But if readers can feel justified in ignoring any analysis for which one can make such a complaint, then readers can feel justified in ignoring pretty much any such data analysis. That is way too low a standard for ignoring data.
But Phil isn’t saying we can ignore the study just because it uses a linear regression. He’s giving good, and what should be obvious-to-experts, reasons why a linear regression will be deceptive on this question. Once you know dosage matters and that
The mean values used in the study of both A and E are in ranges known to be toxic. The maximum values used were ten times the known toxic levels, and about 20 times the beneficial levels.
then linear regression looks like a really bad choice.
The references were a couple of sentences before. Miller et al. 2004, “Meta-Analysis: High-Dosage Vitamin E Supplementation May Increase All-Cause Mortality”, “Randomized Trial of Vitamin A and Vitamin E Supplementation for Retinitis Pigmentosa.” Though I see the formatting made it look like 1 reference instead of 2, and the link was broken.
Also, this is something you can easily google if you question it.
People familiar with vitamin studies would know right away that 200,000IU of vitamin A and 5,000IU of vitamin E per day are both extremely high, and not in the same category as “vitamin supplementation”.
Sure. “Known to be toxic” was probably too glib a way to put it, Phil should provide a cite and I shouldn’t have repeated it uncritically. But even if this was just someone’s hypothesis without much experimental evidence behind it: the concept of vitamin poisoning isn’t a new one. There are publicized daily intake tolerable upper levels for lots of vitamins. Hypervitaminosis A, E. I don’t know what kind of evidence backs these claims up but presumably people in the field are aware of this kind of thing. I’m not saying “These are the toxicity levels. This is why the meta analysis is wrong.” I’m saying “People are hypothesizing vitamin toxicity at certain levels. Why the hell would you run an analysis that couldn’t even in principle take that into account?”
One thing is the fat soluble vitamins (A, E, D & K2-mk4) are [cofactors]. Vitamin A (retinol) toxicity directly depends on Vitamin D3 status.
Vitamin A is used short term at high dose 50,000 IU to 100,000 IU adjunctly to augment cancer therapy as part of core integrative nutraceutical programs (incl natural beta-carotene, high dose vitamin D 25(OH)D 75ng/ml, high dose fish oil (4-20g/day), glutamine, butyrate, etc)
Why is Vitamin A used together with Vitamin D? Why are they found in potent quantities together in nature (ie, fish liver, oily fish, salmon, oysters, trout, catfish, egg yolk, zooplankton, butter, pate, fish eggs/roe/caviar, breastmilk)? All the best foods in life… (breastmilk—my kids were really into that stuff). Pasture-raised cows indeed produce butterfat brimming with a wealth of cardioprotective vitamins K2, A, D and E! I wonder why??
A synergistic effect has been observed for nearly all benefits studied. This makes absolute sense since they exist co-dependently physically located in the nucleus of our cells.
But Phil isn’t saying we can ignore the study just because it uses a linear regression. He’s giving good, and what should be obvious-to-experts, reasons why a linear regression will be deceptive on this question. Once you know dosage matters and that
then linear regression looks like a really bad choice.
But no citation is given for this “known to be toxic” claim. Known by whom how and how confidently?
The references were a couple of sentences before. Miller et al. 2004, “Meta-Analysis: High-Dosage Vitamin E Supplementation May Increase All-Cause Mortality”, “Randomized Trial of Vitamin A and Vitamin E Supplementation for Retinitis Pigmentosa.” Though I see the formatting made it look like 1 reference instead of 2, and the link was broken.
Also, this is something you can easily google if you question it.
People familiar with vitamin studies would know right away that 200,000IU of vitamin A and 5,000IU of vitamin E per day are both extremely high, and not in the same category as “vitamin supplementation”.
Sure. “Known to be toxic” was probably too glib a way to put it, Phil should provide a cite and I shouldn’t have repeated it uncritically. But even if this was just someone’s hypothesis without much experimental evidence behind it: the concept of vitamin poisoning isn’t a new one. There are publicized daily intake tolerable upper levels for lots of vitamins. Hypervitaminosis A, E. I don’t know what kind of evidence backs these claims up but presumably people in the field are aware of this kind of thing. I’m not saying “These are the toxicity levels. This is why the meta analysis is wrong.” I’m saying “People are hypothesizing vitamin toxicity at certain levels. Why the hell would you run an analysis that couldn’t even in principle take that into account?”
One thing is the fat soluble vitamins (A, E, D & K2-mk4) are [cofactors]. Vitamin A (retinol) toxicity directly depends on Vitamin D3 status.