Grass-Fed Pork? Not Really. Still the Difference in Fatty Acid Composition & Micronutrient Content Are Profound & Not Accounted for by Food Databases - Let Alone Epidemiology

You often hear that pigs are pretty closely related to us humans, but "are all pigs created equal"? Or what may be a more appropriate question for the SuppVersity: Is all pork really created equal?

If you like databases like nutritiondata.com or the USDA's very own detailed nutrient database in order to evaluate whether your diet is actually delivering all the nutrients you need you are probably missing half of the picture. At least as far as the more sophisticated details go, a recent paper from the Instituto de Ingeniería de Alimentos para el Desarrollo at the Universidad Politécnica de Valencia clearly indicates that you would at least have to consider what the animals, in this case pork, were fed and from which muscle of the animal the piece of meat you are eating has been cut, in order to get an approximate idea of how much of unquestionably health relevant micronutrients, such as coQ10, carnosine, anserine, taurine, creatine glutamine or haem you get - and in some cases the differences can be way larger than 100%!

If pizza salami equals pork...

... in epidemiological studies, how can these studies on the fallacies and advantages of eating red meat, which usually get a hell lo of media attention, be accurate, given the fact that the amount of unquestionably beneficial coQ10, for example, would differ by 60 percent, even if you would only ignore the difference between loin that was cut from the trapezius (= high coQ10 content) and the longissimus dorsi (=low coQ10 content)?

Figure 1: Content of selected amino acids and micronutrients in cuts from different muscle; data expressed relative to respective mean (total value is given in mg/100g above the bars) of all tested muscle samples (data based on previous studies by the co-authors that have been compiled for Reig. 2012).

Moreover, if you take a look at the complete data in figure 1 it should be clear that coQ10 is only one of several micro-nutrients / amino acids that are highly dependent on which muscle your particular steak or whatever you are about to eat was cut from. Let's take taurine as yet another example. A prolonged low dietary intake of taurine has been observed to be linked to a number of disorders including retinal degeneration, retardation of growth and development, cardiovascular dysfunctions, CNS abnormalities, immune impairment and hepatic disorders (Abebe. 2011). If you eat meat (fish & other animal products) only occasionally and are therefore at risk of not getting adequate taurine in your diet, eating sausages from a butcher you trust would be a better choice than a piece of ham, since the former do include the high taurine meat from the masseter (cheeks) of the animals, while ham does not.

Let's get to the obvious: Grass-fed is... ah, wait a minute

"Grass fed is best" as you will people say about beef obviously won't be the case for pork, because pigs, just like humans, by the way, are omnivores. The simple formula, grass-fed = most beneficial fatty acid and micronutrient profile that may (in general) be valid for beef doesn't apply and we will have to take a closer look at the actual data first to decide what would be the "best" feed for pigs, if the goal was not a maximal yield of lean meat (in that case adding some clenbuterol, like the Chinese like to do it would be the least you should do; cf. The China Post. 2011), but rather to produce the meat with the most beneficial fatty acid  composition.

Figure 2: Fatty acid composition (primary axis) and omega-6 to omega-3 ratio of pork from pigs fed different diets (corrected version of data Reig et al. re-pupublished based on previous studies; spec. the figure for the n6:n3 ratio in the "standard feed" group that's based on Enser et al. was off - a ratio of 1.54 is obviously unrealistic)

I we define "most healthy" as having the lowest omega-6 to omega-3 ratio - a practice that seems appropriate given that 95% of the inhabitants of the so-called 'Westernized World' consumes way too much of the former and (comparably) way too little of the latter type of polyunsaturated fatty acids, the data in figure 2 clearly argues in favor of *surprise* the standard feed - at least if you define that by the feed the animals the meat of which (50 samples) Enser et al. bought in British supermarkets in 1996 (note: these values are still higher than for the conventional beef samples from the same study, which had a n-6:n-3 ratio of ~2.2; cf. Enser. 1996). There are however more intricate patterns that are not evident from the overview in figure 2, but could have implications as far as the direction into which "pork production" could or should head to in the future is concerned (summarized based on Reig. 2012):

Do you notice a pattern? I guess even based on the data in figure 2 you will already have noticed that the "grainier" the diet, or in other words, the more corn and soy there is in the diet of the swine the less favorable is the fatty acid composition of their meats going to be. Now, I am asking an outrageous question: If swine are such a good model for human metabolism, what do you believe your belly was going to be made of, if you copied the pigs' diets and lived on "healthy grains", their oils and the uber-healthy soy beans for the (probably pretty short) rest of your life?
• more food (yet no excess) can produce overall leaner muscle meat in the type II fibers, while the total body fat is increasing
• aside from local desaturation and elongination effects, the overall muscular fatty acid pattern does (much like in humans, by the way) mirror the dietary intake
• canola or linseed oils produce a substantial increase in the content of linolenic acid (C 18:3), and slightly increase the eicosapentaenoic (EPA, C 22:5) and docosahexaenoic (DHA, C 22:6) acid contents in pork mea
• soy, peanut, corn, and sunflower increase the content of linoleic acid (C 18:2; omega-6), increase the n-6:n-3 ratio and reduce the content of mono-unsaturated fats (MUFAs)
• fish oils or algae added to the feed substantially increases the content of EPA and DHA and thus reduce the n-6:n-3 ratio
• a high saturated fat content as in tallow (see figure 2) increases the levels of palmitic, palmitoleic, stearic and oleic acids in pork meat and reduces the PUFA:SFA ratio 
• CLA supplementation can increase the CLA content of the fatty portion of the meats (1% CLA results in 5.5 mg CLA/100g) and the adipose tissue (2% CLA yields 1,490mg CLA/100g fatty acids).

As you can see, the same rule applies for humans, pigs and, as you know from a previous SuppVersity post, mice who are fed inferior, since soy-fed salmon, as well: You are what you eat, folks!

Wallowing, roaming, routing: Work out like a pig

Since pigs make a pretty decent model of human metabolism and in view of the fact that - aside from our diets - the amount of exercise we get is one of the fundamental determinants of the total and relative levels of body fat, it should not be forgotten that "exercise" or rather the ability to range freely and be as active as any swine should be, is another determinant of the quality of the meat you are buying at the supermarket, grocery store, butcher or your local farmer. In this context, Reig et al. point out that

If you have no idea of the different cuts and location of the individual muscle, I suggest you download the "Meat Cuts Manual" from the website of the Canadian Food Agency. It's free and bilingual.

"[i]t has been reported that pigs maintained in free-range conditions in the Mediterranean forest had subcutaneous and intramuscular fats with higher monounsaturated fatty acids and lower saturated fatty acids than those pigs housed individually and receiving acorns as feed. The subcutaneous fat depth increases with exercise being 15.9 mm for exercised pigs in comparison to 11.5 mm depth for those kept in confinement. The same applies for the intramuscular fat content where 3.36% for extensive vs 1.44% for intensive raised pigs have been reported in the semimembranosus muscle." (Reig. 2012)

And if you really intend to overcomplicate things, you would also have to ask your butcher, whether the sausages you are about to buy were made of the meat of male of female pigs. After all, meat from barrows typically contain more fat and marbling and a thicker subcutaneous fat layer than meat from gilts (Armero. 1999). But let's face it: If you start stressing about things like this, the quality of your meat is probably your least problem.

If you want to know read more about epidemiological overgeneralization andthe effects of "pork" and red meat on your health (spec. the prostate) I suggest you go back to the Meat-Ology post.

So what's the bottom line, then: I guess the bottom line of the above insides is twofold. As far as you as an individual are concerned, it would be yet another argument for getting your meats (pork or whatever else) from a farm nearby, where you know what you are getting. It is yet also evidence of the fact that meticulous nutrient counting as I often see it in former calorie counters who have nor grasped the notion that "a calorie is not a calorie" is of little avail - at least if you expect to be able to calculate them as precisely as you can read them on the nutrition labels of the 90% artificial and 100% standardized convenient foods that's probably much more the answer to the question "Why are we fat?" than the non-descript statement "insulin".

In fact, the real significance of these results lies elsewhere. It concerns the way epidemiological studies are conducted (I may remind you of the metaphorical pizza salami being red meat or pork), their over-generalizing interpretations and the conclusions on what the optimal human diet should look like. So, once the next study is telling you "red meat" or "pork" is bad for you - you may want to remind yourself of some of the things you have learned in today's blogpost and ask yourself (and if you incidentally have the chance, the researchers as well): What kind of "pork" are we talking about?

References:

• Abebe W, Mozaffari MS. Role of taurine in the vasculature: an overview of experimental and human studies. Am J Cardiovasc Dis. 2011;1(3):293-311.
• Armero E,  Flores M,  Toldrá F,  Barbosa JA,  Olivet J,  Pla M,  Baselga M.Effects of pig sire types and sex on carcass traits, meat quality and sensory quality of dry-cured ham.  Journal of the  Science of  Food  and  Agriculture. 1999; 79:1147-1154.
• Enser M, Hallett K, Hewitt B, Fursey GA, Wood JD. Fatty acid content and composition of english beef, lamb and pork at retail. Meat Sci. 1996 Apr;42(4):443-56.
• Reig M, Aristoy MC, Toldra.Variability in the contents of pork meat nutrients and how it may affect food composition databases. Food Chemistry. 2012 [ahead of print]
• The China Post. Clenbuterol-tainted pork latest China food scandal. March 18, 2011. < http://www.chinapost.com.tw/china/national-news/2011/03/18/295146/Clenbuterol-tainted-pork.htm > retrieved Dec 06, 2012.

Demonized N-6 Pufas Surprisingly Ergogenic: Safflower Oil More Than Doubles Swimming Endurance of Aging Mice.

Image 1: Unexpectedly ergogenic - Carthamus tinctorius L., better known as "safflower", a highly branched, herbaceous, thistle-like annual.

As a regular visitor of the SuppVersity and/or listener of SuperHumanRadio, you will be familiar with my skepticism towards fish oil supplementation as the "good for all" wonder-supplement in an athletic population. You will also be familiar with studies such as Filaire et al. (2010) which showed increased MDA (malondyaldehide) levels (and thus more, not less toxic waste) in athletes receiving 600mg of EPA and 400mg of DHA for 6 weeks. Thusly, it may not come as a total surprise that Guihua Zhang and his colleagues the National Food Research Institute and the National Institute of Vegetable and Tea Sciences in Japan found that 12 weeks on a diet containing 6% fish oil reduced endurance performance in aged mice by -20%. What may be more surprising, though, is that the vilified n6-pufas from safflower oil more than doubled the rodents' endurance performance.

Video 1: Not the swimming test performed in the study, but maybe an explanation why mouse-oil might be good for fish, but not vice versa - or have you ever seen a mouse eating a fish?

In view of the fact that the mice in the lard group suffered a similar loss in endurance performance, it should be said that the overall effect of fish oil, as well as lard, could in fact have been a null-effect. In other words, contrary to safflower oil, fish oil and lard had no beneficial effect on swimming endurance, so that an age-related decline in swimming endurance would have become obvious. After all, the average mouse-life is no longer than ~100-150 weeks, so that another 12 weeks are quite a time-span for 52 weeks old mice. On the other hand, previous studies such as Shimomura et al. (Shimomura. 1990) and Rustan (Rustan. 1993) would point toward an overall negative effect of high SFA+MUFA (lard) and high N3-PUFA (fish oil) on fatty acid oxidation in skeletal muscle and subsequently (endurance) exercise performance.

In the study, 40 male Crlj:CD-1 (ICR) mice had been randomly assigned to one out of three groups with the 6% of fatty acids of their experimental diet coming from either lard (n=13), safflower oil (n=13) or fish oil (n = 14) for 12 weeks.

Figure 1: Effect of 12 weeks on diets with 6% lard, fish oil and safflower oil on swimming endurance of aged mice (data calculated based on Zhang. 2011).

As the data in figure 1 goes to show, the fat content of the diet, i.e. low PUFA (lard), high N3-PUFA (fish oil) and high N6-PUFA (safflower oil) had a profound impact on the swimming performance of the animals. In view of the fact that we cannot completely rule out that the "negative effect" of lard and fish oil were simply due to an age-induced decline in swimming performance (cf. red box above), the most important finding of this study is however the +113% endurance increase in the safflower group, and not so much the -20% performance decreases in the other groups in swimming endurance [if you asked me, it's a pitty that there is no control group on a mixed diet]

Figure 2: Effect of 12 weeks on diets with 6% lard, fish oil and safflower oil on lactate levels pre and post endurance exercise in aged mice (data calculated based on Zhang. 2011).

As Zhang et al. point out, this increase in endurance performance cannot be explained based on increases in muscle or liver glycogen stores, because scientists measured "[s]imilar glycogen storage and plasma glucose levels in sedentary mice in the three diet groups suggest". A better explanation relates to the significant differences in the accumulation of plasma lactate following swimming (cf. figure 2), where lactate levels were "significantly lower" in the safflower oil group than in the lard (+57%) and non-significantly higher in the fish oil (+14%) group.

These results imply that the improved endurance associated with dietary safflower oil may be due, at least in part, to glycogen sparing. The working skeletal muscle is not only the major site of lactate production but is also important for utilization of lactate, which is mainly removed by oxidation. The decreased accumulation of lactate observed in aged mice fed safflower oil could be due to increased lactate oxidation and subsequent utilization as an additional energy source during swimming.

Yet the effect on accumulation or utilization of lactate was not the only difference that may have contributed to the increase in swimming performance that was observed in the safflower oil group. As the researchers point out,

the significant increase in muscle and liver CPT activities and decrease in plasma NEFA levels observed following exhaustive swimming in mice fed safflower oil implies an upregulation of fatty acid metabolism in these mice.

The absence of these effect in the lard or fish oil fed animals suggest that "the safflower oil group may have increased fatty acid utilization for energy than the other diet groups". In that, it is particularly noteworthy that we are talking about a localized increase in CPT activity and consequent fatty acid oxidation in muscle tissue. The increased liver CPT in the fish oil group, on the other hand could have contributed to an overall negative effect of fish oil consumption on endurance performance that would have been corroborated by the established suppressive effect of N3PUFAs on fatty acid synthesis (Kim. 1999; Nakatani. 2004)  and lipid oxidation (Rustan. 1993), against the backdrop of which less fatty acids became available for and subsequently oxidized in skeletal muscle.

Image 2: Biological activities of IL-6 (illustration by Prof. Dr. Heinrich)

Not directly relevant to the endurance aspect, but nevertheless interesting is another result of the study, which is the absence, respectively statistically insignificant elevation of elevations in the inflammatory maker IL-6 in the exercised (non-existent) and sedentary (non-significant) mice on the safflower oil diet. A result the anti-n6-faction in the diet-guru camp will probably find surprising and which goes against previous findings by Moon et al. (Moon. 2003) and Garcia-Escobar (Garcia-Escobar. 2010) - on the other hand, this also means that it was not the increase in IL6, which has in human studies been shown to selectively stimulate lipolysis in skeletal muscle (Wolsk. 2010), that facilitated the increase in endurance performance.

If and in what extent the reduction in plasma ferritin (fe) levels in the fish oil group (-13% sedentary; -24% exercised; both compared to lard, with slightly greater reductions compared to safflower oil) could have been an additional factor in a complex equation of substrate availability, usage and enzyme activity which could eventually explain the perfomance increases and decreases in the different groups is questionable. After all, the fe levels in the lard and safflower oil groups were virtually identical.

So, what would be the overall lesson, we can learn from the results of this study? Fish oil is poison, safflower oil liquid gold? Probably not. Yet, while it may still be questionable in how far the mouse metabolism is a good model for the human one, the inhibition of fatty acid synthesis and the increased fatty acid oxidation observed in mice as a consequence of fish oil feeding is present in humans, as well. Moreover, I assume you would agree that not everything that would be beneficial for the average sedentary borderline to morbidly obese inhabitant of the Western Hemisphere, is equally beneficial for performance-oriented athletes - or would you suggest 200 meter sprinters start swallowing statins and blood pressure medications? So, wouldn't it be remotely possible, then that a physical culturist (as I hope you would consider yourself to be one) would be much better off with a reasonable amount of those "nasty" n6-PUFAs in his/her diet to keep the fire in the mitochondrial furnace of his/her muscles in full blast? If you want to, ask your guru about it ;-)

Body Fat Modulation with Corn Oil & L-Carnitine: What You Can Learn From Your Schnitzel

Its quite remarkable that, primates aside, swine are among the best models of human metabolism. So, even if you do not feel piggy at all, the fact that pigs just as humans are omnivores, makes them a much better model for metabolic disease than rodents. It is thus not too unrealistic to assume that we can learn something about ourselves from the results of a very recent study published in the Journal of Animal Science (Apple. 2011).

Figure 1: American Pork Cuts; quality is determined by corn-oil and carnitine intake of the swine.
What lessons can you learn from our pink relatives?

Investigating the effects of l-carnitine supplementation on the quality characteristics of fresh pork bellies from pigs fed three levels of corn oil, J.K. Apple and his co-workers observed a linear trend towards decreased belly-firmness with increasing amounts of corn oil (0, 2 or 4%) in the diet. If you look at the average American, his/her high corn oil consumption and their respective (pot-)bellies, this should not surprise you. All aesthetic considerations aside, those feisty pot-bellies are nothing but the outward sign of metabolic derangements that - without appropriate lifestyle interventions - have their owners suffer from diabetes, high blood pressure, chronic inflammation, and all the other players in the (eventually) deadly "game" of metabolic syndrome.

[...] belly firmness decreased linearly (P < 0.001) with increasing dietary OIL, but there was no (P ≥ 0.137) effect of CARN on any belly firmness measure.

Now, did the touted fat-burner l-carnitine prevent these effects? No, it didn't. Yet, what it did do is it increased the amount of saturated (SFA) and mono-unsaturated (MUFA) fatty acids and decreased the amount of polyunsaturated fatty acids (PUFA) in the belly tissue:

Dietary CARN increased (P < 0.05) the proportion of total SFA in the intermuscular fat layer, increased (P < 0.05) the proportion of total MUFA in the primary and secondary lean layers, and decreased (P < 0.05) the proportion of total PUFA in the intermuscular fat and secondary lean layers of pork bellies.

In view of the finding that increasing the amount of corn oil in the diet tended to increase the PUFA content of the belly tissue, while depositing the highly oxidative polyunsaturated fatty acids preferentially in fat and not lean layers, one must acknowledge that L-carnitine, despite not being able to prevent the outwardly visible (and touchable) negative effects of a diet high in omega-6 rich corn oil, was yet able to modulate the effects of excess PUFAs on intra-tissue body fat composition.

Against the background of the recent changes in the scientifically accepted perspective on the previously vilified saturated fatty acids and possible beneficial effects on cell stability and inflammation the significance of these results goes beyond profane insights into the management of pork quality and solidify the foundation of my previous recommendation to avoid omega-6 instead of increasing the overall PUFA load by additional omega-3 supplementation. What's new, however, is the role l-carnitine supplementation may play in your efforts to get rid of overly high tissue levels of omega-6, since the reduced storage in fat tissue and the increased storage in muscle could be able to (a) decrease inflammation of the fat tissue and, at the same time, (b) increase oxidation of PUFAs in exercised muscle tissue. Yet, without appropriate dietary changes and the incorporation of regular exercise sessions into your  new, healthier lifestyle all carnitine in the world won't help you, if you insist on eating too many breaded and fried schnitzel with French fries and a boatload of mayonnaise and ketchup.

Scientists Probe the Interaction Between Saturated and Unsaturated High Fat Diets and Their Corresponding Carbohydrate Sources (Cornstarch vs. Fructose)

This add is a perfect example of how saturated fat, in this case lard has always been blamed for the "lard" on ones hips.

Any hypothesis that tries to blame for our "fat misery" on a single nutrient is short-sighted. After years of fat-bashing, carbophobia and fructose hating in the course of which the situation progressively, we are now seeing the first studies which investigate what the Polish researchers, Adam Jurgoński, Jerzy Juśkiewicz and Zenon Zduńczyk from the Institute of Animal Reproduction and Food Research at the Polish Academy of  Sciences call the "biological interactions among these dietary factors" in their latest paper in the peer-reviewed open-source journal Nutrients (Jurgoński. 2014).

With the publication of the data of a their latest rodent study, the scientists have already taken the first step to a new, an "interactionist" perspective on the obesogenic effects of saturated vs.unsaturated and simple vs.complex carbohydrates and their interaction with another previously overlooked factor that has gotten quite some attention in the past months: The gut and its inhabitants.

Goodbye! Nutritional scapegoatism 

It goes without saying that this model study is nothing but a first step on a long road we still have to travel, but the differential effects the four diets (see Table 1)...

• 

  Table 1: Composition of the diets.

  the soybean powered high cornstarch diet (OS),
• the lard-laden high cornstarch diet (LS), 
• the soybean-powered high fructose diet (OF), and
• the lard-laden high fructose diet (LF)

...had on the health, caecal short-chain fatty acid concentrations, cholesterol and triglyceride levels are revealing, to say the least.

World premiere! I know it sounds hilarious, but this is actually the first study I have seen that focused on nutrient interactions, instead of individual (macro-)nutrients in diets that are not even suitable to isolate the effects of the nutrient of interest - most prominent example the "high fat diet"  which is high in fat (45% of the energy is the standard; there are yet also "high fat" diets with only 32% of the total energy from fat; Gajda. 2008) but leaves enough room for carbohydrates to complement, some would say "trigger" the obesogenic effects by providing a pro-insulinogenic stimulus that will blunt the oxidation of the dietary fat and help drive it into the cells.

If you take a closer look at the actual study outcomes, you will see that the answer(s) the study provides are about as complex as its design.

In contrast to the dietary fat which had no independent effect on any of the measured markers of gut function, the carbohydrate source, i.e. cornstarch vs. fructose lead to significant differences in total small intestinal mass, mean pH of the ileal digesta and the mucosal activity of sucrase, all of which were increase on the high fructose diet.

Figure 1: Serum lipid levels of the rodents after 4 weeks on obesogenic diets containing different forms of dietary fat and carbohydrate (Jurgoński. 2014)

Interactive effects were observed for the mass of the cecum itself (the tissue) and the digesta with opposing effects of fructose on when it was administered in conjunction with lard (reductions) vs. soybean oil (increases in cecum mass). Slightly different effects were observed for the short-chain fatty acid composition (SCFA):

"Both the dietary fats and carbohydrates contributed to changes in the total SCFA concentration in the caecal digesta of rats (p < 0.05 and < 0 0.001, respectively). The highest total SCFA concentration was in group LS, while group OS had a significantly lower concentration (p ≤0.05). Similarly, the acetate concentration in the caecal digesta was influenced both by dietary fats and carbohydrates (p < 0.05 and p < 0.001, respectively) with a similar span of differences among particular groups (p ≤0.05). The type of dietary carbohydrate had significant influence on the propionate and isobutyrate concentrations in the caecal digesta (p < 0.001 and p < 0.05, respectively); however, both dietary factors had an interactive effect on their concentrations (p < 0.05). The highest propionate concentration was observed in the LS and OS group, whereas significantly lower concentration was found in the OF group. The lowest isobutyrate concentration was in group OF and it was significantly higher in group OS (p ≤0.05)." (Jurgoński. 2014)

The serum lipid profiles were influenced by both, the types of fats and carbohydrates as shown in Figure 1. What's particularly striking, here, is the nasty effects of a combined lard + fructose feeding on the triglyceride levels.

A similar fat-dependence as for the fructose induced triglyceride boost can be observed for the levels of total and HDL cholesterol, which were increased only by the combination of fructose + saturated fat. In the rodents that received soybean oil with their coke, ... ah, I mean with their fructose, the researchers observed the exact opposite trend and a 5x lower yet similarly increased artherosclerosis risk (as evidenced by the 5x higher atherogenic index).

Suppversity Suggested Read: "EGGS - A Four-Letter Food Improves Both Cholesterol Particle & Phospholipid Profile + HDL-Driven Lipid Reverse-Transport" | read more

The results are still difficult to place. The complementary increases in total and HDL cholesterol in the lard + fructose group for example could be interpreted as unproblematic in view of the contemporary social media trend to depict high cholesterol as absolutely irrelevant. In view of the concomitant 2.3x increase in the ratio of triglycerides to HDL-cholesterol, of which we do know for sure that it predicts extensive coronary disease (Luz. 2008), it is still warranted to conclude that the combination of fructose and saturated fats is even worse than the combination of a high fructose intake with unsaturated fats, which had almost no effect on the triglycerides to HDL ratio and left the rodents in the corresponding group with a trig:HDL ratio what was >2.5x lower than that of the lard + fructose rodents.

Yes, I know - that's only rodent data, there is no information on body weight, or the gut microbiome and even the impact on glucose metabolism wasn't measured (you can predict from the triglyceride levels, though, that the animals lard + fructose diet had the lowest insulin sensitivity), the reason I still spent a whole article on this paper is that this is the kind of study, we'd need if we actually want to understand "why we are fat" from the inexplicably popular (macro-)nutrient perspective... I mean, let's be honest: On the level of food items, the complexity is not a problem and we all know the food items that propel the obesity epidemic, don't we?

References:

• Gajda, Angela M. "High fat diets for diet-induced obesity models." A Report for Open Source Diets (2008).

High MUFA Diets are (Heart-)Healthy and Probably Superior to High PUFA Diets

Ever since the "Mediterranean Diet" was/is the talk of the town, more and more people become aware of the potential benefits of the formerly largely ignored mono-unsaturated fatty acids (MUFAs). In spite of that, the majority of consumers (probably due to the misinformation coming from the marketing machinery of the food industry) still focuses on avoiding the "bad" saturated fats and consuming as much "healthy" polyunsaturated fats (PUFAs) as possible in order not to fall victim to an obesity epidemic which is inseparably intertwined with these kind of black-and-white approaches to nutrition.

In an extensive review (Jones. 2011) scientists from the Department of Human Nutritional Sciences at the Richardson Centre for Functional Foods and Nutraceuticals (University of Manitoba, Canada) evaluated data from over 50 years of research to come to the conclusion:

Consumption of dietary MUFA promotes healthy blood lipid profiles, mediates blood pressure, improves insulin sensitivity and regulates glucose levels. Moreover, provocative newer data suggest a role for preferential oxidation and metabolism of dietary MUFA, influencing body composition and ameliorating the risk of obesity. Mounting epidemiological and human clinical trial data continue to demonstrate the cardioprotective activity of the MUFA content of dietary fat.

In fact, they found MUFA rich diets to be superior even to diets enriched in PUFAs, which have lately oftentimes been hailed as the saviors of the fat and unhealthy:

When PUFA and MUFA rich diets were compared for replacement of dietary SFA in healthy adult subjects, those consuming MUFA rich diets demonstrated a preservation of HDL-C levels to a greater extent with only a 4% decrease in HDL-C levels compared to those consuming PUFA rich diets, which decreased HDL-C levels by 14%.

What is interesting, however, is that there still seems to be an initial bias against saturated fatty acids. This can also be seen from the fact that the general questions the authors pose throughout their review always come back to the idea of replacing saturated fatty acids by either carbs or MUFA, PUFA or MUFA etc. I would be interested to see a study or a review without this initial bias against saturated fats - the results could be very interesting... what do you think?