Health
High LDL Cholesterol on a Ketogenic Diet: What You Need to Know | William Cromwell, Dave Feldman
Some people follow a ketogenic diet seeking to lose weight, feel more energised, or gain control over their eating habits. Others …
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Some people follow a ketogenic diet seeking to lose weight, feel more energised, or gain control over their eating habits. Others …
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@davidzip8841 I quote "Dave, aren’t you being a little disingenuous? A number of participants were excluded from your study solely because they had positive CAC scores. Let that sink in. Excluded because of their CAC scores. You know this and never seem to mention this. And then you have the temerity to draw positive conclusions from the fact that the people you did enroll had low plaque scores"
I hope I did catch the meaning of your comment. It's not an attack but I have to highlight that your comment is a prime example of why people on either side of the argument need to gain more clinical/scientific knowledge and understanding in this day and age where health information is so abundantly available. You have clearly missed the whole point of this study.
I have yet to fully dive into the study myself, so I don't claim to fully understand all of it as of yet, But as a general rule, one of the reasons you want to remove people already presenting with the very conditions a study is addressing is so you can investigate one variable without interference from other pre-existing factors that already caused the condition such as previous lifestyle/eating habits that may be carried over a certain period of time in individuals (hence the importance of a "washout" period when assessing different diets using the same participants). It's like using a blank slate so you can see what ONE variable does on its own with as little interference as statistically/realistically possible. I hope that makes sense. I'll try and come back to this if I got anything wrong (happy to admit this should that be the case) upon further diving into that study.
We want more trials on Carnivore and different diseases
Another interesting conversation ! I've never heard of either of them but I'm not in the keto camp either. Interesting subject matter though it seems like a very small percentage of the population – eating keto years on years and wondering what the CV impact is if you are otherwise metabolically healthy. I can see why someone would want to do it if it was to treat a very specific illness otherwise idk why someone would ever risk living their life on an elimination diet. From a nutritional standpoint and possible impact on the microbiome it seems- at least at this point with current research- to be unnecessary risk. It is entirely possible to be metabolically healthy eating carbohydrates so why go to such extremes? Just my own opinion. I know we all respond to foods, patterns, exercise differently. So many different factors at play and genetics a huge part of that as well as the composition of the microbiome. I hope they get some answers to their questions even if they are short term results. I have a good friend that has eaten high fat for years and has extremely high cholesterol so I hope they are right :/
Interesting discussion but I have real problems with the idea that our body creates a Lipoproteins – Appo B that will cause death… this would imply a fundemantal problem with our biology. The question is what causes Appo B to become a problem? The idea that it effects some and not others or that its only at certain levels all adds to the problem of the analysis.
Man, you're ruining this podcast with the ads you place every 2 seconds!
“Therapeutic carbohydrate restriction is the best way to deal with insulin resistance”
Adapt your life academy YouTube with Dr Eric Westman and Dr Philip Ovadia
“Insulin resistance is a bigger factor for heart disease than smoking” Dr Philip Ovadia, heart bypass surgeon
This was difficult to listen to.
BMI for Simon is not surprising. He lifts and is fit. He has more muscle. A better question would be adipose % if he was looking for health info.
Also it would have been helpful to spell out metabolic syndrome. I listened but nowhere did I hear why Mr Feldman was pre-diabetic. Did he have metabolic syndrome which includes obesity, high blood pressure, high abnormal lipid profile, and diabetic/diabetics. N=1 is not at all interesting to me. And no control with his study design. Now many lean mass hyper-responder are there out there? Why so they can eat a high fat diet?
Also why risk it? What is the draw for a high fat diet? Is he unable to control his eating unless he limits it to low or no carb?
Obviously I am not as mature as you Simon.
“It’s a lottery bet.”
Of course epilepsy is a different question all together.
But what concerns me is the group of people going keto who has a family history of serious heart disease with family members dying in their 40 and 50s but a way for them to lose weight.
Dave Feldman is hypothesizing that those with atherosclerosis have genetically different macrophages whereas Dr. Cromwell is saying that the macrophage’s phenotypical expression is dependent on its environment, elevated apo B and other chronic metabolic states that elevate inflammation. A common factor that would bridge the two hypotheses to genetically modify macrophages/monocytes are chronic infections diseases such as HIV, hepatitis C, and other viruses, which are known to accelerate vascular inflammation via many mechanisms. For example, normal macrophages infected with HIV have impaired cholesterol efflux due to HIV Nef protein and the HIV rna can bind to toll-like receptors. Both of these mechanisms result in increased foamy macrophages. Both treated and untreated HIV infections can accelerate atherosclerosis, a process that can be further exacerbated by factors such as dyslipidemia, opportunistic infections, drug abuse, and smoking. HCV infection alters receptors, inflammatory mediators and mitochondria function resulting in hepatocyte lipid accumulation and accelerated atherosclerosis and fatty liver. Kawasaki’s disease, a syndrome well known to cause accelerated atherosclerosis in children and can increase their long term atherosclerosis risk, is caused by a number of viruses (adenovirus, coronavirus, rhinovirus and enterovirus) however the exact mechanisms are unclear as there has been a lack of funding in virology. An important unifying factor that could explain differences in long term morbidity and mortality in those with high LDL cholesterol is a person’s acute and chronic infectious disease burden.
Maybe take a look at the Samburu people in Africa that drink just meat and blood, they have done some cardiovascular studies on their people
I think the part I really have a hard time with is thinking that something human beings have evolved with to this point, which is LDL has this set point where the body decides it’s going to use it against us and kill us, to me what makes more sense is man made chemicals and ingrediants and quality of life have more to do with our health than LDL. It’s just hard to wrap my head around the idea that this LDL thing is what has been killing us all along throughout evolution, it’s like, how did we evolve to this point then, just on agriculture ? I’m having a hard time with this, did humans eat mostly vegetables and pasta ?
Any summary, take away? Particularly, if high LDL / apoB is independent (partially) mono-causal risk factor? And why Daves body responds differentenly to (saturated) fatty diet?
(Am not able to listen all currently and found no summary at outro)
FH is phenotype with different mechanisms and genotypes. There are FH people with high LDL and no plaque during their whole life and FH people with devlopping plaque during their childhood.
High LDL can be associated with plaque formation but is it always causal ? or can it be a symptom of a dysfunctionnal ApoB/receptor problem ?
The way Peter Attia treated Dave on his podcast was memorable for its hostility and ambush-like quality.
I’m hoping a big fat slice of Humble Pie and a side of Crow is publicly served to Attia and Dayspring when Dave wins a Noble Prize.
Dave's new model(s) went right over the heads of Simon and Bill. I see where Dave is going but they don't.
Transcytosis is an active process for the immune system. Macrophages (foam cells) are part of the immune system. LDL fuels the immune system and LDL is an opsonin for the immune system. Inflammation is step 2 of the 4 steps of healing. Healing from what?…infection. When you plug in "infection" then it answers all the questions. Transcystosis occurs in the presence of an infection.
Great interview, thank you. The only thing harder to get than a fasting insulin from my doctor is imaging for plaque!! I can buy the blood tests, but other than a CAC I can’t get advanced imaging without a doc. Frustrating. 65 yo F, keto/LMHR for 6 years, otherwise metabolically healthy, no inflammation, CAC 0 for past 5 years, worried about what I can’t see and don’t know.
I'm not sure if you will get a chance to read this Simon, but thank you for hosting such an interesting conversation. It is nice to see balanced conversation around this topic.
I have got two questions/points..
Firstly, the concept of 'metabolically healthy', as alluded to, is such a difficult thing to define. I do feel that simply the absence of a marker of metabolic ill health still leaves a lot on the table. Therefore within the 'lean mass hyper-responders' there is likely significant heterogeneity in their metabolism. I hope that exercise capacity and determinants of health beyond simply a normal BMI and normal glucose parameters are considered by Dave in future research.
Secondly, while I recognise the end point in question has mainly been the presence or absence of atherosclerosis on non-invasive imaging. The hard endpoint on coronary events will at some point need to be considered more. In this regard I have for some time felt there is already evidence towards a more complex answer to the question of ASCVD. In as much as 1/3 of cases of ACS there is plaque erosion rather then plaque rupture. These plaques typically do not have rich lipid cores and are seen in patients without high lipids. Thus when we lump both ruptured and eroded plaques together we do run the risk of 'watering down' the strength of associations. Ultimately I would like to see more understanding in this area which maybe important to tease apart the lipid and inflammatory risk associated with ASCVD events.
This was a great episode as I have been following interviews of Dave and Dr. Cromwell since adopting a low carb (but not necessarily keto diet) due to rising A1C levels. So glad to see them both on your podcast in particular as you are a great interviewer. I am curious if @realDaveFeldman or you have seen discordance between ApoB and LDL levels (e.g. dropping ApoB but high LDL levels) and why that occurs. Also curious if @realDaveFeldman has tested whether he is still insulin resistant and whether one needs to be on a Keto/low carb diet long-term if their previous pre-diabetic condition seems to be in remission.
Listening to Malcom Kendrick, I would love to this Dr and Kendrick compare differences on apob.
Thinking blue light of screens and less natural light #sunrisesunshinesunsetrepeat exposure add epegentic influences
Zero plaque in keto dieters with 600 LDL. The study was long enough for plaque to form. If LDL causes atherosclerosis plaque would have formed.
Interesting. I remember my dad(non keto) had high sky LDL to the point when I took him to the doctor to review his blood work, his doctor was genuinely concerned and was questioning him on whether he was short of breath or had breathing problems. The doctor told him he had never had any patient he had ever seen with such a high LDL level. He immediately prescribed him statins and told him to return in two weeks after another blood test to review. Just for context, my dad had T2D, was a chain smoker, had a poor diet and lived a sedentaryy lifesyle. Being old school, he did not take tge meds, he consumed a whole head(yes whole head not a few cloves) of chopped up garlic he swallowed with water. He did not change anything else. When he went for a follow up and had my dad go for blood tests again as he did not believe test results and felt the lab had erred. Finallly as puzzling as the results were, his doctor had no choice but to accept the results. His doctor asked him if he had done anything else but taken the meds. My dad lied and said no, just meds, why? The doctor said that he had never in all his many years of practice come across anyone whose LDL had dropped so low and normalized in two weeks of the prescribed meds. He said it often takes years for him with the meds prescribed to see LDL drop to that level in his patients. Again my dad did not take up exercise, put his T2D in remission, adopt exercise or healthier diet. In fact he remained a sugar addict during that period and remained a chain smoker. The only change was consumption of a head of garlic a day for the two weeks. No keto, no consumption of 12 oreos daily
It's a pity that MGP wasn't mentioned as it plays a critical role in calcification of the arteries.
It prevents the cacium forming on soft tissues and allowing calcium yo form on bones and teeth as part of the mineralisation of them.
The gene expression gets suppresed when visceral fat toxins get involved.
Vitamin k plays a role in it's activation. When the body immune function is compromised by inflammatory markers, oxidative stress then the allocation of vitamin k goes to immediate survival needs, like blood clotting. See Bruce Ames Triage Theory.
A study was done in 1998 on knocking out the MGP gene in mice.
All were healthy.
100% of them died early with calcified arteries. Not parts of their arteries, all of them.
Both mice and humans have the MGP gene.
@realdavefeldman Insipired by your research me and my husband did TC scan last year and again this year, one year later. My husband last year had the score of 143, this year – 109. How would doctor Cromwell explain this… Please let me add that he is very thin, 76 years old and has LDL of 270. I thought it was KNOWN that calcium score never regresses, and certainly not with such high LDL count. I truly wonder what will the trial show for the cohort of LMHR.
Love this quote by William Cromwell, "people share one thing; it is their metabolic vulnerability and inflammation which significantly distinguishes who lives and who dies"
All I can say is, 66 years old, was told over 27 years ago, go on statins, never did, Iam still here no issues. In the gym 5 to 6 days a week, sauna 5 days a week, do plenty of cardio, either in the gym or in the yard. Changed diet even further 3 years ago, I use to eat lentils and quinoa for lunch everyday, oatmeal for breakfast. Doctor says your anemic, so I changed diet to include more whole eggs, meat and fish, stopped the lentils, quinoa, no processed anything, no sugar, the only sugar is small amount of fruit on weekends only. Fast more then 16 hours everyday, last cholesterol test after 22 hours no food and gym, was over Tc- 300, triglycerides-49. Doctor said was to high, I said, I can reduce it back to 200 if I go back to ice cream, bread and pasta, and by the way, checked the glucose 2 hours after eating organic sprouted oatmeal, glucose shot up to 205, after 2 hours, it should be below 140, I usually range in the 80 to 90s. Could I have plaque, I dont know, but then again, at 66, I can hit the bag 5 days a week, a thousand times, and do 8 sets of 100 push ups straight, once a week and never out of breath.
This was a really interesting episode and great that Dave has done so much research. However, it worries me that as someone who doesn't have a good grounding in how the human body works and how all systems interact with each other, has the potential to influence the general public to make very consequential choices about their health.
We will only see in years to come the impact of a ketogenic diet!
An issue that's important on a population basis is the massive change in diet in the Western world with highly processed foods, refined carbohydrate and frequent consumption of high sugar/high fat foods .They have influenced the huge increase in heart disease, insulin resistance, inflammatory and metabolic conditions.
It would be interesting to see the impact of a high fibre diet including carbohydrates such as brown rice, quinoa, freekah, bulghar wheat, potatoes with skins on, which contain protein, fibre and vitamins and minerals and are broken down slowly would have on ldl and plaque. As well as a range of protein and vegetables containing polyphenols.
Excercise is another factor affecting metabolic disease.
We have epidemic proportions of metabolic and inflammatory disease linked to poor quality diet and a sedentary life style, which is not present in tribes leading a hunter gatherer lifestyle.
Loved listening to the wisdom of Dr Cromwell. I didn't know who Dave Feldman was and while listening to this podcast I looked at his web site. I don't understand how a software engineer (& entrepreneur) is considered "an expert" on lipids?? To me it seems that his entrepreneur side found a catchy way to create a business that caters to the keto crowd. Sorry, I just don't get it?
Feldman is a GENIUS!
It seems that there is a lot of wishful thinking, on the part of Mr. Feldman, to justify the proposition that high fat animal based diets are not harmful.
I don't understand why the body would produce a toxic particle. LDL is there to repair damage due toxins or pathogens.
When you look at huge population data across countries and LDL and All cause mortality, the U-shaped curve makes it obvious that its not a good idea to ask all asymptomatic humans to lower LDL with statins once their LDL is above 100, without considering a whole bunch of other factors (presence of plaque, metabolic syndrome, etc.) It's irresponsible but that's whats happening in the U.S.
There was a study done in Sweden that followed over 4000 people for 35 years. Over 1200 of them lived to be over 100 years old and had higher levels of total cholesterol than the people who died much younger. I'm not going to worry about ldl cholesterol.
Amazing episode! It was super interesting! This is state of the art knowledge. So much inside that's amazing at the edge of knowledge.
I have found it hard to understand sometimes when they geek out on it. I'd love to read more about what they've mentioned, their views and arguments. If you could give ressources that'd be great!
I think a bit more of an introduction with the basics is quite necessary to understand the depth of this. I wonder if you recommend it like a beginner's knowledge video (maybe by you).
Thanks a lot!
Best interview of Simon’s I have watched to date. Big fan of the research that Dave is doing
I'm hearing a lot of talk about the extreme ends here. People with genetic mutations that lead to levels of both extreme highs and lows. If you let them inform your experiments or most of the time even your theories, that's a guaranteed failure. There are so many epistemological errors in that way of thinking there are even idioms for how bad they affect all parts of science. Survivor bias, not seeing the forest for the trees, hearing hooves and thinking zebras etc. etc.
This is not how the scientific method works and for this discussion in particular it's not how you defend a new hypothesis. If you're not automatically discounting the bottom end and the top end of your distribution curves in your hypothesis I don't care what it says because none of it will ever apply to a generalized theory and most importantly it won't apply to me. The answer to someone mentioning something as inconsequential as familial hypercholesterolemia in a discussion about atherosclerosis is "Well most people don't have that and human physiology is too complex to ethically or realistically draw any informed conclusions or even a hypothesis out from an extreme disease, it's a different topic altogether. We have to focus on the majority at this point, not on the extreme exceptions."
I can see the excitement and I am fully convinced that the lipid hypothesis is 99% wrong because clearly doctors and pharma are not helping, everything is getting worse, and it's not people getting worse, it's doctors, pharma and our "food" making it worse. But if you spend time debating genetic freaks as a valid factor or consider them at all really within this current pursuit, all you'll end up replacing it with is most likely going to be equally dogmatic and biased as what we have now. I could only make it about 1h20 into the episode before the fallacies were overwhelming me. The man that came up with the steel man idiom (seemed apt since it was mentioned) fell into this pit already, I'm not following more people down that hole. If you make that turn, no matter the experience or the education or prior status or work, I'm staying on the road.
To me this is nothing more than people talking about the mechanisms of tree diseases while the forest is burning down. You can claim it would be just more iatrogenesis to do a heel turn, but at this point if you can't see the reality that the doctors, pharma and our "food" is killing us, just move the fucking apple.
I am so confused now! Been doing carnivore 5 months. My CAC score was 7. I’m 56 and have had high cholesterol my entire life and never used meds. I smoked and was around secondhand smoke (nana smoked). Triglycerides were 116 and HDL 50.7 LDL was 245.1 and that was the first week of starting diet. I’m going back in a month to check bloodwork. My A1C was 5.8 so I hope that went down. Total cholesterol was 319. Now I’m freaking out. I’ve heard people who have been carnivore their entire lives and are perfectly fine 🤷🏼♀️. BP is always perfect 100% O2 great HR as well. Had a hysterectomy in 2019 for uterine cancer no chemo or drugs.
Great conversation! As a likely LMHR with a non-zero CAC score (BMI 21.0, 130 LDL before LCHF and 350 after, HDL 40 before and 80 after, Trigs 300 before and 70 after), I would ask that the advice to "reintroduce some carbs to lower LDL" consider the fact that some of us are no longer considered metabolically healthy if we do so (trigs shoot back up and HDL goes down). Add to this that increasing carbs brings back chronic migraines for me and I feel forced to select a pharmacotherapy.
Carnism is disease, death, and denial. Why are people so desperate to eat dead animal flesh?
Feldman has a cult following who actually believe eating meat only is healthy even after 100 plus years of scientific evidence. Will he be responsible for all the death?
LMHR is another statement of denial, similar to claiming we are carnniovores. Humans are not designed to consume road kill and dead animal flesh like carnivores are. Common Sense?
1:04:16 terrain theory vs germ theory!