1/ #ListeningThread for @PeterAttiaMD's new podcast with @DrSarahHallberg

Full disclosure, I have tremendous respect for Sarah and all the incredible mountains she has moved in nutrition and health, not to mention just being an incredible human being.

2/ Oh boy -- just 1 minute in and Peter is asking Sarah about dietary fat vs observed composition in vivo! I have a feeling I'm really going to like this episode...
3/ Sarah: "Fatty acids play a critical role, study after study, in cardiovascular risk." -- Love this line...

(Though I'd add a few caveats with regard to lipid profile, but more on that another time)
4/ "...right now we're at the tail end of our five-year data collection of the longest and largest trial looking at nutritional ketosis as a means of reversing type 2 diabetes..."

Okay -- this is worth a moment of pause all on its own given it's staggering significance...
5/ In some alternate universe where there wasn't a Sarah Hallberg or Steve Phinney taking this crucial initiative, would we have anything like this massive, longitudinal @virtahealth dataset?

I think it's fair to point to other aspects of their program with regard to process...
6/...Such as the constant communication and care through their app and its platform.

But I remember a lot of assumptions about why long term keto wasn't feasible that aren't typically asserted anymore given this hard data. Credit Sarah for opening this new, important chapter.
7/ Yes! Happy to hear Peter considers fasting triglycerides of over 100 is considered "elevated" [instead of the guidelines of 150]*

(*To be sure, TG is a noisy marker, so I don't get overly concerned about a single test of, say, 115 when typically below 100 for most)
8/ Yes! At 26:00 Peter is talking about looking at microvascular damage as early indicators of risk [example semi-NSFW, but highly relevant]

Also mentions retinal imaging for the same early warning sign purposes. Couldn't agree more.
9/ More Peter: "...let's look at the actual place where the damage is taking place and make the assessment on an individualized basis as opposed to using these sort of population-based metrics which move in the right direction but for any one individual can be quite misleading."
10/ Again, couldn't agree more.

Nothing trumps the actual detection of disease outcome, period.
11/ 27:45 "Okay, with that background, let's kind of dive into this nerdy, nerdy fatty acid stuff..."

Me in joyful anticipation... 👇
12/ Sarah goes into why increased *dietary* saturated fatty acids doesn't typically result in increased *serum* saturated fatty acids.

Cites very interesting stepwise study here: journals.plos.org/plosone/articl…
13/ So this definitely gets a big geeky as they are getting into POA, SCD-1 driving increased VLDL (via increased cholesterol and TG synthesis pathways), and how this all results in a different fatty acid composition found on these lipoproteins in the bloodstream...
14/ But this is *extremely* relevant to me as it provides an important clue on the synthesis of lipids in the liver relative to those provided to it. That distinction is very important as the former is tightly correlated to disease and the latter is not.
15/ I'll concede I have some disagreements with how the liver function / role is described a little while after that, but I want to put a pin in that for now.
16/ It looks like second half Sarah is discussing her personal journey with lung cancer. I'll concede I want to stop here for now and pick this up tomorrow when I'm in a better space to listen to it. I don't want to be part way in and then having to pause as I head to bed.
17/ But as a heads up, when I first learned of the news it hit me a bit hard as I'm one of the many, many, many people who has benefited from Sarah's kindness. Specifically, she has helped me make many key connections with my research and offered great advice many times over.

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More from @DaveKeto

17 May
1/ Big Update Thread for OwnYourLabs

If you didn't already know, @siobhan_huggins and I launched OwnYourLabs.com last year as a means of ordering private blood work directly. (Feel free to visit the site and for our short intro video)

We have some cool news to share...
2/ In the last few months we've been growing... *a lot*

When we started this originally, it was to help others not only get the labs, but to help encourage them to contribute their anonymized data to help #CitizenScience by given a special discount for opting in (at checkout)...
3/ A few months ago we overhauled the site to include all the features we've been wanting all along (advanced searching/sorting, single page lists, multi-add, bundles, etc)

But even better, checkout is now more streamlined for the anonymous data submission (for those opting in).
Read 7 tweets
24 Apr
1/ Reminder: "Lean Mass Hyper-responder" is literally defined as a combination of LDL ≥ 200, HDL ≥ 80, and Triglycerides ≤ 70.

In other words -- by definition -- #LMHRs are not hypertriglyceridemic (high triglycerides). They are the opposite. (See CholesterolCode.com/lmhr)
2/ For example, in the first of this case series a woman is identified as hypertriglyceridemic (triglycerides of 1109). This is if 15 fold higher than the TG max cap of #LMHR.

lipidjournal.com/article/S1933-…
3/ Moreover, we actually addressed this particular case of hypertriglyceridemia in our Letter to the Editor of this very case series. In fact, it's how we set up the question on what to consider when triglycerides are low instead

Read 4 tweets
17 Apr
1/ It’s ironic, I came across an email I wrote almost 3 years ago when I was first pushing for a “Study on atherosclerosis in LMHRs”. For that first 1.5 years I tried to raise interest and money from inside the system. Some of these details I’ll go into with the book eventually..
2/ Not at all calling anyone out — just noting that it took me a while to realize it was likely a dead end.

For almost all of them, the answer to this question was already known: High LDL LMHR = high atherosclerosis

(And FWIW, it’s possible they’re right— we’ll soon see...)
3/ Then I had the crazy idea to start a charity and announce at #LowCarbHouston in Oct 2019 that we’re going to just try to straight up raise the money to do this study through crowdfunding.

And you know what?

The community stepped up.
Read 4 tweets
15 Apr
I saw this paper linked by @BioLayne (hat tip!) in a twitter discussion and had to stop and read most of it. Basically SFA vs PUFA infused muffin RCT. There's quite a lot of interesting data within. And it's publicly available, btw (no firewall)...

ncbi.nlm.nih.gov/pmc/articles/P…
... The lipid profile changes for the SFA group are unsurprising to me, ofc. But I was surprised they went with ALT as the proxy for "liver fat accumulation". Relative change 53%, but I didn't find the absolute values listed for ALT between groups? Maybe in the supplement...?
... They had a subgroup of 10 (5 of each) where the did PET-MRIs (need more of this in studies) to detect "change in hepatic palmitate uptake" -- which tends to be a stronger proxy for liver fat accumulation, but it showed no association.
Read 4 tweets
14 Apr
Presentation Polls
—————————-

1/ Your current LDL cholesterol is:

(All units are mg/dL)
2/ Your current HDL cholesterol is:
3/ Your current triglyceride (TG) level is:
Read 9 tweets
9 Apr
1/ Whether in agreement or not, @DBelardoMD's statement does represent the existing position of mainstream medicine, particularly lipidology. (Tho she's adding a bit more "color" to it, ofc :) )

My retweets like these are to further generate cross exposure to other voices...
2/ ... Think of it as working toward breaking down some of the echo-chamber-ism.

If you follow me, you're going to get this on a regular basis because I feel hearing every side is important (I have many friends who are LDL skeptics who definitely don't agree with me on this!)
3/ And while we're at it -- here's a list of people I've had excellent, cordial conversations with who are likewise concerned about high LDL whether LMHR or not:
@DrNadolsky
@ethanjweiss
@lansberg
@Lpa_Doc
@NutritionMadeS3

Listen to them as well -- I do...
Read 5 tweets

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