal products as part of their diet based on the body of evidence showing a general lack of relationship between animal protein consumption and selected health outcomes (DGAC, 2010).
    In view of the fact that there are still epidemiological trials, which do suggest that increased consumption of red meat could pose an increased cancer risk, it will be all the more important to try and eliminate methodological shortcomings, such as
    • heterogeneous definitions of red and processed meat (is Pizza Salami really "red meat"?),
    • variable and unreliable measures of meat consumption, and
    • profound inter-study differences in the analytical evaluation of the data
    as well as confounding factors such as physical activity, body mass index, body fat levels, alcohol intake, or adherence to screening recommendations, in order to pinpoint any allegedly meat-related increases in cancer risk in the future.

    The non-health related ethical dilemma

    By now, I have hopefully encouraged my fellow carnivores and maybe even convinced some skeptics (you know I love you ;-) that the allegedly conclusive data on the potential health hazards from an average, let alone increased consumption of real (unprocessed) red meats are at least not conclusive, and, from my naturally biased reading of the available evidence, non-justifiable and to a great extend the result of paradigmatic ignorance towards contradictory research.

    Yet whatever your take on the health effects of red meat consumption may be, now that you have reached the end of this article, it is still up to you to decide if you want or don't want to eat formerly living creatures. I have made my decision and ask you to accept mine, just as I will accept yours - whatever it may be. Thank you!

      Meat-Love: You May Have Pork, Too. Eating More Lean Chicken, Beef & Pork Builds 3.6kg of Lean Mass + Cuts Abdominal Obesity by 7% in Obese Australians

      It's often cited as the source of all nutritional (and environmental) evil and still: The experimental evidence informs us that the epidemiologically instigated politically subsidized meat hating is unreasonable.
      I wanted to start this article with the words "I actually don't know why" and follow it up with the statement "pork has gotten such a be rep," but that would be incorrect: After giving it a brief thought, I do know why pork has gotten such a bed rep as the unhealthiest meat source there is. It's not a religious question as some of you may believe.

      It's rather a matter of the end-consumer products that are made of pork. sausages & co are not good for your health, but that's not because they are made of pork, but rather because they consist of highly processed waste no one of you would eat, if it was served in its original form - and that in spite of the fact that the unprocessed garbage would probably be healthier than the final hot dog.
      "Meat" and "Pork" are not the problems: That pork per se is not a problem and pork-consumers can - probably to the great astonishment of the average dietitian - improve their body composition without diet and exercise by its regular consumption is the results of a recent 6-months study by researchers from the University of South Australia in Adelaide (Murphy. 2014).
      The participants, , 49 overweight or obese adults were randomly assigned to consume up to 1kg/week of pork, chicken or beef, in an otherwise unrestricted diet for three months. To avoid the "saussages" effect the male and female participants were given seven (men) or five (women) portions of "their" meat per week and told to incorporate it into their habitual diet.

      Table 1: Energy & Nutrient intake at baseline and during the meaty intervention period (Murphy. 2014)
      As the meats were matched on energy per serving, the portion sizes varied slightly (pork 140 g/serve, chicken 150 g/serve, beef (red meat) 150 g/serve).
      "All participants were seen fortnightly to monitor body weight, discuss any issues arising in the intervention and collect a selection of frozen meat products including lean beef or pork steak or chicken breast, stir fry, diced and mince. All participants kept a weekly log of study meat consumption" (Murphy. 2014)
      Next to their food intake, the subjects also had to log their physical activity in three-day logs (2x week + 1x weekend).

      This data was then used by the researchers to calculate the energy expenditure (kcal) for every 15 min period in a 24 h day according to nine categories of different types of activity (e.g., sleeping, playing sports, gardening etc.) and multiplied by the appropriate physical activity level factor for the reported intensity of exercise.
      Just to clarify things: There was no energy restriction and/or exercise regimen involved and the data the scientists gathered confirms that the only meaningful changes that occurred were the intended substitutions / additions of lean pork, beef and chicken meat!
      As it turned out, there were no differences in either the total energy or macronutrient intake between the groups; and on the micronutrient side of things, the only measurable difference was a minimally (but statistically significantly) elevated zinc intake in the beef group.
      Figure 1: Changes in body composition during the 6 months pork, chicken, beef phase (Murphy. 2014)
      Against that background it is not surprising that the main outcome, i.e. the changes in body composition I plotted in Figure 1 were (from a statistical point of view) identical as well. What is surprising (certainly for Colin T. Campbell), though, is that
      • Figure 2: Lean mas at baseline and after the meaty intervention (Murphy. 2014)
        ... the weight loss occured in the absence of prescribed energy reduction and / or increase in activity level or the total protein intake (see Table 1) of  the 50 ± 2 year-old overweight male and female participants , 
      • ... there was an extremely health-relevant 7% increase in lean mass (that's +3.5 ± 0.1kg (!); see Figure 2) in and all women
      • ... the researchers did not observe any negative side effects in either of the groups.
      In other words: Simply eating more - not less - lean and mostly "clean" (=unprocessed) meat lead to a significant and unquestionably health-relevant reduction in abdominal fat and corresponding increases in lean mass.
      Bottom line: The significance of the decrease in fat and increase in lean mass, the researcher observed in the study at hand can hardly be overestimated. Unfortunately, there are still way too many men and even more women who consider the "weight loss" their main "health goal" - a goal, of which Allison et al. (1999) have been able to show that it increases all-cause mortality, which a loss of body fat, as it occured in the study at hand, lowers all-cause mortality!

      Suggested read: "Reduced Weight Gain, Improved Insulin Sensitivity and No Adverse Side Effects from 'Red Meat Supplementation' Even in Rodents!" | read more.
      In that, it should not be surprising for you as a SuppVersity reader that an increased intake of (mostly) lean + unprocessed red meat can be the driving force of corresponding changes in body composition. I have, after all, written about the unwarranted over-generalized assault on meats repeatedly (" The Meaty Gritty on the Red Meat Debate: A Comprehensive Rebuttal of the Constant Assault On My Beloved Steaks " | read more); and in view of the data German researchers presented in a 2011 paper (Petzke. 2011), it should be clear that similar benefits of meat in general and lean pork in particular will occur in lean women, as well (see "Additional(!) 200g Pork/Day Build Lean Mass + Improve Blood Lipids & Glucose Levels" | read more)
      References:
      • Allison, D. B., et al. "Weight loss increases and fat loss decreases all-cause mortality rate: results from two independent cohort studies." International Journal of Obesity & Related Metabolic Disorders 23.6 (1999).
      • Murphy, Karen J., et al. "A Comparison of Regular Consumption of Fresh Lean Pork, Beef and Chicken on Body Composition: A Randomized Cross-Over Trial." Nutrients 6.2 (2014): 682-696.
      • Petzke, Klaus J., Susen Lemke, and Susanne Klaus. "Increased fat-free body mass and no adverse effects on blood lipid concentrations 4 weeks after additional meat consumption in comparison with an exclusion of meat in the diet of young healthy women." Journal of nutrition and metabolism 2011 (2011).