1/ Have you seen the New Non-Nutritive sweeteners paper in Cell making the rounds!?! Fantastic!
Here's a video rundown:
And this thread contains a brief tweetorial...
2/ This study took 120 young health people who didn't consume non-nutritive sweeteners (NNS) and broke them into 6 groups, n = 20/group
👉 Control (no supplement)
👉 Glucose
👉 Sacchrin
👉 Sucralose
👉 Aspartame
👉 Stevia
7 day baseline, 14 day exposure, and 7 day follow-up
3/ There was a clear individualized response across NNS, with Sucralose and Saccharin having the largest impact on glucose tolerance on oral glucose tolerance test.
There were "responders" (who had worse glucose tolerance in response to NNS) and also non-responders.
4/ B = week 1, C = week 2, and D = follow-up (no sweetener)
Note how the pink and orange distributions get vertically squeezed in C compared to B. This appears to suggest that, overtime, non non-responders converted to responders
5/ Also, note in D (follow-up), that responders tended to revert to baseline, meaning the negative impact was reversible... PHEW!☺️
6/ The researchers were also able to show the effect was MEDIATED BY THE MICROBIOME
When then transferred fecal/microbiome transplants from participants to mice without microbiomes, the mice adopted the metabolic profiles of the responders/non-responders
7/ There were many brilliant nerdy nuggets throughout the paper. I'll highlight just one
When they look at profiles of responders vs non-responders for Sucralose, a major difference the popped out was baseline #ketone (BHB) levels
Look at top row...
8/ Responders (impaired glucose tolerance after Sucralose) had LOW ketone [dark blue]at baseline vs. non-responders had HIGH ketone [dark red] at baseline.
Then, levels went in opposite directions after exposure to Sucralose!
What gives?!
9/ While they data certainly do not confirm this, one might SPECULATE, that baseline metabolic state/dietary choice (re #ketogenic diet) could influence whether one is a responder/non-responder to Sucralose, which incidentally is the sweetener in @ketochow
10/ Speaking more broadly, I think it's possibly - if not likely - that dietary choice could influence how one responds to NNS
For example, it's previously been shown carbs + NNS might be worse than NNS alone
11/ Again, here's a link to a verbal video rundown. Certainly a stellar paper. The @Elinav_Lab group always produces incredible research! Very grateful for them!
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2/ The story behind this study started back in the fall, when a grass-roots group of my peers expressed interest in designing a "Metabolic Health Immersion" program to help us learn about how lifestyle impacts metabolism and health...
3/ 40 students wore CGM for 10-40 days, and a subgroup also engaged in journal clubs, patient panels, dietary tracking, and took intake and completion questionnaires with qualitative and quantitative components 👇
1/ Medical Case
👉53y M, #LMHR w LDL 394, HDL 111, TG 40 for 4y on #keto diet
👉BMI 21.6
👉Prior to keto LDL was 98 mg/dl
👉CCTA shows no plaque, CAD-RADS = 0
👉Parents both lived to >80y w/o cardiac events Family hx of neurodegenerative diseases, including 2x of 👉Parkinson’s
2/ Patient doesn’t want to abandon diet because it makes them “feel my best.”
You’ll notice, there’s no poll associated with this case. Medicine isn’t a democracy and not all medical opinions on Twitter are equally informed. However, I wanted to share this case ...
3/ ...as a juxtaposition to the extremism I’m seeing ON BOTH SIDES: LDL/ApoB is benign v. lower is better (period). Neither is the case. A bit of nuance…
With respect to “LDL/ApoB is benign,” all things being equal, the data don’t support this view. It’s a risk factor...
2/ 2:45 I talk about how 30g inulin/d can increase inflammatory markers and markers of liver damage, here are those data. Look at the pink arrows and I explain what's going on.
3/ At 3:38 I discuss how Arabinoxylan fiber specifically, but not inulin fiber lowers LDL #cholesterol. You can see that very clearly here as the red line represents a plummeting of LDL vs. green line no real change. They are both fibers, but differentially impact lipids
Lipids & associated proteins have previously been identified as biomarkers of infection, including VLDL, HDL and various apolipoproteins, while both TAG and (serum) PUFA have been implicated as markers of severe disease outcomes
But what this paper adds
3/ Is an investigation (using mostly HEK293T-ACE2 and A549-ACE2 cells) of how the virus alters the lipidome and the importance of these changes in viral proliferation ... They found virus ⬆️TAGs, and PUFA chains were 2-8-fold more than saturated or monounsaturated species ...
2/ First and foremost, what did my diet look like?
Vegan and w/o no coconut to maintain low sat fat % <15% total fat. These are data from a day of soy protein, 1/4c tahini, 1lb eggplant, 100g broccoli, 6 Tbsp EVOO, 4 Tbsp avo oil, 2 oz ea macadamia and pecans, 200g asparagus
3/ I’m an example of an LMHR that eats a relatively low saturated fat diet at baseline. Even when >80% of my fat intake is MUFA/PUFA, my LDL can run >500. Thus, it’s not simply the sat fat. Even when fiber intake has been >30g with net carbs <30g, my LDL can easily run >350