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marylin monroe
Showing posts with label n3. Show all posts
Showing posts with label n3. Show all posts

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

Image 1: Kids who drink more milk, tend to be leaner... and that despite (?) the fact that this stuff comes out of an animal and is full of bad cholesterol and fat - outrageous ;-)
Plenty of interesting news, lately, so this one - just like the recently released hypertrophy / hormone correlation study by Stuart Phillips, about which I have been talking in yesterday's installments of the Intermittent Thoughts got somewhat delayed. With the Christmas holidays and the approaching and all those New Year's weight loss resolutions (I would prefer the term "fat loss resolution", though ;-) already on your mind, I do yet think that it is about time to break the news on the "fat" reason for the purported beneficial effects an increased consumption of dairy products during periods of caloric restriction appears to have on weight and more specifically body fat loss (Linn. 2000; Peirara. 2002; Shahar. 2010).

Dairy, calcium or simply the right macronutrient composition?

The scientific results I am going to present are taken from a study that was published in the Journal of Nutrition and Metabolism a few weeks ago (Smilowitz. 2011). In a randomized, placebo-controlled study Jennifer T Smilowitz and her colleagues from the USDA-funded (keep that in mind, when interpreting the results, or rather the scientists interpretation of the latter ;-) Western Human Nutrition Research Center assigned their 62, against the background of the rampant obesity epidemic, only slightly overweight young subjects (mean age: 25y; BMI ~28) to a calorically restricted diet (-500kcal) that was specifically designed to "provide comparable levels of macronutrient and fiber, to approximate the average consumption in the US" (35% fat, 49% carbohydrate, 16% protein and 2-3g fiber), which contained either
  • 0-1 servings of dairy, with 500mg dietary calcium (from the whole diet) + placebo,
  • no dairy (still 500mg calcium from diet), 900mg of supplemental calcium carbonate, or
  • 3 servings of dairy, with 1400mg of dietary calcium (from the whole diet) + placebo
Thusly, the study basically mimicked, what would happen if you told the average American to just keep their usual sedentary life-style (the subjects were instructed not to start to exercise or anything like that) and either just reduce his caloric intake by 500kcal, to do the former and to make sure to have three servings of dairy per day, or to just take an additional "healthy" calcium carbonate supplement.

Eat dairy + whatever you want and lose weight?

Now, interestingly, the subjects were not only free to chose whether they wanted to consume the dairy from low or normal fat cheese, milk and/or yoghurt, they were also relatively free as far as the rest of their dietary choices were concerned so that the detailed analysis of their food-logs allowed for conclusions to be drawn that went beyond the initial scope of the study... but let's take one thing after the other.
Figure 1: Dietary intake (macronutrients in kcal/day) of the subjects before and at the end of the 12-week study period and relative changes in carbohydrate, protein and fat intake (data calculated based on Smilowitz. 2011)
If you take closer look at the analysis of the dietary records the subjects had to keep, you will notice that the minor differences in the dietary prescriptions induced quite profound changes as far as the macronutrient composition of the respective diets was concerned. While the subjects in the non-dairy groups, regardless of whether they received a calcium supplement or placebo, cut back on all the three major macronutrients, the requirement to incorparate three servings of dairy into their meal-plan, alone appeared to suffice to keep the protein intake of the dairy group at a reasonably high level (~72g; which would be 0.96g/kg body weight). The protein intake of the two non-dairy groups, on the other hand dropped to 57g (0.75g/kg) and 54g (0.7g/kg) for the calcium and placebo supplemented groups, respectively.
Figure 2: Changes in body composition and measures of insulin sensitivity after 12-weeks on the high dairy, calcium supplemented or placebo supplemented diets (data calculated based on Smilowitz. 2011)
In view of the facts that the subjects had to stick to the calorically restricted diet for 12 weeks, it should not surprise you that all of them lost a statistically significant amount of body weight (cf. figure 1) and improved their insulin sensitivity (as indicated by reduced insulin levels and HOMA-IR values).What should yet strike your eye are the increased reductions in body fat and waist circumference and the greater increase in lean mass-% in the high dairy group. Now, you will probably assume that this was a result of the higher protein intake, and that may in fact have been the case, as one of my beloved model calculations by which scientists "adjust" their data for whatever they want (usually until the result is in accordance with their hypothesis ;-) revealed that
Dairy product consumption was found to be significantly associated with reduced WC [waist circumference] and %BF [percent body fat], however, these relationships were no longer significant after adjustment [my emphasis ;-] for protein and energy intake and physical activity.
Figure 3: Scatterplot of the partial correlations between reported 12-week mean dietary fat intake expressed as % of total energy and changes in lean body mass (LM) and body fat % (taken directly from Smilowitz. 2011)
Assuming that this "adjustment" yielded valid results it is all the more interesting what a subsequent analysis of the "adjusted" data revealed:
When expressed as a percent of total energy, dietary fat composition was correlated with changes in anthropometrics. Reported MUFA at 12 wk was inversely and positively associated with changes in % LM and % BF, respectively.
Or, in the words of the layman: The greater the relative monounsaturated fatty acid (MUFA) content of the subjects' diets, the more lean mass was lost and the more body fat was retained during the study period (cf. figure 3). Similarly, a higher intake of polyunsaturated fatty acids (PUFA) was associated with lower reductions in waist circumference, and while  the scientists claim that the n3:n6 ratio did not matter, it should make you wonder if it could actually be coincidental that the n6:n3 ratio in the dairy group was 6.6, while the ones in the calcium and placebo groups were 8.7 and 7.9, respectively.

And what about saturated fats? 

Moreover, the USDA scientists mention only "in the small print" that most fundamental (and statistically significant) distinguishing feature of the dairy group, who unquestionably had more favorable weight loss results despite an overall greater caloric intake, was (and I am quoting this from the paper) "a significantly higher intake of SFA [saturated fats] and lower intakes of MUFA and PUFA compared with the calcium supplement and placebo groups". Now, guess where this "bad" saturated fat came from? Well, probably from full-fat dairy! And guess why those "good" MUFAs and PUFAs were missing from the diets of the high dairy group. Well, probably because the subjects ate less "healthy vegetable oils"... ah, and did I already mention that the dairy group also ingested disproportionally (relative to their caloric intake) higher amounts of biotin, vitamin B12, vitamin D and - God forbid! - cholesterol?
Image 2: Even if you like animals, eating their eggs and full-fat dairy products won't hurt them.

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

Caffeine Protects Brain Function Against Stress & SAD Diet; Coffee Withdrawal, Anxiety & More; Giardia, Messy Subtenant W/ Gusto For Arginine; Vit B6 & n6:n3 PUFA Ratio

19 Billion Euro that's the estimated 2011 financial burden due to lung cancer, alone, here in Europe and the On Short Notice figure of the week (information based on ESMO2012 press release)
Those of you who are also following the SuppVersity facebook news, will probably recognize the figure on the right: 16,000,000,000€ or $24,419,000,000, that's the estimated economical burden due to lung cancer, alone, here in Europe (cf. "Who cares if people are dying as long as the economy is thriving?"). An enormous financial loss, and still not the reason that this is my figure of the week. Rather than the financial damage, itself, it is the tragic fact that only the latter, yet not the fate of the patients and their families, would make a valid argument, when policy makers were debating a long overdue, total and all-encompassing public smoking ban... but now for a couple of more sciency, yet not less intriguing news from the past week.



Problems thinking straight? Guess what: 3-4 cups of coffee could help :-) According to a soon-to-be-published paper by scientists from the Jordan University of Science and Technology in Irbid, Jordan, the ingestion of the human equivalent of approximately 3.8mg caffeine per kg body weight or 3-4 cups of coffee per day, can inhibit both, the stress, related as well as diet induced (we are talking of the "typical" Western diet (WD), that's both high in carbohydrates and fat) cognitive impairments (Alzoubi. 2012)... well, at least in the researchers 3-months rodent study it worked like a charm
  • learning trial: animals in the caffeine/stress, caffeine/WD, and caffeine/stress/WD groups made fewer errors, than non-supplemented stressed or WD animals; overall their performance was comparable to those of the control
  • memory tests: treatment reduced the number of error and restored short-term memory and long-term memory during chronic stress and/or WD (P < 0.05) to normal levels
With respect to the underlying mechanisms the scientists speculate that caffeine may "act mainly by inhibiting adenosine receptors" (Alroubi. 2012), which has in turn been shown to to inhibit long term potentiation (LTP) in rat hippocampal slices and disrupt the process of learning and memory at the synaptic level by blocking release of glutamate (de Mendonca. 1994).

Additionally, caffeine has also been shown to increases the expression of hippocampal brain-derived neurotrophic factor (BDNF) and its receptor, which is impaired in response to chronic stress and a hypercaloric Western diet (Aleisa. 2006; Molteni. 2004) and leads to deteriorations in cognitive performance. In the long run those effects could also contribute to the anti-dementia and anti-Parkinson's effects, I mentioned in the recent SuppVersity post on the insulin sensitizing effects of coffee.



Figure 1: While the Hedonic tone and alertness reduced to baseline on day 5 of caffeine withdrawal, the habitual caffeine consumers had >15% higher anxiety scores on day 7 after giving up on their daily dose of methylxanthine (data calculated based on Smith. 2012).
Don't worry, caffeine will also work for humans. And what's best, upon short-term withdrawl (8 days) your cognitive performance is not going to suck - at least not as much as when you are stressed or living on pizza and French fries, only. All that and a couple of interesting other results have been published ahead of print in the online version of the Journal of Pharmacology (Smith. 2012).

To probe the effects of acute caffeine ingestion on cognitive performance and the influence of previous caffeine consumption and withdrawal, Andrew P Smith, Gary Christopher and David Sutherland recruited 70 volunteers (25 male, 45 female; mean age 22.8 years). The 35 consumers (>100mg caffeine /day, mean 300mg; range 110–600 mg) were put on withdrawal and tested on day 2, alone and without caffeine, and day 8 together with the non-consumers in a double-blind placebo-controlled fashion. During the caffeine challenge, the cognitive performance was tested twice, once before and once 30min after the provision of the caffeinated beverages.

Anxious, but smart: Caffeine gives you the edge

The results of the trial clearly indicate that the ingestion of 2 mg/kg of caffeine, which were served in decaffeinated coffee or tea 30min before the testing procedures, were associated with faster simple reaction times, fewer long responses, greater detection of targets in the cognitive vigilance task, and faster encoding of new information.
"The results confirmed previous findings, with ingestion of caffeine being associated with a faster simple reaction time, fewer long responses, more targets detected and faster encoding of new information. There were no main effects of consumer status, nor were there any significant interactions between caffeine and consumer status." (Smith. 2012)
Notwithstanding, I believe that many of you will probably be more interested in the effects of caffeine withdrawal on overall withdrawal symptoms (figure 1, top), as well as the alertness, hedonic tone and anxiety (figure 1, bottom) and the cognitive performance on day 2 of the withdrawal period (figure 2, left), than in any of the well-established performance cognitive performance boost, right?
Figure 2: Performance on day 2 of withdrawal phase (w/out caffeine) and on day 8 before (w/out caffeine) and after (w/ caffeine)the ingestion of decaffeinated tea or coffee with 2mg/kg caffeine in it (data based on Smith. 2012)
As you can see on the left-hand side of figure 2 there was a minimal performance decline on day 2 of the withdrawal phase, but the latter was statistically not significant and all measured markers of cognitive function had returned to normal on day 8 (remember longer response times = worse performance!), when the resumption or first time provision of caffeine spiked the reaction times and lowered the mistakes in all tests, irrespective of whether the subjects were former habitual consumers on withdrawal, or not.

Outside of controlled experiments "real" coffee and tea do at least as well

Since a large cup of coffee contains about the same amount of caffeine the scientists simply added to decaffeinated beverages, to ensure that the drinks could not be distinguished (by their smell for example), you can simply stick to your regular coffee and if you want to enjoy similar benefits. And to be honest, in view of the plethora of benefits of chronic low dose coffee consumption, I would not even think for a second about whether or not you may be missing out on the occasional boost, when you are not "going on withdrawal" from time to time...



Figure 3: W/out arginine (Arg-) intestinal epithelial cells can't proliferate (graph based on Stadelmann. 2012)
Giardia eats away your guts arginine supply and makes itself at home within an increasingly morbid digestive tract! As a group of scientists from Sweden and Argentina reports in their latest paper, the protozoan parasite, Giardia intestinalis, feasts on the arginine your gut cells need to proliferate (Stadelmann. 2012). This will lead to reduced polyamine levels and upregulated cell cycle inhibitory genes, which will eventually disrupt the the cell cycle of the intestinal epithelial cells. The reduced intestinal epithelial cell proliferation, on the other hand, allows the gut pathogen to thrive and will, in the long run, disrupt the intestinal tissue homeostasis and thus initiate the decay of the intestinal epithelium  - a central feature of so many of the wide-spread gut pathologies.

Provision of additional arginine + citrulline can help ... in the short run

Now, the good news about all that is that the in-vitro data in figure 3 clearly suggests and anecdotal, as well as the effective therapy of diarrhea patients with arginine/citrulline actually confirm that the provision of supplemental arginine (or citrulline) constitutes a cheap and readily available way to ameliorate the decay, until the bugs have been eradicated by antimicrobial drugs.

A pros pos, antimocrobial drugs, with regard to latter, Noa Tejman-Yarden and Lars Eckmann write in a recent review of the latest drug innovations, that despite the fact that metronidazole and other antimicrobials are usually effective, "treatment failures are common and antimicrobia resistance occurs" (Tejman-Yarden. 2011), so that it would appear as if complex derivatives of 5-nitroimidazole and benzimidazole, which form the core structure of the most widely used antigiardial drugs, will replace them in the short-run. At least for so long, until several new classes of antigiardial drug candidates that have already been identity by high-throughput screening of large compound libraries, will eventually hit the market (Tejman.Yarden. 2011)




More about vitamin B6: Helps with neurotransmitters synthesis; is involved in nerve function and necessary for normal brain development & function; influences mood, and melatonin production; effects circadian clock; is needed for B12 absorption and thus red blood cell production
When low: "Pins and needles" in extremities, mental disorders, seborrheic dermatitis, estrogenic PMS, dizziness, irritability, kidney stones, abnormal EEG, anemia, convulsions, edema (water retention), hypothyroidism, migraine-headaches, glossitis, lymphopenia
When high: Depression, suicidal tendencies, severe fatigue, mood swings, low blood sugar, migraine-headaches, heart palpitations, thyroid abnormalities (hyper- in the short, hypo in the long term), numbness in hands and/or feet, spinal / nerve degeneration, muscle spasms / cramps, osteoporosis, arthritis, higher blood pressure (short-term suppl.), lower blood pressure (long-term suppl.), mineral imbalances (high phosphor & magnesium vs. low sodium & calcium), restlessness, insomnia, vivid dreams, decreased estrogen & prolactin, depressive PMS.
RDA (adults): 1.3 mg*
*higher for pregnant women & >50y
Upper tolerable limit: 30-100mg*
*depending on the source of information
Food sources: chicken, turkey, tuna, salmon, shrimp, beef liver, milk, cheese, lentils, beans, spinach, carrots, brown rice, bran, sunflower seeds, wheat germ, and whole-grain flour
n6:n3 ratio does not depend on dietary intake alone: A marginal deficiency in vitamin B6 will skew your serum PUFA levels towards the N6-side That's the long and short of the results of a study that's going to be published in the October issue of the Journal of Nutrition.

Mei Zhao and her colleagues analyzed the fatty acid profiles in plasma, erythrocytes, and peripheral blood mononuclear cells (PBMC) of healthy men and women who had been fed a low-vitamin B-6 (pyridoxine) diet for 28 days and observed that contrary to the plasma HDL and LDL cholesterol concentrations, the amount of free fatty acids (FFA) in the blood and the erythrocyte and PBMC membrane fatty acid compositions, neither of which showed any statistically significant changes, the amount of all long-chain polyunsaturated fatty acids, i.e. arachidonic acid (n6) and EPA and DHA (n3) decreased from 548 ± 96 to 490 ± 94 μmol/L, 37 ± 13 to 32 ± 13 μmol/L, and 121 ± 28 to 109 ± 28 μmol/L, respectively.

The subsequent 8% increase in the total n6:n3 PUFA ratio from 15.4 to 16.6 is not alarming, but if this trend would continue linearly, it would certainly become problematic, in the long run. Moreover, the decrease in both n6 and n3 long-chain PUFAs (of which people tend to forget that the "inflammatory" arachidonic acid is as vitally important as its "anti-inflammatory" omega-3 counterparts) could provide an alternative / complementary mechanistic explanation for the increased cardiovascular disease risk that has been associated with vitamin B-6 deficiency.

In view of the fact that the RDA is not exactly high and can easily be achieved from dietary sources, along (as long as you follow a diversified whole foods diet), and considering the fact that high levels of B6 have been associated with more negative side-effects than B6 deficiency (see infobox on the right; please note that I collected the information on a couple of trustworthy websites on RDAs & co and did not verify the research on each of them!), I would however caution against the typical Western "more helps more" supplementation mentality.





Figure 4: Easy come, easy go - the mass you gain and the fat you lose by doing nothing than simply injecting testosterone is lost / regained within 6 months after discontinuation of the "testosterone therapy" (Forbes. 1992); read more about the role of testosterone in skeletal muscle hypertrophy in the Intermittent Thoughts on Building Muscle
In view of the fact that (a) today's short news items are pretty long(ish) and you still got a couple of interesting facebook news to check out, such as...
... and a plethora of additional gems from the realms of health, exercise, nutrition & supplementation, I will call it a day for today and save the exercise and a couple of other exciting On Short Notice items for later next week.


References:
  • Aleisa AM, Alzoubi KH, Gerges NZ, Alkadhi KA. Chronic psychosocial stress-induced impairment of hippocampal LTP: possible role of BDNF. Neurobiology of Disease 2006;22:453–62. 
  • Alzoubi KH, Abdul-Razzak KK, Khabour OF, Al-Tuweiq GM, Alzubi MA, Alkadhi KA. Caffeine prevents cognitive impairment induced by chronic psychosocial stress and/or high fat-high carbohydrate diet. Behav Brain Res. 2012 Sep 20.
  • ESMO. Press releases related to the ESMO 2012 Congress of the European Society for Medical Oncology in Vienna.
  • Forbes GB, Porta CR, Herr BE, Griggs RC. Sequence of changes in body composition induced by testosterone and reversal of changes after drug is stopped. JAMA. 1992 Jan 15;267(3):397-9.
  • de Mendonca A, Ribeiro JA. Endogenous adenosine modulates long-term potentiation in the hippocampus. Neuroscience 1994;62:385–90.
  • Molteni R, Wu A, Vaynman S, Ying Z, Barnard RJ, Gomez-Pinilla F. Exercise reverses the harmful effects of consumption of a high-fat diet on synaptic and behavioral plasticity associated to the action of brain-derived neurotrophic factor. Neuroscience 2004;123:429–40.
  • Smith AP, Christopher G, Sutherland D. Acute effects of caffeine on attention: a comparison of non-consumers and withdrawn consumers. J Psychopharmacol. 2012 Sep 19.
  • Stadelmann B, Merino MC, Persson L, Svaerd SG. Arginine Consumption by the Intestinal Parasite Giardia intestinalis Reduces Proliferation of Intestinal Epithelial Cells. PLoS ONE. 2012; 7(9): e45325. 
  • Tejman-Yarden N, Eckmann L. New approaches to the treatment of giardiasis. Curr Opin Infect Dis. 2011 Oct;24(5):451-6.

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 ;-)

The Quest For the Best N6:N3 Ratio. Swine Study Suggests: 5:1 is Healthy, 1:1 Will Also Cut Fat and Build Muscle

 Yes, this study is about omega-3s, but it is not about the beneficial effects of fish oil.
Ok, I see you are totally excited, so I am not going to beat around the bush for long: According to a soon-to-be-published study from the Hunan Provincial Engineering Research Center of Healthy Livestock, Institute of Subtropical Agriculture at the Chinese Academy of Sciences  a 5:1 ratio of n-6:n3 (as in omega-6 to omega-3) is good enough to keep pigs healthy.

Kicking out another couple of grams of omega-6 fatty acids, on the other hand, had pretty intriguing effects on the body composition of the ninety-six male cross-bred (Large White£
Landrace) pigs who happened to weigh about as much as an average human being (another advangate, of swine - HED calculations are not necessary; learn more).
Did you know that pigs are opportunistic omnivores just like us and provide a better model of human metabolism than our little, furry remote cousins with the big round eyes and the long tails who are populating the laboratory cages of scientists all around the world (cf. Miller. 1987)?
Lineseed or soybean - that makes all the difference

I hope you did not already start popping fish oil, while you are reading this. After all, in this case the glorified residual waste from the fishery industry did not contribute to either the health or weight loss benefits Duan et al. observed in their pigs who were fed one of the four isoenergetic diets with n6:n-3 PUFA ratios of 1:1, 2·5:1, 5:1 and 10:1 for 2 months.

Table 1: Ingredients, nutrient and fatty acids composition of the diets the pigs received; † vitamin premix (Duan. 2013)
As the ingredient profiles of the different diets (table 1) tell you the major source of omega-3 fatty acids was lineseed oil. The latter is basically devoid of long-chain omega-3 fatty acids (EPA & DHA). Instead, it contains the short-chain variety aka alpha-linolenic acid that is often laughed at in the health and fitness community as being the useless precursor to the powerful "fish oils" EPA and DHA (note: the level of DHA was identical in all diets!).

So, no fish oil, just ALA

Although the allegedly more potent LC-PUFAs were missing, the changes in body composition and the overall improvement (=reduction) of the activity of the potentially pro-carcinogenic PI3K-alpha gene and the fat storage genes FATP-1 and PPAR-gamma (learn more about PPAR-gamma) were still impressive.

If you take a closer look at the data in figure 1, though, you will realize that the effects on body composition require a reduction to 2.5:1, better 1:1 to become significant.
Figure 1: Feed conversion rate, muscle mass, adipose tissue mass, lean to fat mass ratio expressed relative to the levels of the pigs in the 5:1 n6:n3 group after 2 months on the different diets (Duan. 2013)
At the same time there is a clear relationship between increased adiposity and the amount of soybean oil in the pig diets. Thank god that the USDA in their incredible wisdom lists it among the top dietary sources for fat *sarcasm*.

Ah, I'd better not get political here, but let me point out one thing: In view of the currently available scientific evidence it borders physical injury resulting from negligence that the "guidelines" do not put an emphasis on the reduction of the the crazily high n-6:n-3 ratio of the Standard American Diet (16-17:1).

Unlike this pig study, a previous rodent study suggests you should pick EPA over DHA over ALA for weight loss purposes (learn more)
Bottom line: This is one of the most convincing well-controlled animal studies we have that would support that the purportedly "paleolesque" 1:1 ratio of n-6:n-3 fatty acids entails highly significant health benefits,  even if those omega-3 fatty acids don't come from fish, but from lineseed oil.

One thing we must not forget, though, is the fact that the beneficial changes in health and body composition were brought about by the concomittant reduction in omega-6 and increase in omega-3 fatty acids. Simply drinking a bottle of lineseed or cod liver oil everyday could thus do more harm than good, because with ~3g of oil per 100g the diet was also low in total fat and almost devoid of saturated fats and whether the same results would occur in a high fat scenario is beyond what the study at hand can tell us.

References:
  • Duan Y, Li F, Li L, Fan J, Sun X, Yin Y. n-6:n-3 PUFA ratio is involved in regulating lipid metabolism and inflammation in pigs. Br J Nutr. 2013 Aug 15:1-7. [Epub ahead of print]
  • Miller ER, Ullrey DE. The pig as a model for human nutrition. Annu Rev Nutr. 1987;7:361-82. Review.

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

Learn more about the fatty acid and nutrient composition of grass-fed vs. regular beef this SuppVersity article is for you... and make the first step to reduce your CVD risk by 20% irrespective of whether or not you're going to eat grass-fed in the future!
I remember that I wrote a previous post about the detrimental effects of growing salmon on a high omega-6 diet. The result is a fish with an omega-3 to omega-6 ratio that is totally different from that of the wild-caught salmon everyone is raving about. Bad news, I know and to be honest, I am fed up with bad news.

Luckily you can rely on the scientists over at the Leibniz Institute for Farm Animal Biology in Germany: Dirk Dannenberger and his colleagues have just published a paper that sheds some light on the beneficial side of this ostensibly nasty link between the fatty acid make-up of the feed and the fatty acid composition of the meat of the animals we eat.

N6 in N3 out, N3 in N6 out - you see, it works both ways!

In their quest to find a way to change the fatty acid composition of beef products (German Corned beef (GCB), tea sausage spread (TSS), scalded sausage (SS)) the scientists simply replaced the regular maize silage + concentrate  and soybean meal based diet with a diet containing grass silage + concentrate with added rapeseed cake (12%) and linseed oil (3%) and *surprise* the amounts of short chain and long chain omega-3 fatty acids increases by 160%, 130% (EPA) and 70% (total long-chain PUFA = EPA, DHA, DPA).
Figure 1: Detailed comparison of the fatty acid content (mg/100  g) in Longissimus muscle of German Holstein bulls fed the regular corn + soy based (control) vs. grass + linseed based (experiment) diets  a different diet (Dannenberger. 2013)
Now that's cool, but in view of the fact that the major part of beef products is not bought as a raw steak of in form of ground beef, etc. what really counts is the net omega-3 gain in the previously mentioned beef products and that did not work as well as the enthusiastic
"n-3  PUFA  from  beef were  found  to  be  product-specifically  transferred  into  the  corresponding  beef  products"(Dannenberger. 2013)
 would suggest. After all, the increase in short chain and total long-chain omega-3s in the corned beef was only 40% and 50% and thus 75% and 29% lower than the increase in the "raw material".

So where did the good omega-3s go?

Well, I guess some of you will already have got it. German Corned Beef if freakin' lean. With only 2% fat the reason for the absence of omega-3s is thus simply that the fatty cuts don't even make it into the end product.
Figure 2: While the "grass-fed + enhanced" meat has identical amounts of iron, copper, zinc and selenium (not shown) it lacks the additional "vitamin E"-s that are in the corn-based chow; furthermore both forms are devoid of the fat burning isomer of CLA, this does yet also imply they don't entail the corresponding diabetes risk (Dannenberger. 2013)
So, despite the success of the study at hand, we would initially have to take up eating the whole animal, or rather all the cuts instead of throwing away the fatty ones just to be take the lean parts, fry them in plant oils and drown them in soy- or sunflower-oil based sauces to "water" the dry meat and spice up the blatant taste (with the decrease in total fat content in grass-fed cattle this effect will be even more pronounced, by the way).

Once we have made that important step from thinking that all animal fat must be bad, a simple change in the ingredient profile of our animals' feed could make a big difference to our health... what? No, you can already buy meat like that... you must be kiddin' me, right?  ;-)

This is not what you want: Farmed Atlantic salmon - raised with & fried in soy *yummy* (learn why)
Bottom line: I hope today's SuppVersity article did not just provide you with more information about the fatty acid profile of "grass fed, omega-3 pimped meat", but also made you smile. And if it did that I did already contribute to a 22% reduction your personal heart disease risk before you even ate one of the omega-3 steaks from the German cows.

How? Well, that's the CVD risk reducing effect of positive affect that was established in a large prospective study with 10 years of follow-up by Karina Davidson from the Department of Medicine, Center for Behavioral Cardiovascular Health at the Columbia University Medical Center in 2010 - I know I am so caring, but you don't have to thank me for that. I mean who would ready my stuff if it was not for you?

References:
  • Dannenberger D, Nuernberg K, Herdmann A, Nuernberg G, Hagemann E, Kienast W. Dietary PUFA Intervention Affects Fatty Acid- and Micronutrient Profiles of Beef and Related Beef Products. Foods. 2013; 2(3):295-309.
  • Davidson KW, Mostofsky E, Whang W. Don't worry, be happy: positive affect and reduced 10-year incident coronary heart disease: the Canadian Nova Scotia Health Survey. Eur Heart J. 2010 May;31(9):1065-70.

Turning Bad Into Good Fats, AHA Style: How the American Heart Association (Ab-)Uses Scientific Research According to Their (Hidden?) Agenda

As a diligent student of the SuppVersity, you are well aware that the absolute and relative overabundance of n-6 fatty acids (also known as omega-6 or linolic acid) in Western diets literally lies at the heart of heart disease. It is thus dear to my heart to turn your attention to the recent advances of the American Heart Association Nutrition Subcommittee of the Council on Nutrition to reestablish the myth of the heart-healthy omega-6 polyunsaturated fatty acids.

Image 1: You better watch out, other
than the American Heart Association
wants you to believe
, one of the
"better fat sisters" (Poly, the one in the
middle) turns out to have a very dark
six-times unsaturated side ;-)
Back in 2009, already, the American Heart Association had published an article (AHA. 2009 Omega-6 Fatty Acids and Risk for Cardiovascular Disease), the putative intention of which was "to summarize the current evidence on the consumption of omega-6 PUFAs, particularly LA, and CHD risk". Cleverly, selecting only those studies that fit their (hidden?) agenda, William S. Harris from the Sanford School of Medicine , who is a speaker for GlaxoSmithKline and a consultant to several other companies, including Monsanto, Acasti Pharma, Unilever and Omthera (Ramsden. 2011), and the other members of the committee put together seemingly conclusive evidence (if you solely rely on the studies the commitee selected, their argumentation is in fact very conclusive) supporting their objectively questionable, if not dangerous advice to the American public to obtain "at least 5%-10% of [their daily energy intakes] from omega-6 PUFAs [in order to] reduces the risk of CHD [chronic heart disease] relative to lower intakes." The board even went so far to conclude that...
[t]he data also suggest that higher intakes appear to be safe and may be even more beneficial (as part of a low–saturated-fat, low-cholesterol diet). [...] To reduce omega-6 PUFA intakes from their current levels would be more likely to increase than to decrease risk for CHD.
As it seems, neither Harris, nor his colleagues Ingeborg A. Brouwer or Dariush Mozaffarian stuck to their own advice, because, now, two years later, they are obviously still healthy enough to defend their sponsors messages against the results of a paper by Ramsden et al. (Ramsden. 2010), who had addressed the very same topic somewhat more objetcive-, or, I should say "scientifically" in December 2010. In a sneaky letter to the editors of the British Journal of Nutrition with the tell-tale title "n-6 Fatty acids and risk for CHD: consider all the evidence" Harris, Brouwer and Mozaffarian indirectly accuse Ramsden, who happens to work for the National Institute of Health in Bethesda, and his colleagues of unscientific practice due to "not considering all the evidence".

In fact, Ramsden et al. had, as Harris and his collaborators point out "stratified studies by whether the vegetable oil intervention included any n-3 PUFA", or not, but other than the guys from the agro-lobby... ahh, pardon me, the American Heart Association would have it, this is the way a meta-analysis of the CHD outcomes of randomised controlled trials (RCT), in which oils were used that contained a natural mix of both n-6 and n-3 PUFAs, must be designed, in order elucidate the individual effects of n-6 and n-3 polyunsaturated fatty acids on heart health. Any other approach, such as the one cited by the authors themselves (Mozaffarian. 2010),  apparently overlooks the "significant different effects on risk of non-fatal myocardial infarction (MI) and CHD death", Ramsden et al.  found in their heterogeneity analysis (Ramsden. 2010) of all the available data. In their aptly titled response "Don't disregard the essential distinction between PUFA species" (Ramsden. 2011) Ramsden, Hibbeln, Majchrzak-Hong and Davis, state:
Harris et al. have not fully appreciated the essential distinction between n-3 and n-6 PUFA species in attributing benefits from our pooled analysis of mixed n-3/n-6 PUFA RCT datasets to ‘vegetable oils rich in n-6 PUFA’ or simply ‘soybean oil’, despite substantial increases in n-3 EPA+DHA in two of the four datasets.
They also point out that the influence of n-3 fatty acids has been (I would say purposefully) underestimated by Harris and elsewhere, and provide the famous Oslo Diet Heart Study as an example:
The experimental dieters in the Oslo Diet Heart Study (ODHS) were actually provided with ‘substantial quantities of Norwegian sardines canned in cod liver oil’ and not simply ‘encouraged’ as Harris et al. state here and elsewhere. Oslo dieters consumed about 5 g EPA+DHA per d (thirty times the average US intake); therefore it is not valid to attribute CHD benefits to LA or soybean oil.
They go on to mention that interventions "specific to n-6 LA", on the other "provide no indication of benefit and a relatively consistent signal toward harm" and draw the yet to be validated conclusion that "lowering dietary n-6 LA [Ramsden et al. suggest to 2% of energy, which would be consistent with evolutionary and historical US diets] is likely to potentiate the benefits of n-3 PUFA and/or have independent CHD benefits".

Guess where I found this advertisement,
right within the official Fats 101 of the
American Heart Association.
The advertisement banner on the left, taken directly from the official Fats 101 of the American Heart Association shall remind you of this blogpost, the next time you read about what the American Heart Association has to tell you about "healthy eating" practices. It may be remotely possible that those are healthy first and foremost for the corn- and soy-driven American economy.

Want to Boost Hormone Production? POP Crude Cod Liver Oil or Industrial Waste: Persistent Organic Pollutants (POPs) in Crude Cod Liver Oil Modulate Steroidogenesis.

Image 1: If you are concerned
about the hormonal side(?)-effects
of persistent organic pollutants,
better make sure you buy pharma-
ceutical grade cod liver oil.
I know, what you are thinking now: "Not again, the ProfDrAndro anti-fish oil rant." Yet, this is neither about your beloved fish oil, nor is it ranting. Its an unfortunate fact that environmental poisons such as persistent organic pollutants (POPs) find their way into the food-chain of fish. The fish your shiny cod liver oil pills are made of are no exception from this rule and if the producers did not take (costly) measures to remove these toxins from the crude cod liver oil, chances are the non-dioxin-like POPs have already begun to accumulate in your adrenal coretex (Colby. 1994; Ribelin. 1984). So, even if you are a fish-oil enthusiast, give this blogpost a chance and read on...

Still ahead of print is a study by Montano and some European colleagues (Montano. 2011). In their paper which will be published in the Journal of Food and Chemical Toxicology, the authors describe the effects of crude cod liver oil, pharmaceutical grade cod liver oil and the industrial waste that is produced in the manufacturing process of the former on human adrenocortical adenome cells. The latter are considered a valid tool to model the general effects of exogenous toxins on steroidogenic key pathways in humans. They will yet not provide quantitative dose response relationships between oral intake of "contaminated" fish oils. It would thus warrant further investigations how much of the "Crude Atlantic Cod Liver Oil" that was used in the study you would have to consume to achieve the (un-)desired(?) hormonal "boost" both the crude cod liver oil and the industrial residue induced even at the lowest (dilution factor 1/10000), the pharmaceutical grade oil only at the highest concentrations (dilution factor: 2.5/1000):
‘‘Cod’’[crude cod liver oil] mixture significantly increased cortisol and P4 [progesterone] production at all concentrations tested. It also increased T [testosterone] production at 1E-3-dilution and E2 [estradiol] at the two highest concentrations. ‘‘Pharm’’ [pharmaceutical grade cod liver oil] mixture in contrast, was unable to significantly trigger changes in hormone production, with the exception of increased E2 production by the highest concentration tested (2.5E-3-dilu-tion). However, the production of E2 triggered by the highest ‘‘Pharm’’ concentration was half from that produced by the exposure to ‘‘Cod’’ and ‘‘Ind Res’’ at the same dilution. ‘‘Ind Res’’ mixture significantly induced the production of E2, P and Cort at 1E-3-dilution.
Assuming that you do not consume the industrial waste (God knows what is in all those cheap fish oil products out there, though), the data in figure 1 shows that you would still ramp up your hormone production significantly (i.e. statistically significantly), as long as you bath your steroidogenic cells in high enough concentrations of polluted crude cod liver oil.
Figure 1: Induction in hormone expression in human adrenocortical adenoma cells after incubation with crude cod liver oil (Cod) or pharmaceutical grade cod liver oil (Pharma) at doses of 1/10000 (E-4) and 1/1000 (E-3) relative to control (DMSO)
(data adapted from Montano. 2011)
These results shed a new light on some of the studies showing ergogenic / anabolic effects with fish oil supplementation - what if it was not the fish oil, but rather the pollutants in the oil that increased hormonal output and lead to small, yet statistically significant effects in terms of muscle gain, fat loss or whatever else was measured in these studies? Well, I guess if you want to take "advantage" of these toxins you just have to keep buying the cheapest fish oil out there from the most shady supplement company you can find. If, however, you insist on having fish oil as a source of supplemental n-3 PUFAs (instead of just reducing the overload of n-6 fats in your diet), these results would indicate that it may be wise to invest a few more bucks into some legitimate pharmaceutical grade fish or cod-liver oil, regardless of whether or not you believe that oral dosing would elevate tissue concentrations of POPs enough to replicate the effects observed in this in-vitro study. Afterall, with daily ingestion of polluted fish oil, tissue accumulation would certainly be an issue.

Fish Oil Compromises, Fish Improves Adiponectin Levels in "Overweight, But Healthy" Individuals. Neither Promotes Weight or Fat Loss Within a 4-Week Study Period

Fish are smart, they tell you about the good things "omega-3" fatty acids will do, without pointing you to the fact that eating them will yield a more favorable DHA:EPA ratio than popping pills that are made from the same remnants of their deceased relatives the fishery industry has dumbed for decades.
With the vitamin D news the other day (go back), you are now probably thinking "hell, no Adel's other favorite topic to rant about"... an yes! You are right: I just like to rant against mainstream stupidity and one-size-fits-it all approaches everybody loves because they are so "easy"! Take your fish oil! And everything is going to be all right. Much easier and so much more compelling, than my advice to eat fatty fish at least once, better twice or thrice a week to promote, not magically achieve metabolic health.

And while you've heard about the anabolic and blood pressure lowering benefits of fish protein in previous articles, here at the SuppVersity, it is more than unlikely that you've already gotten wind of the latest study from the Smart Foods Centre, School of Health Sciences (you got to love that name!) at the University of Wollongong, New South Wales, Australia (Neale. 2013)... and that despite the fact that it took - just as with the egg study, showing only beneficial effects on blood lipids (learn more) - suspiciously long for the study to make it from an "accepted manuscript" into a print article in the scientific journal Metabolism.

Scaled fish or capped oils - is that even a question?

In what is by no means the first, and certainly not going to be the last paper comparing the metabolic effects of fish oil caps to the food item, the oil is supposed to be delivered with (the fish ;-), Elizabeth P. Neale and her colleagues recruited 18–65 year old volunteers, who were willing to consume fish, but had a low- or moderate habitual fish intake to begin with (<3x per week). The subjects had to have a BMI somwhere in-between 25 and 37 kg/m² and a chubby midline with awaist circumference of >94 cm for men, >80 cm for women. Exclusion criteria were pregnancy, diabetes mellitus, impaired renal function, smoking, not weight stable for the past six months, food allergies or habits inhibiting compliance with the study design, illiteracy and inadequate conversational English; plus, they were excluded if they were currently taking medications including thiazolidinediones, valproic acid, ACE in-hibitors, and glucocorticoids.This left the researchers with N=30 subjects who were randomized to consume either
  • fish providing 1.86 g of LC n-3 PUFA (812mg EPA +1044 mg DHA)per day -- three serves of 135 g salmon (Birds Eye Atlantic Salmon Fillets, Simplot Australia), two serves of 66 g sardines (adjusted for percentage fish in total canned product; John West Sardines in Tomato Sauce, Simplot Australia) and one serve of 55.1 g tuna (adjusted for percentage fish; John West Tuna Tempters Lemon and Cracked Pepper, Simplot Australia) per week, or
  • supplemental fish oil (Blackmores Omega Daily) containing the same amount of LC n-3 PUFAs, yet - and this is a consequence of the low DHA/EPA ratio in fish oil vs. real fish - 1055.1 mg EPA and only 744.9 mg DHA
for 4 weeks, on a daily basis. And while the participants in the supplement group were "not expressly told to avoid fish", they were not "encouraged to consume it in preference to other protein sources", either (Neale. 2013).

What did the scientists want to measure?

The primary outcome parameter of the study were the differential effects of fish and fish oil on the plasma total and high molecular weight adiponectin levels in overweight humans and, secondary, to identify the genetic variations in participant's ADIPOQand FTO genes that may influence that response.
Figure 1: Relative changes in weight, BMI, waist, body fat (%), glucose, insulin and EPA + DHA levels in serum from t = -2 weeks (i.e. before the 2-week run in in which the diets and activity levels were standardized to 25% protein, 45% carbohydrate, and 30% fat) to t = 4 weeks (Neale. 2013)
As the data in figure 1 goes to show you this did not stop the scientists from evaluation the effects the intervention had on anthropometric parameters (waist, body fat, etc.) of their subjects, as well. Neither of these, nor the effects on blood glucose and insulin showed any significant inter-group difference. If we discard the identical changes in the EPA and DHA levels of the subjects, the dietary / supplement intervention had absolutely zero effects on any of these "extra-parameters" - no weight loss, no visible improvement in glucose metabolism.

No reduction in body fat or waist circumference in with fish or fish oil

Reason enough to ask yourself, whether we should not go back to baseline and ask "is fish / fish oil even good for you"? Certainly not - or I should say, only if you put faith in the hilarious promises of "instant weight loss, improvements in glucose metabolism" and what not, if you finally jump aboard and take your "essential fish oil supplements" that are plastered all over the Internet. If you discard these advertisment claims or simply apply some critical thinking skills, it should be obvious that you got to content yourself with changes in your potential to shed fat / improve glucose metabolism by simultaneously committing to lifestyle that's juxtaposed to the way of living that has gotten you into all the trouble to begin with.
Figure 2: Total and high molecular weight adiponectin levels expressed relative to the levels after the 2-weeks run-in (left) and the ratio of the absolute values after 4 weeks (right; Neale. 2013)
The changes in adiponectin expression in figure 2 are such an indicator of a change in the potential of getting rid of the blubber, the high blood glucose - and it is obvious to see that fish oil is inferior to fish, when it comes to inducing these changes.
"The results of this study suggest that short-termconsumption of fish and fish oil supplements does not have the same effect on HMW adiponectin levels in overweight humans. [...] This was due to a small increase in HMW adiponectin in the ‘fish’ group, whilst the ‘supplement’ group exhibited a significant decrease in HMW adiponectin concentrations. A similar pattern was seen for total adiponectin; however this did not reach statistical significance." (Neale. 2013)
As mentioned in the previous paragraph, these changes were not associated with differential effects on body weight, insulin levels and body fat mass, all of which "remained relatively constant" (Neale. 2013)



Fatty acid content in g/100g of wild and farmed salmon (left) and respective omega-3 to omega-6 ratios; learn more about making the "right fish choices", here
Unfortunately(?), the underlying mechanisms behind the differential effects on HMW adiponectin are as of now not known. Neale et al. do yet also subscribe to the "synergy hypothesis" I alluded to earlier in the first paragraphs of this article. The proven benefits of fish protein on insulin sensitivity and chronic inflammation (Soucy. 1999; Ouellet. 2007; Pilon. 2011), as well as the "other components present in fish such as selenium and vitamin D [, which] have also been associated with a range of health benefits in humans" [Rayman. 2000; Garland. 2006)...

...Oh, no! I know what you are thinking now. "I got all those in my multi! And I guess whey will do just as well as fish protein..." - come on, are you serious? Synergy is about ratios, about competition, about ups and downs, about co-factors and adjuvants. It's not about a kitchen sink supplementation approaches that try to reunite what has been ripped apart in a helpless effort to "make things easier" for the lazy consumer who does not like his fish and does not want to spend some of his daily screen time on buying fresh foods and preparing them... sorry, now I am really ranting ;-)

Handpicked suggested reads:
  • Study on Krill Powder Suggests: There is More to Seafood Than Fat - Can Krill Give You What Fish Oil Can't? Plus: Krill Protein's EAA Content More Than an Able Match to Whey (read more)
  • Phospholipid or Triglyceride? What's in Your Fish Oil Caps? Only Phospholipid Based DHA+EPA Reduces Fat Cell Growth & Elevated Insulin Levels Despite Obesogenic Diet (read more)


References:
  • Moroi M, Akter S, Nakazato R, Kunimasa T, Masai H, Furuhashi T, Fukuda H, Koda E, Sugi K, Jesmin S. Lower ratio of high-molecular-weight adiponectin level to total may be associated with coronary high-risk plaque. BMC Res Notes. 2013 Mar 6;6:83. 
  • Neale EP, Muhlhausler B, Probst YC, Batterham MJ, Fernandez F, Tapsell LC. Short-term effects of fish and fish oil consumption on total and high molecular weight adiponectin levels in overweight and obese adults. Metabolism. 2013 May;62(5):651-60.
  • Ouellet V, Marois J, Weisnagel S, et al. Dietary cod protein improves insulin sensitivity in insulin-resistant men and women: a randomized controlled trial. Diabetes Care 2007;30(11):2816.
  • Pilon G, Ruzzin J, Rioux L-E, et al. Differential effects of various fish proteins in altering bodyweight, adiposity, inflammatory status, and insulin sensitivity in high-fat–fed rats. Metabolism 2011;60(8):1122–30. 
  • Rayman MP. The importance of selenium to human health. Lancet 2000;356(9225):233–41.
  • Soucy J, LeBlanc J. The effects of a beef and fish meal on plasma amino acids, insulin and glucagon levels. Nutr Res 1999;19(1):17–24.

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.