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Re: Albino2 post# 90413

Tuesday, 08/30/2016 8:06:25 AM

Tuesday, August 30, 2016 8:06:25 AM

Post# of 448129

Can you help me understand how you can hold the view that the supplement is too small to affect the outcome and also site DHA as working and therefore better? How is it possible to maintain both positions? --Alb



I don't think 4g--or even 8g of EPA *with* 8g of DHA (16g/d n-3), will do much of anything for these patients, wrt reducing MCE risk. The reason being is because it isn't so much more fat is needed for these patients (the good kind), it's that bad fat needs to be *reduced*. Their bodies are simply not as good at dealing with all of that dietary fat.

My fam history has 0 incidence of heart disease. They were all active, ate pretty well, etc. But take me, a genetic result of these, and give me a very high sat fat/ trans fat diet for 15 years, and take someone else who is equally fit as me and has a terrible genetic history of CVD, and make him do the same. Guess whose arteries will look better at the end of that? His, of course. Why? Genetics. So that's one part of this equation, and a big one. Better off that these individuals eat *only* n-3/n-9. But that is very difficult to achieve.

It's like a smoker and lung cancer. More oxygen may be good for him, and his tar-filled, damaged lungs, but he *really* freaking needs to just stop smoking if he wants to lower his risk of getting lung cancer at all.

n-3 do get preferential treatment, meaning your body will use these in preference of other fatty acids, but a few things here--it's not a perfect system. If I dose an individual with 40g of mammal fat and trans fat and 2g of Vascepa, he will not use 38g of mammal fat and 2g of Vascepa. Fat is excreted unused as well, though much of it gets stored. You would like to think it is a perfect system and the body will usher that 2g of Vas right where it's needed but that just doesn't happen.

The other problem is, it doesn't matter if you are ingesting 2g of Vas when you, a pre-diabetic, etc., are also eating 4 eggs, a bowl of cereal with whole milk, and a danish. And then a bacon double cheesburger with salty oil soaked fries and a coke (and no Vas with that meal, took it already). Then Wendy's dollar menu fried chick sandwiches as a snack. Then chinese food for dinner (the oil soaked fast food variety, not authentic). Then meat lovers pizza for late snack (44g sat fat), and take your next 2g Vas pill with it. Then a half pint of ice cream as midnight snack. And the most physical exertion you did all day was slow pace walking here or there.

Who cares if DHA is beneficial? Yep it is, so what? You're doomed if you do the above regularly. You will have no better chance at reducing MACE if you pop Lovaza or Vascepa twice a day or not.

Now contrast this with the person who decides (like Whal) to make significant changes. He swaps out most meat for fish, esp salmon, decreases overall caloric intake, cuts out sugars, exercises regularly, quits smoking if he smokes, etc., and takes a high dose statin daily and low dose aspirin. And also takes 2g of Vas twice a day. Does that Vas matter now? Imo no it doesn't. What matters is all the rest. The *decrease* of what is negative. Does Vas contribute to the increase in what is positive? Sure, I think so. Would Lovaza be better? Yes, I personally think so (due to DHA). But if he took neither, would it matter much? No, I don't think it would.

We're talking about something that is so small. It's like... Two groups that exercise, and one walks 0.05 miles further than the other every day. Which one will have lower MACE? Uhm. I *guess* the one that walks further? But, would I bet on a company totally dependent upon that being proven true to *exist*?

Hellllll no.

I'd short em though.

Jmo

GL


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