No worries. Family time is much more important than Twitter arguments If you want to know the criticism I'd personally make of the study, I did a quick thread herehttps://twitter.com/GidMK/status/1032390899995557888 …
-
-
Replying to @GidMK @bokkiedog and
I see two related reasons for the outcry against this study from low carb advocates (hereafter LCAs). First, the authors have implicated "low carbohydrate diets", when they have not studied any carb intake remotely like low carb diets (LCD). This matters, because 1/
1 reply 0 retweets 2 likes -
Replying to @KetoCarnivore @GidMK and
not only is there a huge gap between their lowest quartile at 38% and the <5% that LCDs entail, but the difference is critical physiologically. Only at those very low levels are symptoms of MetS demonstrably reversed, including the dyslipidemia of triglycerides and HDL. 2/
1 reply 0 retweets 2 likes -
Replying to @KetoCarnivore @GidMK and
This framing has caused harm to public perception of LCDs, exacerbated by inappropriate but predictable headlines such as "LCDs take four years off your life." It is difficult not to attribute deliberate deceptive intent, and this generates ill will and lack of trust. 3/
1 reply 0 retweets 2 likes -
Replying to @KetoCarnivore @GidMK and
The deeper conflict is what we were discussing. It is precisely that we don't agree on the causal pathways in the first place, that makes LCAs see this kind of study as fundamentally worthless. These assumptions affect how the statistics are analysed. 4/
1 reply 0 retweets 2 likes -
Replying to @KetoCarnivore @GidMK and
LCAs came to be advocates because of effects like the ones cited above. Even if you don't take carbohydrates as a primary driver of metabolic syndrome, once MetS has developed, risk factors can be drastically, favourably changed by LCDs. 5/
1 reply 0 retweets 2 likes -
Replying to @KetoCarnivore @GidMK and
The LCA model of causality is that (chronic high carb intake & some other factors) → chronic hyperinsulinemia → (MetS & diabetes & CVD), whereas the HCA model seems to be: (gluttony & sloth & genetics & some other factors) → overweight → (optionally MetS & diabetes) → CVD 6/
2 replies 0 retweets 2 likes -
Replying to @KetoCarnivore @GidMK and
Therefore to a LCA, adjusting for diabetes is tantamount to adjusting for the outcome, but it shouldn't be warranted under the other model either, as it is still at least sometimes on the path. 7/
1 reply 0 retweets 1 like -
Replying to @KetoCarnivore @GidMK and
In any case, the essential conflict is a disagreement about the causal model, and therefore epidemiological studies that have causal assumptions from the HCA model baked in cannot possibly contribute evidence that would be compelling to someone with a different causal model. 8/8
1 reply 0 retweets 1 like -
Replying to @KetoCarnivore @bokkiedog and
It's interesting, because while I can see where you're coming from, it's extremely to take any of this seriously given the low-carb reaction to the PURE study 6 months ago
3 replies 0 retweets 1 like
I was having the exact same arguments with low-carb advocates about epidemiology and residual confounding, except in the other direction, despite the fact that every criticism you've made applies equally to that study as this
-
-
Replying to @GidMK @KetoCarnivore and
I think
@AlanLevinovitz said it best. To paraphrase: if only people would apply the same level of rigor in their analysis of studies they like as those they dislike2 replies 0 retweets 0 likes -
Replying to @GidMK @KetoCarnivore and
Smug sanctimonious straw manning. Many of us do just that.
0 replies 0 retweets 0 likes
End of conversation
New conversation -
Loading seems to be taking a while.
Twitter may be over capacity or experiencing a momentary hiccup. Try again or visit Twitter Status for more information.