Hi, well organized papers and arguments, Tucker. 1. Flanagan was referring to Yki-Järvinen study 1:17, which Peter dissects so nicely. http://high-fat-nutrition.blogspot.com/2018/07/butter-gives-you-fatty-liver-again.html You referred to Swedish muffins "study". Frozen logic in both...
2. Gura and Omegaven. From Europe this intralipid omega-6 poisoning ongoing trial is like not washing your hands from corpses room to babies delivery room. Gura is your "Semmelweiss". This data is priceless, and as you say, it would be unethical to random test it anymore. They turn yellow on Intralipid, and pink again with Omegaven? However, I read Gura's own handed version, and the producer has a fat mix for the IV purpose, they do not use omegaven for total parenteral nutrition. I would like to speculate that Omegaven works in context of long-time poisoning before it is being applied? Of course, TPN has also glucose fed, and it requires insulin (due to incretin effect and intralipid O-6 as a background fat does not induce insulin response?). Why glucose IV anyhow, should be not needed...? Sure this has been studied?
Yes, overfeeding is a significant confounder, it's not a physiological model if it's voluntary (vs driven by some food component.
TPN guidelines recognize that benefit of n-3 may only be apparent compared to n-6, and may be harmful independently. But less so, so it's still an improvement. I covered that in my COVID19/ARDS post, with links to the papers/studies.
While I sincerely appreciate the admirable angles and numerous valid points Mr. Flanagan's topics revolved around (for instance the concern for those that may or may not have resources to significantly impact their choice of foods and particularly their consumed fats), I do think much of his argument was obliterated by the literature that you so eloquently cited and defended. His concerns are well founded, but that really wasn't the topic at hand. The topic (my take) was the increase of dietary PUFA consumption and if they are contributing to the large increases of modern disease we are seeing (all our metabolic dysfunction friends, T2DM, CVD, Alzheimers, etc). And with this as the base of the discussion, a great segue into those probable mechanistic pathways which was backed up by significant literature on these topics.
This was a great one to listen too. And most definitely, as you said, "I thought it was very productive". Couldn't agree more. Thank you so much for this. Keep up the great work. I will be in the audience!
I haven't listened yet.....but I can say....love LMNT.
ReplyDeleteOK - just need to find a spare couple hours....
ReplyDeleteHi, well organized papers and arguments, Tucker.
ReplyDelete1. Flanagan was referring to Yki-Järvinen study 1:17, which Peter dissects so nicely. http://high-fat-nutrition.blogspot.com/2018/07/butter-gives-you-fatty-liver-again.html
You referred to Swedish muffins "study". Frozen logic in both...
2. Gura and Omegaven. From Europe this intralipid omega-6 poisoning ongoing trial is like not washing your hands from corpses room to babies delivery room. Gura is your "Semmelweiss". This data is priceless, and as you say, it would be unethical to random test it anymore. They turn yellow on Intralipid, and pink again with Omegaven? However, I read Gura's own handed version, and the producer has a fat mix for the IV purpose, they do not use omegaven for total parenteral nutrition. I would like to speculate that Omegaven works in context of long-time poisoning before it is being applied? Of course, TPN has also glucose fed, and it requires insulin (due to incretin effect and intralipid O-6 as a background fat does not induce insulin response?). Why glucose IV anyhow, should be not needed...? Sure this has been studied?
3. Nice and polite discussion, congrats.
JR
Thanks JR.
DeleteYes, overfeeding is a significant confounder, it's not a physiological model if it's voluntary (vs driven by some food component.
TPN guidelines recognize that benefit of n-3 may only be apparent compared to n-6, and may be harmful independently. But less so, so it's still an improvement. I covered that in my COVID19/ARDS post, with links to the papers/studies.
Thanks, I thought it was very productive.
While I sincerely appreciate the admirable angles and numerous valid points Mr. Flanagan's topics revolved around (for instance the concern for those that may or may not have resources to significantly impact their choice of foods and particularly their consumed fats), I do think much of his argument was obliterated by the literature that you so eloquently cited and defended. His concerns are well founded, but that really wasn't the topic at hand. The topic (my take) was the increase of dietary PUFA consumption and if they are contributing to the large increases of modern disease we are seeing (all our metabolic dysfunction friends, T2DM, CVD, Alzheimers, etc). And with this as the base of the discussion, a great segue into those probable mechanistic pathways which was backed up by significant literature on these topics.
ReplyDeleteThis was a great one to listen too. And most definitely, as you said, "I thought it was very productive". Couldn't agree more. Thank you so much for this. Keep up the great work. I will be in the audience!