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 ;-)

Vitamin D & PUFA - Is There an Overlooked Antagonism Between Polyunsaturated Fatty Acids and Vitamin D3?

Image 1: Do not write off all the "good"
foods until you read the full blogpost,
including my comment at the end
(image by ADAM)

Hah... I knew a newsitem the title of which joins everybody's contemporary "pet supplements", would get your attention. Quasi as a byproduct of one of the hilarious vitamin D + calcium trials in which scientists seek to prevent bone loss and fracture in men and women age 65 and older by supplementation with 700IU (no I am not missing a "0", here) and 500mg calcium per day, Sathi Niramitmahapanya and his colleagues from the  U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University found an interesting and previously not thought of negative correlation between their subjects' plasma levels of 25-hydroxyvitamin D (25OHD) levels and the ratio of poly- to monounsaturated fatty acids in their diets (Niramitmahapany. 2011). Could it be that you have to choose, when it comes to high vitamin D or PUFA intake?

Since this was not a specifically designed experiment, Niramitmahapany et al. had to rely on the data that had already been gathered in a 3-year, randomized, double-blind, placebo-controlled trial, originally designed to determine the effect of supplemental vitamin D + calcium on rates of  bone loss and fractures in 152 men and women (age &amp;gt;65years). Consequently, the study relies heavily on the accuracy of complex regression analysis, by the means of which the Tuft researchers tried to figure out which of the handful of confounding variables they had surveyed, had the greatest influence, or I should say statistically measurable explanatory value for the effect of vitamin D3 supplementation on serum 25-hydroxyvitamin D levels in their elderly subjects.

In essence a regression model consists of a system of several sets of loosely predefined partial differential equations (e.g. logarithmic, linear, polynomial, etc.), the scientists, or rather their computers (in this particular study, the SPSS software package was used for statistical analyses) solve using the experimentally established data. Although statistical analyses like this allow for literally unlimited adjustments for confounding variables, such as body weight, total energy intake, etc., the underlying models are still in and out of themselves theoretical constructs that are based on certain hypothesis and assumptions. Thus, any "associations" of parameter A and outcome B, which are usually expressed in the form of regression coefficients (larger coefficient = greater explanatory power), are valid only if all the underlying assumptions hold true.

Out of the parameters Niramitmahapany et al. evaluated, the only independent variable with a significant impact on the effect of supplemental vitamin D3 on serum levels was the composition (not the absolute amount!) of the fats in the subjects' diets.

Figure 1: Statistically modeled regression coefficients of total fat intake and MUFA/PUFA ratio; adjusted for baseline BMI, 25OHD levels, total energy intake (data adapted from Niramitmahapany.. 2011)

As the regression coefficients in figure 1 clearly show, neither the absolute amount of fats nor the absolute amount of an individual type of dietary fat (monounsaturated, MUFA; polyunsaturated, PUFA; saturated fatty acids, SFA) are adequate predictors of serum 25OHD levels. The ratio of monounsaturated to polyunsaturated fatty acids (MUFA / PUFA ratio) on the other hand turned out to be a pretty reliable predictor of the amount of active vitamin D in the sera of the study participants. This was all the more the case if possible influences of saturated fatty acids were taken into account in the model, as well.

Now, statistics and "associations" are one thing, mechanisms and "causations" are yet another; and obviously the latter, i.e. cause-and-effect relations and determinisms, are what humans, in general, and natural scientists, in particular, have been striving for even before the early days of natural science in the ancient times. Thus, I assume you will be interested to hear, what the scientists have to say with regard to the underlying mechanisms of the statistical "association" they observed:

The mechanisms by which fatty acid intake may influence vitamin D3 absorption have not been completely delineated. Most of the available evidence comes from early work by Hollander and colleagues (Hollander. 1981). Their gut perfusion studies in the rat revealed that vitaminD3 is absorbed by passive diffusion in the proximal jejunumand the distal
ileum (10). Absorption of physiological doses of vitamin D3 in rats was reduced by 30%in the presence of a 4-fold increase in luminal fat (Hollander. 1978; 1981), and consistent with our findings, the PUFA, linoleic and linolenic acids, were particularly effective in decreasing vitaminD3 absorption (Hollander. 1978). Hollander offered several potential explanations for why these fatty acids impaired vitamin D3 absorption. They may have increased the solubility of vitamin D3 in the micelles and changed the partition coefficient such that the vitamin D3 stayed in the micelle. Alternatively, they may have increased the size of the micelle and thereby reduced its diffusion rate and increased its difficulty in crossing the unstirred water layer lining the intestinal mucosa. 

I suppose, what you just read about how dietary fat impairs the absorption of vitamin D goes against all you have hitherto heard from the same "experts" and "gurus" who have been telling you to take 20g of fish oil and 20.000IU of vitamin D, each day. Well, in their defense, it should be said that small amounts of dietary fat are actually beneficial, probably even essential for the uptake of the so-called "fat-soluble" vitamins A, D, K (and probably even E), BUT its obviously not the fat that "drives" or "carries" the vitamins into your blood stream, but the bile acid that is secreted in order to digest the former, which helps with / is necessary for the absorption of these, in the true sense of the word, vital nutrients. Moreover, as Niramitmahapanya et al. state, even evidence for the general accepted claim that vitamin D from small amounts of fish oil "produced a greater increment in 25OHD than vitaminD3 as a powder or dissolved in ethanol" is "inconclusive", ...

because the starting 25OHD levels, study durations, and dosing schedules in the available studies weren’t matched and because increment in 25OHD rather than absorption of parent vitamin D3 was measured.

And studies by Holvik (2007) and Maalouf (2008) which compared identical doses of vitamin D as a powder or in ethanol vs. vitamin D in oil found no difference.

The authors of the study at hand obviously did not look close enough at the data of the Maalouf study, because they state that Maalouf had "found the serum 25OHD increment to be greater with the oil vehicle", which may be correct, but the difference was small and mainly the result of a single 'hyperresponder' within the small study population (N=9 in the respective group). The "greater increment" in the oil group of the Maalouf study is thus statistically irrelevant.

So, while it appears quite clear that the general effect of large amounts of fat taken with physiological doses of vitamin D is a negative one, the scientists cannot explain why mono-unsaturated fatty acids seem to be an exception to the way the other fats (and PUFAs in particular) appear to negatively affect micelle content or migration rate of fat-soluble vitamins in the intestines. Yet, whatever the mechanism may be, an increase or, after all, a reduced decrease in vitamin D3 absorption from the gut may yet be another of the hitherto established health benefits of the long-overlooked mono-unsaturated fatty acids.

Dr. Andro's comment: If you want my personal assessment of these results, take them with an appropriate amount of skepticism. After all, eating meat, fish, liver, eggs, dairy etc., all rich sources of dietary fat and fat soluble vitamins, is the way nature intended us to get part (remember we would synthesize most of our vitamin D from sun exposure) of our vitamin D. So, the only way it would make sense that fat reduces its absorption would be the close association of cholesterol, which is the building block our body uses to manufacture vitamin D, and fatty foodstuff. It would thus be more prudent to say that "fat starvation", which would naturally be associated with low cholesterol intake, is a signal for you body to increase vitamin D uptake, in order to save the valuable cholesterol for the production of other hormones. Instead of avoiding fatty foods, you should thus rather get your lazy ass off the couch and into the sun to put the cholesterol from your 10-egg-breakfast-omelet to good use ;-)

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).

Making the Right Fish Choices: Fatty Acid Contents of 33 Different Fish Species. Plus: What Are the Implications?

Pollachius virens (Photo: Tino Strauss) is king, when it comes to the n:3/n:6 ratio, but with <1% of fat you will still be hard pressed to get tons of omega-3s from eating pollock... but is more really better, let alone necessary?

I have already broached the issue of the differences in the fatty acid composition of fish - even those of the same species - in past articles such as the one(s) on fish as a potential source of mercury in your diet (read more). When I saw the recent paper by Claudia Strobel, Gerhard Jahreis and Katrin Kuhnt in Lipids in Health and Disease, I thought that it was about time to supply you with some real data on the actual n:3/n:6 ratio of different fish and its implications for the purported health benefits and anti-obesity effects of regular fish intake. Is there a "super fish" or is it as so often a matter of "mixing and matching" to achieve the right balance?

Fish? Of course, I have fish & chips or fish sticks every other day!

I guess I don't have to tell you that both the fish part of "fish and chips", as well as the "healthy" fish sticks that are pretty popular at least among German kids, should actually be sold at the bakery, right? I mean the ratio of the bread crumb coating to the pressed fish fillets inside, is hilarious and in view of the fact that these products are 'pre-fried' with cheap vegetable oil before they end up in the freezer cabinets of supermarkets all around the world, you cannot avoid the increased (partially oxidized) omega-6 intake, even if don't (as most people do) fry them at home.

So, if the fast-food version of "fish" is not an option to gear your polyunsaturated fatty acid ratio more towards the n-3 side of things, which fish shall you go for? Well, according to the data the scientists from the Friedrich Schiller University in Jena, Germany, collected Pollachius virens is the n3:n6 king among the seven most frequently consumed fish species, which are herring, tuna, pollock, alaska pollock, salmon, rainbow trout and iridescent shark (at least according to Strobel, 2013).

Figure 1: Content of EPA & DHA, other omega-3 and the sum of omega-6 fatty acids in percent of total fat of the 33 tested species in the study; ordered according to n3:n6 ratio, fish with the highest n3:n:6-ratios on the left; note: the anchovies and sardines were in a tin with oil and while they were drained before the analysis this will have decreased the n-3:n-6 ratio (data calculated based on Strobel. 2013)

On the other hand, the total fat content of pollock (<1%) is so low that you will be hard pressed eating enough of it to elicit any significant health effects. As far as the most frequently consumed fish species go, this does bring us back to our good old friend, the salmon.

Figure 2: Comparison of fatty acid content in g/100g of wild and farmed salmon (left) and respective omega-3 to omega-6 ratios (right; based on Strobel. 2013)

Unfortunately "salmon" does not equal salmon, these days. The dripping orange stuff you can buy for a few bucks (the orange color is artificially added to the feed by the way) at every supermarket, for example, is farmed salmon and contains only 2-3x more omega-3 fatty acids than omega-6s. The reddish, lean cuts of wild salmon on the other hand, have a 12-13x higher relative omega-3 content and in fact almost no omega-6 fatty acids (0.05g / 100g). With 0.53g /100g omega-3 fatty acids, wild salmon is yet just like pollock not the "bulk" source of omega-3 fatty acids you would be looking for, if you fell for the stupid idea that you could undo the damage you are doing by eating tons of (oftentimes oxidized) omega-6 fatty acids by simply throwing an even greater amount of omega-3s into the equation.

So what do we make of all that information?

The very latest on the effects of fish consumption on body weight comes from a study in the latest issue of the British Journal of Nutrition and shows that there is no effect of higher intakes of total, lean or fatty fish on 5-year risk of becoming obese in the 344,757 male and female participants of the European Prospective Investigation into Cancer and Nutrition (Jakobsen. 2013). Now, this does not exclude the existence of non-body weight related benefits, but it certainly puts the myth of the "anti-obesity" effect of fatty fish into perspective. After all, every 10g of additional high fat fish in the diets of the female study participants was associated with a 5x more pronounced increase in body weight than an equal amount of low fat fish. The general trend towards increasing BMIs was yet countered by none of the two.

In view of the fact that we are suffering from a relative deficiency in omega-3 fatty acids, only (relative to the exubarant amount of omega-6 fatty acids the average Westerner consumes on a daily basis), I see the data presented in this post not as a "shopping guide", but rather as a means to conduct a reality check of how realistic it really is that someone who follows a no fast- and convenient-food diet and keeps a non-neurotic eye on his overall n-6 intake will benefit from omega-3 intakes in the multiple gram range.

Specifically when it comes to supplementation, previous trials such as Filaire et al. did in fact find increases in oxidative stress in perfectly healthy athletes (judo) in response to 6 weeks on 600mg EPA + 400mg DHA per day (Filaire. 2010). If you also take into consideration that these negative effects on lipid oxidation were not ameliorated by higher alpha-tocopherol (vitamin E) levels, the message this and other studies are sending is clear: The putative increase in omega-3 requirements is a result of an abnormally high intake of omega-6 fatty acids.

The easiest way to escape any negative effects while still reaping the benefits therefore is to reduce (not totally avoid!) the intake of omega-6 fats (specifically from processed foods) - full stop! If you do that by incorporating a large variety of whole foods into your diet and include grass-fed beef, dairy from pastured cows and, obviously, fish on a regular basis, you won't have to increase your intake of omega-3 fatty acids by picking the orange colored, disgustingly tasting, fat dripping farmed salmon from the super market over its delicious red wild cousin, just because it has 4.5x more omega-3 fatty acids.

Bottom line: It's food quality and fatty acid ratios that make the difference; not the absolute numbers of allegedly good and bad fats, carbs and whatever else has recently fallen victim to the over-generalization that appears to be necessary to render dietary advice suitable for the masses. If there is any one thing that's to blame for the health crisis these days, it's this kind of black-and-white thinking that's behind the overgeneralized and faulty "expert advice" which is by no means propagated exclusively via supposedly unreliable sources on the Internet.

References:

• Filaire E, Massart A, Portier H, Rouveix M, Rosado F, Bage AS, Gobert M, Durand D. Effect of 6 Weeks of n-3 fatty-acid supplementation on oxidative stress in Judo athletes. Int J Sport Nutr Exerc Metab. 2010 Dec;20(6):496-506.
• Jakobsen MU, Dethlefsen C, Due KM, May AM, Romaguera D, Vergnaud AC, Norat T, Sørensen TI, Halkjær J, Tjønneland A, Boutron-Ruault MC, Clavel-Chapelon F, Fagherazzi G, Teucher B, Kühn T, Bergmann MM, Boeing H, Naska A, Orfanos P, Trichopoulou A, Palli D, Santucci De Magistris M, Sieri S, Bueno-de-Mesquita HB, van der A DL, Engeset D, Hjartåker A, Rodríguez L, Agudo A, Molina-Montes E, Huerta JM, Barricarte A, Amiano P, Manjer J, Wirfält E, Hallmans G, Johansson I, Khaw KT, Wareham NJ, Key TJ, Chajès V, Slimani N, Riboli E, Peeters PH, Overvad K. Fish consumption and subsequent change in body weight in European women and men. Br J Nutr. 2013 Jan;109(2):353-62.
• Strobel C, Jahreis G, Kuhnt K. Survey of n-3 and n-6 polyunsaturated fatty acids in fish and fish products. Lipids Health Dis. 2012 Oct 30;11:144.

Saturated Fat Makes You Fat! You Read the Press Release - Here is the Whole Story: A Story of Muffins, SFA, MUFA, PUFA, Body, Liver & Visceral Fat and N6s & Lean Mass

I have to admit: Whether a conclusion as general at this is warranted based on the data from a recent study is questionable.

Somehow I knew that people would freak out, about a press release I reposted on the SuppVersity Facebook page earlier today (read it!). Next to saying that you can eat fructose and not get obese saying that you can eat PUFAs without getting fat is probably as heretic as saying that saturated fat makes you fat... what? Oh yes! You're right, it can be even worse. I mean, imagine you'd say that unsaturated fatty acids are less obesogenic than saturated fats.

Ah, come on! That's so mainstream it must be propaganda from the "pharmaceutical enteprise/ cholesterol lowering drug entreprise" [sic!], right?

Well, I am just looking at the acknowledgements of the study the press release refers. Let's see: "None of the authors have any conflicts of interest to disclose" and "This study was funded by the Swedish Research Council (project K2012-55X-22081-01-3)." No, I wouldn't say this sounds like there had been a "pharmaceutical enteprise/ cholesterol lowering drug entreprise" funding the study

Just as an aside: Discarding the results, because the results are not inline with your own indoctrictinat like the guys who sponsored it, is pretty pathetic. If you want to argue that the results Fredrik Rosqvist and his colleagues from the Uppsala University, and the Center for Clinical Research Dalarna are b*s*, you better take a look at the study design to identify flaws and shortcomings - and guess what?! That's what we are about to do now.

Now that we have all calmed down a bit, let's see what exactly we could freak out about - or, to put it differently, let's take a closer look at the study design, the results, and their interpretation.

I - The Research Question

I know that many of you don't care about questions. That's a mistake. In science, questions are everything. Answers are secondary. The motto of a true researcher is thus - just as the Greek philosopher Euripides had it -  "Question everything. Learn something. Answer nothing." In the end, we've already made a very good start by questioning the scientists' conclusion that

"[...] overeating SFA promotes hepatic and visceral fat storage whereas excess energy from PUFA may instead promote lean tissue in healthy humans." (Rosqvist. 2014)

What we are interested in part I of our analysis are not our questions, though. What we want to look at now, is the question that worried the researchers, the questions, whether ...

"[...]liver fat accumulation during moderate weight gain could be counteracted if the excess energy originate mainly from PUFA rather than from SFA." (Rosquist. 2014)

This question, as logical as it may seem for the average individual who has been sucking up the "good fat (PUFA) vs. bad fat (SFA)" mantra with his PUFA-enriched formula ever since he was born, is obvious a reason to freak out for the meanwhile almost as average black-and-white thinking inhabitant of the blogosphere.

Don't interpret this article as incentive to follow all dietary recommendations to the "T" before you've read my 2012 article on the effects of an allegedly heart healthy low fat diet on the LDL particle profile of healthy volunteers | read more

What this question is not, though, is pure invention. The idea to investigate whether liver fat accumulation during moderate weight gain could be counteracted if the excess energy originate mainly from PUFA rather than from SFA was born, when the researchers observed an isocaloric diet rich in PUFA given for 10 weeks reduced liver fat content and tended to reduce insulin resistance compared with a diet rich in SFA in individuals with abdominal obesity and type 2 diabetes (Bjermo. 2012) - the differences were not earth-shattering, but statistically significant (-1% total fat in PUFA vs, +0.6% body fat in SFA); and the "improvements" in the visceral fat to subcutaneous fat ratio (a marker of a healthier fat distribution) in the PUFA group of the Bjermo study were brought about (mainly) by increases in subcutaneous body fat in the PUFA group.

In view of the fact that the alleged improvements (in many cases the values simply worsened less) of the blood lipids, glucose and insulin levels, the hypothesis that "liver fat accumulation during moderate weight gain could be counteracted if the excess energy originate mainly from PUFA rather than from SFA" (Rosquist. 2014) is legitimate, but probably optimistic.

II - Study Design

So, if the underlying hypothesis is valid, the next thing we could target to debunk the claim that saturated fats are more fattening / unhealthier than unsaturated fats would be to have a closer look at the design of the LIPOGAIN study:

• 

  Figure 1: Rel. changes in liver, visceral and subcutaneous fat in subjects over-consuming a high vs. low (white) saturated fat diet.

  the subjects were randomly allocated to the two intervention groups
• the scientists made sure that the subjects gained weight at identical rates (3%) (the amount of muffins consumed per day was individually adjusted weekly, i.e. altered by +/- 1 muffin/day depending on the rate of weight gain of the individual)
• the dietary intervention was based on highly standardized food items 
• muffins containing sunflower oil (high in the major dietary PUFA, linoleic acid, 18:2 n-6) or 
• muffins containing palm oil (high in the major SFA, palmitic acid, 16:0). 
• the muffing were baked in large batches under standardized conditions in a metabolic
  kitchen at Uppsala University
• except  for  the type of fat, the  muffins  were  identical  with  regard  to  energy,  fat (51%),  protein (5%), carbohydrate (44%; sugar to starch ratio 55:45), and cholesterol content, as well as taste and structure.

I guess you will agree that there are no major design flaws, here. If anything, you could speculate that the changes in SFA and PUFA intake (-1.6% and +4.9% SFA intake and +7.9% and +0.3% PUFA intake in the PUFA and SFA group, respectively) were pretty pathetic and insufficient to produce significant results.

Figure 2: Relative contribution of saturated (SFA), monounsaturated (MUFA) and polyunsaturated (PUFA) fatty acids to the total energy intake of the subject before and after the study (Rosquist. 2014)

If you take a look at my plot of these differences (you should be aware that they are expressed in terms of the total energy intake), you will have to concede, though, that the difference between SFA/PUFA ratios, i.e. 0.9 and 3.6, is pretty significant.

Figure 3: There is a distinct correlation between the relative amount of omega-6 fatty acids in the blood and the change in lean mass - a beneficial one!

More or less flawless, but still questionable: Whether that's enough for you to accept that the Rosquist et al. used their results to make a general statements about the effects of saturated vs. unsaturated fat intake is up to you. The same goes for the real-world significance of the different body and liver fat trajectories in Figure 1.

In view of non-negligible increases in total, liver and visceral body fat and the absence of the often-touted pro-anabolic effects of saturated fats (mind the proportionality of an increase in the allegedly bad omega-6 concentration in the blood and the lean mass increases / decreases in Figure 3), it's difficult to keep nibbling on a chunk of bacon without at least taking into consideration that the "bad PUFAs" may not be as bad after all.

"Whut?" Calm down, I am not suggesting that you have to go back to the "saturated fat is bad for you" mantra, but I would like to invite you to take a parting look at Figure 2 (right) and note that the main characteristic of the "PUFA" diet is not its high PUFA content, but it's balanced fat content. Maybe the sentence "The optimal diet is characterized by a balanced intake of all three main types of dietary fat" would thus be a conclusion we can agree on - ha?

References:

• Bjermo, Helena, et al. "Effects of n− 6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial." The American journal of clinical nutrition 95.5 (2012): 1003-1012.
• Rosqvist, Fredrik, et al. "Overfeeding Polyunsaturated and Saturated Fat Causes Distinct Effects on Liver and Visceral Fat Accumulation in Humans." Diabetes (2014): DB_131622.