Discover and read the best of Twitter Threads about #LEM
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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.)
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
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.
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.
#Vegan🌱#keto (low sat fat, 0 cholesterol)
vs.
Meat and Egg heavy diet + 120g net carbs
N=1 Crossover experiment
Surprisingly, LDL >300 mg/dL on vegan keto and ~100 mg/dL on meat and egg plus carb diet 🤯
👉 If this doesn't make you curious, I don't get you
vs.
Meat and Egg heavy diet + 120g net carbs
N=1 Crossover experiment
Surprisingly, LDL >300 mg/dL on vegan keto and ~100 mg/dL on meat and egg plus carb diet 🤯
👉 If this doesn't make you curious, I don't get you
2/ This contradicts the explanation that sat fat is the primary driver of ⬆️ LDL on low-carb
While it may represent an outlier case (& sat fat may primarily drive⬆️LDL in others), that these lipid results can present in anyone requires an explanation beyond conventional wisdom
While it may represent an outlier case (& sat fat may primarily drive⬆️LDL in others), that these lipid results can present in anyone requires an explanation beyond conventional wisdom
3/ 2022 has been a good year for study of the Lean Mass Hyper-Responder phenotype with 5 manuscripts published:
-Demonstrating presence of the phenotype
-Providing explanation in the form of the Lipid energy model #LEM
-Calling for further research
-Demonstrating presence of the phenotype
-Providing explanation in the form of the Lipid energy model #LEM
-Calling for further research
📍Big milestone!📍
The Nov/Dec @LipidJournal just dropped!
🚨Featuring the #LMHReditorial 🚨
via @nicknorwitz et al
It focuses on #LMHRs, both in consideration of their high #LDL and an urgent call for expanded #research.
Why is this important?... /1
doi.org/10.1016/j.jacl…
The Nov/Dec @LipidJournal just dropped!
🚨Featuring the #LMHReditorial 🚨
via @nicknorwitz et al
It focuses on #LMHRs, both in consideration of their high #LDL and an urgent call for expanded #research.
Why is this important?... /1
doi.org/10.1016/j.jacl…
2/ Certainly the biggest impact is bringing this phenotype well into the spotlight.
If you've been following my work from the beginning, you can appreciate just how much energy I've put toward putting this phenotype in front of Lipidologists.
If you've been following my work from the beginning, you can appreciate just how much energy I've put toward putting this phenotype in front of Lipidologists.
3/ But this is understandably a challenge given how much progress on this research has been accomplished outside typical channels ("Citizen Science").
-- Until now.
-- Until now.
🧵 Dec 9th anniversary thread
On this day in 2015 I received a lab result that would alter the course of my life.
Just two weeks earlier I had gotten my very first bloodwork after half a year on #keto that showed my total and #LDL #Cholesterol had nearly doubled (!)… /1
On this day in 2015 I received a lab result that would alter the course of my life.
Just two weeks earlier I had gotten my very first bloodwork after half a year on #keto that showed my total and #LDL #Cholesterol had nearly doubled (!)… /1
2/ With that first test I was overcome with shock and curiosity — much more former than the latter.
I wanted to get a repeat test to confirm this wasn’t a lab error.
I wasn’t ready to give up #keto, but I was miserable enough that I ate considerably less.
I wanted to get a repeat test to confirm this wasn’t a lab error.
I wasn’t ready to give up #keto, but I was miserable enough that I ate considerably less.
3/ At the same time I learned as much as I could about Lipidology - which focuses on how the body moves lipids (like cholesterol) in the blood.
And to my surprise, this system is already very familiar to me as a software engineer given it is a distributed object network.
And to my surprise, this system is already very familiar to me as a software engineer given it is a distributed object network.
🚨Cool New Study!
Omega-3 fats have sex-specific impacts on lipids, LDL, HDL & TG!
Thread + video breakdown...
1/ In this new paper published in the @LipidJournal, researchers performed a Double-Blinded Randomized Crossover to see how EPA & DHA imapct lipids and mean dn women
Omega-3 fats have sex-specific impacts on lipids, LDL, HDL & TG!
Thread + video breakdown...
1/ In this new paper published in the @LipidJournal, researchers performed a Double-Blinded Randomized Crossover to see how EPA & DHA imapct lipids and mean dn women
2/ The study was a has 21 subjects each with at least 1 marker of Metabolic Syndrome
There was a 4 week run-in period, followed by 10w on 3g/d of EPA or DHA, a washout period, and then the other long-chain fatty acid. Again, order was randomized and study was double-blinded...
There was a 4 week run-in period, followed by 10w on 3g/d of EPA or DHA, a washout period, and then the other long-chain fatty acid. Again, order was randomized and study was double-blinded...
3/ Researchers found:
(1) EPA and DHA both ⬇️ TG.
(2) EPA and DHA both ⬆️ LDL-C/ApoB ratios, suggesting more large fluffy healthy buoyant LDL-C
(1) EPA and DHA both ⬇️ TG.
(2) EPA and DHA both ⬆️ LDL-C/ApoB ratios, suggesting more large fluffy healthy buoyant LDL-C
🧵1/8 Here's an easy thread for reference on our current papers. 👇👇👇
🔖 Bookmark this!
We cover:
- High #LDL on #lowcarb/#keto
- Lean Mass Hyper-responders (#LMHR)
- The Lipid Energy Model (#LEM)
- And, ofc, our #LMHRstudy underway right now
🔖 Bookmark this!
We cover:
- High #LDL on #lowcarb/#keto
- Lean Mass Hyper-responders (#LMHR)
- The Lipid Energy Model (#LEM)
- And, ofc, our #LMHRstudy underway right now
2/8 The #LMHRpaper was our first describing the #LMHR phenotype
- #LDL #Cholesterol of 200 or higher
- #HDL #Cholesterol of 80 mg or higher
and
- #Triglycerides of 70 mg or lower
Which is actually common for lean, very folks on #lowcarb/#keto folks. doi.org/10.1093/cdn/nz…
- #LDL #Cholesterol of 200 or higher
- #HDL #Cholesterol of 80 mg or higher
and
- #Triglycerides of 70 mg or lower
Which is actually common for lean, very folks on #lowcarb/#keto folks. doi.org/10.1093/cdn/nz…
3/8 Our second paper brings a case report on a single #LMHR with extremely high #LDLc (~500 mg/dL) for 2.5 years, their eating patterns, and current CT angiography.
(⚠️Please note this is a single case report and should be considered anecdotal, ofc) doi.org/10.3389/fendo.…
(⚠️Please note this is a single case report and should be considered anecdotal, ofc) doi.org/10.3389/fendo.…
🧵 New paper on comparing advanced lipid testing (NMR) with body fat (adiposity) - ht @nicknorwitz
High adiposity associates with:
- ⬆️ #ApoB & #LDL-C
- ⬆️ #triglycerides
- ⬆️ levels of all fatty acids
How does this relate to #LEM? Let's unpack... /1
nature.com/articles/s4385…
High adiposity associates with:
- ⬆️ #ApoB & #LDL-C
- ⬆️ #triglycerides
- ⬆️ levels of all fatty acids
How does this relate to #LEM? Let's unpack... /1
nature.com/articles/s4385…
2/ "Adiposity-related hypertriglyceridemia is mainly driven by increased numbers of triglyceride-rich VLDLs (which carry the largest proportion of triglycerides in blood). Concurrently, the cholesterol in these lipoproteins also seem to be higher at higher adiposity levels."
3/ And these next sentences are key -- take special note of the underlined text...
If I went #vegan #keto for 3 weeks, do you think I’d still be #LMHR? @realDaveFeldman @siobhan_huggins @drscottyk @AlbertSyMD
1/ Okay, I'm putting a bow on this. And, short answer is... yes, the 37% have it. You can be on a 0 cholesterol #vegan #ketogenic diet and be #LMHR. Now for a debrief with some reflections. @realDaveFeldman @AlbertSyMD @siobhan_huggins @drscottyk ...
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
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
1/3 Okay, here's my daily breakdown for the #IsItSaturatedFat Experiment.
I'm going to consume 1,000 calories for @KerrygoldUSA! 🧈🧈🧈
That's 140g of butter per day!
I'm going to consume 1,000 calories for @KerrygoldUSA! 🧈🧈🧈
That's 140g of butter per day!
2/3 However, I'll be likewise supplementing 728 calories from dextrose, thus consuming much of my remaining dietary energy from carbs.
Per the #LEM, I believe this will have a substantial lowering impact on my LDL-C relative to the increasing influence via ⬇️LDLr of butter
Per the #LEM, I believe this will have a substantial lowering impact on my LDL-C relative to the increasing influence via ⬇️LDLr of butter
3/3 Note I'm performing this experiment in the spirit of both learning and keeping it fun. ☮️
While I'll concede I might have been caught off guard for a moment yesterday, I'm now thankful this can provide us a new opportunity for discovery and furthering the discussion. 🔬🔬🔬
While I'll concede I might have been caught off guard for a moment yesterday, I'm now thankful this can provide us a new opportunity for discovery and furthering the discussion. 🔬🔬🔬
1/ 🚨New N=1 Experiment: #IsItSaturatedFat🚨
🙏retweet🙏
Yes, I'm doing a new N=1 -- and it's going to be a biggie!
My good friend and colleague, @DrNadolsky completed his recent #MakingLMHR experiment concluding the added 2 sticks of butter as the reason for his LDL increase.
🙏retweet🙏
Yes, I'm doing a new N=1 -- and it's going to be a biggie!
My good friend and colleague, @DrNadolsky completed his recent #MakingLMHR experiment concluding the added 2 sticks of butter as the reason for his LDL increase.
2/ He's already conceded he's left out all the context on aiming for #LMHR profile, the relevance of RER, and the #LEM (so no need for people to keep pinging me on the IG video). I've chatted with him privately and we'll leave it at that. 👍
3/ However -- this actually affords us a huge new opportunity.
@DrNadolsky's claim isn't just his own, it's just about everyone else's outside the low carb community.
Simply stated: high #LDL #cholesterol seen in #LMHRs is predominantly due to high consumption of saturated fat.
@DrNadolsky's claim isn't just his own, it's just about everyone else's outside the low carb community.
Simply stated: high #LDL #cholesterol seen in #LMHRs is predominantly due to high consumption of saturated fat.
1/ I want to give huge props to @DrNadolsky for doing this #MakingLMHR experiment!
Yes, I know some of my followers may be blocked -- so I'm including an image as well.
If you're interested in how this experiment came about -- read on... 🧵
Yes, I know some of my followers may be blocked -- so I'm including an image as well.
If you're interested in how this experiment came about -- read on... 🧵
2/ We've had an ongoing debate on how much (or little) #saturated fat consumption is responsible for high #LDL #cholesterol levels we typically see for #LMHRs.
Whereas I (we) believe #LEM to have greater relevance overall.
Which led to the experiment👇
Whereas I (we) believe #LEM to have greater relevance overall.
Which led to the experiment👇
3/ Could @DrNadolsky emulate the #LMHR phenotype while *not* being fat adapted? (or at least, to get his #LDL #cholesterol that high?)
He consumed two sticks of butter a day to test this! 🧈🧈
Yes, the experiment went more toward my prediction, so alas, I won't be flying there.
He consumed two sticks of butter a day to test this! 🧈🧈
Yes, the experiment went more toward my prediction, so alas, I won't be flying there.
🚨 #LeanMassHyperResponder lowers LDL 🚨
#LEM #LMHR
1/ First off, this thread is long with lots of nuance.
But here’s the bottom line:
👉 I dropped my #LDL by over 400 mg/dL
👉 Previously ~500
👉 Now it is under 100
(Yes, you read that correctly)
Here’s how I did it…
#LEM #LMHR
1/ First off, this thread is long with lots of nuance.
But here’s the bottom line:
👉 I dropped my #LDL by over 400 mg/dL
👉 Previously ~500
👉 Now it is under 100
(Yes, you read that correctly)
Here’s how I did it…
2/ The method was quite simple:
Add in some carbs.
This shouldn’t be a news flash for anyone following our work on the Lipid Energy Model
We published on this intervention with the #LMHRpaper case series here: doi.org/10.1093/cdn/nz…
Add in some carbs.
This shouldn’t be a news flash for anyone following our work on the Lipid Energy Model
We published on this intervention with the #LMHRpaper case series here: doi.org/10.1093/cdn/nz…
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
1/ It begins...
Naturally, the #LEM would be a bit suggestive of this outcome where a diet is mid to moderately higher carb for this context.
Low TG typical of metabolic health.
Lower turnover of VLDL-TG = lower total cholesterol, lower LDL cholesterol, and lower HDL...
Naturally, the #LEM would be a bit suggestive of this outcome where a diet is mid to moderately higher carb for this context.
Low TG typical of metabolic health.
Lower turnover of VLDL-TG = lower total cholesterol, lower LDL cholesterol, and lower HDL...
2/ If replacing M/PUFA with SFA but keeping all else equal (including -- importantly -- carbs) for this exact context, this might have a marginal impact on TC/LDL/HDL. But would it command a higher magnitude of increase? I'd be doubtful...
However, if replacing carbs with fat...
However, if replacing carbs with fat...
3/ ... Thus going lower carb, we get closer to the model around LEM and its explanation regarding TC/LDL-C/HDL-C changes toward the outcome magnitude of the LMHR phenotype.
Hence the value of looking to RER for this experiment to confirm/disconfirm fat-adaptation.
Hence the value of looking to RER for this experiment to confirm/disconfirm fat-adaptation.
1/5 This is BIG & I've really been looking forward to it. @DrNadolsky will be looking to see if he can reach a #LMHR phenotype while not being low carb or keto (or at a minimum, increase LDL-C to 200)
In short, can high consumption of saturated fat w/o being fat-adapted = #LMHR?
In short, can high consumption of saturated fat w/o being fat-adapted = #LMHR?
2/5 There's a bit of back-and-forth that originated this experiment which you can read about here 👇
And yes, this could literally result in my flying to him to confirm results directly with advanced bloodwork & RER (Respiratory Exchange Ratio)
And yes, this could literally result in my flying to him to confirm results directly with advanced bloodwork & RER (Respiratory Exchange Ratio)
3/5 But more importantly, this gets to a very common assumption regarding #LMHRs -- that their phenotype can be mostly explained by higher consumption of saturated fat.
1/ I'd love to take an opportunity to expand on this important topic, and if I may, suggest something important to watch for with some newly emerging data.
To @MichaelMindrum point, I too believe the #ApoB will demonstrate higher association with #ASCVD than #LDL #Cholesterol..
To @MichaelMindrum point, I too believe the #ApoB will demonstrate higher association with #ASCVD than #LDL #Cholesterol..
2/ But to be sure, ApoB can be best represented as:
(1) Non-LDL ApoB lipoproteins
- and -
(2) LDL ApoB lipoproteins
The first category is predominantly chylomicrons, VLDL, and IDL -- which associate very highly with ASCVD.
(1) Non-LDL ApoB lipoproteins
- and -
(2) LDL ApoB lipoproteins
The first category is predominantly chylomicrons, VLDL, and IDL -- which associate very highly with ASCVD.
3/ You can think of category (1) as "Triglyceride Rich Lipoproteins" (TRL, aka "remnants") and category (2) as "Triglyceride Poor Lipoproteins" (TPL)
The population of #LMHRs have extremely high levels of ApoB. But this pattern is a mix of very *low* TRL and very high TPL.
The population of #LMHRs have extremely high levels of ApoB. But this pattern is a mix of very *low* TRL and very high TPL.
Design a VLC diet that is low in fiber with the goal toward reaching a low respiratory exchange ratio on a cohort of lean, fit athletes (but no other exercise confounding like resistance training or diet confounding like meds/sups, etc).
I’d likewise bet big majority = #LMHRs
I’d likewise bet big majority = #LMHRs
Full disclosure - @DrNadolsky and I took to some of this discussion via direct texting. However, it did lead me to a good question that I decided to turn into a poll out of curiosity...
1/2 Another great prop bet @DrNadolsky and I were discussing:
He proposed he could emulate the #LMHR phenotype by consuming a lot of butter and coconut oil while not keto and fat-adapted (thus, high RER). I'd predict the opposite.
He proposed he could emulate the #LMHR phenotype by consuming a lot of butter and coconut oil while not keto and fat-adapted (thus, high RER). I'd predict the opposite.
1/ Two weeks ago we released our paper on the #LipidEnergyModel (#LEM) along with our video abstract for it. I'm pleased to say it has led to many great connections and expanded discussion.
I'm going to recap on a lot of these in this thread. 🧵 ...
I'm going to recap on a lot of these in this thread. 🧵 ...
2/ First and foremost, thanks to everyone for their extraordinary support in retweeting our announcement, sharing our paper, and letting researchers know of this model.
3/ As we state many times (including within the video abstract), this model doesn't describe all possible influences on cholesterol levels. For example, other things can impact LDL-C such as M/PUFA-to-saturated fat composition, fiber, genetics, medication, etc.
WOW! >300 retweets in first 24 hours!
1/ Now for a thread from the first author on the #LEM Paper:
👉What it IS
👉What it ISN'T
👉👉and What's NEXT...
doi.org/10.3390/metabo…
Read on... @realDaveFeldman
1/ Now for a thread from the first author on the #LEM Paper:
👉What it IS
👉What it ISN'T
👉👉and What's NEXT...
doi.org/10.3390/metabo…
Read on... @realDaveFeldman
2/ What it IS:
We provide the first description of the long-awaited #LEM hypothesis, a model that attempts to explain:
(i) the inverse association between BMI and LDL-C on #lowcarb diets
(ii) the #LMHR phenotype, in which lean people on low carb exhibit very ⬆️LDL-C⬆️HDL-C⬇️TG
We provide the first description of the long-awaited #LEM hypothesis, a model that attempts to explain:
(i) the inverse association between BMI and LDL-C on #lowcarb diets
(ii) the #LMHR phenotype, in which lean people on low carb exhibit very ⬆️LDL-C⬆️HDL-C⬇️TG
3/ These phenomena, presently, have no complete competing explanation:
If effect were purely genetic, the🧬s would need 2explain:
>how macronutrient change can alter, not just LDL-C, but HDL-C+TG as part of a triad
>correlation between BMI and lipid changes
That's a tall order
If effect were purely genetic, the🧬s would need 2explain:
>how macronutrient change can alter, not just LDL-C, but HDL-C+TG as part of a triad
>correlation between BMI and lipid changes
That's a tall order
1/4 Retweeting via @Lpa_Doc -- click within to read 3 part thread. 👇
Also, per our video abstract:
"We remind viewers that existing guidelines and every major scientific institution around heart disease strongly advises against high cholesterol levels."
Also, per our video abstract:
"We remind viewers that existing guidelines and every major scientific institution around heart disease strongly advises against high cholesterol levels."
2/4 And,"While these data on our patient are comprehensive and provide potential new insights, they are limited in scope and timespan. It’s certainly possible this patient is an outlier, or that their progression of plaque will take place later, or many other such possibilities."
3/4 In short, while we appreciate the opportunity to explore the Lipid Energy Model (#LEM paper forthcoming) and share novel data (such as this case study), we continue to emphasize this is uncharted territory and largely considered substantially risky within Lipidology.
1/ Reminder: I realize it’s the single hardest concept to get across, but for all these years I have and continue to suggest there’s a crucial case of lipoprotein profiles as often more a reflection of disease than the independent drivers of it. (ie — from 2018 re general👇)
2/ For example, I certainly know so much more on the workings of #LEM* than when I tweeted this from 2018, but does the foundation still hold up… do I think this is more relevant or less? Definitely more!
(*Obligatory mention of @nicknorwitz here and others re coming paper!)
(*Obligatory mention of @nicknorwitz here and others re coming paper!)
3/ The bottom line is that while the independent causal role of lipoproteins (whether LDLp, sdLDL, oxLDL, glLDL, etc) are well worth examining. We should likewise investigate how *both* lipid profiles and CVD can be downstream of poor lipid metabolism.
1/ It's been quite a week on Twitter regarding #lowcarb and LDL
I have been on the fence about weighing in, not wanting to add to the dog pile, but decided 2drop my thoughts in this thread
If u don't have time to READ THE WHOLE THING IN CONEXT, ignore& consider me🪰 on the wall
I have been on the fence about weighing in, not wanting to add to the dog pile, but decided 2drop my thoughts in this thread
If u don't have time to READ THE WHOLE THING IN CONEXT, ignore& consider me🪰 on the wall
2/ I'll first address @deirdre_tobias analysis of LDL and all cause mortality. With the caveats that I'm not an epidemiologist &hope to have more insightful questions when time passes and the dust settles, I am not in disagreement w/ the main results: high LDL associated with ACM
3/ That's actually old news, isn't it?Not so say that the analysis doesn't bring something to the table, but on a population level v high LDL levels (will get to low LDL in a minute) are generally undesirable. Thus, all things being =, a conservative gambler would pick low-is LDL
1/ Yes -- if you're curious as to why @nicknorwitz and I are chatting so often about ANGPTLs, it's worth working our way backwards...
If you're powered by fat, your tissues are getting it from free fatty acids or triglycerides (which is really three FAs bundled together)...
If you're powered by fat, your tissues are getting it from free fatty acids or triglycerides (which is really three FAs bundled together)...
2/ Recently I was much more focused on fasting (see ) and lipoprotein lipase (LPL) dynamics (see )
3/ And indeed, the regulatory strings behind LPL up and down regulation is a much bigger part of the story with regard to VLDL turnover -- and thus potential resulting effects on LDL-C, HDL-C, and Triglycerides (TG).
1/ As a #LMHR and close colleague of @DaveKeto I feel compelled to jump in here and clarify my own stance on LDLp and ASCVD risk because I feel that our positions are usually misrepresented by others. Here we go…
2/ To cut to the chase, outside the low-carb lipid triad of high LDL and High HDL and low TG, I would absolutely personally consider elevated LDLp an issue. Where I to have high LDL and atherogenic dyslipidemia I would both take an LDL lowering med and, more importantly IMO…
3/ change my lifestyle to improve the atherogenic dyslipedmia. Personally I do have concerns about longterm safety use of statins specifically and would preference Zetia/PCSK9i. But that’s besides the point. I won’t speak for @DaveKeto but for my part the LMHR phenomenon & LEM…
1/ New #LipidEnergyModel video on ANGPTL proteins via @nicknorwitz
And a few added thoughts...
ANGPTLs are *all* inhibitors. They are applying the breaks to the Lipoprotein Lipase (LPL) in particular.
So consider this analogy...
And a few added thoughts...
ANGPTLs are *all* inhibitors. They are applying the breaks to the Lipoprotein Lipase (LPL) in particular.
So consider this analogy...
2/ Imagine a room full of people at tables being served with trays of food regularly coming from the kitchen moved around the room by waiters.
No one is particularly famished, but they aren't especially full either, so they are absently taking food off the trays to maintain...
No one is particularly famished, but they aren't especially full either, so they are absently taking food off the trays to maintain...
3/ However, a few guests at one table leave to get some exercise and return quit hungry.
And here's the catch: You can't tell specific people to do specific things (including the waiters), but you can say things to the entire room. Is there a way to solve this puzzle?
And here's the catch: You can't tell specific people to do specific things (including the waiters), but you can say things to the entire room. Is there a way to solve this puzzle?
