Tuesday, August 14, 2012

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.