Friends Don’t Let Friends Eat Farmed Salmon

By Lewis Perdue

Salmon is on a lot of plates when people resolve to make healthy changes in their diets.

Many articles have emphasized the benefits of fatty fish, citing the heart-healthy benefits of Omega-3 fatty acids and other micro-nutrients. Those benefits have been gradually narrowed down to salmon because other mild, oily-fleshed fish like tuna have grown notorious for accumulations of mercury and other environmental contaminates absorbed during long life spans.

Life span varies from species to species, but most species of salmon live 3 to 9 years while some species of tuna can live up to 50 years. The average age of tuna is about 15 years.

So, salmon has become a “miracle fish” to many health conscious consumers thanks to the presence in the flesh of LC n-3 PUFA a (long-chain n-3 polyunsaturated fatty acids) including a high proportion of docosahexanoic acid and eicosapentaenoic acid.

However, a study of wild versus farmed salmon found significantly higher levels of pesticides and endocrine disruptors in farmed versus wild caught salmon. (1)

A second study, this one of farmed Atlantic salmon(2) found that organic pollutants in the salmon feed  (primarily PCBs and metabolites of DDT) functioned as endocrine disruptors and caused insulin resistance as well as excess adipose tissue in laboratory rats despite identical energy intake.

The levels, according to the study were enough to more than offset any potential health effects.

The laboratory rats were divided into groups, one fed a very high fat (VHF) diet containing  commercially available farmed salmon fillet (VHF/S) and the other a VHF containing farmed salmon fillet with reduced POP concentrations (VHF/S-POPs).

According to the authors of the study, “We have previously reported that POPs may counteract the benefits of salmon oil and impair insulin action in both in vivo and in vitro models. To determine whether the presence of POPs modulates the outcomes of farmed salmon fillet intake, we compared the metabolic profile of mice challenged with VHF/S to those fed VHF/S-POPs.

“In epididymal fat, mice fed VHF/S-POPs had about 20% and 50% lower concentrations of 7 PCBs and dichlorodiphenyltrichloroethanes (DDTs), respectively, than animals fed VHF/S , thereby indicating that mice fed VHF/S-POPs had reduced body burdens of POPs. Interestingly, mice fed VHF/S-POPs had reduced body weight gain and visceral fat compared with animals fed VHF/S.


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“This decrease in adipocity [fat] was correlated with reduced adipocyte [fat] size and macrophage infiltration….There were no significant differences in energy intake and fat absorption between groups.”

NOTE: Words in [brackets] have been added to the original text.

Macrophages are a type of immune cell that, along with T cells can infiltrate adipose tissue and are responsible for the majority of inflammatory proteins that can cause insulin resistance and are suspected of helping to drive the development of Type 2 diabetes. (3)

In addition, inflammation from macrophage cell destruction has been established as one of the mechanisms that support cancer cell invasion of healthy tissue.(4)

 

Finally, the study found decreased metabolic activity in the rats fed the standard feed and improved  Consistent with enhanced insulin action, animals consuming VHF/S-POPs had improved insulin-stimulated glucose uptake in soleus [muscle], which was accompanied by reduced muscle TAG (triacylglycerol also known as triglyceride — fat] accumulation, and tended to have less hepatic TAG concentration.”

Insulin resistance, fatty liver, decreased metabolism, increased fat and inflammation are hallmarks of metabolic syndromes that may develop into Type 2 diabetes.

(1) Preliminary examination of contaminant loadings in farmed salmon, wild salmon and commercial salmon feed. M.D.L. Easton, D. Luszniak, E. Von der Geest,) Chemosphere 46 (2002) 1053–1074

(2) Chronic Consumption of Farmed Salmon Containing Persistent Organic Pollutants Causes Insulin Resistance and Obesity in Mice. Ibrahim MM, Fjære E, Lock E-J, Naville D, Amlund H, et al. (2011)PLoS ONE 6(9): e25170. doi:10.1371/journal.pone.0025170

(3) Macrophage infiltration into adipose tissue: initiation, propagation and remodeling

Bonnie K Surmi, Alyssa H HastyFuture Lipidol. Published in final edited form as: Future Lipidol. 2008; 3(5): 545–556. doi: 10.2217/17460875.3.5.545

(4) Douglas Hanahan and Robert A. Weinberg, Hallmarks of Cancer: The Next Generation, 646 Cell 144, March 4, 2011, DOI 10.1016/j.cell.2011.02.013

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