LDL-P Drops by 27nmol/L With Every 1% Reduction in Trans Fat Intake. Plus: "Trans-Fat Free" Does Not Mean Risk Free!

In contrast to the message "trans fats = bad". The information that cookies and bakery, not cooking oil, margarine, chips & co are the main trans fat offenders in our diet has reached only a very small group of people.

There are only few 'nutritional wisdoms' out there that are actually 'wise'. One of them is the notion that "trans-fats are bad for you". By now that's something every fifthgrader knows. What most people don't know, though, is how bad "bad" actually is and whether the small amounts of trans fatty acids, the industry is cleverly hiding in their products by downsizing them in a way that "one serving"contains less than 0.5g of transfats - that's the magic loophole in the FDA regulations according to which transfats don't have to appear on the label, as long as the total amount per serving is less than 0.5g.

The question I would like you to remember, when you read more about the most recent strudy from the Preventive Cardiology Program at the Columbia University Medical Center/New York-Presbyterian Hospital in 2013 is: 

Do those 0.5g/serving the FDA is turning a blind eye on matter?

Within the past decades, the ill health effects of transfats have been addressed by countless studies. The study at hand, however, is the first one to directly assess and quantify the influence of transfats on LDL particle number (LDL-P = particle number, not LDL-C = LDL content!).

This is not about CLA & Co: Most of you will be aware that the "bad" trans-fat this article is not about CLA, but about the trans-fats from partially hydrogenated vegetable oils and other industrially processed fats and oils. If you want to know how much trans-fats (in % of total fat) the french fries and chicken nuggets at "your" Mc Donald's or KFC contain, just take a look at the table on the left (data from Stender. 2006)

As Garshik et al. point out, compared to the standard measure LDL-C the exact number of LDL particles, i.e. LDL-P, has been found to be a superior indicator of heart disease risk compared.

"Studies have suggested that increased LDL-P leads to progression of CVD and that the predictive value of LDL-P for future CVD events is equal to or greater than more traditional lipid measurements such as LDL-C." (Garshik. 2013)

That alone is a huge plus, but guess what: M. Garshick, H. Mochari-Greenberger and L. Mosca have been working with real patients - no rodents.. ah pardon, strings attached ;-)

This is not just another rodent study

Having the advantage of actually working in a hospital, not a sterile lab setting, the researchers picked participants from the Family Intervention Trial for Heart Health (FIT Heart), a National Heart Lung and Blood Institute (NHLBI) sponsored randomized controlled clinical trial that enrolled 501 family members of patients who were admitted to the cardiovascular service of the New York Presbyterian/Columbia University Medical Center, as their subjects. In the course of a previous study, the subjects had been assigned to two different groups:

• 

  Table 1: Subject characteristics at baseline (Garshik. 2013)

  An intervention group, the members of which were invormed about the CVD risk factor screening results and education about diet and physicalactivity to prevent CVD, with regular contact and feedback by a health educator for up to 1-year, and
• A control group, that did not receive the information about their own CVD risk factor and was not part of the organized education program that did obviously include the advise to reduce your trans-fat intake as much as possible

In the course of this study the control group made similar lifestyle changes as the intervention group - despite a lack of formal information / education (Moska. 2008). The reduction in trans-fat intake, in particular, was virtually identical. Therefore, the scientists could pick any of the men and women from the original cohort, as long as there was no lack of information or implausible dietary data for the 1 year study period.

Is it bad, if you get 2.5% of your daily energy intake from trans-fats?

When all was said and done, M. Garshick, H. Mochari-Greenberger and L. Mosca ended up with a "participant pool" the characteristics of which you I've summarized in Table 1. If you stop gazing at Table 1 and take a look that the data in Table 2, you will see that the average subject consumed approximately 2.5% of his or her daily energy intake from trans-fats.

Table 2: Dietary intake (% of kcal/day) and corresponding serum lipid measures in the subjects of the Garshick study.

"Is 2.5% much?" I guess it depends on what you take as a reference. If your reference is the "average" European in the TRANSFAIR study from 1999, this is much. Only the Icelanders, who have the highest trans-fat consumption of all Europeans (2.1% of total calories) come remotely close.

The Greeks on the other hand, live up to their reputation as the fathers of the often-hailed Mediterranean Diet: With a mean trans-fat intake of 0.5% and 0.8% in men and women, respectively, they are compliant with the recommended maximal daily allowance (RDA) of 2.2g trans-fats per day (this statement is based on the assumption that their average caloric intake was 2,000kcal).

You don't have to move to Greece though, to reduce your personal trans-fat intake even further. It is, after all, another flawed urban nutrition myth that you could produce trans-fatty acids in your kitchen by heating whatever type of oil / fat you use to cook (if you never change the oil you use to fry at very high temperatures, things look different, though). Industrially produced junk... ah, pardon "food" - specifically cakes, cookies, etc. - is thus your most if not only significant source of dietary trans-fats. Eliminate those and you are good to go.

Remember: Higher baseline intake = greater relative effect size!

Figure 1: Linear associations between baseline dietary composition and LDL particle number (top) and between change in dietary trans-fat intake and LDL particle number in the course of 1-year (bottom); data based on Garshik, 2013.

Assuming that you are not the cookie monster and consume mostly fresh foods, your transfat exposure is probably much lower than 2.5% of your total calorie intake. The average reduction in LDL particle count per for each 1% of trans-fats you cut from your diet is thus most likely less pronounced than it was in the study at hand.

If we discard the effect size and focus on the general trend, the results of the Garshik study are still highly relevant for all of us; and what's more, most of us will have friends or relatives with similar transfat intakes, a low activity level, a low MUFA and omega-3 intake and way too little protein in their diets - and as Figure 1 can tell you, MUFAs, n-3s, protein and obviously exercise / physical activity are all factors that have been found to be associated with low(er) LDL particle counts and a correspondingly increased risk of arteriosclerosis and heart disease in the Garshik study (see Rosenson. 2002 & 2010; Prado. 2011 for the link between LDL-P and heart health).

Eggs are trans-fat free and heart-healthy | learn why.

So! How dangerous are those 0.5g of trans-fat in "trans-fat free" foods? If we consult the results of a 2011 study by Prado et al., symptom-free individuals with LDL-P levels in the 1953–3560 nmol/L tertile are 3.7x more likely to exhibit coronary artery calcification than those in the 620-1530 nmol/L tertile and take into consideration that the RDA for trans-fats is < 2.2g/day, it should be obvious that those 0.5g of trans-fats, i.e. ~25% of the your maximal daily allowance, are a problem we must not ignore.

If we assume that there is a linear relationship between LDL-P and trans-fat intake (obviously this is a gross simplification) and make a rough and scientifically highly questionable estimate of the consequences, we will find that those unlabeled 0.5g of transfats could boost your LDL levels from the first into the third tertile of LDL-P values in the Prado study (+by 675nmol/L).... that this would also mean that a daily dose of only 0.5g of hidden trans-fats could triple your likelihood of arteriosclerotic plaque should be obvious, right?

References: 

• Cromwell WC, Otvos JD, Keyes MJ, Pencina MJ, Sullivan L, Vasan RS, et al. LDL particle number and risk of future cardiovascular disease in the Framingham offspring study-implications for LDL management. J Clin Lipidol 2007 Dec;1(6):583-92. 
• Cromwell WC, Otvos JD. Low-density lipoprotein particle number and risk for cardiovascular disease. Curr Atheroscler. Rep 2004 Sep;6(5):381-7.
• Garshick M, Mochari-Greenberger H, Mosca L. Reduction in dietary trans fat intake is associated with decreased LDL particle number in a primary prevention population. Nutr Metab Cardiovasc Dis. 2013 Oct 4.
• Hulshof KF, van Erp-Baart MA, Anttolainen M, Becker W, Church SM, Couet C, Hermann-Kunz E, Kesteloot H, Leth T, Martins I, Moreiras O, Moschandreas J, Pizzoferrato L, Rimestad AH, Thorgeirsdottir H, van Amelsvoort JM, Aro A, Kafatos AG, Lanzmann-Petithory D, van Poppel G. Intake of fatty acids in western Europe with emphasis on trans fatty acids: the TRANSFAIR Study. Eur J Clin Nutr. 1999 Feb;53(2):143-57. Review.
• Mora S. Advanced lipoprotein testing and subfractionation are not (yet) ready for routine clinical use. Circulation 2009 May 5; 119(17):2396-404. 
• Mosca L, Mochari H, Liao M, Christian AH, Edelman DJ, Aggarwal B, et al. A novel family-based intervention trial to improve heart health: FIT Heart: results of a randomized
  controlled trial. Circ Cardiovasc Qual Outcomes 2008 Nov; 1(2):98-106.
• Prado KB, Shugg S, Backstrand JR. Low-density lipoprotein particle number predicts coronary artery calcification in asymptomatic adults at intermediate risk of cardiovascular disease. J Clin Lipidol 2011 SepeOct;5(5):408-13.
• Rosenson RS, Otvos JD, Freedman DS. Relations of lipoprotein subclass levels and low-density lipoprotein size to progression of coronary artery disease in the Pravastatin Limitation of Atherosclerosis in the Coronary Arteries (PLAC-I) trial. Am J Cardiol 2002 Jul 15;90(2):89.94.
• Rosenson RS, Davidson MH, Pourfarzib R. Underappreciated opportunities for low-density lipoprotein management in patients with cardiometabolic residual risk. Atherosclerosis 2010 Nov; 213(1):1-7. 
• Stender S, Dyerberg J, Astrup A. High levels of industrially produced trans fat in popular fast foods. N Engl J Med. 2006 Apr 13;354(15):1650-2.

2.1kg Muscle From Fast Food Supplement; No Prolactin, No Fat; Oleic Acid Counters CLA's Inflammatory Effect; Spicy Marinades vs. Salmonella; Flaxseed, Estrogen & Penis Size; TTA in the Emergency Room; Alcohol & Binge Eating

Image 1: Scientifically proven muscle builder - 2.1kg lean mass in 3 months, no post-cycle therapy necessary!

I was just about to write another one of my artistic introductions, trying to incorporate all the exciting On Short Notice news I've piled up for you into a brief narrative, when I realized that you probably don't really appreciate those introductions (I guess, I would skip them myself, so don't worry, this is more of an objective assessment than an accusation). So, I listened to my gut and decided to skip this part of this series, today, and rather spend the time to edit another item I did actually not want to post today. It's the one on the "IIFYM slightly gone wrong fast food bulk" in the Hambre study, to be precise; and I would venture the guess that you won't mind taking that instead of a longer introduction, once you've read and digested the impossible: You cannot only gain muscle with "fast food supplements", you won't even get fatter than you would if you just used a classic whey protein... oh my, I see, you are already scrolling down: What I said, I would have been wasting my time, had I written a longer introduction. But dare you, if you don't at least read the other items, as well!

• 

  Figure 1: Food intake (top, lef) and energy expenditure (bottom, left) as well as body fat % (top, right) and body weight development of the normal vs. prolactin negative mice after 14 weeks on standard chow (SC) or high fat diet (HFD; Auffret. 2012); btw: taking super-doses of vit. B6 will induce nerve damage, not fat loss!

  Without prolactin mice can't get fat! If that is true for humans as well, this would mean that Julien Auffret and his colleagues would have made a very important finding that could help us solve at least part of the diabesity pandemic, if we found a way to mimick the effects the "beigening" (=making white adipose tissue behae similar to the fact burning brown adipose tissue) effect the genetic ablation of the prolactin receptor on the fat cells of the mice in the Auffret study had on their susceptibility to diet induced obesity (Auffret. 2012).
  In particular, the scientists found that the ablation of the prolactin receptor gene in the mice results in profound increases in the expression of master genes controlling brown adipocyte fate (PRDM16) and mitochondrial function (PGC1α, UCP1), which allow - and this is the actual caveat,, here - for an inrease in thermogenesis.
  The latter, in turn, allows the rodents to burn off a major part of the fat they would otherwise store and thus keeps them relatively lean despite HFD feeding. Aside from the fact that the hyperphagic rodents on the high fat diet were still fat (there is no debating that!), you may savely assume that the effects will be way less pronounced in human beings, where 9/10 "thermogenic" agents that have been successfully tested in rodents do nothing at all, anyway. Against that background the hunger-promoting effects of the prolactin recetor ablation would suggest that it is almost as likely that a drug that block prolactin completely would make obese individiuals even fatter, since that's usually what happens if you eat more - like the mice in the prolactin (-/-) group did (see figure figure 1), without burning more.

• 

  Figure 2: Comparison of MUFA : CLA ratios in steak and mince from grass fed or conventional beef and milk from mares, sows, women (human milk ;-), goats and cows (based on Dhiman. 1999; Jahreis. 1999; McAfee. 2011); higher values indicate more MUFA per unit of CLA, but more must not necessarily be better - in fact too much MUFA could completely block the fat loss effects of CLA and thus maybe explain why it rarely works in humans - our diets are pretty high in oleic acid and thus the ratio will be much lower, than in the high dose CLA rodent trials

  Conjugated linoleic acid needs oleic acid to work without side effects. That's the main take-home message from a recent study conducted by researchers at the at the University of North Carolina at Greensboro, who found that oleic acid, the mono-unsaturated fatty acid from olive oil & co, does prevent the expression of inflammatory genes in adipocytes treated with the "anti-fat fat CLA"..
  So, until my friends from the supplement industry read this post and come out with yet another SuppVersity science powered product with CLA in olive oil* you simply make sure to have a spoon of the liquid gold from time to time, when you feel that you need to take CLA to burn more fat. Unfortunately, this could not just mean that you can rid yourself of the nasty side-effects as discussed in "CLA Destroys Body Fat! But at Which Costs?", but also that the "body fat destruction" will at least be ameliorated if not totally absent :-(
  * I had hardly written this post, when I browsed the web and found that a certain newcomer and as of late very succesful "yellowish green" company has already a CLA + Olive Oil + Avocado Oil combination on the market, for them this would mean that they didn't even have to change their formula

• 

  Image 2: It's funny how so many things people (or at least chefs) have been doing forever, here marinating meats, simply make sense, isn't it?

  Antibacterial marinades for your meat! Don't worry this is not yet another dysfunctional functional food that's going to make you sick, but an all-natural mixture of green tea, lemon and turmeric you will have to smear onto your chicken meat if you want to make sure to get rid of the C. jejuni and S. enteritidis it may be contaminated with.
  All it takes are 24h of "incubation", but that's nothing else than leaving your meat lying in the marinade in your fridge and thus something you would do anyway, right? That's what I would call a convenient, effective and above all totally natural and healthy way of gettting rid of Samonella and Campylobacter :-)
• Tons Flaxseed flour in your diet will increase estrogen, but won't decrease the size of your penis, well at least not visible ;-) That's probably the most straight-forward summary of the results, Ludmila Ferreira Medeiros de França Cardozo and her colleagues present in the latest issue of Food and Chemical Toxicology after analyzing the effect of a flaxseed flour containing diet on the expression of hormone levels and penis morphology of male rats (de Franca. 2012)

  

  Image 3: Flaxseed bread won't turn you into an hermaphrodite overnight, don't worry.

  While the rats that were maintained on a diet containing 25g of flaxseed flour per 100g for 250days had significantly elevated estrogen levels in the blood 39.5 vs. 32.5 pg/mL (+22%), the minor drop in testosterone did not reach statistical significance and the reduced diameter of the corpus spongiosum, which helps to maintain the urethea as a viable channel for the ejaculation was obviously no problem for the fertility, either - at least the scientist don't mention anything in this regard; unfortunately, they did not really test it, either, as the poor male Wistar rats that were abused in this experiment were bachelors against their will.
  In view of the fact that flaxseed ain't the best source of omega-3s, anyway, and there appears no other good reason (for men and women!) why you would eat them in large quantities (I am not talking about the occasional tablespoon of flaxseed, here), I would still suggest to stay away from it.

• 

  Image 4: In farm-raised salmon chronic TTA administration has been shown to improve cardiac function and immune activity; it does however also lead to cardiac growth during viral infections, so that the benefits of chronic administration are still by no means certain (Grammes. 2012a & 2012b); long-term human studies, on the other hand, are not yet available.

  Acute TTA administration soothes the flames and keeps the coronary vessel open You will unquestionably remember my previous posts about the fat burning fatty acid tetradecylthioacetic acid (TTA) and how it's ability to accumulate in various tissues of your body could potentially become problematic. In the short term however, it's anti-inflammatory effects can come very handy. So handy, in fact, that the a recently published study by Pettersen et al. would suggest that we are soon going to see TTA balloons being inserted into coronary vessel walls, in order to deliver the sulfur-containing fatty acid right to an obstructed vessel that's being operated on, in order to suppress the local expression of inflammatory cytokines, as well as the subsequent macrophage infiltration and the unwanted collagen formation, which would precipitate restenosis (=further clogging) of the very heart vessel that has only just been opened operatively.
  You may now rightly ask yourself what this has got to do with you? Well, if it works locally, it could work similarly systemically and other studies such as Bjørndal (2012) do confirm just that: 0.4% TTA reduce TNF-α, IL-1β, and IL-6 in an experimental model of colitis and render the rodents guts more of less bullet..., ah, pardon, dextran sulfate sodium (DSS; a chemical used to induce cholitis) proof. The long-term effects of the continous consumption of ~3g of TTA, which would be the human equavalent of those 0.4% TTA in the rodent diets is yet still not fully established (re-read: "TTA & Fish Oil" and "TTA & Fish Oil - Revisited").

• 

  Figure 3: Alcohol overrides the inhibitory control over food intake (Chapman. 2012)

  Of TV watching, sleep deprivation and alcohol consumption, booze has the most pronounced negative effect on reward saliency and inhibitory control of food intake! That's the conclusion Colin Daniel Chapman, Christian Benedict, Samantha Jane Brooks, and Helgi Birgir Schiöth mkae based on their latest meta-review of pertinent studies from pubmed (N=23). With an impact factor of 1.03 on a scale from -4 to 4, alcohol is by far the worst the greatest effect on food intake and shows the highest correlation with obesity (Chapman. 2012).
  Compared to booze, both sleep deprivation (50% less) and TV watching (20% less) appear almost harmless. Their contribution in the non-drinking part of the population may yet still not be underestimated, also because the urge to do the latter, i.e. watch TV, when you ought tho sleep, precipitates the former and subsequent derangements in the circadian rhythm (suggested read: "The SuppVersity Circadian Rhythm Series").
• IIFYM was yesterday, ROWFYM is today, but what's going to be tomorrow? If that's all Greek to you, let me first bring you in the loop on the acronyms. While IIFYM designates "If It Fits Your Macros", implies (in the most extreme case) that you give a sh*t about what you eat, as long as you hit your macronutrient ratios for the day ("Carbs? Gimme that pizza!") and is getting increasingly popular among those who are fed up with broccoli and chicken breast and either unwilling or unable to see that those are not the only, and I would say, by far not the most healthy foods you can eat, ROWFYM is my own invention, means "Regardless Of Whether It Fits Your Macros" and would probably end up for way too many trainees in a protocol similar to the one 12 of the 24 subjects in a recent study from the Linköping University in Sweden were following for 12 weeks (Hambre. 2012).

  

  Image 5: "WTF do you want, I am doing ROWIFYM, here! That's serious bulking, man. Scientifically validated." If you want to follow his example, go ahead... but 3 months really is the absolute max and only if you are still healthy - regardless of whether the blood markers return to normal in the course of your next diet.

  While those lucky (?) twelve healthy young men (aged 19–32 years) in what I will from now on call the "fast-food arm" of the study had to add a delicious (???) fast food menu (1350 kcal, 41 g protein) on top of their diets, the other twelve participants had to contend themselves with a blatant protein shake (33g of whey) as their bulking supplement of choice. The reasoning behind this at first sight unquestionably highly questionable experiment was that the Swedish scientists wanted to elucidate, whether it would really make a difference whether you are eating "clean" (=adding a whey protein shake) or simply stuffing yourself with the next best, allegedly protein-laden fast food you can find during a 3-months bulking cycle (at least three lifting sessions per week) and the results were, ... well, let's say surprising.
  As you would expect, subjects in both groups managed to gain some weight. The first surprise is that subjects in both groups gained identical amounts of weight, namely 3.6kg. That's not all, however. Even the lean mass increases 2.1kg did not differ between the groups (measure by DEXA scans) and the sophisticated (compared to a similar calories in vs. calories out calculation) measurement of the resting metabolic rate, the scientists had conducted yielded that both groups had compensated for the overeating by a statistically highly significant (p < 0.0001!) + 10% increase in resting metabolic rate!

  

  Figure 4: Kaplan-Meier plots indicating the percentage of patients that made it to time-point X (see horizontal axes) without adverse event after their first coronary event - patients w/ (thin line) vs. w/out (bold line) metabolic syndrome (top), patients with high (thin line) vs. low (bold line) ApoB leves (bottom; based on Corsetti. 2005); ApoB turns out to be a way better risk predictor than having metabolic syndrome

  Before you do now jump into your car and head for the next drive-in "restaurant" with a big yellow "M" in front of it, you may want to take into consideration that this extended ROWIFYM version of the IIFYM approach, where you may hit the protein but overshoot on the carbs and fats (and certainly not  the good ones), did lead to statistically significant increases in fasting insulin and ApoB, a building block of LDL that has been associated with increased risk of arterial plaque formation (Gebel. 2008), compared to the "clean bulk" (= whey only) group. And while those changes (as well as the increase in RMR) were reversed on the 12 months follow-up, I am not sure if especially those people, who are most fond of bulking approaches like that, i.e. men (and very rarely women) who have been following a junk food diet for way too long already, should take the results of this study as an incentive to do a 3-month fast food bulk during the winter. After all, it could be that one additional LDL molecule that nests in the already existent arterial plaque which will eventually break the camel's, no your neck - or for those who like it more explicitly, which won't let the next mini blood clot pass by and causes a stroke, which could, in the worst case, end deadly!

That's it as far as the official On Short Notice items go, for today. If you don't have enough yet, I suggest you take a glance at the 6-10 news-items I've piled up on the SuppVersity Facebook Wall for you to review. Maybe you've read that sleeping with wife and children in a room would decrease your testosterone levels? False! Maybe it decreases the intellectual capacity of the reporter who wrote the respective news-item you may have read, but what really happens, is an increase in the amplitude of the circadian pattern with higher morning and lower evening testosterone levels (click here to read more). And if you neither have or plan to have children or don't care about your or your significant other's testosterone levels, you may be interested in a study that debunks the use of a "slim belt" for weight loss purposes, the idiotic idea to counter BPA toxicity with soy, the way working out can make depressed old people happy again, and more... ah, I almost forgot, there will also be an exercise special of On Short Notice very soon - and I am not talking about next Saturday, here - so stay tuned, it could be published anytime (Tip: If you subscribe to the SuppVersity Facebook Page you won't miss it ;-)

 References:

• Auffret J, Viengchareun S, Carré N, Denis RG, Magnan C, Marie PY, Muscat A, Fève B, Lombès M, Binart N. Beige differentiation of adipose depots in mice lacking prolactin receptor protects against high-fat-diet-induced obesity. FASEB J. 2012 Sep;26(9):3728-37. 
• Bjørndal B, Grimstad T, Cacabelos D, Nylund K, Aasprong OG, Omdal R, Portero-Otin M, Pamplona R, Lied GA, Hausken T, Berge RK. Tetradecylthioacetic Acid Attenuates Inflammation and Has Antioxidative Potential During Experimental Colitis in Rats. Dig Dis Sci. 2012 Aug 2.
• Chapman CD, Benedict C, Brooks SJ, Birgir Schiöth H. Lifestyle determinants of the drive to eat: a meta-analysis. Am J Clin Nutr. 2012 Sep;96(3):492-7. Epub 2012 Jul 25.  
• Corsetti JP, Zareba W, Moss AJ, Sparks CE. Apolipoprotein B determines risk for recurrent coronary events in postinfarction patients with metabolic syndrome. Atherosclerosis. 2004 Dec;177(2):367-73.
• de França Cardozo LF, Boaventura GT, Brant LH, Pereira VA, Velarde LG, Chagas MA. Prolonged consumption of flaxseed flour increases the 17β-estradiol hormone without causing adverse effects on the histomorphology of Wistar rats' penis. Food Chem Toxicol. 2012 Aug 25.
• Dhiman TR, Anand GR, Satter LD, Pariza MW. Conjugated linoleic acid content of milk from cows fed different diets. J Dairy Sci. 1999 Oct;82(10):2146-56.
• Gebel E. Meet LDL's partner in plaque. ApoB puts the "bad" in bad cholesterol. Diabetes Forecast. 2008 May;61(5):39-40.
• Grammes F, Rørvik KA, Takle H. Tetradecylthioacetic acid modulates cardiac transcription in Atlantic salmon, Salmo salar L., suffering heart and skeletalmuscle inflammation. J Fish Dis. 2012a Feb;35(2):109-17. 
• Grammes F, Rørvik KA, Thomassen MS, Berge RK, Takle H. Genome wide response to dietary tetradecylthioacetic acid supplementation in the heart of Atlantic Salmon (Salmo salar L.). BMC Genomics. 2012n May 11;13(1):180.
• Hambre D, Vergara M, Lood Y, Bachrach-Lindström M, Lindström T, Nystrom FH. A randomized trial of protein supplementation compared with extra fast food on the effects of resistance training to increase metabolism. Scand J Clin Lab Invest. 2012 Aug 30.
• Jahreis G, Fritsche J, Möckel P, Schöne F, Möller U, Steinhart H. The potential anticarcinogenic conjugated linoleic acid, cis-9,trans-11 C18:2, in milk of different species: Cow, goat, ewe, sow, mare, woman. Nutrition Research. October 1999; 19:10. 1541–1549.
• McAfee AJ, McSorley EM, Cuskelly GJ, Fearon AM, Moss BW, Beattie JA, Wallace JM, Bonham MP, Strain JJ. Red meat from animals offered a grass diet increases plasma and platelet n-3 PUFA in healthy consumers. Br J Nutr. 2011 Jan;105(1):80-9.
• Murali N, Kumar-Phillips NS, Rath NC, Marcy J, Slavik MF. Effect of Marinating Chicken Meat with Lemon, Green Tea and Turmeric Against Foodborne Bacterial Pathogens.International Journal of Poultry Science. 2012; 11(5): 326-332.
• Pettersen RJ, Salem M, Rotevatn S, Kuiper KK, Larsen TH, Bohov P, Berge RK, Nordrehaug JE. Effects of local delivery of Tetradecylthioacetic acid within the injured coronary vessel wall. Scand Cardiovasc J. 2012 Aug 30.
• Reardon M, Gobern S, Martinez K, Shen W, Reid T, McIntosh M. Oleic Acid Attenuates trans-10,cis-12 Conjugated Linoleic Acid-Mediated Inflammatory Gene Expression in Human Adipocytes. Lipids. 2012 Sep 2.

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)

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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 ;-)

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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.