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Apr 27

Presenting the Lipid Energy Model to Stanford University

I was incredibly honored to be invited by Annelise E. Barron, Associate Professor, Dept. of Bioengineering, to present my research to her class and discuss the Lipid Energy Model in depth. Originally, I was going to be flying to the campus to give the talk directly, but with the current Covid-19 crisis all speakers were presenting via Zoom.

This proved to be an excellent opportunity provide an overview for general (not low carb) audience. Overall, the presentation was well received, maintained strong retention, and there was quite a bit of discussion afterward. (Discussion not included in the video)

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skp
skp
2 months ago

Hi, I like your post really I have read first-time Thanks for sharing keep up the good work.

Randy Neufeld
Randy Neufeld
2 months ago

What were the hardest questions in the follow-up discussion?

Su-Chong Lim
Su-Chong Lim
2 months ago
Reply to  Dave

Dave:

I just stumbled onto your site, after frantic search following a half remembered comment or description from a Peter Attia presentation, trying to rapidly digest the available information before urgent Cardiologist appointment and treadmill testing tomorrow morning.

Quick summary — I am 72 yr old retired Physician retired at 64. Had been running since age 50, and decided on retiring to learn to swim and bike (how hard could that be) and compete in Triathlon. After a brutal and humbling learning curve finally completed an IronMan in 2018 (lots of 1/2 IronMan events over the years). Along the way I learned so many strange things I didn’t expect. I was the usual lipid- ignorant Family Doctor during my years of practice, so I was really offended when my coach suggested I try lowering my Carbohydrate Intake to boost my fat burning, because I knew that ketosis was dangerous etc. etc. Long story short, I was astounded to find during a Treadmill Respiratory Gas Analysis in 2015 that my fat burning at Zone 1 intensity was only 11%. I tentatively went on a restricted Carb diet (I was totally uncontrolled full-on CHO consumer prior to that) and 12 weeks later repeat testing showed fat burning at Zone 1 was 62%. I continued on restricted carbohydrate intake, and got increasingly knowledgable and consistent in my diet; for the past 3 years have been in dietary ketosis (confirmed by regular blood glucose and beta-hydroxybutyrate testing, and more recently by breath acetone sampling device). I was actually already quite lean before, possibly 53-53.5kg (height 162 cm) and am now 50-51 kg, >> Lowest Risk Third
—-> Go to https://tinyurl.com/ycccmmnx for more on AIP

Framingham Offspring: 0.7 Odds Ratio >>> Low Risk
—-> Go to https://tinyurl.com/y5fc5adl for more on this Framingham study

Jeppesen: >>> Lowest Risk Third
—-> Go to https://tinyurl.com/y63xp7lj for more on the Jeppesen study

Cholesterol Remnants: 14 mg/dL >>> 0.15 mmol/L >>> Low Risk
—-> Go to https://tinyurl.com/y84u92wm for more on Cholesterol Remnants

——CONVENTIONAL MARKERS AND RATIOS——
Friedewald LDL-C: 244 | Iranian LDL-C: 207
TC/HDL Ratio in mg/dL: 3.41
TG/HDL Ratio in mg/dL: 0.64 | TG/HDL Ratio in mmol/L: 0.28

AND SHE JUST ABOUT HAD A FIT!! Hence the urgent Cardiology consultation. The cardiologist has already suggested I should be on a Statin aiming for a target of LDL-C of 2.0 mmol/l. I’m in a bit of a dilemma. I know where he’s coming from, and I used to be in that camp, but I’ve seen the light, and I think the lipid hypothesis is deeply flawed. My wife thinks I’m arrogantly over inflating my self-expertise and that I’m the typical Internet Patient taking my life in my own hands in a bad way.

I’m really trapped. It doesn’t help that my family history is positive for maternal premature death by stroke and hypertension, and hypercholesterolemia and hypertension in a sibling (but he’s obese!) Oh, yeah, in 2014 I got a pelvic CT scan to reveal an avulsion fracture on my femur after being hit by a car while biking — but the CT showed “Atherosclerotic Streaks” (no quantification specified) in my Aorta and Iliac vessels, so, as far as the cardiologist is concerned, it’s established that I have evidence of arterial plaque already.

An interesting tid-bit is that I had a blood test at age 32 in 1980 showing normal cholesterol and lipid ranges including an HDL-C of 41mg/dl (we were using US units then). In 2015 HDL-C had risen to 1.66 mmol/l, and in 2018 HDL-C was 2.12 mmol/l.

But if I can decipher the Feldman Code as precisely as you describe it to be, perhaps I can drop my serum LDL without Statins and keep everyone happy. I don’t mind taking low dose ASA though, and have started that.

Sorry to go in so much detail, but I wanted to establish that I’m a genuine flaming LMHR, and I want to join the team, and I’d do anything you ask me to do. But I’m in crisis mode right now, and anxious lest I piss the Cardiologist off, uppity ex-Doctor patient and all.

Su-Chong Lim
Su-Chong Lim
2 months ago
Reply to  Su-Chong Lim

Follow up — it was even worse than I feared. The Exercise Treadmill Test was trivial. I got up to Level 5 with no issues at all, and they cut off the test as my HR got up to 153, way higher than their calculated Max HR of (220 – age), which for me was 148, even though I had carefully explained that I regularly achieve 175 bpm at my top exertion levels without issue, and I have actually measured as high as 182. My 2014 CT was reviewed and shows a small calcification at the aortic bifurcation that I would guess represents an occlusion of 2% of the luminal area. I was given a prescription for Crestor 20mg, no discussion at all, I guess LDL of 6.32mmol/l is cut and dried to her meaning I have familial hypercholesterolemia and I am in immediate danger until I treat with Crestor to lower LDL to 2.0 mmol/l.

I just reviewed my original comment, and noticed there is a large chunk missing in the middle section, most of which probably doesn’t matter, except maybe my lipid profile drawn on April 30, 2020, which I’ll paste below.

No, wait, I must have originally included the values for my lipid profile because there are comments and conclusions based specifically and precisely on my results — so the values were stripped by the moderator, I’m not sure why, but I’m sure there’s a good reason, so I’m ok with that.

Now to figure out what to do. I’m not filling the Crestor prescription, but I have to come up with a response. I filled the Nitroglycerine prescription, but I can’t imagine needing to use it. I’ve got an Echocardiogram booked tomorrow and a Thallium Stress test sometime in the future.

Siobhan Huggins
Admin
2 months ago
Reply to  Su-Chong Lim

Hi – thanks so much for providing the details! It can help a lot to establish some context for your concern and where you’re coming from.
Regarding your results – it just looks like they didn’t copy/paste properly, we didn’t remove anything. The only things we remove from the comments are spam, or personal information (e.g. email, or phone numbers) and in the case of the latter we insert a note that personal information has been removed by an admin.
No worries though! Based off what you said, and that you’re a LMHR I can guess what the results would have been anyway (but it would also be great if you could re-post the number – just plain numbers is fine like LDL, HDL, triglycerides, total cholesterol).

Although I’m not a doctor, so can’t give medical advice, from what you said it seems as though the calcification was already there prior to going low carb, correct? From what Ivor Cummins has stated after looking into the research of CACs (coronary artery calcium scoring) he found that if calcification was already present, then the next best thing would be to follow up after two years or so to get another score and check the rate of progression. Progression under 15% (if I remember right) was comparative to a low score from the start. He has a couple different videos on this that might be worth looking into, I’ve linked one with the relevant information timestamped.

Regarding Familial Hypercholesterolemia, as far as I know if earlier in life you had expected values, and cholesterol increased from diet, then this would suggest it’s not genetic – although I’ve heard from a couple people that high levels alone are assumed to be genetic. If it were me, if I were to make diet changes and it went back down to “normal” levels I’d presume it were the diet resulting in the profile (as we’ve seen in quite a few lean mass hyper-responders). But that’s just my own interpretation – perhaps you could discuss with your doctor for clarification given your prior numbers?

If you’re not comfortable with your LDL levels as is, then one thing that people in the Lean Mass Hyper-responder facebook group have noted seems to work pretty consistently is to increase carbohydrates and (this is super important) proportionally decrease fat. This is a diet change that seems to work over the longer term for people who would like to move away from the profile, and fits with the general idea of the lipid energy model.
Some others in the group (which you might want to join if you haven’t already) opt instead for thorough testing over time – including not only CAC, but other blood markers to look at inflammation, metabolic health, etc, CIMT (looks at thickness of the artery in the neck), carotid doppler (visually checks for plaque and measures bloodflow), etc. This is for people who want to monitor their health fairly frequently to see the trend and verify nothing outside lipid numbers is going sideways (or if it does, to alter diet however they feel most comfortable).

If wanting resources for discussion, you could also check out this presentation from Dave about a cautiously optimistic perspective on risk, and this post by Dr. Nadolsky showing a cautiously pessimistic view. This way you can read up on both sides and see which is more compelling to you based on the evidence, and use the studies discussed to talk to your doctor about where your viewpoint is coming from, if you wish.

However, it’s also worth noting that your doctor’s job is to give you advice they think will help you reach better health, but it’s ultimately it’s up to you to decide if their suggestions will help you reach your personal health goals, and help you achieve what you’re wanting to. Although it does get infinitely more complicated when spouses or family is involved, it is you who has to live with whatever decision you ultimately make (or the path you decide to follow to experiment and find what works for you – a decision doesn’t have to be permanent if you later change your mind). So, hopefully you can find something that you feel comfortable with, and work as a team with your doctor to make sure what you’re doing is working for you.
Obviously, because it depends on what you’re comfortable with, your interpretation of the data, etc, I can’t say what you should or shouldn’t do. Only point you to resources which may help you decide for yourself with your healthcare team.

Apologies for my own reply being very long, but hopefully this provides a little something you can use to help orient yourself as you continue to learn and decide what you feel you should do. If you have any further questions please do feel free to check back, and if you’d like to discuss with other lean mass hyper-responders the facebook group is a place worth checking out to hear from others in similar positions (and with similar cholesterol profiles) as your own.

Su-Chong Lim
Su-Chong Lim
2 months ago

Siobhan:

Thanks for reply, and for your very helpful opinions. Rest assured, after weighing all the evidence I will take full responsibility for my own decisions, whatever they will be. However, there will be no further discussion with the cardiologist — she is as cut and dried and literal minded as they come regarding high LDL is fixed in stone as being synonymous with established high cardiac risk until it is lowered, almost certainly with a Statin tried first, or if not tolerated, with some other pharmaceutical. (She had no patience with any idea that dietary intervention or fasting might have had any effect on the lipid results, even though I had explained to her that the week prior to testing was extremely chaotic and stressful from me, I had not slept well and had not eaten regularly prior to the test, then had occasional binge meal to compensate, then fasted for the test.) That is why my plan is not to fill the Crestor prescription, and to do an end run and repeat the lipid panel, hopefully after thoroughly understanding, then emulating the Feldman Protocol.

Regarding my age, the calcification is not just in my aorta, but also in my internet and computer competence. Given that the Admin had nothing to do with the lost part of my first comment, I’m sure that what actually happened was that I tried to edit, unknowingly highlighted some already inputted text and just as unwittingly deleted that block of text.

Firstly I will try and remember what I had said and deleted. — In March this year I was one day aware of an odd discomfort in my chest while running uphill into a cold winter wind with slippery snow underfoot during the first mile of starting a run that felt like a very mild pressure in my sternum and left 3rd-4th adjacent rib. There was no radiation of the discomfort to anywhere, but being a doctor in my prior life, I was sensitized to the idea that heart disease was common in my age group, notwithstanding the fact that at other times I was capable of much greater exertion and heart rate. The circumstances were suspicious, too, although the discomfort, such as it was, was very mild, almost trivial, and may even have been aggravated by deeper breathing, which was not typical of angina. Then the discomfort went away as I reached the top of the hill, and I sprinted the rest of the run, as usual. I reached the swimming pool, did my swim, then ran home again with no further incident.

On thinking about it, I thought that perhaps I had experienced something similar perhaps on 2-3 occasions in the the prior 4 months or so (with hundreds of other extreme exertional sessions with no discomfort at all), but had forgotten about it. I was undergoing a lot of stress, and shortly after this episode the COVID 19 lockdown started in Calgary, Alberta, Canada where I live, and while still under further stress, I experienced another single mild recurrence of this vague chest discomfort running uphill early in a run one day in cold weather. I was inclined to write this off as a stress phenomenon, but with an abundance of caution, I thought I should run this by my own doctor (an ex-colleague in my old practice).

She ordered a lipid panel which was drawn on April 30. (I will paste what I saved onto my clipboard after filling in the data from your beta testing report tool.)

–===== CholesterolCode.com/Report v0.9.5.15 =====–
• Male • 72 • Coffee: 1 cups/day •
• 4 on years on Keto (less than 20g carbs) •
• 18h water fasted • Cholesterol Rx: false •

Total Cholesterol: 365 mg/dL 9.43 mmol/L
LDL Cholesterol: 244 mg/dL 6.32mmol/L
HDL Cholesterol: 107 mg/dL 2.76mmol/L
TG Cholesterol: 68 mg/dL 0.77mmol/L

———RISK REPORT———
Atherogenic Index of Plasma: -0.554 mg/dL >>> Lowest Risk Third
—-> Go to https://tinyurl.com/ycccmmnx for more on AIP

Framingham Offspring: 0.7 Odds Ratio >>> Low Risk
—-> Go to https://tinyurl.com/y5fc5adl for more on this Framingham study

Jeppesen: >>> Lowest Risk Third
—-> Go to https://tinyurl.com/y63xp7lj for more on the Jeppesen study

Cholesterol Remnants: 14 mg/dL >>> 0.15 mmol/L >>> Low Risk
—-> Go to https://tinyurl.com/y84u92wm for more on Cholesterol Remnants

——CONVENTIONAL MARKERS AND RATIOS——
Friedewald LDL-C: 244 | Iranian LDL-C: 207
TC/HDL Ratio in mg/dL: 3.41
TG/HDL Ratio in mg/dL: 0.64 | TG/HDL Ratio in mmol/L: 0.28

THIS IS WHERE MY DOCTOR PANICKED REGARDING MY LDL-C AND REFERRED ME URGENTLY TO THE CARDIOLOGIST.

By the way, I just had an echocardiogram today (ordered by the cardiologist because of a mild outlier feature in my EKG, that is, slightly increased voltage in the anterior leads, that is, the electrical sensors on the front wall of the chest, which is sometimes an indicator of Left Ventricular Hypertrophy ( a thickening of the heart muscle due to hypertension, which I don’t have, or sometime unexplained). In my case I am a bit of an age group high performance runner, so I might have slightly more developed heart muscular than average, but particularly, I have very diminished body fat all over, including my chest wall, which will allow more electrical voltage to show on the EKG. (I know these things because I used to read EKG’s for other doctors).

The echocardiogram was very enlightening because I ran into the cardiologist who was to read it, and we recognized each other’s names from when I used to practice medicine, and she very graciously invited me into her office and carefully stepped through the interpretation with me. So it turns out that I have a very efficient heart with a high ejection fraction but no ventricular hypertrophy. I may have an aortic diameter at the upper limit of normal or possibly at early stage of dilatation, and very mild regurgitation (leakage) of the aortic valve (seen quite commonly in the normal population). A reasonably cautious recommendation would be to repeat the echocardiogram in 1 year. I would call that essentially normal.

Without coercing her to contradict or support another cardiologist’s opinion, I asked her point blank at the significance of some very mild (non-encroaching on the lumen) calcification in the lower aorta and iliac vessels revealed in an incidental CT of the pelvis obtained in May 2014, long before the low carbohydrate diet was started, and she said almost every 70 year old would have some, so it didn’t mean much.

BTW, the other Cardiologist’s “familial hypercholesterolemia” idea comes from my reported Family History of Mother having hypertension and a stroke at age 72, and my 73+ year old brother reporting hypertension since age 30, and treatment with statins for elevated cholesterol. But both my mother and brother were/are your typical sedentary chubby Chinese lard-asses, with a lifelong high carb diet. I really doubt we all carry the familial hypercholesterolemia gene. Although, it’s reasonable to get my children tested, I suppose.

But the Cardiologist’s intransigence from the get go is a bad prognostic indicator for any flexibility in treatment options. It’s gonna be the Crestor way or the highway. She doesn’t even want a repeat of this single testing given above. She wasn’t impressed with my diet history, nor, apparently of my High HDL, low TG, so the Jepessen study would be seen as irrelevant, I guess, because the Pharma sponsored group consensus would not have considered this a credible study, because, well, that’s how it works.

Peggy Heppelmann
Peggy Heppelmann
2 months ago

Dave, My husband and I fund research investigating diet and chronic disease. I would like to talk to you about your lean mass hyper responder research. I think I can clarify a piece of the puzzle that you are missing with LMHRs, and would like to discuss supporting your research program. Please contact me at the email below.

Reese
Reese
1 month ago

Dave and Siobhan, have you looked up anorexia and high cholesterol before? I found a few interesting papers on the subject. It looks like anorexics often have high LDL, high HDL, and low triglycerides. This goes along with elevated ketones. It’s not a great comparison since anorexia is going to cause a bunch of health challenges too like being malnourished and actually starving, but I thought it was interesting. Here is one paper https://pubmed.ncbi.nlm.nih.gov/16791856/. Have you ever checked your CEPT before?

Siobhan Huggins
Admin
1 month ago
Reply to  Reese

Hi Reese! Yes, I’m not sure if it’s been brought up in a presentation, etc but it is something Dave has discussed with me in regards to what he’s looked into before. I’ll see if he’s seen the paper you’ve linked in particular, as more info on this is appreciated, regardless with regards to the lipid energy model.
Regarding CETP (if that’s what you meant? If not, please correct me!) I’ve not seen a blood test available to measure it through common resources, so I haven’t.

Reese
Reese
1 month ago
Reply to  Reese

Oh! Hah! You mentioned anorexia in your presentation. I should have watched the whole thing first. I thought I’d discovered something new. 🙂

Adam
Adam
28 days ago

Hello Dave, The last year I have been severely sick and suffered from several infections and neurological issues. The only thing that has brought about genuine relief is supplementing with Zinc Sulphate, I have heard that supplementing with zinc if you are relatively healthy and not obese can cause atherosclerosis as it has been shown through several meta analysis that Zinc significant lowers HDL and raises both TC and Triglycerides,

I would love you’re opinion on the impact of Zinc because it has helped me but I don’t want to risk heart disease since relatives have it.

Article below finds different conclusion on the impact of zinc on healthy and non healthy individuals.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4523910/#:~:text=The%20present%20meta%2Danalysis%20demonstrates,cholesterol%2C%20LDL%20cholesterol%20and%20triglycerides.

Matthias
Matthias
28 days ago

Hi Dave, Hi Everybody!

I am a Senior SW Developer who felt and found out that the mainstream energy model of the “medical science” must be wrong.

As you I started to do blood tests at a private lab to find correlations.
It all started in 2016 with an antibiotic which almost killed my liver.
I was then told not to eat fat and suger, but carbs.

With my own data points I could proove that eating low carb helps my liver (lowers GGT).
I read everything out there about the topic. Back from Otto Warbung, Krebs Cycle until
the metabolic pathways poster and “Metabolism at a glance” from Hallway.

I want to suggest the follwing.
Let’s put the energy model into a program:

Simple rules define the behavior of
organs and their interaction. Entities are “Glycogen Store”, “Liver” …

Liver: “if (!gylcogen.isEmpty():
release steady blood sugar from gylcogen store
else
if (in fight and flight)
trade body tissue for sugar
else
access fat for ketons

Cells: “if (Vit B1 around and Floride not present)
do gylcolysis”

“if ( flight and fight OR !oxygen)
burn pyruvate into lactate
else
burn pyruvate in krebs cycle”

Then we define some Test-Cases which reflect different energy demanding scenarios
for the body and are backed up by empiric science

“Steady state, 24h walking” -> Expected result: “glycogen empties, afterwards ketons get burned. Uses krebs cycle for pyruvate”

“Emergceny, 24h running” -> Expected result: “glycogen empties, afterwards body tissue traded for energy. uses pyruvate to lactate (until ….tissue if full with lactate then die)”

Another test case would of course be the feldman protocol. We tune the rules until the
model can quantitavely and qualitatvely fullfill your obeservations.

Out “program” would be then be the Unit-under-Test.
A correct energy model would just satisfy all test cases.

In the end we can more and moe finetune parameters and rules.

Finally we get the get the nobel price.

BR

Matthias

Mari
Mari
20 days ago

Hi. I went Keto and my LDL P doubled and triglycerides lowered. I’m afraid, what to do?

Siobhan Huggins
Admin
17 days ago
Reply to  Mari

Hi Mari – could you post your actual numbers (total cholesterol, LDL cholesterol, HDL, triglycerides, and any other relevant info)? It’s hard to comment without the details.