Taubes: “One of the defining characteristics of pathological science is — people commit themselves publicly to a result based on premature evidence…”
2/ “…So it’s not ironclad, they haven’t locked it down, there’s still a chance they could be wrong and they don’t understand the likelihood of that chance, no one ever does until you get very good at this when you realize that chance is enormous.”
3/ “And so once you go public, science is supposed to be hypothesis and test, right? You’re supposed to rigorously test your hypotheses and ideally you’re trying to prove that you’re wrong..."
4/ "Richard Feynman – first principle of science – is that you must not fool yourself, and you're the easiest person to fool."
(So incredibly true!)
5/ "When we talk about pathological science, people tend to think of fraud, right? When you're committing fraud in science, you're knowingly trying to fool other people by manipulating the evidence...
But there are two ways you can manipulate the evidence...
6/ "You can create a signal, or you can do an inadequate job of studying the background.
Remember it's a signal-to-noise problem.
So you can fudge a signal or create a signal, or move a signal...
...or you could ignore the background.
7/ "... and do a poor job in the background you'll still end up with a big signal-to-noise ratio. You haven't technically committed fraud.
You're not actively trying to fool anyone else, you're fooling yourself."
8/ Naturally, this speaks to me very personally.
As mentioned above, the first major endeavor is to seek proving yourself wrong -- which is exactly the value of the coming #LMHRstudy for us.
9/ I continue to hypothesize lipid profiles are often in large part a consequence, not a cause of metabolic health and disease.
FWIW, I've been doing so for years, but I think this could be the "background" that keeps getting overlooked (or maybe it's not relevant after all)
10/ I likewise believe populations of genetically normal, metabolically healthy populations and their LDL assoc with CVD are surprisingly understudied. Healthy LMHRs will provide a new window of study given very high LDL effect size against resulting CVD outcome. Hence the study.
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2/ First, I definitely DO NOT want anyone to interpret anything I've said as reflective of analysis with secondary prevention. I'm quite upfront that I prefer looking to lipid research with regard to so called, "primary prevention" (populations without prior heart attacks)...
3/ Second -- and as always -- I want everyone to work with your doctor. Yes, I do think your doctor needs to likewise work with you and your health goals, but this is a given.
If I had a heart attack, I'd definitely be working with my doctor and considering all the options...
2/ For me, this journey started 6 years ago with alarmingly high total and LDL cholesterol following my going on a ketogenic diet. I became obsessed with trying to understand why and begin reading everything I could on lipidology...
3/ I found through a series of experiments there was quite a bit of change I could induce based on dietary patterns. As I developed and executed this "citizen science" research, I turned it around back to the community to hopefully help us in advancing this important topic.
2/ Let's have some fun and use a relatable analogy...
Imagine you had exactly two kinds of stores in the neighborhood: bakeries and butcher shops.
You normally get groceries from both, but recently the bakeries were closed down, so now you just get meat only for meals...
3/ Now that the bakeries are down, there's more demand on the butcher shops, so they are having more inventory sent to them.
But then, the neighborhood increased while the number of butcher shops actually decreased, and this required an even higher rate of shipments to restock.
1/ This would be a good opportunity to clear the air on a few things...
Per @DrNadolsky's tweet, we don't know everything we want to know about #atherosclerosis. Almost everyone would agree it is multifactorial, and most of Med would ascribe the central risk driver to LDL/ApoB..
2/ First, I agree glucose going up and down -- in and of itself -- is not inherently a mechanism of concern.
The key questions of interest are by how much and for how long -- and from this, can we determine if there is a dysregulation?
3/ I was listening earlier in a Clubhouse chat to @Dr__Guess discuss her recent study and how "all over the map" glucose levels were for these T2D patients -- which is unsurprising given the nature of the disease.
2/ @BioLayne “… if you torture the data enough, you can get it to show what you would like it to show.”
This is actually a variation I was one of my favorite quotes of all time.👇
3/ it’s also very prescient in its timing. I was actually just talking with @NutritionMadeS3 yesterday, and why I tend to be more interested in studies that work off open or shared data sets given the level of transparency in the statistical instruments being used…