|Image 1: Micrograph of non-alcoholic fatty liver disease, caused by the same kind of lipid accumulations |
Shirazi et al. observed in the rats receiving fish oil treatment (image by Nephron)
|Image 2: In the aorta of rats on a diet rich in fish oil, fatty streaks like that|
formed in the aortae (image source www.heartsite.com)
[...] fatty streak in fish oil fed pups were significantly more than that in the other group. [... liver] ductular cell hyperplasia in pups fed with fish oil was significantly more than that in animals fed with standard diet. There was a positive relationship between fatty streak in aorta and ductular hyperplasia in liver (r = 0.470 and p= 0.037)
Although the animals had free access to food (ad-libitum feeding) the pathological changes cannot be a consequence of differing calorie intakes. Both groups consumed roughly 16g of the respective diet. According to Shirazi et al., a feasible explanation for these observations and their inconsistency with previous studies by Saraswathi et al. (Saraswathi. 2009), Bringhenti et al. (Bringhenti. 2010), Zampolli et al. (Zampolli. 2006),and Casós et al. (Casos. 2008) would be the lower total amount of dietary fish oil, different (more varied) overall fat compositions of the diets and shorter study periods, respectively:
One possible explanation for this discrepancy is that in our study animals faced higher amounts of dietary fish oil; Saraswathi et al. used 209 g/kg of mixed oils (including coconut oil, olive oil, corn oil and soy bean oil) plus 60 g/kg fish oil, while we used 70 g/kg fish oil which was the only dietary fat source. The dosage of fish oil used in Zampolli et al. and Casós et al. studies were 1% and 5%, respectively, which was lower than 15.9% used in the present study. In the study performed by Bringhenti et al. animals were fed with fish oil containing diet from weaning till puberty which is a shorter period comparing to ours.On the other hand, the results of this study stand in line with those of Ritskes-Hoitinga et al. (Ritskes-Hoitinga. 1998), Verschuren et al. (Verschuren. 1998) and Brenner et al. (Brenner. 1990), which, in parts (e.g. Ritskes-Hoitinga) observed even more severe aortic atherosclerosis and hepatic steatosis than Shirazi and his colleagues. [ Something to think about: Isn't it telling that all those studies have been published before the fish oil craze? And before GlaxoSmithKline started making big bucks by selling is "pharmaceutical grade fish oil" Lovaza. Add to that the fact that Shirazi et al. obviously did not find an American publisher for their study and make up your own thoughts. ]
So what? In essence these results only confirm what I have been saying before. Supplementation with reasonable amounts of fish oil (~2g) may make sense, especially if your diet is naturally low in omega-3 fatty acids in general and DHA, in particular. Mega-dosing on the other hand, or trying to compensate for fatphobia by overconsumption of fish oil, i.e. consuming a low- to no-fat diet, while supplementing huge amounts of fish oil >5g), falsely believing that you would do your body a favor by providing him exclusively with the "good essential fatty acids", will do more harm than good. After all, the "best" (do we really think low total cholesterol is good) serum cholesterol and triglyceride levels are useless, if you die from clogged arteries and a liver defect.