Farmed vs. Wild-Caught: Pollutants and A Low Omega-3/6 Ratio - Is Wild Caught Fish Always the Better Choice? Plus: Krill, Fish Oil, or Whole Fish - What's Best for Your Health?

Wild caught or farmed? If you google it, it appears to be as if eating farmed  fish could be worse than eating no fish at all, but is this actually true?

Farmed fish is the ugly duckling in the "superfood" family. It is - at least that's what you'll read on the Internet - low in omega-3s, full of "bad" omega-6 fatty acids and laden with all sorts of pesticides. But wild caught fish is expensive and if we all ate it day in and day out not exactly eco-friendly, right?

In today's SuppVersity special parts of which you may have recently seen pop up for a few hours in interview form over at www.fighterdiet.com, before Pauline Nordin and I decided that due to its length and complexity it was rather an article than an interview and should thus be published as such, I am going to tackle the issue of "farmed vs. wild-caught" and "fish vs. fish oil" from all possible angles.

Do not underestimate fish as a protein source - fish is more than just omega-3!

Salmon Better Than Whey?

Cod protein for recovery

Krill = Super Protein?

High EAA protein for fat loss

Fast vs. slow protein

5x More Than FDA Allows

I would like to start my elaborations with the results of a recent paper by Nichols et al. (2014). A paper, in which the scientists investigate whether the existing differences of the fatty acid profiles from farm-raised vs. wild-caught cold-water fish would depend on what the fish were fed.

The general consensus on the Internet appears to be that wild-caught salmon is in all ways superior to its "industrially produced" counterpart from the large fish farms. In that, the opponents of farmed fish consumption usually highlight the (I quote) "exorbitant" amount of allegedly unhealthy omega-6 fatty acids in farmed fish.

Now it is certainly undebatable that the ratio of omega-6 to omega-3 fatty acids in wild-caught vs. farmed salmon differs significantly. The previously mentioned study by researchers from the Commonwealth Scientific Industrial Research Organization does yet also show that this effect is not a result of "farming", per se. Rather than that, the increase in omega-6 and decrease in omega-3 fatty acids in today's industrially produced cold-water fish is a result of the ongoing reduction of the fish(oil) content in the fish food.

Figure 1: Fatty acid profile of farmed and wild-caught baramundi in 1998, 2002 and 2010 (left) and the corresponding omega-3 to omega-6 ratios (right) – it's worth noticing that "back in the day" of high fish oil diets, the farmed barramundi had a more favorable omega-3 to omega-6 ratio than their wild-caught relatives (Nichols. 2014)

In 2001, for example, when farmed barramundi (Lates calcifer | another cold-water fish that is raised in large aqua-farms these days) were still fed a high percentage of dietary fish oil, the farmed fish actually had a more favorable omega-3 to omega-6 ratio than its wild-caught counterpart (see Figure 1).

Over the past 13 years, the fish farmers have yet replaced large amounts of the increasingly expensive fish oil in the feed by cheap poultry oils. The consequences are obvious: While this practice may reduce the levels of dioxins and dioxin‐like PCBs (Berntssen. 2005), the substitution of fish oil with vegetable oil in the feed lead to decreases in the total amount of PUFAs, most specifically omega-3s, though. Thus, the originally highly favorable omega-3/omega-6 ratios of 5:1 for farmed salmon and 3:1 for farmed barramundi has declined to a meager 1:1 (Nichols. 2014).

High omega-6 in today's farmed cold-water fish - a problem? For the average physical culturist who is following a diet that is comparatively low in potentially pro-inflammatory omega-6 fatty acids (they are only bad for you, when they are consumed in excess), tehe deterioration of the omega-3 to omega-6 fatty acid ratio in modern farmed vs. wild caught fish is relatively unproblematic. Unlike it is the case for the average Westerner, who is in dare need of high omega-3 and low omega-6 foods to balance his or her excessive omega-6 intake from vegetable oils and industrially processed foods, farmed salmon is thus still a good source of protein and fats for those of us who are following a whole foods diet with a balanced fatty acid profile.

So, if the relatively high omega-3 content is not a problem, because the effects of "high omega-6" farmed fish on your omega-3 to omega-6 ratio is still neutral (that's the case if the ratio is approx. 1) there is no reason to avoid farmed fish, right?

From "high omega-6" to high levels of organic and inorganic pollutants

Unfortunately the high omega-6 content is not the only problem farmed fish is supposed to have.  Next to the previously discussed issue, the occurrence of various pollutants in farmed fish is another of the topics that will be mentioned in almost every online- or gym-debate on the consumption of farmed fish. Rumors have it that farmed salmon was loaded with toxic chemicals. And guess what!? To a certain extend that is absolutely true.

Figure 2: Fish is by far not the only POP source in our diets. Each 0.5 serving of the above foods is associated with the given increase in µg of urinary phthalate and phenol biomarkers in the urine of 6-8 year old girls and may thus increase their breast cancer risk later in life (Mervish. 2001)

When we are taking a closer look at the latest scientific evidence on the real world effects of thes persistent organic pollutants (POPs), it turns out that a high fish consumption has no measurable impact on the concentration of this potentially cancerous endocrine disruptors (they mess with your hormones) in our blood and adipose tissue. In fact, the latest study by Hausken et al. clearly indicates that the POPs in the blood of their fish fed subjects and the corresponding control group have different food products as their main sources (Hausken. 2014).

It is thus no wonder that the researchers from the University of Bergen did not find any change in serum or adipose tissue POP levels, when they had their subjects, 42 outpatients with different metabolic disorders, increase their intake of farmed salmon or salmon oil and compared their subjects' serum and fat pollutant levels to a non-fish eating control group.

The results were unambiguous: The consumption of farmed fish did not affect the steady-state of organic pollutants in either the blood or fat tissue of the subjects.

High levels of persistent organic pollutant (POPs) - a problem? The ever-increasing amount of POPs in our diet and other consumer goods (deodorants, perfumes and cosmetics are another source of POP) is a problem and a potential threat to our health, but farmed fish is not the item on your plate or cupboard that will tip the scale.

Due to the ever-increasing pollution of the oceans, rivers and lakes, POPs and other pollutants are no "farmed fish" phenomenon, anyway. If you look at the results of a recent study from the Hong Kong Baptist University, for example, you will have to concede that "eating wild caught only" is not going to protect you from being exposed to chemicals like BPA (Wei. 2011).

Figure 3: Polycyclic aromatic hydrocarbon (PAH) content of farmed and wild-caught salmon samples (Easton. 2002).

Moreover, the amount of organic pollutants in farmed fish could be easily reduced if the producers were willing to invest more money into quality fish food. The results of a 2002 study by Easton et al. clearly indicate for example that the increased polycyclic aromatic hydrocarbon (PAH) content of farmed vs. wild caught salmon could be easily reduced if these organic pollutants were not already present in hilariously high quantities in the feed the fish are fed. Buying uncontaminated fish food would thus give the farmers a degree of control fishers whose wild caught chinook salmon can contain up to 4.8x  more PAH than farmed salmon (see Figure 3) will never have.

Fish oil can be POP free, but not everything that glitters is gold

Fish oil is a highly processed substance. If the processing is done right, it is possible to remove large parts of the previously discussed POPs, as well as inorganic pollutants like mercury from the fishy sludge. The fact that it can be pollutant-free, however, does not necessarily mean that your fish oil caps will actually be free of any harmful substances.


The fact that fish oil producers may not do their job properly is yet not the only reason I am a strong proponent of consuming whole vs. "capped fish" and a whole foods vs. processed "supplement diet.  Why? Well, fish is by far not the only so-called "superfoods" for which we have seen time and again that the isolation of certain ingredients, of which we think that they are what makes these foods so "super", is not going to yield the results we are looking for.

In fact, recent studies which highlight the benefits of fish proteins for man and women who strive to build and maintain a muscular physique (learn more in a previous SuppVersity article) clearly suggest that the often-cited high selenium content of fish is not the only "good thing" you'd miss if you ditch your salmon, tuna and other fatty fish for cheap and convenient fish oil caps.

Warning! "Whole fish" does not include fried fish as you will find it on a "fish mac" or fish & chips and/or fish sandwiches. An increased consumption of these "fish" meals has been shown not to influence the cardiovascular mortality risk of 3910 adults aged 65+ years in a 2003 study by Mozaffarian et al. Moreover, the previously discussed amount of environmental pollutants in the fish is another determinant of its beneficial health effects.

In an editorial comment in the Journal of Internal Medicine Jacobs, Ruzzin & Lee highlight that "[t]he evidence that environmental pollutants can affect the health benefits of fish is supported by previous experimental studies" (Jacobs. 2014). In rodent studies, only decontaminated farmed salmon oil ameliorated the negative effects of high fat feeding. A POP-laden salmon oil from Atlantic salmon, on the other hand, accelerated the development of insulin resistance-related disorders in the lab animals (Ibrahim. 2011). The question, whether we should eat fish and take fish oil supplements is thus intricately related to the question whether we can obtain POP-free fish and fish oil products.

Table 1: The amount of organochlorides in various types of fish oil supplements bought on the Canadian market can be significant - similar results have been found on other markets | ^aΣ of 1,2,3,4 tetrachlorobenzene, 1,2,3,5 tetrachlorobenzene, and pentachlorobenzene; ^bΣ of α-HCH, β-HCH, and γ-HCH; ^cΣ of oxychlordane, trans-chlordane, trans-nonachlor, and cis-nonachlor; ^dΣ of p,p′-DDT and p,p′-DDE.(Rawn. 2009).

And even if you're not interested in being muscular, a recent study by Brazionis et al. clearly suggests that getting your 1g of long-chain omega-3 fatty acids from fish vs. fish oil supplements "may have additional cardiovascular benefits beyond the omega-3 effect". Effects which lead to a significant reduction in blood pressure the scientists observed only in those subjects who consumed fresh salmon (two 150 g servings per week of John West fresh Atlantic salmon), but not in their peers in the fish oil arm of the study (Brazionis. 2012).

Is fish oil the safer alternative? If you buy your fish oil from a manufacturer who can prove that each and every batch is tested for its POP and heavy metal content, it may be safer, but in view of the synergistic effects of protein, fat, certain peptides and a plethora of micronutrients you will be missing if you scrap your two weekly servings of fatty fish and turn to fish oil caps instead, this does not mean that it will be healthier.

When we are talking about toxic substances in fish and fish oils, we obviously cannot dismiss the heavily debated issue of heavy metal contaminations.

Heavy metals are clearly no farmed-fish exclusive!

While the heavy metal issue is still a matter of open scientific debate, the epidemiological evidence in favor of the profound health effects of regular fish consumption appears to suggest that it is less of an issue for the general population than the hysteric news on the Internet may make you believe.

Figure 4: Mean (bottom axis) and max (top axis!) mercury content (mg/kg) in fish (FDA Monitoring Program. 1990-2010 from a 2012)

For fitness junkies and bodybuilders who are trying to satisfy their alleged protein "requirements" of 3-4g of protein per kg body weight by shoveling down one can of tuna after the other, however, the heavy metal content of the cheap fish cans may become a problem.

Or maybe I should say: I personally would not use canned tuna as my primary protein source, when aiming for a protein intake of 3-4g per kg of body weight.

And this goes regardless of the fact that I believe that the risks associated with consuming tuna containing 0.10-0.75ppm methyl mercury (Yess. 1993) may be overblown in some of the sensationalist articles on the Internet and other mainstream media.

Similarly, I am reluctant to rely on the purported protective effect of the high amounts of cysteine and selenium in seafood. A protection, by the way, of which scientists have recently shown that is cannot mitigate the loss of cardioprotective effects of high omega-3 intakes in individuals with high hair mercury levels (Virtanen. 2009 | learn more).

So mercury is less on an issue than people claim? Probably yes. I would subscribe to the FDA recommendation to limit your fish intake to 2-3x fish meals a week. More specifically, you should forget about the idea of tuna as a "healthy snack" you can eat as often as you want to and stay away from more than one fish meal if you are pregnant or trying to become pregnant. In this case buying either mercury controlled fish or fish oils may in fact be the better choice  – I mean: "Better save than sorry", right?

Speaking of fish oil, there is an increasing trend towards krill oil as the "hype" omega-3 supplement. A trend of which you, as SuppVersity readers know that it appears to be unwarranted, although krill oil has the advantage of providing a large amount of the omega-3 fatty acids in their phospholipid-bound form (learn more in a previous SuppVersity article).

Figure 5: Plasma, liver and white adipose tissue (WAT) levels of triglyceride (TL) and phospholipid varieties of DHA+EPA after 9 weeks on HFD diet with (w3TL or w3PL) or  w/out 30mg/kg chow DHA + EPA (Rossmeisl. 2012)

Compared to triglycerides, the phospholipid-bound version is easier to assimilate. Accordingly, it is not very surprising that Rossmeisl. et al. (2012) were able to show that phospholipid-bound long-chain omega-3 fatty acids increase the plasma and liver omega-3 content to a significantly greater degree than the same amount of triglyceride-bound omega-3 fatty acids. An effect that was – at least in rodent studies – associated with a significantly more pronounced reduction in fat cell size and insulin sensitivity (Rossmeisl. 2012).
A more recent study by Tillander et al. (2014) adds to the evidence that krill oil may have an edge over fish oil, as an anti-NAFLD agent, because it will epigenetically reduce the fatty acid synthesis in the liver (read more).
 
The very ability to reduce the synthesis of fatty acids in the liver makes krill oil particularly interesting for overweight and obese people.

The increased fatty acid oxidation in response to the ingestion of fish oil (vs. krill oil) the researchers observed in the same study, on the other hand, may be something that could be of interest for lean individuals who are trying to lose weight (learn more in previous SuppVersity article).

Fish or krill? It depends... The previously presented evidence does thus make one thing very clear: It is more than likely that it will depend on your goals and current health status which of these omega-3 sources you should prefer. Overall, there is yet still a paucity of independent research, which is why I would not be surprised if the previously made conclusions were refuted by future studies.

If not weight loss, but muscle gains and fat loss are your goal, though, neither fish nor krill oil will do - at least not in the absence of one of the previously mentioned synergists: Fish protein!

Fish protein, an overlooked anabolic?

What wanna-be bobybuilders need is protein. Fish protein, to be precise. In 2009, for example, Ramel et al. were among the first to observe that using fish, or more specifically cod protein as the major protein source in the diet of their overweight subjects would yield improved outcomes in terms of fat loss and lean mass retention (Ramel. 2009; see Figure 6).

Figure 6: Decreases in anthropometric measurements after the 8-week intervention with isocaloric energy reduced diets having in obese subjects consuming no, three or five servings of lean fish per week (Ramel. 2009).

It is thus quite obvious that there must be something special to fish proteins more common dietary protein sources do not provide.

This hypothesis is also supported by previous evidence from rodent studies. One of these studies that was conducted by Frédéric Tremblay et al. (2003) at the Laval University Hospital Research Center suggests that the benefits may be related to the potent anti-inflammatory effects of fish proteins, which will thus increase the muscular insulin sensitivity and favor fat over muscle loss and muscle over fat gain.

A more recent study by Vikøren et al. (2013) seems to confirm this hypothesis.

The overweight adults who participated in the corresponding experiment experienced significant improvements in glucose metabolism, increases in lean and decreases in fat mass, when the scientists added 3 g of fish protein per day to their diets for the first 4 weeks and 6 g/d for the last 4 weeks of the 8 week intervention.

Figure 7: Macronutrient composition of the diets at baseline, after 4 weeks and 8 weeks and changes in body composition compared to baseline (Vikøren. 2013 - learn more in a previous SuppVersity article)

What is particularly noteworthy about this study is the fact that these effects occurred in spite of the fact that "[p]hysical activity and energy and macronutrients intake did not change during the course of the study" (Vikøren. 2013).

More recent evidence from a rodent study by Kawabata et al. (2014) strengthens the "anti-inflammatory" hypothesis. In their experiments, the researchers compared the effects of casein and fish protein in a tightly controlled dietary intervention and found similar increases in muscle mass and improvements in glucose metabolism in their hairy subjects as Vikøren et al. did one year before in overweight adults (learn more in a recent SuppVersity article).

Why don't we use our consumer money to force producers to make a change? I hope my previous elaborations have made it clear that living off fish as your only protein and fat source in the diet is probably not the best idea. On the other hand, similar issues with antibiotics (ab)use, persistent organic pollutants (POP) and even mercury exist for other foods, as well – with the exception of antibiotics which are only used to produce animal products all these pollutants can also be found in veggies and fruits (so no "vegan advantage").

We would thus be good advised to use our most powerful weapon, i.e. consumer money, to steer the food industry away from doing everything to cut the production costs and buy fish from those farms that don't use cheap poultry instead of fish oils, intoxicate the water with antibiotics and buy the cheapest, yet POP-laden food from questionable sources in China to feed their fish.

Time to draw some conclusions: Based on the existing evidence there is no reason to shy away from either fish consumption, in general, or the consumption of farmed fish, in particular. The overwhelming majority of epidemiological evidence indicates that consuming two servings of fatty fish a week will have nothing but beneficial effects on your overall health and that in spite of the fact that the fish was not controlled for organic or inorganic pollutants in any of these studies.

Whether it makes sense to consume large quantities of fish on a daily basis is yet as questionable as the routine use of fish oil supplements. Most of us will be able to cover our fundamental omega-3 needs with the previously mentioned two servings of fish per week. Consuming more than that in supplemental form is – in my humble opinion – not necessary for healthy individuals, unless they need to balance their exuberant intake of omega-6 fatty acid from large quantities of vegetable oils and processed foods in their diets –both products of which I highly recommend that people limit their intake to a minimum.

Moreover, imbalanced diets that are dominated by a single food source have repeatedly been shown to increase one's risk of running into severe health problems in the long run. So why don't we combine fish with dairy products, grass fed beef, pork and vegetable protein sources to create a varied, tasty, health and physique promoting high protein diet we can follow for the rest of your lives, instead of looking for the one "superfood", of which I would hope that most of the people who read this interview will know by now that it doesn't exist, anyway.

References:

• Brazionis, Laima, et al. "The effects of fish or fish oil on the omega‐3 index." Nutrition & Dietetics 69.1 (2012): 5-12.
• Berntssen, Marc HG, ANNE‐KATRINE LUNDEBYE, and Bente E. Torstensen. "Reducing the levels of dioxins and dioxin‐like PCBs in farmed Atlantic salmon by substitution of fish oil with vegetable oil in the feed." Aquaculture Nutrition 11.3 (2005): 219-231.
• Easton, M. D. L., D. Luszniak, and E. Von der Geest. "Preliminary examination of contaminant loadings in farmed salmon, wild salmon and commercial salmon feed." Chemosphere 46.7 (2002): 1053-1074.
• Hausken, Trygve, et al. "High Consumption of Farmed Salmon Does Not Disrupt the Steady State of Persistent Organic Pollutants (POP) in Human Plasma and Adipose Tissue." Journal of Toxicology and Environmental Health, Part A 77.20 (2014): 1229-1250.
• Ibrahim, Mohammad Madani, et al. "Chronic consumption of farmed salmon containing persistent organic pollutants causes insulin resistance and obesity in mice." PloS one 6.9 (2011): e25170.
• Mervish, Nancy, et al. "Dietary predictors of urinary environmental biomarkers in young girls, BCERP, 2004–7." Environmental Research 133 (2014): 12-19.
• Mozaffarian, Dariush, et al. "Cardiac benefits of fish consumption may depend on the type of fish meal consumed the cardiovascular health study." Circulation 107.10 (2003): 1372-1377.
• Nichols, Peter D., et al. "Readily available sources of long-chain omega-3 oils: is farmed Australian seafood a better source of the good oil than wild-caught seafood?." Nutrients 6.3 (2014): 1063-1079.
• Rawn, Dorothea FK, et al. "Persistent organic pollutants in fish oil supplements on the Canadian market: polychlorinated biphenyls and organochlorine insecticides." Journal of food science 74.1 (2009): T14-T19.
• Rossmeisl, Martin, et al. "Metabolic effects of n-3 PUFA as phospholipids are superior to triglycerides in mice fed a high-fat diet: possible role of endocannabinoids." PLoS One 7.6 (2012): e38834.
• Tillander, Veronika, et al. "Fish oil and krill oil supplementations differentially regulate lipid catabolic and synthetic pathways in mice." Gene expression 24 (2014): 28.
• Tremblay, Frédéric, et al. "Dietary cod protein restores insulin-induced activation of phosphatidylinositol 3-kinase/Akt and GLUT4 translocation to the T-tubules in skeletal muscle of high-fat-fed obese rats." Diabetes 52.1 (2003): 29-37.
• Vikøren, Linn A., et al. "A randomised study on the effects of fish protein supplement on glucose tolerance, lipids and body composition in overweight adults." British Journal of Nutrition 109.04 (2013): 648-657.
• Virtanen, Jyrki K., et al. "Serum long-chain n-3 polyunsaturated fatty acids and risk of hospital diagnosis of atrial fibrillation in men." Circulation 120.23 (2009): 2315-2321.
• Wei, Xi, et al. "Assessment of risk to humans of bisphenol A in marine and freshwater fish from Pearl River Delta, China." Chemosphere 85.1 (2011): 122-128.
• Yess, N. J. "US Food and Drug Administration survey of methyl mercury in canned tuna." Journal of AOAC International 76.1 (1993): 36.

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

What do you need for a high 25OHD picnic on day at the beach? Eggs!

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

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

Are Eggs the Best Dietary Vitamin D Source We Have?

"Eggs? The best vitamin D source?" I don't have the hubris to say that eggs are the absolute #1, but considering the fact that eggs are the #1 source of "actual", preformed 25OHD, aka 25-hydroxyvitamin D*, in our diets, you are probably going to agree that eggs may well be the most underrated source of vitamin D in our diet (25OHD is what doctors and scientists will measure in your blood stream; most essays measure total 25OHD, so I will not differntiate the different forms here).

Preformed vitamin D? Isn't that dangerous? No, quite the opposite: Pharmacologic doses of 25OHD do not change or may even decrease plasma levels of 1,25(OH)D, aka calcitriol, which can potential cause calcification (Trummel. 1669; Heaney. 1997). When you are D-ficient, though, your body will retain the 25OH. This is particularly interesting for people with intestinal malabsorption, for whom 'regular' vitamin D supplements, i.e. vitamin D3, aka cholecalciferol, or vitamin D2, aka ergocalciferol, don't work (Francis. 1983)

When it comes to vitamin D, eggs, fish, dairy, meat and offal are quite unique. All of them contain "vitamin D" in the still-to-be-converted D3 form you all know. What only few people know is that they also contain the celebrated vitamin D metabolite 25-hydroxyvitamin D (25OHD). This is not only the form your doctor will measure, when you ask for a "vitamin D test", it's also the "vitamin D" that has been linked to all sorts of health benefits in the aforementioned epidemiological studies.

If you want to increase or maintain your 25OHD levels, it is obviously an advantage if you don't have to rely on your body to transform the dietary D2 + D3 into 25OHD. It is even better though, if the efficacy of this "supplement" (as of now I have not seen 25OHD in caps, so you better stick to eggs) has a higher bioavailability than its non-polar precursor, vitamin D3, which is absorbed mainly into the lymph (Thompson. 1966; Blomstrand. 1967).

"[T]he more polar metabolite 25OHD at physiological concentrations is also absorbed directly, and more rapidly and efficiently, from the proximal jejunum into the portal vein independent of fat absorption. These findings are consistent with results from clinical studies, which have found better absorption of 25OHD versus vitamin D in patients with fat malabsorption. Also, in healthy subjects and in patients with bone disease  25OHD is absorbed better and faster than vitamin D." (Ovesen. 2013)

I would hope that you are by now at least considering to eat an egg instead of popping dozens of vitamin pills. For those who still need actual data before they subscribe to the egg-ological approac to vitamin D 'supplementation', I have compiled a couple of figures in Table 1:

Table 1. 25OHD content (µg/100g) of chicken & egg, pork, beef, fish, dairy (various sources; cf. Oveson. 2013)

With respect to fish it's worth mentioning that the exact concentrations vary from species to species. Moreover  25OHD content of fish is distributed relatively evenly in muscle, fat and organ mass of the fish - much in contrast to vitamin D3, by the way, which is contained mostly in the organs, specifically the liver. For the average human being this means that he or she will actually get his / her share of 25OHD with every serving of fish. For vitamin D3 that's clearly not the case, because few of us actually eat cod liver on a regular base.

The sentence "You Eat What You Feed" is not new to SuppVersity regulars - it's also the title of an older article discussing how you can use food additives to increase the Omega-3 content of your steaks, milk and other animal products | read more

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

If you ate the bacon of the pigs in the Thompson study from the late 1960s, for example, you would get a whoppy dose of 0.7–2.0µg 25OHD per 100g and thus max. 10x more than from regular bacon. Why? Easy: The sows were on a(n extremly) high vitamin D diets (total D-intake was 2–3mg/day for 2-3 weeks; Thompson. 1966).

What's the "minimal" vitamin D level: If we take the most recent study by Tepper as our guide, you need much less vitamin D to keep your heart disease risk, or rather the markers that have been associated with the latter in check.

In their study, the scientists measured the vitamin D levels of 400 healthy men (age 25-65 years) and identified their relationship to fasting plasma insulin (FPI), fasting plasma glucose (FPG), triglycerides (TG), high sensitive C-Reactive Protein (hs-CRP), blood pressure and triglycerides and found that (a) vitamin D status is related to cardiometabolic indicators in healthy men and that (b) their data would suggest that 11−14 ng/ml should be defined as the minimal vitamin D threshold. So, if you are below that mark you are in for trouble and supplementation actually necessary.

Egg yolks instead of pills? The question, whether you can trash your vitamin D3 (or D2) supplements, as long as you make sure you get your daily dose of egg yolks (the 25OHD is in the yolk, not the egg white!), is difficult to answer. The 'potency' of oral 25OHD is estimated to be 1.5-5x higher than the one of 'regular vitamin D3' the form of 'D' you will find it in the majority of OTC supplements. Since we don't even know how much D3 a given individual actually needs the best thing you can do is to get tested, even if the estimated equivalent values and bioactivity were accurate.

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

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

References: 

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

Obese Vegan Salmon!? Vegetable Oils and Proteins Reduce DHA and EPA Content by -28% and Increase Overall Adiposity and Triglyceride Levels in Atlantic Salmon.

Image 1: Could this be made of obes vegan
salmon? (img from littlesteps.eu)

If you listened to yesterday's episode of Carl Lenore's Super Human Radio, you may remember that I repeatedly pointed out that "not all milk is created equal" and that milk quality is determined by food quality (if you want to read more about milk in general and colostrum in particular, I suggest you read last week's Ask Dr. Andro, as well). Today I am going to tell you about another of the industry's economic (in the monetary sense) ways of reducing the quality of animal foods in our foodchain - and we are talking about a food with a much better reputation than milk or beef: Salmon, the "heart-healthy cold-water fish" that is literally in on (or rather between) everyone's lips, lately.

Note: Salmon is explicitly mentioned in the "sample one-day menu" scientists at Colorado State developed according to the USDA dietary guidelines (Dietary Guidelines for Americans), so don't tell me you are not supposed to eat Norwegian fish, anyway, because you, my American friends, are supposed to have Grilled salmon, steamed broccoli, barley pilaf, low-fat milk and cake with fresh berries for dinner ;-)

Bente E. Torstensen and his (her?) collegues from the National Institute of Nutrition and Seafood Research and the Skretting Aquaculture Research Centre in Norway conducted an interesting experiment (Torstensen. 2011). For about a year, the researchers fed 6,000 smolt of Atlantic salmon (mean weight 355g) which had previously been randomly assigned to one out of three experimental + one control groups with diets containing...

• maximal amounts of fish meal and fish oil (Control)
• the "safe maximum replacement" of both fish meal and fish oil with plant meal (80% plant protein) and vegetable oil (70% vegetable oil) (80PP70VO)
• half the maximum replacement with plant meal (40%) and maximal replacement with vegetable oil (70%) (40PP70VO)
• maximum replacement with plant protein (80%) and half of the maximal replacement with vegetable oil (35%) (80PP35VO)

While the control diet obviously resembles what salmon, which primarily feeds on other fish, would naturally eat, the diet composition of group 2 remotely reminds me of what the food-industry has been feeding the less health-conscious masses in the US and Europe over the last decades. What... as a animal-loving vegan you are more interested in the fate of the poor salmon than in that of your sick and obese fellow human beings? Ok, here is what happened:

Maximum dietary VO [vegetable oil] and PP [plant protein replacements] increased visceral lipid stores, liver TAG, and plasma VLDL and TAG concentrations. Increased plasma TAG correlated with an increased expression of apoB100, indicating increased VLDL assembly in the liver of fish fed the high-plant protein- and VO-based diet.

Veganism, it turns out, ain't the preferable diet for salmon. Depending on which end of the dietary spectrum you belong to - the carnivorous hunter or the vegan gatherer -  you will probably now be asking yourselves one of the following questions:

1. Hunter: "What does that have to do with me? I always knew plant proteins and oils are bad for you!"
2. Gatherer: "What does that have to do with me? I don't eat salmon and the results from a 'fish-model' certainly won't apply to human beings!"

In isolation both the carnivorous hunter as well as the vegan gatherer appear right, when they ignore a prick like me citing the results of an insignificant fish study, the amalgam of both of these trains of thought does yet bring up a more unsettling question: What happens to the average health-conscious customer on a budget who thinks he is doing him/herself good by frying his economically raised, i.e. vegetable oil and protein fed, salmon in "healthy" vegetable oils and finishes dinner with a tofu dish? To be honest, I don't think we really need a study to answer that question. You just have to look at your peers to see the health consequences of eating sick animals and other vegetables that were either never intended for human consumption or have been (over-)processed beyond all recognition.

Figure 1: Relative changes in the fatty acid profile compared to "real", i.e. fish-fed, salmon after 1 year on vegetable oil and protein (data calculated based on Torstensen. 2011)

A pros pos "beyond recognition" if you have a closer look at the combined effects of vegetable oils and proteins on the fatty acid (figure 1) of the fish you will notice that industrially produced salmon fed with the "safe maximum replacement" dose of vegetable oils and proteins has little resemblance with the healthy food most consumers believe they were eating, when they buy "salmon" at the grocery store. Most obviously, the beneficial n3:n6 ratio of 7.6 in "real" salmon changed for the worse and ended up at roughly 3.0 after one year on a 80% plant protein 70% vegetable oil diet. Moreover, the individual composition of the fatty acids changed, as well. These changes include -28% reductions in EPA and DHA levels. After all, customers are left with something that looks like salmon, because it has been artificially colored, and tastes like "salmon", simply because 99% of the customers do not even know how "real" salmon would taste, because since the 1980s the ratio of wild-caught (real) salmon to farmed (fake ;-) Atlantic salmon has declined from 10:13 to 1:480 and fewer and fewer people have even had the chance to taste non-industrially produced salmon.

You Are What You Eat? Not Really! Rodent Study Shows Mice Are What the Salmon Ate That's in Their Chow

Image 1: Farmed Atlantic salmon - raised with & fried in soy *yummy*

Health conscious as you are, you will probably make sure to get grassfed beef, pay extra for the delicious Kerrygold butter and ask your farmer whether the chicken that lay the eggs you are just about to buy were pastured or received the standard feed and tons of antibiotics... right? Ok, but do you know what the fish that's lying there right in front of you had as his last supper? No? Well, after reading today's SuppVersity news, you will probably give your fish monger the third degree... but one thing after the other.

We are what that what we eat ate!

In a soon to be published study in the British Journal of Nutrition, Anita R. Alvheim and her colleagues from the National Institute of Nutrition and Seafood Research, the Department of Biomedicine  at the University of Bergen in Norway, the National Institute on Alcohol Abuse and Alcoholism in Rockville, USA, and the Department of Biology at the University of Copenhagen in Denmark, report which astonishing (or should I say frightening?) downstream effects it can have when the fish farmer who supplies your local fish monger with salmon wants to save a couple of bucks and replaces the fish oil in the diet of his farm-raised Atlantic salmon with some cheap (and hip / at least among vegans ;-) soybean oil.

Table 1: Fatty acid composition of rodent chow (top) and change in fa content of salmon due to soy oil feeding (rel. fish oil fed salmon, bottom; Alvheim. 2012)

To elucidate the downstream effects of this practice, the researchers raised Atlantic salmon on either soy or fish oil based diets (250g of each added to the diet), slaughtered the animals, filleted them and used the fillets to prepare two calorically identical rodent chows. A practice, by the way which was not as easy as it may sound, after all the salmon that had received the soy-based diet was significantly fatter (33% fat in the fillet of the soy fed vs. 26% fat in the fish oil fed salmon), so that the scientists had to make up for the lack of fat. The 6-week old mice were then randomly assigned to one of the two experimental diets to which they had ad libitum access for 6 weeks.

As the data in figure 1 goes to show the rodents on the "soy-salmon" diet had a significantly elevated hepatic alpha linoleic acid and arachidonic acid (AA) content in the hepatic phospholipids. After 9 weeks on the diet, there was a trend towards increased body weight gains that reached statistical significance in week 15 - and that in the absence of statistically significant differences in energy intake. 

Figure 1: Linoleic acid, Arachidonic acid and Arachidonoylglycerol (endocannaboid) content of liver phospholipids (left, data expressed relative to fish oil diet group), body weight development (right; Alvheim. 2012)

Moreover, compared to the rodents on the diet that contained the "normal" salmon the rodents on the soy fed salmon diet had significantly lowered EPA and DHA levels in the phospholipid fraction of their liver, erythrocytes and white adipose tissue. This lead to an overall decrease of the omega 3-index from 23 to 16 and increased the relative abundance of n-6 highly unsaturated fatty acids from 19 to 39 % percent. The histological analysis of the adipose tissue did also reveal that the rodents who received the diets with the soy fed salmon exhibited significantly more of the so-called crown-like structures which are remnants of macrophage (immune cells) invasion into the inflamed and partly necrotic (=dead) adipose tissue. The presence of this structures is associated with major increases in local and systemic inflammation and their has been implicated as one of the major driving forces of obesity induced metabolic disturbances in mice and humans (Bremer. 2011). Furthermore the adipocyte size in the groin area (=inguinal WAT) was increased.

Figure 2: I must admit I did not check if AP got the data in this chart right, but if they did, the increase in AA and AA-related endocannaboids is only part of the problem and you better stick to grass-fed beef if you can't afford wild salmon.

Implications: Overall, the weight gain may be negligible, the intricate differences in the phospholipid structure of various cells and even the presence of the crown-like structures relatively harmless and still, with the overall increase in soybean oil consumption in the US (from 2.2% of the total energy to 7.3% of the total energy intake) and the constant decline of natural (not supplemental!) DHA and EPA in the diet of the average US citizen, in the course of the 20th century (Blasbalg. 2011), the indirect or "second feed" assault from all sorts of animal products may well be the literal "last straw that brakes the camels back". After all, there is accumulating evidence for a direct relation between the diet-induced increase in arachidonic acid derived endocannaboids like 2-arachidonoylglycerol (cf. figure 1) in rodents and humans and the modulating effects of dietary fat intake on the latter.

With the study at hand, Alvheim et al. show pretty conclusively that the effect of certain foods, specifically oils, can be "handed down" in the food chain an effect that is hitherto largely ignored by scientists and nutritionists. In conjunction with reports that show that the DHA and EPA content of Atlantic salmon is already on the decline, while the linolic acid content has increased from 1.1 g/100 g in 2005 to 1.6 g/100 g in 2010  (NIFES. 2011), this raises the question of whether salmon, which is still considered to be the go-to protein and fat source for health-conscious customers, has not already been turned into another Frankenfood and puts another emphasis on the importance of knowing not just what you eat, but also what whatever you eat ate or grew on... but the latter is, I guess a topic for another blogpost ;-)

References: 

• Alvheim AR, Torstensen BE, Lin YH, Lillefosse HH, Lock EJ, Madsen L, Hibbeln JR, Malde MK. Dietary linoleic acid elevates endogenous 2-arachidonoylglycerol and anandamide in Atlantic salmon (Salmo salar L.) and mice, and induces weight gain and inflammation in mice. Br J Nutr. 2012 Aug 10:1-10.
• Blasbalg TL, Hibbeln JR, Ramsden CE, Majchrzak SF, Rawlings RR. Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am J Clin Nutr. 2011 May;93(5):950-62. Epub 2011 Mar 2.
• Bremer AA, Devaraj S, Afify A, Jialal I. Adipose tissue dysregulation in patients with metabolic syndrome. J Clin Endocrinol Metab. 2011 Nov;96(11):E1782-8. Epub 2011 Aug 24.
• Massiera F, Saint-Marc P, Seydoux J, Murata T, Kobayashi T, Narumiya S, Guesnet P, Amri EZ, Negrel R, Ailhaud G. Arachidonic acid and prostacyclin signaling promote adipose tissue development: a human health concern? J Lipid Res. 2003 Feb;44(2):271-9.
• NIFES. National Institute of Nutrition and Seafood Research. Research on nutrition;
  feed for fish and fish as food. < www.nifes.no/sjomatdata > retrieved Aug 14, 2012.

Whey Protein Hydrolysates Were Yesterday! Study Shows Salmon Protein Hydrolysate Can Deliver Protein Even Faster, But Does This Also Mean They Are More "Anabolic"?

That's salmon, yes, but it's not processed enough to compete with any hydrolysate. Well, unless you decide to eat and regurgitate it - after some time, obviously, 'cause "hydrolyzed" proteins are in the end only pre-digested proteins.

As a SuppVersity reader you know that the amount of protein is not the only determinant of the potential muscle building effects of a given protein source. The digestion time and thus the amount of protein that is released into the bloodstream on a "per minute"-basis, as well as the amino acid profile (preferably all essential amino acids (EAAs) and a high amount of leucine) are also important determinants of the "anabolic" qualities of a given protein source.

Using a quite unique multi-compartmental dynamic model that closely simulates in vivo gastrointestinal tract digestion in humans scientists from the Institute of Nutrition and Functional Foods (INAF) at the Université Laval in Quebec, did now determine that salmon not whey protein hydrolysates are the "numero uno", when it comes to digestion speed.

You can learn more about protein intake at the SuppVersity

Are You Protein Wheysting?

Cod protein for recovery

Protein requ. of athletes

High EAA protein for fat loss

Fast vs. slow protein

5x More Than FDA Allows

If you take a closer look at the data in Figure 2 at the bottom of the article, you will notice that salmon and whey hydrolysates were not the only products the scientists tested (I would love to help you along with the amino acid compositions, but unfortunately the full text does not provide any details and Hofseth  Biocare the producer of the salmon protein hydrolysate does not disclose if it's made from fish heads or salmon filets... I am not kidding, scientists have been investigating methods to produce salmon protein hydrolysates from the waste material for years; cf. Gbogour. 2004).

In view of the fact that we don't really know if salmon has similar real-world pro-anabolic effects, it may thus be at least as interesting to compare the digestion speed of whey hydrolysates and isolates.

Figure 1: Nitrogen distribution throughout the TIM-1 compartments at the end of the 2 hour digestion. SHP, salmon protein hydrolysate; WPH-High, whey protein hydrolysate extensively hydrolysed; WPH-Low, whey protein hydrolysate weakly hydrolysed; WPI, whey protein isolate (Framroze. 2014)

The latter is, as you can see in Figure 1, only significant if the hydro-whey is "extensively hydrolyzed". The difference between regular hydro-whey and the two whey isolates, on the other hand, is too to assume that it may - by any means - be relevant.

Figure 2: Data shows how much of the protein content is released in the course of a 120min digestion period (Framoze. 2014).

Let's not jump tp conclusions, here: In spite of the fact that the nitrogen digestibility data in Figure 2 supports the notion that salmon is not just the faster digesting, but also the more bioaccessible protein source. The currently available evidence on the effects of salmon protein hydrolysates on skeletal muscle hypertrophy, fat loss, blood pressure and inflammation - all things where we have plenty of evidence for beneficial effects of whey protein - is non-existent. Considering the fact that salmon protein hydrolysates are probably even more disgusting than their whey counterparts, I would thus not go and buy the next best product you can possibly find on the Internet.

Reference: 

• Framroze, Bomi, et al. "Comparison of Nitrogen Bioaccessibility from Salmon and Whey Protein Hydrolysates using a Human Gastrointestinal Model (TIM-1)." Functional Foods in Health and Disease 2014; 4(5):222-231  
• Gbogouri, G. A., et al. "Influence of hydrolysis degree on the functional properties of salmon byproducts hydrolysates." Journal of food science 69.8 (2004): C615-C622.

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.

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

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

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

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

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

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

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

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

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

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

So what do we make of all that information?

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

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

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

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

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

References:

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