Recently, Mark Lightell, a 29-year-old endurance athlete, took it upon himself to try to convert to the LMHR phenotype with a two-week n=1 experiment. You can find Mark’s post about this experience here. Mark and Dave invited me to do a little commentary on Mark’s experiment. Here it goes…
First, I want to reinforce my respect for Mark’s scientific curiosity. As I wrote in my closing note to Mark’s post, “[T]he fact that Mark’s personal hypothesis leans towards isolated high LDL-C being sufficient to drive atherosclerosis (and, thus, less in line so with some in the LMHR community) does not preclude him from sharing a genuinely scientific interest in the LMHR phenomenon, nor should it. This n =1 experience is a testament to how those with different hypotheses can share scientific curiosity and collaborate in genuine attempts at pursuing scientific truth.” In fewer words, “GO Mark!”
With that, some thoughts…
Mark’s hypothesis was that “adherence to a very low carb ketogenic diet will produce a LMHR profile within a timespan of 2 weeks.” While the half-life of LDL particles would suggest a full conversion to the LMHR phenotype (LDL-C ≥ 200, HDL-C ≥ 80, and TG ≤ 70 mg/dL) could be possible in two weeks, I think it’s first important to consider the impact and timeframe of fat-adaptation.
The Lipid Energy Model (manuscript for publication in production) proposes that the high LDL-C observed in LMHR is driven by dependence on fat as fuel and on the LPL-mediated turnover of hepatically secreted VLDL. That’s a jargony way of stating that the LMHR phenotype is most likely to be exhibited in those who are fully fat adapted.
While Mark’s endurance exercise regimen suggests that his body should be good at oxidizing fat at baseline, the fact that his body was completely naive to carbohydrate restriction also means he probably did not achieve full fat adaptation within 14 days of starting a ketogenic diet. Of course, he did see a trend towards the LMHR phenotype (a doubling of LDL-C from 68 to 139 mg/dL) consistent with what the LEM would predict in an individual who is in the process of fat adapting, and upregulating VLDL secretion and peripheral turnover.
There are, of course, other explanations. For instance, synthesis of ApoB could have been rate-limiting, creating a metabolic bottle neck for the repackaging and export of non-esterified fatty acids upon VLDL, to be converted into LDL by LPL. Again, this is a jargony way of stating, metabolic change takes time, and I’m not sure one should expect full conversion to LMHR in two weeks.
Vegan Diet Baseline
The choice of both the baseline diet and the ketogenic diet were interesting. With respect to the baseline diet, it was Mark’s choice to consume a vegan diet to lower his LDL-C as much as possible as a run-in phase, although he doesn’t regularly consume a vegan diet. As he has disclosed, his normal resting LDL-C on a mixed macronutrient diet rests at ~130 mg/dL. Thus, the transformation observed in his experiment could be interpreted as a reversion to his personal baseline.
It is pertinent to contrast this scenario (vegan diet to keto-carnivore diet) against much of the current LMHR community who have converted to the phenotype from a standard mixed diet after changing to many forms of ketogenic diets (standard to ketogenic). In other words, in this case, we can’t distinguish between the putative contributions of the ketogenic diet raising the LDL-C or the vegan diet lowering it. That evidently creates a major confound in data interpretation that is important to highlight.
As I was not consulted on the formulation of the baseline diet, neither was I consulted on the formulation of the on the ketogenic diet. Mark’s ketogenic diet reflected Dave’s standard diet and included Colby Jack Cheese, Beef Franks, Hard boiled eggs, Diet Coke, with the addition of uncured bacon… for variety (that’s a laugh line folks). Mark explains that he “found the diet intolerable” and “had a miserable time.” All I have to say to that is, I probably would have reacted the same way.
Quickly, for those of you who don’t know, Dave and I are quite close and I love him like a brother. So, what I say next is written with a comedic tone (but with honesty): Dave’s diet makes me sad. Sometimes, after a nice dinner of smoked salmon with capers, roasted garlic, buffalo mozzarella and extra virgin olive oil, and dark chocolate with coconut manna for dessert, Dave and I will get on a Zoom call and I’ll see him munching on a piece of string cheese with a Diet Coke and my tongue will cry a little for him.
Point being, I don’t blame Mark for quitting the Dave diet after two weeks, especially when his gut had recently been adapting to veganism. (Talk about a shock to the microbiome! – It’s like tossing a giraffe into the arctic). The fact that he lasted two weeks is a testament to his strength. But the more serious point I want to make is that Dave’s diet is not necessary or typical of LMHR. You can be an LMHR while eating vegetables or without eating meat or eggs.
So, to Mark: I’m sorry.
To Dave: You and I need to have a little chat about both your diet and – more pressingly – sleeping habits.
And to readers: We will shortly have for you a rather striking demonstration of how the LMHR phenotype can occur in the context of a low-saturated fat ketogenic diet. Let’s put a pin in that…
“Picking up the torch”
In his post, Mark expresses a desire for someone to “pick up the torch” and replicate his attempt to prospectively convert to LMHR, albeit over a greater time frame. I can here confirm that is being done. We have another community member who has self-selected to attempt to convert to LMHR over the next couple of months. Like Mark, she’s young, athletic, and by all measures metabolically fit with a baseline LDL-C on a mixed diet (not vegan) of 50 – 79 mg/dL. (Some other markers: HDL-C 73 mg/dL, TG 50 mg/dL, HbA1c 4.8%, insulin 4.9 uIU/L, BMI 24 kg/m2.) I think we will all be interested to see what happens.
Of course, these n = 1, while prospective, are not properly designed clinical trials. Hopefully, we will acquire the partnerships and resources to conduct these after publication of the Lipid Energy Model manuscript. Already, I’m noting more serious researchers within academia approaching us about this work. The ball is starting to pick up steam…
But, circling back to the point I made above, the most notable thing to me about individuals like Mark and our anonymous second subject is that their self-directed efforts represent an interest in a scientific curiosity (the LMHR phenotype) sufficient in magnitude to compel them to put their tongues, guts, and bodies on the line to pursue science. If that’s not being a citizen scientist, I don’t know what is.
Other Lab Abnormalities
As a final comment, Marks labs were also notable for several abnormalities, including but limited to leukopenia (WBC 2.2 – 3.0 x10e3/uL) and elevated bilirubin throughout the vegan and keto-carnivore stages, and thrombocytopenia while vegan (PLT 127 x10e3/uL). These abnormalities were largely pre-existing and we have reinforced his doctor position that he pursue a hematology consult. It’s important to acknowledge these other abnormalities, not only for their potential interaction with the results, but also to strongly caution others against embarking on dramatic lifestyle changes without professional consultation when one is aware of pre-existing conditions, especially dietary changes that may exacerbate pre-existing nutrient deficiencies.
Note from Dave: I laughed out loud when I read Nick’s comment above, “Dave’s diet makes me sad.” To be sure, Nick, that’s not actually my normal diet at all. The “baseline diet” is strictly for experiments and doesn’t include Diet Coke and bacon. But the three baseline components (+ vitamins & electrolytes) were selected against many criteria that includes availability and consistency when traveling, avoidance of preparation and/or cooking oils that could be confounding, and zero fiber – to name just a few. I wanted to get as few components as possible to achieve this baseline, and that’s where I landed. In short, it’s my version of a “ketovore chow” that has been very successful for replication of baseline bloodwork as well (such as with OxLDL Replication Experiment). We can discuss more in depth when we do a podcast on this experiment — should be fun! 😉
Note from Dave: Mark Lightell is actually a frequent commenter at the LMHR Facebook group, but he is notably an advocate for reduction of LDL cholesterol and ApoB, and a firm believer in the Lipid Heart Hypothesis. However, he’s also interested in our work and saw a clear opportunity to make a contribution with this experiment. I think you’ll find this guest post on his experiment very interesting. Also, see Nick’s companion analysis for this experiment, and our added note at the end.
Vegan Diet vs Keto/Carnivore Diet – My Attempt to Create a LMHR
The LMHR phenotype paper by Nick Norwitz, Dave Feldman, and colleagues suggests that LMHRs, rather than being a genetic anomaly, may be a reproducible metabolic phenomenon. If this is true, it should be possible to recreate this LMHR lipid profile in most people who are metabolically healthy (low TG/HDL ratio) and lean, and in whom dietary energy is derived primarily from fat with minimal carbohydrate intake. Due to LDL particles having a half-life of 3 days, I further expect the LMHR phenotype could be seen over the course of 2 weeks.
In people who are lean, metabolically healthy (exhibiting a low TG/HDL-C ratio), and with lower BMI, adherence to a very low carb ketogenic dietwill produce a LMHR lipid profile within a timespan of 2 weeks.
I fit these criteria, with the added benefit of having a high energy demand due to my daily exercise (50+ miles of running per week). According to the Lipid Energy Model, proposed to mechanistically explain the phenotype, this should amplify the effect due to my body requiring a greater volume of lipoproteins (LDL) to traffic triglycerides for energy. I’ve never done a low carb diet, but given that I should be the ideal candidate for this effect, I decided to give it my best shot.
General Health and Physical Fitness
I’m a 29 year old endurance athlete, 5′ 9″ with lifelong weight around 130-135 lbs. I’m in good health with no known medical conditions. I take no medications or supplements. My most recent race (January 2022) was a 10k in 40:11 (~6:28 min/mile pace).
Step 1: Reduce LDL-C as low as possible with a carb-based Vegan diet.
Step 2: Immediately switch to a 2 week Keto-carnivore diet to maximally increase LDL-C.
3 weekly lab draws as follows: March 3 (Vegan), March 10 (Keto), March 17 (Keto).
Lab draws will be ~14 hours water fasted.
All food weighed via food scale.
Maintain aerobic training (50+ miles per week).
In case you’re pressed for time, here’s the summary:
Over the two week experiment my LDL-C increased over 2-fold, albeit not quite to the LMHR LDL-C threshold of 200. Specifically, my LDL-C increased from 68 to 139, which suggests to me that it is very much possible to induce the LMHR metabolic phenomenon, but that 2 weeks is not a sufficient time frame. I suspect 3-4 weeks would have shown LDL-C of 200 or more.
Main Lab Results
Lab changes greater than 20% are shaded gray
Sample Meals & Daily Routine
I wanted to begin the experiment by establishing a low baseline LDL-C. After the conclusion of my December 2021 Vegetarian experiment (where I brought LDL-C down to 64) I was enjoying the freedom of “no diet,” eating frequently at restaurants. I’ve always been weight stable so it wasn’t that I had gained weight, but rather that it was extremely likely my LDL-C was far above the 64 I got in December.
So starting February 5, 2022 I began the work to reduce my LDL-C. I went back to my proven Vegetarian diet, but was tempted with ideas to achieve an even lower LDL-C than last time, so I changed it to a Vegan diet. I removed animal products, got dietary cholesterol down to 0mg, reduced saturated fat as much as possible, while maximizing PUFA intake via walnuts, and increasing fiber.
At the time, I thought the PUFA-to-saturated fat ratio was key to getting my LDL-C even lower, ideally to 50s. I had promising results going from a 3:1 to a 6:1 PUFA-to-saturated fat ratio during my December 2021 Vegetarian experiment, so naturally I thought increasing the ratio to 9:1 would produce an even greater effect.
Week 1 – Vegan Routine
Two meals a day
Wake up at 11am
Breakfast of ~2800 calories. Finish breakfast by ~1pm
Go to work at 2pm
Lunch at 7pm, just Diet Coke or water
Get off work at 11pm
Run after work at ~11:30pm
After run, Dinner at ~1am, ~400 calories
I found this diet easily tolerable and enjoyable, even if fairly restrictive and mundane. I ended up running 52 miles this week, with total carbs averaging 418g/day.
So March 3, 2022 arrives and I have labs drawn.
Results: Week 1 – Vegan
Pft, 68?? Where’s my 50? I found this result disappointing, as I really thought my “improvements” would beat my last result of 64 from December 2021 to give me my lowest LDL-C yet. From this result I’ve concluded that the PUFA-to-saturated fat ratio is not as powerful as I thought for reducing LDL-C. While LDL-C did not behave as I predicted, it was not the goal of this experiment (just an “along the way” project).
It was time for the Keto/Carnivore arm of the experiment.
I tried Dave Feldman’s baseline diet of Colby jack cheese, beef franks, and hard boiled eggs but found the diet intolerable after 2 days, primarily due to the hard boiled eggs. So I switched to uncured bacon, Colby jack cheese, and diet coke for the remaining 5 days.
Week 2 – Keto/Carnivore Foods
Day 1 & 2: Colby Jack Cheese, Beef Franks, Hard boiled eggs, Diet Coke
Day 3 – 7: Uncured Bacon, Colby Jack Cheese, Diet Coke
Week 2 – Keto/Carnivore Routine
3 Meals a Day
Wake up at 11am
Breakfast of ~2000 calories. Finish breakfast by ~1pm
Go to work at 2pm
Lunch at 7pm, ~800 calories
Get off work at 11pm
Run after work at ~11:30pm
After run, Dinner at ~1am, ~600 calories
The switch to bacon had a promising start but eventually became difficult to tolerate, which is to be expected after consuming 12 packs of bacon in 5 days. I managed to stick with it until the first Keto lab draw. I ended up running 74 miles this week, with total carbs averaging 5g/day.
LDL-C increased an additional 54% in 7 days.(104% increase over 2 weeks.)
Better, but at the start of this I fully believed it was going to be a slam dunk of an experiment with LDL 200+. Instead, what I feared most ended up happening: A middling result that effectively demands a longer experiment. What would have happened in just one more week? I was this close to finding out, but wow was this diet difficult and absolutely unenjoyable. Maximal carb elimination made the diet so restrictive to the point that I could not continue it past 2 weeks. I had so much drive and motivation at the start, but that was largely sapped from me on this diet. Food became a chore that gave me no enjoyment, I was not hungry most of the time, and generally did not feel great. It was made worse by the fact that, given my activity levels, I needed to consume ~3400+ calories per day of food that I did not care for just to maintain my weight.
All that to say: Yes I had a miserable time, and yes I fell short of my goal to create LMHR lipids at will, but I’m still glad I did it. Now hopefully someone else can take the torch and try for 3-4 weeks to see what would have happened.
Why did you do this experiment in the first place?
I find lipids and biomarkers pretty fascinating. Especially the nature of LDL and its function in the body. I know it’s a controversial topic, so to clarify my position I will say that I’m convinced of LDL/apoB being causal in cardiovascular disease. My main interest is the quantification of that risk.
If LDL/apoB is the only risk factor, what is the risk forsomeone like me? An athlete with high HDL, low triglycerides, and low body fat, but on an “anything goes” diet of restaurant food my LDL-C will rest at around ~130. How much risk do I have between 68 and 130? I don’t think anyone has an answer to that, other than the basic binary answer of “yes it’s more atherogenic”. I think it matters if we’re talking months to a year vs years to a decade+ in life expectancy. Some people may be willing to make that trade of not having to limit their food choices for a lifetime if the cost is “minimal” with regard to elevated LDL/apoB.
That’s why I find Dave Feldman’s research into this topic interesting, because he is essentially exploring a niche where increases in LDL may not be a pathological response, but rather a benign adaptive one. While I would like for that to be the case, I’m also aware that the preponderance of evidence we currently have is stacked against that idea, but that doesn’t mean it’s not an idea worth exploring. If it did end up being true, it would be a fascinating discovery if only because literally, “how does that work?”. And for those of us in good health with high HDL and low triglycerides, where elevated LDL/apoB is our only risk factor, we would no longer have to limit food choices to keep this marker within range.
In summary, I think there is something interesting happening here with this massive increase in LDL, and this was my attempt at adding my piece to the puzzle.
hsCRP – Increased to 1.45 on Keto/Carnivore, compared to my baseline in the 0.17-0.39 range. I think it’s interesting how my hsCRP perfectly matches how unwell I felt without carbs.
Platelets – Arguably the most unusual result. Platelets were below ref range (common for me) in Week 1 – Vegan and Week 2 – Keto. Only Week 3 – Keto showed normal platelets.
HDL-P – Increased to the 35.9umol/L on Week 3 – Keto/Carnivore, which is the highest it’s ever been. I’m usually quite low in HDL-P, even when I’ve had 92 HDL-C.
Bilirubin – Decreased linearly with the duration of the keto diet. Bilirubin went from my normal of 3.2 down to 1.7 by Week 3 – Keto, which is the lowest I’ve ever seen it.
Resting HR – The Keto/Carnivore diet resulted in a higher resting HR. At first I thought it was because I went from 50 to 70 miles in one week, but my HR was at its highest after reducing my mileage down to 50 in the final week of the experiment, so this is clearly an effect from diet and not training load.
Insulin – This behaved as expected. Insulin was already low on a carb-based diet, and went even lower on a Keto diet.
Note from Nick: I want to begin my concluding remark by repeating two quotes from Mark: (i) “I find lipids and biomarkers pretty fascinating,” and (ii) “If LDL/apoB is the only risk factor, what is the risk for someone like me?” These quotes represent questions I and other LMHR ask themselves every day. Notably, the fact that Mark’s personal hypothesis leans towards isolated high LDL-C being sufficient to drive atherosclerosis (and, thus, less in line so with some in the LMHR community) does not preclude him from sharing a genuinely scientific interest in the LMHR phenomenon, nor should it. This n=1 experience is a testament to how those with different hypotheses can share scientific curiosity and collaborate in genuine attempts at pursuing scientific truth. For more thoughts, read my commentary here.
Note from Dave: this guest post from Nick Norwitz discusses our #LMHRpaper, which as of today, is now finalized. Thanks again to the many wonderful readers who contributed their efforts in our final edit.
The final version of the Lean Mass Hyper-Responder (LMHR) paper was just released!
I’m pleased to report that, even in the early days since the initial release of the unedited accepted manuscript (on November 30, 2021), this paper has stimulated vigorous discussion, risen to the top of its journal for all time reads, and is among the top 15 trending papers across all American Society of Nutrition associated journals for the year 2021. So, what’s all the fuss about? This blog is intended to get you up to speed so you can be part of the discussion and follow this exciting line of biomedical research as the conversation continues to heat up.
But the elevations in LDL exhibited by these lean persons on low-carb diets had two peculiar features that set it apart from other forms of high LDL.
Extreme LDL Increases
First, the LDL increases were much larger than those typically associated with living an unhealthy lifestyle. When most doctors think about high LDL related to being unhealthy and eating a poor diet, they think about levels in the high 100s. But lean people on carbohydrate-restricted diets were anecdotally observing LDL levels of 200, 300, 400, and even 500 mg/dL or more.
In fact, some LMHRs exhibit LDL levels as high as persons with homozygous familial hypercholesterolemia, a rare and devastating genetic condition (1 in 1,000,000) that likewise associates with very early heart disease.
Very High HDL and Very Low Triglycerides
Second, when lean people do see increases in LDL on a carbohydrate-restricted diets, they tend to be accompanied by high HDL (so-called “good cholesterol”) and low triglycerides (TG), fat in the blood. This pattern of high HDL and low TG is exactly opposite the profile of “atherogenic dyslipidemia,” which is defined by low HDL and high TG, and is, at present, the predominant risk factor for cardiovascular disease (Libby, 2021).
Simply put, when lean people on low-carbohydrate diets saw increases in LDL they were quite often in the context of otherwise excellent metabolic health markers. Therefore, Dave created a set of three cut points that combine to define what would become the LMHR phenotype:
LDL cholesterol ≥ 200 mg/dL
HDL cholesterol ≥ 80 mg/dL
TG cholesterol ≤ 70 mg/dL
Now for a couple comments on the definition of LMHR. First, why these cut points? Well, in addition to approximating threshold levels Dave Feldman was empirically observing in the world around him for lean athletic people who went low-carb, these triad of cut-points were chosen for just how extreme they are.
To meet someone with LDL ≥ 200 is rare. To meet someone with HDL ≥ 80 is rare, and to meet someone with TG ≤ 70 is rare. Thus, the probability of meeting someone who meets all the cut points by chance is highly unlikely. Otherwise put, if someone presents with this triad, it seems reasonable to hypothesize that the markers are associated with each other.
Other important point is that LMHR are only defined by this triad, and NOT by any measure of leanness. This is confusing because “lean” is in the name of the phenotype, but that’s only because the triad – at least in Dave’s point of view in 2017 – tended to occur in people who were lean and athletic. In other words, the name LMHR is the hypothesis – that this triad present in lean people who go low-carb.
Study Suggests that LMHR Exist!
Being Leaner & Having Lower TG/HDL Predicts Larger LDL Increases on a Low-Carb Diet
It was a long time coming, but we finally put that hypothesis to the test in a scientific study.
In this new study, published in Current Developments in Nutrition, we collected survey data from people who were low-carb, who were not on statins, and who had lipid data from before they started their low-carb diet as well as recent lipid data from on their lowcarb diet.
Then, rather than massaging the numbers to conform to our hypothesis, we engaged in a “hypothesis-naïve exploratory analysis” in which we took all the data we had on respondents — including age, sex, BMI, and current and pre-low carb LDL, HDL, and TG levels — and asked a computer to tell us which factors were most strongly and reliably associated with increases in LDL after starting a low-carb diet.
The results were clear. No matter how we approached the question (be it multivariate linear regressions or hypothesis-naïve computer-generated decision trees [Supplemental Figure 3]) we found that having lower BMI and a lower TG/HDL ratio associated with larger increases in LDL.
The relationship can be clearly seen in the bar graph below. The further you go to the left, the lower the BMI. The further you go to the back, the lower the pre-diet TG/HDL ratio. And the height of the bar is the median increase in LDL.
Picking out the LMHR
After establishing that those who are leaner with lower TG/HDL ratios exhibited larger increases in LDL with carbohydrate restriction, it made sense to try to separate the true LMHR (those who met all three cut-points) from the larger cohort and see how different they really were…
Of the 548 participants that met the inclusion criteria, 100 were bona fide LMHR (which is a lot, considering many people don’t believe LMHR exist). And, true to their name, they were Lean!
The average BMI of a LMHR was 22.0, as compared to 24.6 for the rest of the low-carb sample in this study (between group p = 1.2×10-11). Furthermore, LMHR exhibited higher LDL, higher HDL, and lower TG, with mean values of 320, 99, and 47 mg/dL respectively.
And, importantly, LMHR did not differ in terms of their pre-diet LDL when compared to the non-LMHR population. In fact, median pre-diet LDL was 135 mg/dL in non-LMHR and 133 mg/dL in LMHR. No difference!
A LMHR Case Report Shows the Phenotype is Reversible
Now, you’ve probably sensed a lot of enthusiasm from me, but don’t mistake intellectual excitement about a fascinating observation for a suggestion that high LDL levels in LMHR are benign.
Setting my own hypotheses aside, we do not yet know if the risk associated with high LDL is any different in the context of LMHR as compared to any other context. And most experts would agree that high LDL is dangerous, regardless of cause.
Nevertheless, for the time being, many or most LMHR patients and their doctors are concerned about their high LDL. That said, many of those same people find a low-carb way of life to be tremendously beneficial for their various metabolic disorders. This begs the question, can you “fix” the LDL problem (perceived or true) through lifestyle? The answer, yes — at least partially.
As part of this study, we also wrote up a case series of five patients who were LMHR or borderline LMHR. These patients all exhibited extraordinary increases in LDL upon starting a ketogenic diet. And, importantly, all were tested for genetic mutations associated with high LDL and all tested negative, supporting the notion that being a LMHR is not a genetic condition but a metabolic phenomenon.
One patient saw his LDL increase from 116 to 665 mg/dL (no surprise, he was the leanest).
All of the patients refused, or were intolerant of, statins and instead opted to reintroduce a moderate amount of carbohydrate, ~50 – 100 grams, in order to transition from a very low-carb ketogenic diet to a diet that was still low-carb (<130 grams net carbs per day).
Impressively, all participants saw their LDL drop by at least 100 mg/dL, with larger drops occurring on those with high levels. The patient who saw his LDL increase to 665 mg/dL exhibited a 480 mg/dL drop in LDL by doing nothing more than adding about a small, sweet potato’s worth of carbs per day.
Stop and think about that for a second. In this context, a sweet potato per day could drop LDL by almost 500 mg/dL!
This is only step one, putting the LMHR phenomenon on the map. This paper suggests that LMHR are real and, if I do say so myself, really interesting!
In my opinion, no true student of health and/or medicine can observe this phenomenon and not be intrigued.
But what this paper does not do is explain the “how.” It likewise can’t evaluate the risk. Those are the subjects of upcoming projects.
We are working on formulating an official “Lipid Energy Model” manuscript, explaining the potential mechanisms at work behind the findings of this paper. And, a LMHR study also recently launched out of ULCA, courtesy of Dave’s efforts, that will track plaque progression in the coronary arteries of 100 LMHRs. This paper was just the first domino…
This paper describes a phenomenon. It does not explain the mechanism nor comment on risk.
Saturated fat intake was not measured; however, it seems highly unlikely variations in saturated fat intake can explain the findings as this would assume that, across the study sample of 548 people, lean people and those with good metabolic health preferentially and reliably consumed more saturated fat.
The phenomenon is likely metabolic, not genetic. This is supported by at least three lines of evidence in this study:
LMHR have normal pre-low carb LDL levels. In fact, in the study, pre-diet LDL levels were the same between LMHR and non-LMHR.
It’s been anecdotally observed that LMHR who gain weight exhibit drops in LDL, despite no change in their genetics.
Most importantly, genetic testing in the five patients in the case series were negative. Genetic testing performed on other subjects not reported in this study have also been negative.
Media and Podcasts Around the Paper
For a list of selected podcasts, videos, and media releases that cover this paper, please see the links below (Updated January 28, 2022):
We’ve been quite proud of how well we’ve set up efficient budgeting with our research partners for this important study. Lundquist and our bloodwork providers are providing strong discounts along with Keto Mojo and GB HealthWatch completely contributing their products and services.
Unfortunately, there’s one area of cost we don’t have much control over: travel and lodging.
Rising Costs for Travel, Participants
At the time we were building our projected expenses, it seemed likely we could negotiate packages between plane, car service, and hotel coming in around $250 combined per person, per trip. And to be fair, that was pretty realistic in December 2020 when travel industries were struggling, which was when we published this video.
There have been a handful of other expenses that were unanticipated. One of our bloodwork partners has required us to set up a specialized account for clinical trials that involves greater expense. Another overseas bloodwork partner needs samples shipped as frozen throughout the trip, which costs quite a bit. And we did add a $50 meal voucher per trip for participants as recommended strongly by our research partners to accommodate their stay.
All together, we believe we’ll need to raise an additional $97,000.
The good news is that our other venture, OwnYourLabs.com, has been accumulating proceeds throughout 2021 to contribute directly to the Citizen Science Foundation. I’m pleased to announce this totals $51,000, thus cutting the amount we need to raise to $46,000.
(And also, props to each and every one of you who bought your labs through OwnYourLabs.com as all of them contributed directly to this study!)
How You Can Help
There are three primary ways you can show your support:
Contribute directly to the Citizen Science Foundation. Again, we are a fully qualified, 501(c)(3) Public Charity. Naturally, this is the easiest and most direct way to help. The contribution is generally tax deductible – please talk to your tax preparer for more details. It’s worth noting we have a 0% admin overhead, save third party services (such as credit card processing).
Order your private bloodwork through OwnYourLabs.com. Proceeds are continuing to accumulate for further funding directly to the CSF to support this study. Moreover, if you opt in, you can further help citizen science by volunteering your anonymized data for a discount (see site for details).
Share, retweet, repost – spread the word! Obviously, the more you can help us let others know about this important cause, the better. 🙂
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