Welcome to CholesterolCode.com. This site serves as an information and research hub for emerging data on cholesterol. particularly in the context of a low carbohydrate lifestyle.
If you know little to nothing about cholesterol ->
If you’re looking to better understand the risk associated with high cholesterol on a low carb diet->
Note we are still recruiting for our LMHR study through the Lundquist Institute. Check out our official recruitment page at CitizenScienceFoundation.org/study to find out if YOU qualify!
While several articles on this site present a more “cautiously optimistic” perspective on cholesterol in the context of fat adaptation, we strongly encourage everyone to consider the conventional view as well. Consider reading The Case for Lower LDL on Low Carb by our colleague and co-investigator, Spencer Nadolsky.
If looking to understand the “Lean Mass Hyper-responder” profile ->
If you’d like to learn more about lipoprotein(a), you can watch Siobhan’s presentation on it here
Lastly — you can always just ask us anything our Questions Page. (Just be aware our site does not constitute medical advice and we always recommend consulting with your doctor.)
We’re beyond excited to announce the Lean Mass Hyper-Responder has completed enrollment. Needless to say, this has been a long awaited milestone.
We’ve updated the recruitment page at CSF to let everyone know we are no longer taking participants for the study.
Again, each of our 100 participants will make a total of two trips to the Lundquist Institute. The first will provide the baseline scan, then they will return a year later for their second scan. Once all participants have completed both scans, we’ll move ahead with the final analysis.
We’re still in the process of completing our funding for this study as travel costs have proven more challenging in the current economic environment. Again, thanks to everyone for all their support!
You may have noticed we’ve been posting less frequently here at CholesterolCode.com (CC). This isn’t for lack of interesting things to share and update you on – it’s because Siobhan and I are now fully entrenched in both formal research through the CitizenScienceFoundation.org and expanding our blood testing service, OwnYourLabs.com.
A Quick Recap
Here’s a brief rundown of everything Dave been doing over the last year:
Four papers published on the Lipid Energy Model and the Lean Mass Hyper-Responder phenotype, including one first authored
Produced video abstracts on two of these papers (here and here)
Four presentations and eleven interviews
And, of course, extensive ongoing work with the LMHR Study out of UCLA
Here’s a brief rundown of everything Siobhan been doing over the last year:
Much time spent researching lipedema pathophysiology resulting in the KetoFest 2022 presentation recapping the current working model of how and why lipedema may develop
Additional work as the research specialist for The Lipedema Project including as-of-yet announced research projects, continued work on The Voices of Lipedema Project, helping to coordinate two events per year for the lipedema community (via Lipedema Simplified), and other related side projects such as co-writing an article on lipedema for Keto-Mojo
The Developments We Hoped For
We’ve long used CC as a means to stay close to the community and help promote the research we would like to see happen. But each of these circumstances have changed –– in a good way.
Before, the community was small and it was uncertain how prevalent things like the LMHR phenotype were. Now, as of this writing, the LMHR Facebook group and its sister CholesterolCode Facebook group boast over 9,000 members each(!), and it’s very active in knowledge sharing.
Also, we previously wrote emails and visited NLA conferences in the hopes we could get researchers to help advance this science. Now we’re working directly with researchers on the endeavors we dreamed of, both in the publication of papers and running studies directly.
To put it simply, we’ve replaced our responsibilities in pitching these projects with actually doing them.
What’s Next for CC?
We’re going to continue to be an information hub for our research, such as hosting an active published papers page.
We’ll also continue to post major announcements here.
However, we don’t have the bandwidth we once did for actively responding to all comments. Thus, we’re going to be retiring the Questions Page, and will not be actively responding to comments on CC.
More of the key questions folks are looking for will be answered in our current and ongoing published research, such as the LMHR study. For other questions, consider reaching out to us on social media via Twitter (@realDaveFeldman, @siobhan_huggins), or tagging us in the Facebook groups.
Again, we can’t thank everyone enough for their continued support at getting our research where it’s at — there’s so much more to come!
I’m excited to announce I’ll be heading to the Keto Orlando Summit this weekend.
I’m also excited to announce we made some commemorative magnetic pins for this occasion to help fundraise for the Citizen Science Foundation. If you donate $25 or more (see below), we’ll ship you the pin directly, or I’ll actually hand it to you if you’re attending the conference since I’ll have them on hand there.
It’s a question that comes up again and again: Could Lean Mass Hyper-Responders (LMHRs) just be eating more saturated fat?
Rather than repeatedly answering this question in cumbersome Twitter threads, I thought I’d save both Dave and myself some time by consolidating 5 points that challenge the saturated fat hypothesis of LMHR:
1. Magnitude of effect. Many LMHRs exhibit LDL-C levels of well over 300 mg/dl. Mean levels from the LMHR participants in our cohort study were 320 mg/dl (Table 3), and we certainly have a handful with LDL-C above 500 mg/dl. I’m not aware of any data suggesting saturated fat intake, even at extreme levels, can cause increases in LDL-C to such an extent. If you – the reader – are aware of such data, please do share.
2. LDL-C change has an inverse relationship to BMI. In the same study, we observed that LDL-C change has an inverse relationship to BMI on a carbohydrate restricted diet. If this is the case and saturated fat was the primary driver of the increase in LDL-C observed, then the logical implications are either that there is a dose-response effect of saturated fat on body weight loss (i.e. saturated fat makes subjects leaner) OR that persons who are lean and adopt low-carb diets preferentially eat higher proportion saturated fat diets. For example, if we had three subjects, Jamie, Nicky, Leslie, and Amir with BMIs of 24, 26, 21, and 30, respectively, and they were all to adopt low-carb diets, Leslie would eat more saturated fat than Jamie who would eat more saturated fat than Nicky who would eat more saturated fat than Amir.
3. The triad. A critical point is that LMHR are defined, not by LDL-C alone, but the triad of high LDL-C, high HDL-C and low triglycerides. Therefore, any complete model explaining the LMHR phenomenon must account for this triad. Thus, we must ask, could eating more saturated fat cause to the triad of markers seen in LMHR? (And that’s assuming LMHR eat primarily high-saturated fat low-carbohydrate diets.) In our study, mean levels were 320 mg/dl LDL-C, 99 mg/dl HDL-C, and 47 mg/dl triglycerides.
4. Adding back moderate carbs attenuates the phenotype. In the case series associated with the aforementioned study, six LMHR or near-LMHR subjects were instructed to introduce 50-100g/d carbs to help replenish hepatic glycogen and, via the postulates of the Lipid Energy Model, lower their LDL-C. No further instructions were given, i.e. subjects were not told to lower saturated fat intake. Nevertheless, all subjects exhibited substantial reductions in LDL-C, including one who exhibited a drop from 665 mg/dl to 185 mg/dl. Even if saturated fat intake occurred spontaneously (without instruction), it seems unlikely it could explain the magnitude of the effect.
5. Case series. Although it is an n = 1, we published a case series of an individual consuming a ketogenic diet relatively low in saturated fat (~82% unsaturated, ~18% saturated). His pre-low carb LDL-C was 95 mg/dl. But following carb reduction, LDL-C rose to a peak of 545 mg/dl, despite relatively low saturated fat intake. Furthermore, LDL-C trended inversely with BMI and, when saturated fat intake was altered for experimental purposes, LDL-C remained concordant with the BMI trend and, thus, inconsistent with the prediction that saturated fat drives LDL-C change in this subject. Even if this is only a case report, recall that these data represent a real LMHR patient and are consistent with both the LMHR cohort study and the Lipid Energy Model.
Certainly, none of these 5 points dispute that saturated fat could contribute to the increase in LDL-C seen in LMHR; however, they do suggest that saturated fat is not the primary driver of change. Disregarding point 5, could high saturated fat intake be permissive or even required for the LMHR phenotype? Possibly. However, unless one can explain how saturated fat intake could account for these data, we should assume there is more at play worth investigating.
My primary costs are the many frequent and expensive blood tests I take for this research and data. Any size donation is appreciated. Thank you for your support!
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