Skot, really, you must contemplate the idea that 'mechanistic speculation is bullshit' and that you can't refute strong evidence with weaker, discorcondant outlier studies.
E.g. on ALA you cite case-control when prospective epi exists, you cite an outdated meta-analysis when two recent ones arrive at a different conclusion, you look at ALA in isolation when there is plenty evidence on ALA rich foods and their net effect (I mentioned them in our last discussion!), you think you are addressing MR's argument while he was mainly, though, I suppose not exclusively talking about CRONies.
@MR
...
Similarly, based on its better support of HDL levels is also mechanistically backward, and again rebutted by the evidence from actual health outcomes. There are now several meta-analyses of prospective epidemiology and clinical trials (1-3) all showing that substitution of saturated with polyunsaturated fat (but not, importantly, with carbohydrate) leads to better cardiovascular health outcomes.
...
References
1: Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010 Mar 23;7(3):e1000252. Review. PubMed PMID: 20351774; PubMed Central PMCID: PMC2843598.
2: Skeaff CM, Miller J. Dietary fat and coronary heart disease: summary of evidence from prospective cohort and randomised controlled trials. Ann Nutr Metab. 2009;55(1-3):173-201. Epub 2009 Sep 15. PubMed PMID: 19752542.
3: Jakobsen MU, O'Reilly EJ, Heitmann BL, Pereira MA, Bälter K, Fraser GE, Goldbourt U, Hallmans G, Knekt P, Liu S, Pietinen P, Spiegelman D, Stevens J, Virtamo J, Willett WC, Ascherio A. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr. 2009 May;89(5):1425-32. Epub 2009 Feb 11. PubMed PMID: 19211817; PubMed Central PMCID: PMC2676998.
I would like to draw your attention to a new paper if you haven't seen it yet. Ramsden et al's meta-analysis of Mozaffarian et al. arrives at the opposite conclusion regarding PUFA and may merit revisiting the PUFA discussion. (not so much the SFA discussion, because in either scenario SFA is inferior to n3/n6/MUFA)
The paper is also interesting, perhaps esp. to you, because it is indirect evidence in favour of ALA (and more generally N3 PUFA).
Br J Nutr. 2010 Dec;104(11):1586-600.
n-6 Fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials.
Ramsden CE, Hibbeln JR, Majchrzak SF, Davis JM.
Of course, the only constant remains that MUFA- and polyphenol-rich fatty foods (nuts, EVOO) and some sources of N3 are healthy. Everything else is even more speculative.
and also another study on the topic of ALA and indirectly PUFA:
...hot off the presses:
The PREDIMED trial, implementing a Mediterranean diet somewhat similar to the Lyon study sans PUFA-lowering, now published first results on relevant endpoints, showing reduced Diabetes incidence from an ALA-enriched complex dietary intervention.
http://www.unav.es/d... 2010 Salas.pdf
(tho, honestly the results seem more consistent with a MUFA/other effect than a pure ALA benefit: a similar anti-diabetes effect was seen in the low-ALA olive oil group)
(this was taken from our most recent ALA vs EPA/DHA discussion:
http://www.longecity...310#entry454310 )
---
People tend to forget just how complex the whole issue is when they turn to simplifications like "PUFA increases oxLDL, therefore it must be unhealthy")
Long ago this was meant as a follow-up to
my post about the complexities of Lp(a) metabolism, but I will probably never get around to finishing the post. So here are my
"notes" about the issue.
What follows is a ranting, geeky and most of all unpolished post. Since this is clearly important AND offtopic I suggest we continue the discussion in a new thread:
http://www.longecity...bious-evidence/
Edited by kismet, 29 April 2011 - 08:26 PM.
