1/ My thoughts on #Satiety & @DietDoctor 🧵

If you've followed me a while, you know I try to avoid the "diet debates" (tho not always successfully)

However, I have been getting a high frequency of DMs/messages/calls regarding DD's new endeavor for a #lowcarb alternative
2/ Let me first start off by saying I don't think any diet is inherently superior to all others.

I *do* think the #lowcarb diet is under-utilized for populations that can uniquely benefit from it.

However, I also believe most of us have many more options than is often assumed.
3/ Moreover, I consider @DietDoctor's long history of providing a "one stop shop" platform for all things #lowcarb/#keto with high quality guides, videos, and tools to be without equal.

It made it extremely easy to refer everyone in DD's direction, particularly beginners.
4/ Lately, I'll concede I have been in more of a wait-and-see mode with their new expansion into the Satiety Per Calorie (SPC).

It seeks to provide more flexibility for folks who find #lowcarb isn't working for them by focusing on satiety itself as scored in individuals foods.
5/ Up to now, I haven't commented much on this model or satiety overall.

But I'll concede I actually have a strong opinion on it derived from many of my experiments. I'd like to share a few in the following tweets and others can feel free to share if any of this resonates...
6/ In my original "Added Sugar Experiment" I did identical meals that added Skittles as the intervention -- but it was a crossover where the only thing changed was the order of when I consumed it (before meal vs after) cholesterolcode.com/sugar-and-chol…
7/ Again, same meals, same calories -- everything was the same except the order. This changed the satiety of it substantially for me.

In my famous "Weight Gain" experiment, I literally gained 19lbs (#ForScience) and carefully tracked both entering the mixed diet and exiting.
8/ In the last 5 days of the Standard American Diet (SAD) phase, I was eating 4,217 calories from two footlong subs and a medium pizza -- with a whopping 300g of protein (28%)
9/ Then I went from that phase (May 2-6 2018) to a fixed #keto diet (below) that was 2,437 calories with 128g of protein (21%) and found myself (to my own surprise) much more satiated.

In fact, I was remarking to @siobhan_huggins throughout the 1st day how much less hungry I was
10/ Also note I continued this exact meal plan through to the 19th (hence the Groundhog Day joke in my slide).

It's quite striking when you realize I was only having slightly more fat with the #keto diet (205g vs 177g from SAD), yet carbs were 20g vs 356g, respectively.
11/ Anyway, it's worth noting that while this is strictly anecdotal, these experiments have the benefit of being a planned intervention, as opposed to one that arose from a life event, holidays, etc that typically confound psychological context.
12/ In other words, I don't have any specific personal investment on the topic of satiety -- but the change is unmistakably obvious given it can arise against an otherwise clean baseline.
13/ To be sure, I have many other experiments that touch on satiety which I've commented on (Added Sugar 2, White Bread & Processed Meat, EVOO vs Butter, etc)

And -- as unpopular as it is to say this -- I think satiety is just much more complicated than we'd like to believe
14/ The topic itself is extremely interesting and worth exploring. But I'll concede I'm skeptical of attempts to simplify it substantially to a basic scoring algorithm.

I'm in a wait-and-see mode with these new efforts by @DrEenfeldt and his team.
15/ I readily concede I shouldn't expect DD to remain "all things #lowcarb/#keto" if @DrEenfeldt would like it to cater to other plans as well -- I just loved that level of simplicity in the subject matter alongside varieties of expertise

(I know there's subsections for it, ofc)
16/ If I can finish with one more thought, @DrEenfeldt and @DietDoctor deserve a great deal of respect for remaining very engaged in feedback from the community.

I know there's been a lot of passionate responses on this direction, so I can appreciate Dr. E's effort especially.

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More from @realDaveFeldman

Mar 9
1/ Yes-- I've been meaning to literally do an entire talk on Simpson's Paradox because the concept is really quite simple.

Here's an example:
✅Hypothesis: higher body weight causes higher blood pressure.

💡If we only had scales and BP cuffs, we'd certainly see the relationship
2/ Let's further point out we could demonstrate it over three lines of evidence: observational (epi), interventional (Rx), and genetic (🧬)

Epi: When randomly grabbing a large population of Americans, we find those who generally weigh more generally have higher BP ✅
3/ Rx -- interventions that generally reduce weight, also generally reduce BP ✅

And lastly, 🧬 -- most genes that associate with lower weight will generally have lower BP ✅

Now obviously we have more advanced tools these days than weight scales and BP cuffs...
Read 7 tweets
Mar 5
1/4 "also is the LEM (Lipid Energy Model) mutually exclusive with high LDL being atherogenic?"

Yes and no.

Yes -- in that the two should be treated as separate questions. It may well be that LEM is true, yet high LDL is independently atherogenetic and vice versa.

However...
2/4 No -- in that it was actually metabolic dynamics having an impact on lipid profiles that led me down the road we're at now.

Function vs dysfunction (or successful regulation vs unsuccessful regulation) having an upstream impact on lipid levels should be strongly considered.
3/4 But currently, it is assumed these influences are either irrelevant or the impact known -- at least to the extent that it is commonly assumed high LDL is pathogenic in every context (hence, little need to prospectively study metabolically healthy populations with high LDL)
Read 4 tweets
Feb 7
1/ Got lots of pings on this one (including from @theproof)

But it's worth unpacking just how many variables are in play and why I obsess so much about controlling for them when the shifts are relatively small...
2/ If you're just tuning in, I've done over 50 experiments with many of them hypercontrolled (like below) where I literally eat to an exact meal plan with exact timing, have nearly identical exercise, and try to sync sleep schedule as best as possible. cholesterolcode.com/the-oxldl-repl…
3/ It's because I know there's already a lot of things that can alter lipid levels even in the very short term. Not just days, but *hours*.

Check out this prelim data where I was testing 6 times over each day. And these are the means of the last 3 days...
Read 12 tweets
Feb 2
1/2 Example 1:
🚬 Imagine if the average person from the moment they're born were taught to be 2 pack a day smoker.

⛔️ Now imagine a fraction were born into families that were 0 pack a day smokers.

Would we expect that latter group to have greater longevity than the former?
2/2 Example 2:
Now imagine most people averaged 100 #LDL cholesterol over their lifetime.

But a fraction were born with a genetic mutation that kept their average at 20.

Would we expect that latter group to have greater longevity?
If genetically low LDL/ApoB had universally a net benefit -- this would be strong evidence that indeed this particle is pathogenic -- which is to say, disease-causing overall (not just atherogenic)

But does existing genetic data support this hypothesis? Is there clear longevity?
Read 5 tweets
Feb 1
1/4 Interesting study regarding #LDL-C vs all cause mortality*

✅NHANES -- so it's #OpenScience 👏
✅Lowest LDL-C associates with highest ACM
⚠️ No short term censoring (more on this below)

(*had in my reading list, but forgot until ht
@BobJohnson462) nature.com/articles/s4159…
2/4
A couple notes...

1️⃣ Many assume the higher ACM associated with LDL-C is due to "reverse causality". It's a hypothesis, to be sure, but one I think worth exploring.

Thus, it would have been ideal of the authors tried at least one or more analyses censoring 2-3 years.
3/4
2️⃣ As always, be aware these data are observational.

And as I say often👇

(Always worth a mention of Bradford Hill and his criteria, btw)
Read 4 tweets
Jan 30
Yes, read it when it came out.

For those who've followed my work and know where I'm coming from, WHY would I fully expect LDL-TG (triglyceride content per LDL particle) to closely associate with atherosclerosis?

(By now this should be a very easy question.)
2/ Let's start with causal directionality.

Which of the following are possible?

1) High LDL-TG is causing higher atherosclerosis

2) One or more things are causing both higher LDL-TG and higher atherosclerosis
Answer is: Both are possible.

Now that said, it is way more common for people to only consider (1) and not (2)

I regularly do my best to get folks to consider (2) as well -- and have been doing so for several years now.
Read 7 tweets

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