BREAKING: Our Paper on Low Carb, LDL Cholesterol, and the LMHR Phenotype is Now Available

Note from Dave: This is a guest post from Nick Norwitz on our just released LMHR paper. This post also has a live “Corrections / Clarifications” section (at bottom) which we’ll be updating as needed. We welcome and look forward to all constructive corrections and comments to our paper.

Four of my colleagues and I just published a paper in Current Developments in Nutrition on the Lean Mass Hyper-Responders (LMHR) phenotype.

https://doi.org/10.1093/cdn/nzab144

Now, if you’re familiar with the phrase “LMHR” – or if you are an LMHR yourself – then the findings of this paper will be akin to the statement “water is wet.” Nevertheless, the majority of people, including those in the medical community, are not aware of this fascinating metabolic phenomenon. That’s not a slight against anyone; it is simply the state of affairs.

So, let’s change that. What is a “Lean Mass Hyper Responder?”

Lean Mass Hyper Responders, a History

In 2017, a software engineer, Dave Feldman, made a curious observation: the people who adopted carbohydrate restricted diets who typically exhibited the most pronounced increases of LDL cholesterol (so-called “bad cholesterol”) were often very lean and/or athletic.

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 very high HDL (so-called “good cholesterol”) and very 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:

  1. LDL cholesterol ≥ 200 mg/dL
  2. HDL cholesterol ≥ 80 mg/dL
  3. TG cholesterol ≤ 70 mg/dL

Now, before moving on I want to emphasize that the definition of LMHR is based on these three thresholds and NOT on any measure of leanness or BMI. The word “lean” is in the title because the people who were anecdotally reporting high LDL, high HDL, and low TG tended to be lean.

In other words, the name “LMHR,” posed in 2017 was itself a sort of prediction: maybe leaner and metabolically healthier people are more likely to exhibit increases in LDL on a low-carb diet? The name is the hypothesis.

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 had been low-carb for >2 years, 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.

Hypothesis-naïve exploratory analysis finds that having lower BMI and a lower TG/HDL ratio associates with larger increases in LDL on a low-carbohydrate diet.

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 597 participants that met the inclusion criteria, 112 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 21.9, as compared to 24.5 for the rest of the low-carb sample in this study (between group p = 1.04 x 10-11). Furthermore, LMHR exhibited higher LDL, higher HDL, and lower TG, with mean values of 316, 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 135 mg/dL in LMHR. Exactly the same! This finding is consistent with the notion that, unlike familial hypercholesterolemia, the cause of LDL increases among LMHR is unlikely to be genetic (see more below).

In the Lean Mass Hyper-Responders (LMHR) paper, the average LDL, HDL, and TG of LMHR were 316, 99, and 47 mg/dL on low-carb, respectively. This was despite normal pre-diet LDL levels.

A LMHR Case Report Shows the Phenotype is Partially 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.

That said, this very question — is high LDL harmful in LMHR? — is currently being assessed in a prospective study (data from which are expected to drop in 2023). And I will be vocal about the data when they emerge, whatever they say.

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 nearLMHR. 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 lowcarb 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!

SubjectLipidspre-VLCDVLCDLCDLDLc Decrease
IA*Total Chol214797294-480
LDLc116665185
HDLc8112295
TG845072
TG/HDLc1.00.40.8
MI*Total Chol209698497-223
LDLc122583360
HDLc7297122
TG547067
TG/HDLc0.80.70.5
ROTotal Chol197311180-124
LDLc137239115
HDLc456554
TG625636
TG/HDLc1.40.90.7
NMTotal Chol179387272-122
LDLc113317195
HDLc495961
TG865456
TG/HDLc1.80.90.9
ANTotal Chol218423318-100
LDLc141336236
HDLc576966
TG987464
TG/HDLc1.71.11.0

Future Directions

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 responder 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…

Additional Notes

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 597 people, lean people and those with good metabolic health preferentially and reliably consumed more saturated fat.

So, for those who want to protest that “LMHR just ate more saturated fat” (and we get this a lot), I’d want to ask: what do you think about the flipside of such an assertion. Is it reasonable to assume that eating saturated fat is strongly, and possibly causally, associated with being leaner and with better metabolic health markers? (For more on this, see Supplemental Figure 5 from the paper.)

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 exactly 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 six patients in the case series were negative. Genetic testing performed on other subjects not reported in this study have also been negative.

Corrections / Clarifications

The current publicly available LMHR manuscript is an unedited version
https://academic.oup.com/cdn/advance-article/doi/10.1093/cdn/nzab144/6446805
To facilitate scientific transparency and collegial discourse, we made the full database and
statistical code publicly available, though a link in the manuscript.
We welcome feedback, including any problems in the statistical code, for incorporation and/or
correction in the final manuscript.
These issues have been identified for correction in the final manuscript, some of which relate to
discrepancies between versions of the R-code application:

  • Figure 1. “Potentially unreliable data” should be n=288 and “>130 carb intake” will be
    changed from n=23 instead of n=24.
  • Table 1. % M/F will be changed from 60/40 to 57/42. Data rows for Current TG and
    HDLc were reversed and will be corrected.
  • Table 3. Between group p-value for prior TG/HDLc will be changed from 3.7 x 10-16 to
    3.5 x 10-16. Frequency for male in LMHR group will be changed from 56% to 43%.
  • Supplemental Table 1. Current HDLc p-value will be changed from 4.26 x 10-8 to 4.09 x
    10-8. Current TG p-value will be changed from 0.079 to 0.080. Other minor rounding
    errors will be updated.
  • Supplemental Figure 1. The 2nd (left to right) lower bar will be changed from 76 to 61
    mg/dL.
  • Supplemental Table 2. AIC for the BMI will be changed from 7227 to 7214. AIC for the
    prior TG/HDLc + BMI will be changed from 7230 to 7213.
  • Supplemental Figure 5A should indicate baseline BMI as an effect modifier, not
    mediator, among other forthcoming clarifications.

Additional clarification: Cardiometabolic risk factors are often considered as those comprising
the metabolic syndrome, exclusive of LDLc, such as in this recent CDC study. To avoid
unintended interpretations, we will add the word “otherwise” to the abstract conclusion as
follows:

These data suggest that, in contrast to the typical pattern of dyslipidemia, greater LDLc
elevation on a CRD tends to occur in the context of otherwise low cardiometabolic risk.

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Philippa
Philippa
1 month ago

Your wording of the conclusion is going to continue to be problematic. Suggest more specificity in your wording. E.g. “greater LDLc elevation on a CRD tends to occur in those who appear to be highly insulin sensitive (as indicated by TRG/HDL ratio)”

Nick
Nick
1 month ago
Reply to  Philippa

We do not have data on insulin sensitivity. Thus, the above posed statement would be overreaching the data. “Low cardiometabolic risk” is an accurate statement as “cardiometabolic risk” refers to the TG and HDLc components of metabolic syndrome, not LDcL. The statement is appropriate the the data we collected.

However, we agreed with the constructive comment from another individual that there would be no harm in the addition of the word “otherwise” to provide further clarification. The conclusion of the abstract will now read: greater LDLc elevation on a CRD tends to occur in those with otherwise low cardiometabolic risk.”

Last edited 1 month ago by Nick
Philippa
Philippa
1 month ago
Reply to  Nick

[“cardiometabolic risk” refers to the TG and HDLc components of metabolic syndrome].  This is an incorrect statement, on my understanding (but happy for you to show me any literature where this is stated). On the contrary TG and HDL are two cardiometabolic risk factors. But there are other cardiometabolic risk factors such as blood pressure, fasting blood glucose and waist circumference. If you have not measured these and have no data on them, I do not think you can just take the risk factors that you did measure and make a claim about cardiometabolic risk based solely on them. That’s not how a risk assessment works! You can’t just measure 1 or 2 risk factors and conclude low risk! Just the same as if you had only measured blood pressure, and fasting glucose and no other risk factors, I don’t think it would be justified to state “Cardiometabolic risk refers to the blood pressure and fasting glucose components of metabolic syndrome”, or report a context of low cardiometabolic risk just based on that subgroup having normal blood pressure. 

Philippa
Philippa
1 month ago
Reply to  Nick

You are right, you don’t have data on insulin sensitivity…I was just trying to propose something that would be less of an overreach than what you currently had! Really, your conclusion should simply be “greater LDLc elevation on a CRD tends to occur in those with a lower BMI and lower TG/HDL ratio.” and leave it at that.

Philippa
Philippa
1 month ago

Just out of curiosity..thats a lot of ‘potentially unreliable data’….were these mostly people literally making typos in their data entry, or did you have a bunch of people putting in values in mmol/l or any other trends?

Nick
Nick
1 month ago
Reply to  Philippa

We were quite strict with respect to excluding data in order to minimize bias given the dataset with which we were working. The criteria can be revealed in publicly available R-code linked in the paper. Yes, there were cases of questionable units and entry values that were excluded. To be clear, our exclusion rules were largely automated and set a priori such that we couldn’t intentionally or unintentionally recluse data that we didn’t like.

Philippa
Philippa
1 month ago
Reply to  Nick

Fair enough and good to have a priori rules set

Belle Martin
Belle Martin
1 month ago

Over what period of time did the addition of some sweet potato cause the reduction in LDL – is this a quick fix you can take just before a blood panel, or something to implement over weeks or months?

Nick
Nick
1 month ago
Reply to  Belle Martin

Have you seen Dave’s white bread experiment? If not, search it and let me know your thoughts. I hypothesize that in most cases the reversal of the phenotype is quite quick, given the 2-4 day half-life of LDL. That said, one can not exclude further modifications that may occur over longer periods of time mediated by microbiome changes, epigenetics, or other factors.

Jennifer Holgan
Jennifer Holgan
1 month ago

Is there a differentiation between ‘fit’… ie endurance/strength and percentage body fat?
Are there people fitting criteria who are not lean?

Nick
Nick
1 month ago

First off, nice play on words. As to your question, “fit” is a vague term. In it’s broadest definition, it seemly means that an organism is well-suited to its environment. In that sense, a walrus is far more fit than a lion in the context of Arctic. Colloquially, fit is used to refer to “in good shape” or “sporty” and/or able to perform athletically. As you can see that doesn’t leave much to latch on to in the way of operationalization. Lean, by contrast and at least as I understand it, refers to someone with relatively low body fat and low-normal BMI. The catch is that there are people with higher BMI who still have low-body fat. They have high-lean mass, but are they lean? Take Dwayne Johnson as an example. His BMI is 34.3. He is obese. I wouldn’t call him lean, but he has a lot of lean mass and little body fat. Would he be LMHR if he went low-carb? I’m not sure. It’s still not clear wether BMI or body fat is more tightly linked to the phenotype, as we did not have body fat data for this paper. We hope to assess that question in future. Sorry for the ramble answer.

tom
tom
1 month ago

I am 3 months into Keto Carnivore and over a year into Keto. On Monday I had blood work. Cholesterol of 303, LDL of 213, HDL of 78 and Trig of 58, BMI 21.4. I thought they must have swapped my sample with someone else. 69 years of active lifestyle and 4 to 5 days week in the gym, I was to put it mildly, shocked. My wife, through Dr Berry’s site found this site and I have been following this with great interest. Thank you for your work and some clarity on this issue.

Nick
Nick
1 month ago
Reply to  tom

Thanks for sharing Tom. You reaction is understandable. Dave and I both had similar reactions. For me, I saw an initial increase in LDL from 95 to 321, with my HDL jumping to ~110. My TG run around 40. I was shocked and, coming from a medical family (four doctorates between my two parents) we were all confused and concerned. I never would have guessed that lab value would eventually inspire a scientific interest that connected me to a software engineer, revolutionized my professional network, and redirected my career interests. Life is unpredictable.

Beth
Beth
1 month ago

This happened to me (& I refused the statin). My LDL came down to something more like normal when I started taking thyroid (my TSH was high & my T3 borderline low, but I had antibodies to thyroid).
It’s been probably over a decade since the cholesterol stuff started & I’m still alive anyway. 🙂
FWIW, I wasn’t fat when I started low carb, but I did lose weight & am now at the lower end of normal (bmi of 18.5 & I do exercise regularly). On the last test, HDL 110, LDL 15o & TG 48.

Last edited 1 month ago by Beth
Nick
Nick
1 month ago
Reply to  Beth

Thanks for sharing Beth. Based on the thyroid panels I’ve seen from LMHR (including myself) most don’t have hypothyroidism either clinically or by biomarkers (in particular TSH, although free T3 is also interesting). That’s an entirely different conversation that I’d like to have with a few specific people and a research topic on which I’d like more data.

Ravi Kamepalli
1 month ago

Humans becoming fat-burning beings from high carb fat storage persons.
We ought to help every person figure out how to be able to get rid of the extra inflammatory fat.
#removingbarrierstohealing

Nick
Nick
1 month ago
Reply to  Ravi Kamepalli

Agreed. Let’s remove the barriers and give people a complete array of options. I like that you used the word “help” because I think it’s important to emphasize that this is someone each persons has to figure out on their own. It’s a teach a man to fish situation. It’s about education and self-exploration.

Philippa
Philippa
1 month ago

I’ll make the other point here that I made on twitter, because I also think it was misunderstood, from listening in to the clubhouse discussion. I know that you did not collect ethnicity data and my point has nothing to do with that. My point is that you are claiming to have observed a context of ‘low cardiometabolic risk’ based essentially on the observed TG/HDL ratio. However this ratio is known to not well represent cardiometabolic risk in people of black African descent. Your paper should include this fact as a limitation, in my opinion. https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC5582986/

Nick
Nick
1 month ago
Reply to  Philippa

There are almost certainly factors modifying the phenotype, including polymorphisms roughly linked to geographic ancestry. As an initial observational study describing: the inverse relationship between BMI and LDLc change + the inverse relationships between TG/HDLc and LDLc change + classifying the LMHR phenomenon, it was not within the realm of this paper to generate different thresholds based on genes or ancestry/ethnicity/race (with the latter two not technically having a biological basis) or sex. The LMHR study will have genetic data, and in future we hope that research will be able to link the lipid triad to underlaying lipid dynamics and that different thresholds can be determined in a more personalized manner. Again, once the final manuscript is online, we invite you to compose a letter to the editor.

Philippa
Philippa
1 month ago
Reply to  Nick

Unfortunately, your reply has not addressed the point I made, which was entirely to do with your interpretation of the implication of the low TG/HDL ratio. If you are observing X, which you then claim to mean Y, but X is known to not mean Y in a large section of the population, it would be good practice to discuss this fact in your discussion, IMHO.

Dejan Milanović
Dejan Milanović
1 month ago

Did you test the pattern of LDL particles?

Hermes Carrizo
Hermes Carrizo
1 month ago

Hi Dave, just new here and Im very interested and would greatly appreciate it if you could give me some tips or biohacks to raise my HDL (55) and lower my Trigs (115)….Im on a quasi keto lifestyle considering that one day a week I have no restriction in to what I eat. Thanks for the feedback.

lcp
lcp
1 month ago

I definitely saw this phenomena with myself. Decrease in TG, rise in HDL and LDL. My LDL is not high enough for the study though. Thanks for pursuing and making this a reality!

Peter Bergs
Peter Bergs
1 month ago

Fascinating

Aleksa
Aleksa
1 month ago

To be completely honest, I am here just because I am freaking out and looking for evidence that I am not going to have a heart attack and drop dead any second now. (Reading this site is helping.)

I am a lean and athletic 40-year-old female (rock climber/runner/cyclist/mountaineer) with a BMI of 19. I was recently diagnosed with T1 diabetes, and subsequently stopped being vegetarian (after 20 years) AND started the Bernstein protocol (30g of carbs per day). My ever-evolving (and recently crazy) lipid profiles (and other figures):

  • Before T1D onset (Mar. 2019): TC=4.5, LDL=2.39, TG=0.45, HDL=1.9, A1C=5.7%
  • At diagnosis (Sept. 2021): TC=5.5, LDL=3.22, TG=0.48, HDL=2.06, A1C=12.6%
  • Now-ish (Nov. 2021): TC=9.44, LDL=6.66, TG=0.67, HDL=2.43, A1C=5%

My CRP followed a similar pattern 0.2mg/L – 0.4mg/L – 0.2mg/L. Ketones were 0.48 mmol/L at diagnosis (Oct.) and 0.3mmol/L in the last labs (Nov.).

All else seems to be fine, but I am an emergency room nurse, hence my training makes it impossible for me to not freak out about these numbers. Needless to say, I am freaking out. My endocrinologist, at one of the largest uni/research hospitals in Canada (MUHC), will be doing some follow-up and more detailed lipid tests.

Could I be one of these weird LMHRs?

Siobhan Huggins
Admin
Siobhan Huggins(@siobhanh)
6 days ago
Reply to  Aleksa

Hi Aleksa,
We’re not doctors and can’t give medical advice so can only comment with our thoughts in case they may be of interest.
It does indeed look like you fit the profile of a Lean Mass Hyper-responder e.g. someone who is typically lean, active, and powered by fat (e.g. on a low carb/ketogenic diet). You may be interested in the Lean Mass Hyper-responder facebook group as there are many there with similar profiles who explore the latest research regarding it, their experience, their perspective, and how they’ve approached having the profile (e.g. taking steps to move away from the profile and how they did so, sticking with it but getting additional testing to keep an eye on things, etc). Additionally, you may find the recent Lean Mass Hyper-responder paper of interest as well.

We can’t say whether this profile is of concern or not (as, again, we’re not doctors and can’t give medical advice), but we can offer some resources to explore different perspectives on the topic. For example there’s this presentation from Dave looking at high LDL in the context of high HDL and low triglycerides from a cautiously optimistic perspective, plus this post from Dr. Nadolsky looking at the same topic from a cautiously pessimistic perspective.

Julie Hampson
Julie Hampson
25 days ago

Thoughts?

Screenshot_20220101-061627.png
Siobhan Huggins
Admin
Siobhan Huggins(@siobhanh)
5 days ago
Reply to  Julie Hampson

Hi Julie,
We’re not doctors and can’t give medical advice so can only comment with our thoughts in case they may be of interest.
It looks like you fit the profile of a Lean Mass Hyper-responder e.g. someone who is typically lean, active, and powered by fat (e.g. on a low carb/ketogenic diet). You may be interested in the Lean Mass Hyper-responder facebook group as there are many there with similar profiles who explore the latest research regarding it, their experience, their perspective, and how they’ve approached having the profile (e.g. taking steps to move away from the profile and how they did so, sticking with it but getting additional testing to keep an eye on things, etc). Additionally, you may find the recent Lean Mass Hyper-responder paper of interest as well.

We can’t say whether this profile is of concern or not (as, again, we’re not doctors and can’t give medical advice), but we can offer some resources to explore different perspectives on the topic. For example there’s this presentation from Dave looking at high LDL in the context of high HDL and low triglycerides from a cautiously optimistic perspective, plus this post from Dr. Nadolsky looking at the same topic from a cautiously pessimistic perspective.

For those who decide they are not comfortable with it for the longterm, or would just like to confirm it is dietarily induced, the most consistently effective method (presuming it is dietarily induced) that we’ve seen demonstrated by people thus far is to decrease fat and proportionally increase carbs (e.g. isocaloric carb swapping), which is discussed here.

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