Can you develop Heart Disease if you're not Insulin Resistant? | Dr. William Cromwell
Вставка
- Опубліковано 19 чер 2024
- Can we have plaque in our arteries if we're not insulin resistant? Are "metabolically healthy" people still at risk of heart disease? Does Insulin Resistance raise heart disease risk? How does it do that exactly?
Introductory videos on ApoB and lipoproteins:
• LDL Cholesterol level:...
• Atherosclerosis | Chol...
Connect with me:
Facebook: / drgilcarvalho
Twitter: / nutritionmades3
Animations: Even Topland @toplandmedia
Dr. Cromwell on Twitter: @Lipoprotein
References:
1-www.ncbi.nlm.nih.gov/pmc/arti...
2-www.ahajournals.org/doi/full/...
3-www.ncbi.nlm.nih.gov/pmc/arti...
4-www.ahajournals.org/doi/full/...
5-diabetesjournals.org/care/art...
6-cardiab.biomedcentral.com/art...
7-www.jacc.org/doi/full/10.1016...
8-www.ahajournals.org/doi/full/...
Disclaimer: The contents of this video are for informational purposes only and are not intended to be medical advice, diagnosis, or treatment, nor to replace medical care. The information presented herein is accurate and conforms to the available scientific evidence to the best of the author's knowledge as of the time of posting. Always seek the advice of your physician or other qualified health provider with any questions regarding any medical condition. Never disregard professional medical advice or delay seeking it because of information contained in Nutrition Made Simple!.
#NutritionMadeSimple #GilCarvalho
0:00 Intro
2:03 Insulin Resistance, an independent risk factor?
3:03 Insulin Resistance vs ApoB
9:29 Insulin Resistance, an early risk factor
13:55 ApoB, diet and individual variability
16:52 ApoB and risk
17:52 ApoB production vs clearance
21:09 Components of Insulin Resistance
23:10 Key takeaways
25:09 Recap
Fantastic video, Gil. I'm a big fan of Dr Cromwell, and even if we have some nuanced differences in our hypotheses -- we have quite a bit of overlap on the Venn diagram of metabolic health. I appreciate he presents clear, yet layperson-friendly messaging on the expected risk with ApoB in absence of IR and inflammation. This has definitely been a key consideration in developing our LMHR research, particularly our current study underway at UCLA.
I was just wondering how you find studies to participate in?
0:20: 🔬 Insulin resistance is a significant predictor of cardiovascular events and plaque, with added value on top of ApoB.
3:37: ✅ HOMA-IR and ApoB both significantly predict plaque even when adjusted for each other.
7:47: 🔑 Even if someone is insulin sensitive, they should still monitor their ApoB levels, and vice versa.
23:07: 🔑 The speaker discusses the difficulty of reassembling data on various factors related to health concerns.
11:55: 🔍 Insulin resistance leads to lipoprotein abnormalities before changes in glucose and insulin levels.
15:05: 🔑 Keto diet can affect both the production and clearance of LDL particles, leading to high cholesterol levels.
19:05: 📚 There are agents that work on both the production and clearance sides to decrease ApoB levels in the body.
Recap by Tammy AI
I’ve been on a weight loss journey this year since 1/28/23. I’m down from 432lbs to 300lbs as of today. I had a Cardiometabolic Report done by Precision Health back in July. Dr Cromwell explained my report in a way that I could understand it clearly. I can’t wait for my next report to see how much changes have been made!
That’s awesome! Keep it up.
Especially as you get closer to your goal weight, it may be useful to take diet breaks. It doesn’t have to be one big go.
The channel Renaissance Periodization has some good videos on the topic (and solid info in general)
A affects CVD risk. B affects CVD risk. And C affects CVD risk. A and B and C together would have a compounding effect on CVD risk and just because one factor is missing doesn't make either A or B or C alone less of a risk. The only person who would be considered incredibly low risk for CVD would be the person without A or B or C.
what if A actually causes B and C.
poor diet causes fatty liver causes IR causes high triglycerides and high apob etc.
@@sketchartphoto8117 That is wrong. Insulin resistance is not caused by fatty liver, it is the other way around. Insulin resistance on the other hand is caused by excess visceral - not subcutaneous fat.
Excess visceral fat is caused by inactivity and overeating, like any other type of fat tissue overgrowth, as well as stress.
Genetics determine where your body prefers to store fat, some do on the hips, some do on the butt, some around the chest, and some inside the belly. Men unfortunately tend to get visceral fat more then women for example.
So no, poor diet does not cause fatty liver, isocaloric studies of high fructose and high glucose as well as high saturated fat diets and the development of fatty liver clearly proves that. It is not about what, but how much you eat.
An increase of triglycerides has been shown in insulin resistance, but also is seen in insulin sensitive people eating a high amount of refined carbs.
Same with a diet high in saturated fat and trans fats.
So a poor diet is independently associated with high TG‘s. 😉
So high TG - raise ApoB by raising small dense LDL, so particle number is high while LDL-C might not show that, since small dense particles have very few cholesterol molecules inside.
It is a bit more complicated:
In this case A (high TG‘s) causes B (high ApoB). But B can be there without A, when C (high saturated fat diet) or D (genetics) is causing that. C can be neutralized by specific D‘s so there is no B, and if A not present no increased risk.
C and specific D‘s combined can create extreme B‘s as well and high risk and very high risk if A is there as well.
A does always lead to B, so can‘t be seen as independent risk factor.
B always leads to high risk, wether A is present or not.
B can be caused by C or D
C does not necessarily cause B, and D does not necessarily cause B.
Thank you, Mr. Spock.
I wish I had Dr Cromwell as my stats lecturer. He has a way with words.
I really enjoy when someone can take a very complex topic and boil it down. To be able to simply explain such a complicated and nuanced topic is rare. Wonderful content!
Nicely done, Gil and Dr. Cromwell.
Cheers
Mario
Dr Cromwell is really awesome! Thanks Dr Carvalho for this great interview.
Paul saladino needs to watch this video
I really appreciated Dr. Cromwell's explanation of the relationship between APOB and Insulin Resistance, and how each are risk factors for CVD. Fabulous information!
I remember when I was in medical school (~2015), I was explicitly taught that "insulin resistance" is not actually a thing 😂
Yep 5 yrs after med school 50% of what is taught is now updated or wrong.
So interesting how he broke down the whole data analysis with homIR and apoB in a way that somebody that jnows regression analysis understands what he means, but also someone who never worked with data!! Kudos!!
But i would pay to get more detailed insight into the equations etc...so much to learn there i think!
Thank you! This is simply invaluable in helping to understand the whole picture!!
Terrific video. You do mankind great service Dr Gil. Please keep producing such videos!
The quality of information and presentation on this channel is consistently outstanding!
This was great ! Thanks Dr. Gil awesome guest 👏
That was absolutely fantastic...and actually something I needed to listen to and learn.
Really great video and interview. I’m trying to think of questions but all was so well explained.
Such a great explanation by Dr. William Cromwell! Thank you so much for all your work, Dr. Gil Carvalho! Always learning new things from your channel.
I had a heart attack 10 years ago. Did not have insulin resistance, but did have slightly elevated LDL - enough apparently to cause some artery clogging plaque. Looks to me like ApoB can be a risk factor on its own, in addition, of course, to the ways it can interact as part of a larger landscape with insulin resistance as described by Dr. Cromwell. I reversed the cvd by eating a diet of whole plant foods.
May I ask how did you measure insulin resistance ?
@@kulkarniravi I had no signs or symptoms of insulin resistance - no elevated blood sugar, no elevated triglycerides, no large waist circumference, etc., etc. And, I have no measurable indicators of cvd 10 years after the heart attack, after eating whole plant foods the whole time, which clearly addressed elevated ApoB, and was the correct remedy.
How did you positively conclude you reversed your CVD?
@@alesis100 As I said in the previous comment, I have no measurable indicators of cvd 10 years after the heart attack. And no chest pains, able to exercise vigorously, and a clear ultrasound scan. That good enough? :) Eating whole plant foods over 10 years addressed elevated ApoB, and was the correct remedy. "The proof is in the pudding."
What was your fasting insulin?
Very interesting discussion. I get the impression "inflammation" is critical in all this but that it is also used as something of an umbrella term to explain a number of different physical processes. I'd like to understand that better.
I didn't hear him use the word "inflammation"often (did use at end) It's more of a waste basket term.
Puh, that‘s a big topic, you are right. I‘m not sure if it‘s fully understood in all cases - like for example in autoimmune disease.
You have also to consider that inflammation in general is nothing negative, it only is when it overshoots and or becomes pathological.
It is part of our innate immunity and is the first line response to any kind of pathogens.
It also acts as cleaning process essential for the body to heal and regenerate, for example seen in healing grazes, cuts or bone fractures.
But it also can harm the bodies own tissues while defending the body from pathogens, especially if the immune response is overshooting,
or as chronic inflammation causing little damage over a large proportion of time.
Mechanisms vary, many cells and signaling molecules are involved.
If you haven‘t you could read about the innate immunity, what cells are involved and what mechanisms there are.
Need to do that too again, I already have forgotten things about this topic😅.
Inflammation?
Some search topics
Inflammation and cardiovascular disease
Information and kidney disease
Inflammation and diabetes. Btw, Alzheimer's is often called diabetes type III
Inflammation and neurodegeneration
Inflammation and cancer
Note that a plant-based diet is universally anti-inflammatory
Note that a carnivore diet is universally inflammatory
Take your pick . 😂
FANTASTIC interview! This channel has become a benchmark for solid information.
Thank you Gil for Dr. Bill Cromwell
Excellent! I get so frustrated with people saying it’s all about insulin resistance and others sayings it’s all about LDL as if it is so black and white. If only Biology was this simple. You have a lot of factors that play into the risk and these factors interact with one another. Bottom line! It’s complicated. Coming from an expert like Dr Cromwell we can be assured as to the limits of the current science. Sounds like we have a lot of work to do.
The largest amount of work we have to do is on ourselves and our belief systems. Unfortunately people want simple answers to complex questions. Atherosclerosis is not a simple disease!
i have high triglycerides. when I reduce it through excercise, ldl sky rockets. can you please give an explanation? my ldl is 208, triglycerides is 276. previous it was 160 and 321 respectively.
Wow, fascinating! Thanks to both 😊❤
When the topic has so many moving parts, it makes your head hurt...
Yes, I feel like my head spins when I listen to all the info.
Very helpful! Thanks to you both.
Fantastic video and explanations, thank you.
Bravo Dr. Gill. This is an amazing episode. Finally IR is getting its due attention.
Fantastic work
A good kick in the you-know-what for all those simplistic diet gurus!
Fantastic explanation. It's clear what Dr Cromwell explains. Both ApoB and IR matters for heart disease. And losing weight is the 'simple' way to improve things. Thank you Gil for this valuable video
Another very good video! Thank you
I have watched many of these posts by NMS, and I must admit he seems to adhere to a non-biased approach, although that is impossible. I am grateful for his analysis and interpretations. As an engineer (a different kind of analyst) I think he's mostly correct in his independent analysis. Sometimes I must admit my bias against epidemiological evidence studies versus double blind studies is based on what I've been fed by others. I think he is by nature of being a human being subject to the same kinds of bias. I absolutely love his interviews, which educate us all.
Brilliant video.
FINALLY -!- this puts all of the competing theories of HD into perspective. It's not the simple one sentence answer we all crave, but it's clearly CORRECT and enlightening. Thank-you both.
Epic. Both sides should have learned incredible lesson. Both high IR and ApoB are bad, work on both with diet and exercise and if not to goal, meds could take you rest of the way. Dont stare yourself blind on just one part of the equation.
Too long didn't read version?
All factors will COMPOUND. Doesn't mean if you are great in A means you can ignore B.
They all impact each other one way of the other.
Best way is to keep all factors low.
Dos doctores sumamente inteligentes y respetables. Muchas gracias por compartir esta informacion indispensable.
Very interesting, thank you!
Very interesting video. I have another question regarding cardiovascular/general health besides lipid (patho)physiology.
I see a lot of scientists talking about „lacking“ nutritients in a low meat/vegan diet => Mebicos (meat based bioactive compounds) especially creatine (which we have a lot of evidence of), taurine, carnitin, so on and their influence on health. The main points are that these compounds are fully lacking in a vegan diet and the the body’s synthesis is generally insufficient.
So my question would be: are these compounds really as important as people make them out to be? The scientific literature is a bit overwhelming regarding this topic so it could maybe be an interesting video idea.
Greatings from Germany.
PS: i know about this topic because of an austrian scientist called niko rittenaus. He also held a very facinating lecture regarding this topic, called something like „Mebicos and athletic performance in vegans“ (and it is available in english)
My ldl level was high -151mg/dl .In the same blaod sample, my Apo B level was 67! On the lower end of normal.
There seems to be a big disconnect between apoB levels and ldl levels in some individuals.
yes! the second part of this conversation will cover this (called discordance) in detail
The dietary and medical intervention studies performed on lipid levels should ditch LDL for ApoB. Otherwise it could lead to wrong conclusions.
Hello Dr. Gil. I'm a fan of your work, especially how you evaluate evidence. I was wondering if you could address a vegan diet? I recently saw a film called "what the health" which supported a plant-based diet stating essentially that meat of any variety and eggs were significantly linked to cancer and health issues. Whereas a plant-based diet reversed all manner of maladies. I'd really like to hear your views on the subject.
I appreciate his even handedness and those who think their fitness means they'll never get a heart attack need to see this video. Just wanted to mention that homa-ir is inferior to lp-ir as a measure of IR, and Dugani et al 2019 shows lp-ir as having far more predictive power for cvd than apob. Only mentioning it because he said apob more potently predicts cvd than homa-ir, but that's because homa-ir does not measure IR as well as lp-ir.
Great mention. Dr. Cromwell is one of the creators of LP-IR and would agree 200% with you that it’s better than HOMA-IR.
This sounds very informative, and I'll admit I'm early in the video. Would you be willing to explain your comment in a way that those of us who did not major in the sciences may understand? Thanks
IR raises ApoB, but ApoB is still the stronger predictor. The lesson of this video is that neither one should be ignored.
@@rejoyce318 Sure. For my study reference just google dugani jama association, this should put the jama network heart disease risk study at the top of the results, go to it, then click figures and tables once you found it, then look for Table 2. Sorry youtube does not let me post a link straight to it. I just realized its a 2021 study, not 2019, my bad. Table 2 shows the heart disease predictive power of several factors. The first column is hazard ratios (HR) for women under 55. A 1.0 means something has no predictive power, a neutral hazard ratio. Apolipoprotein B has an HR of 1.89, meaning if your ApoB is high you are at double the average risk of heart disease. yikes. Down near the bottom you see LP-IR has the highest HR, 6.4. That means if you are pretty out of shape your heart disease risk is 6 times higher than average if you are a woman under 55. And it ALSO means if you are in really good shape your risk is only 1/6th of average. lp-ir measures insulin resistance, a low lp-ir score means you are insulin sensitive, which more or less means you are in very good shape. The internet is flooded with people believing their apob does not matter because they are in very good shape, based on research like this. Gil wants to help these people see the bigger picture so he made this video, as there is of course no single item that prevents heart disease. My comment was mainly to point out that while no single item prevents heart disease, a low lp-ir score should be everyone's top priority.
LP-IR is an insulin resistance measurement based on lipoprotein size and number. HOMA-IR is a measurement of tissue insulin resistance. Baked in the LP-IR calculation is a rough measurement of ApoB. Of course it has more predictive power than lipoprotein measurement alone, because it's a combination of both. If you're trying to compare insulin resistance to lipoprotein counts, you can't include lipoprotein in the insulin resistance measure.
I'm 49 and my A1C has just hit 6.4 in the last 6 months (previously 5.7), then I was diagnosed with diabetic retinopathy. I have had PCOS, but was thin most of my life. I've been struggling with my weight in my 40's and now I'm obese at 5'5" 187 pounds. My normal weight used to be 127 to 130. If I'm having all these health issues now, I fear what will happen as I age unless I get my health under control. I've tried intermittent fasting and I must have eaten my calories back when I ate my meals because I just bounced up and down 7 pounds. I'm on Metformin 500 mg to protect my eyes, but I just learned it induces muscle atrophy. My neck is fused and I'm afraid it will make me have more back surgeries since it weakens the muscles. At 49 I'm overwhelmed with my health issues. Never thought it could go like this so fast.
Hello, I hope everything improves for you. Maybe if you ever try intermittent fasting again, maybe have a support person or group that can help you keep on track. As someone who was recently diagnosed diabetic with an A1C significantly higher than yours along with other issues. Believe me I understand what you're going through.
I'm realizing that in some areas having that support group is really beneficial for emotional health. I don't think I'll ever underestimate the importance of emotional support ever again. Once again, best of luck to you and please if it's all possible look for support groups that specialize in the things you're interested in.
I know for me finding groups that mainly focused on the things I'm looking for has given me knowledge and keeps me on track. Best of luck to you.
Forget abt the worries ma'am, and just take ur meds. Eat right and exercise. Got diagnosed with T2D at 24 yrs old (male) on 07/16/23, with an HBA1C of 10. I'm 5.7 and weighed 100kg at first. I didn't take my Metformin meds, said i cud do tins on my own without it, which i did and regret. I Exercise reg, was on low carb at first, but stopped and went back to high cabs 😂. But i peer my foods with veggies and proteins, and I'm also on a calorie deficit.
I didn't check my BS for almost a month wen i went back to high carbs, found out later they where very very high as a result of my blurry visions coming back. So i started taking my Metformin after eating recently, and it sure helped. Currently I've lost 8kg in almost 3months, now i weigh 91kg, and walk for 1 and half hr after breakfast.
The point is, don't stop taking ur meds and doing the tins that are right, just bcus of some side effects it might have u found online. Like me i wished i never stopped, bcus i got back my "neuropathy" that i beat b4 wen newly diagnosed with T2D. Having it back recently was very scary. But the moment i started taking Metformin with my high carb meals, i noticed the symptoms were reduced, and is working.
So ma'am, pls continue what you're doing with ur meds until you've reversed ur T2D. Even after reversing T2D, get off the meds slowly and not once. I know we all don't like taking meds, considering wen they have very many side effects 😂.
Wish u d best ma'am as u fight T2D. We're definitely winning this fight 💪.
@@bbll3729 Well said 👏. I'm also T2D, with an A1C of 10 🤧
Have you tried lowering your carbs? For me intermittent fasting starting working a lot better when I lowered the carbs, controlling the blood sugar and insulin with food makes a big difference for many.
The best explanation I have heard. Maybe I missed it but was the root of the damage essentially inflammation when the other factors were present such as ones of genetics?
No. He said there are many risk factors and trying to divide up which one contributes what to the cardiovascular disease process is extremely difficult.
Thank you Dr. Carvalho, Dr. Cromwell for this invaluable information.
You've provided science - based facts, not some soundbites as certain UA-cam 'doctors' do. They cause confusion. You both helped to clear that.
Bravo 👏 👏👏
These conversations are awesome, and I’m really starting to understand the interactions. I do seem to have some plaque in the lower iliac aorta and traces in the carotids; however my ApoB and Apo(a) are fine, my LDL is kind of okay, and my triglycerides to HDL ration is 1.6 which I understand is good. So it all seems to come down to my pre-diabetes I’m working on now, and another factor you never hear about: I have been taking Fluoxetine and PPI’s for years and I read they both seem to inhibit LDL uptake by the liver. Is that another pharmaceutical scandal coming down the line, and why don’t we hear more about this, since both these medications are and have been heavily prescribed in the US and Europe?
PLEASE make a video discussing the crux of many proponents of plant based: animal protein. If the entire source of nutrition is actually carcinogenic or whatever else we would all be interested!!
Dr greger talks about it a lot but you’ve made me skeptical of him lol
It all goes back to diet + exercise, and maybe a drug or drugs when needed.
How does alcohol consumption affect both glucose and cholesterol levels?
Thank you Gil. Can you please clarify this: In one of your prior videos I believe you indicated if LDL was low enough (like below 70 mg/dl) for long enough (like most of your life), there would be virtually no CVD (backed randomized clinical trials); is this not really the case, as it seems if you are insulin resistant with low LDL, significant CVD risk is still present? The new takeaway is IR is as important as LDL levels (bridging the keto camp with the lipid camp)?
I thought he was saying that if LDL was brought low enough, then atherosclerosis might begin reversing. Also, that people with lifelong very low LDL, had very low CVD risk. in other words, very low LDL reduces risk (but does not eliminate it)?
It makes GHz be that one average people, only reach such an LDL levels when not insulin resistant
Wow. So people in ketosis that have low insulin resistance, are normal weight, and have high APoB are at risk of heart disease due to poor clearance. So how do we better clear ourselves?
In my case, it's Ezetimibe. Just 5 mg (approximately, half a tablet of 10) and my LDL-C is around 40 and my App B around 50. I'm not a canonical LMHR but my LDL-C tends to skyrocket when I lose some (significant) weight.
Allegedly, I'd like to see how they define IR.
Gil, I can't find your two full day of eating videos. Did you take them down?
we took down at least one of those a while back when we did some housekeeping. they were older and just anecdotal so we thought they offered little value. we could easily do an updated version but not sure how useful it is compared to the content we're putting out which feels more informative (?)
Please make a video about vitamin k2 + v D3 and magnesium . Can they lower LDL ? What are the benefits? what is your intake in general?
Toward the end he starts to talk about inflammation and I was wondering in what context he's talking about inflammation?
I tend to have skin inflammation problems and I often wonder if that doesn't translate into arterial inflammation.
Gil, I believe you lumped together esodomibe and statins as methods of clearing. I thoght that ezodomibe is clearing, while statins are decreasng poduction. Am I wrong? I have an issue with clearing, but no cardiologist will start me on ezodomibe. I was proscribed rosuvostatin and about to start it. Thank you.
good question, the immediate effect of statins is to inhibit cholesterol synthesis but as a result, the liver pulls lipoproteins from circulation (increasing clearance) and this is what's thought to lower risk
@@NutritionMadeSimple thank you. Esotomibe inhibits cholesterol absorption. I am a hyper absorber. But the guidelines for cardiologists are to first try statins and only go to esodomibe if the statins are not tolerated. I guess the final result is the clearing in the blood that you are talking about, but the way to achieve it slightly different. That's how I understand now. Thanks for explaining.
Thank you so much this incredible presentation. Did I understand correctly that a rise in cholesterol levels can be an early indication of insulin resistance?
Especially Triglycerides
I can't find a doctor who pays attention to ApoB. My PCP and preventative cardiologist both told me that it didn't matter and they wouldn't even order the test. I had to order my own ApoB test. How can you find a cardiologist who realizes that it's an important measure? I've tried asking around locally but no one knows what I'm talking about.
Wow! In this day and age that is crazy. I had a PCP back in 2016 who was really good and was concerned about my lipid panel given heart disease in my family. He sent me to an endocrinologist who just happened to also have lipidology as a specialty. He's been running Apo B blood work on me since 2016. My daughter is an internist and she said typically PCP's are not ordering Apo B - that it's more typical of cardiologists. My preventive cardiologist will run one if he notices that my lipidologist hasn't done so for him to look at. What neither seems to care about is the PLAC Test for Lp-PLA2 enzyme as a marker for inflammation in blood vessels - linked to increase in plaque in arteries. So, like you I ordered my own.
I sure did develop heart disease without insulin resistance. I was just a speed junkie
What I'd like to know (since apparently in my country NO lab tests for Apo-B) is.... can you have high Apo-B if you have low cholesterol? In particular low vldl and low ldl? Just want to know, as i can't test my Apo-B, but i can test total cholesterol, triglycerides, ldl and vldl. Does anyone know this for a certainty???
It has been stated multiple times that if you can’t check ApoB, the second best test is non-HDL and then LDL.
@@CharlieFader Thanks for the reply. What do you mean by non-hdl? All the lipids except hdl? So total of triglycerides, vldl, ldl?
Edit: OK, I just looked it up. Here's what the Mayoclininc site says:
"Non-HDL cholesterol, as its name implies, simply subtracts your high-density lipoprotein (HDL, or "good") cholesterol number from your total cholesterol number. So it contains all the "bad" types of cholesterol.
An optimal level of non-HDL cholesterol is less than 130 milligrams per deciliter (mg/dL), or 3.37 millimoles per liter (mmol/L). Higher numbers mean a higher risk of heart disease."
It mentioned that this is a better measure of heart disease than cholesterol ratio, and that cholesterol ratio is a better measure than just LDL. Here's what they said with regard to calculating the cholesterol ratio:
"To calculate your cholesterol ratio, divide your total cholesterol number by your HDL cholesterol number. So if your total cholesterol is 200 mg/dL (5.2 mmol/L) and your HDL is 50 mg/dL (1.3 mmol/L), your ratio would be 4-to-1. Higher ratios mean a higher risk of heart disease."
Hope this helps someone else, as it helped me.
@@pragooutube yes, a simple calculation would be total cholesterol minus HDL, but in the actual test the result I think represents the sum of LDL, VLDL, IDL and Lp(a).
You see people...factors amplify together. It's not just one or the other.
Does anyone researched impact of vegan or pescatarian style of keto diet (very low-carb diet) on lipid profile? Assuming for example that lot of your energy would come from SCFAs produced by fermentation of soluble fibers, which we know have quite positive impact on lots of health markers.
I get the impression that the false dichotomy of either factor A or factor B is the sole significant causal risk factor for CVD, is a necessary tool for promoting certain diets and foodstuffs. The confusion is therefore likely to continue since there is a lot of money riding on it doing so.
Great video. However, the mother of all questions is what causes deposition of cholesterol on atrherial walls? LDL is a product of evolution. We can't stay alive without it. So, what causes sticking to walls? How we get from clear atherial walls to cholesterol deposition? Particle number?
LDL oxidizes and creates peroxides and is used as an immune system function dealing with infections and microbiome imbalances. High LDL = Inflammation, and long term is caustic to the arteries which creates scar tissue and can lead to atherosclerosis. That's been known for decades but youtube MDs and keto/carni clowns 🤡 evade, avoid for clickbait videos because of monetization catering to an echo chamber of meat and fat addicts and pigeonholed themselves. Or they simply don't know out of shear ignorance and idiocy. High BMR burning proteins and fats as a main energy/ATP fuel source creates higher uric acid byproducts and ketoacidosis, which then the blood dumps into cells to prevent acidemia, long term that creates cellular acidosis which proliferates bad bacteria (pH below 7) and allows easy viral infections (5.5-6.5 pH). Most viruses require an acidic environment to penetrate cells and can lead to sickness and cancer. BadFad diets that lack Oligosaccharides which are exogenous and used by the immune system to attach to infected cells and remove them and are not created by gluconeogenesis, that long term cycle will raise Oxidized LDL dealing with the infections and by the diets. Google: "Oxidized LDL, Cholesterol, Inflammation and Atherosclerosis" and see all the decades of studies, data and facts.
My LDL is 120-130 mg/dL, A1C ~6 to 6.2%, BP
When he said "a long time", is he talking years, decades?
To me, resistance versus sensitivity are factors in how hyperinsulemic you are. High levels of insulin cause over expression of many things. Joseph Kraft postulated that heart disease and diabetes were two sides of the same coin.
Is Gil Carvalho Brazillian?
No, he is of Portuguese descent but still American.
If your ApoB is below 50 all your life, will there be zero atherosclerosis?
So yes.
Insulin resistance leads to glycosylated LDL particles. ApoB is a great way to measure the number of LDL particles, but whether those particles are glycosylated or oxidized or not is as important as ApoB itself. Also, insulin resistance raises triglycerides which pushes glycosylation by raising blood sugar, AND by shifting equilibrium toward glycosylation events.
I am fairly sure he made videos explaining why oxidation doesn't make a difference.
@@privtprofile24 Let me know if you find one, since there is massive research into oxidized LDL using it as a predictor and cause of atherosclerosis. It is also an explanation for the so called fish oil paradox.
No not really. When hundreds of particles with high pressure and velocity are shot against a thin wall like a bullet repeatedly you don‘t need any additional factors added to those particles to actually penetrate the wall. We do have those - for example Lip(a) attached to the LDL particle. Glycation is not a good example here, because it happens regardless of the presence of insulin resistance or not. The body has to keep blood glucose at a certain level in order to stay alive - and so glycation will happen in any case.
Ox LDL is not that big of a problem as you think it is. We are adapted to them. We do have immune cells recognizing and neutralizing them, there are ox LDL- antibodies. You should not mix up oxLDL circulating in the blood with a LDL getting oxidized due to the immune response it triggered when stuck in the artery wall. The last one is the relevant one in arteriosclerosis. The other one becomes relevant when we already have a first LDL stuck in the wall and getting oxidized and foam cells are forming.
Come on, should I tell my great aunt that it is not scientifically possible that she had a stoke by the age of 47 and a heart attack by 52, because she was not insulin resistant? Well she did have those regardless.
What about those young kids with homozygote familial hypercholesteremia getting heart attacks in childhood? They are not insulin resistant.
Cardiovascular risk for a diabetic is elevated 2-4 times,
For someone with heterozygote familial hypercholesteremia the risk is elevated 10 - 20 times.
The numbers just do not add up either.
I'm sure there's a video on glycated ldl. these glycated ldls got cleared in minutes after they are produced
Go and check, u are watching too much of low carb video
@@lenguyenngoc479i don't watch low carb videos. I'm a research exercise physiologist and my wife is a cardiologist of 15 years. I can't find the video you are referencing. I CAN find 400+ journal articles on glycolytic and oxidative modification of LDL and it's affects on raising Apob and increasing atherogenesis. Decreases reuptake of LDL, raises CHD risk.
I have a CAC of 147 and my insulin response is very good. By definition, I have heart disease.
As he said, it's a multitude of factors that determine heart disease. So many people blabber on about Insulin resistance is the main reason when really it's only a part of the puzzle. Hear this alot from Keto dieters!
My question is mechanistically are insulin resistance and metabolic syndrome the result of the same thing.
My guess is clearance improves with exercise.
Quick someone ping Saladino
This all sounds like the intramyocellular lipids are the cause, since they play a central role in insulin resistance. The saturated fat clogs up the cell where the insulin is supposed to open it, insulin can’t open it, blood sugar can’t get in and it accumulates in the blood stream, more insulin is needed to do the job. This happens in the muscles and the pancreas. And obviously high saturated fat increases apo B in a dose dependent manner. Yet the low carb people don’t tend to see the insulin resistance, since they don’t consume carbs, so their blood sugar is always fine, even though their insulin resistance is probably bad, but masked. An A1C test is not gonna tell you the whole story, but while their diabetes seems “controlled” their lipids show the reality of the situation, those can’t get masked.
This is what vegan doctors have been saying for years, Neal Barnard for instance, and everyone likes to poo poo over him but that theory well explains why both apo B and insulin resistance are avenues for heart disease. This is something Roy Taylor has identified too, lower the calories and clean the fat from the pancreas, you solve your diabetes. And let’s remember that vegans that consume a low saturated fat diet (whole food plant based) tend to have the lowest diabetes and cholesterol numbers.
All this risk factor analysis without any theory is not persuasive. We need to understand mechanisms and why certain things behave the ways that they do to correctly specify and compare models. Does insulin resistance and apoB interact? Might there be a mediated relationship? How do we rule out other obvious confounds?
Mechanisms are difficult and take a long time to figure out because the human body is a complex thing with complex interactions that are hard to understand. Many of these mechanisms may take decades to completely work out through experimentation and randomized controlled testing of various hypotheses. In the meantime, we should take advantage of all of the information that's available instead of waiting on the mechanisms to be fully understood and proved out in a theoretical framework.
@@nichtsistkostenlos6565 Science proceeds by gathering facts in light of hypotheses. Much of medicine is empirical collection of risk factors without regard to hypothesis. If the risk factors are very strong predictors and we have no idea why, then those predictors can be actionable. But then we also end up coming up with interventions that are not as effective as they could or should be. This is a large part of the reason that there are such entrenched camps on health numbers.
👍
Gill , I was starting to believe everything he said right up to the end. He just indicated to me that APOB is more important than anything. Just doesn’t fit the common sense test when you have people with high levels for decades all the way up into the 80s. There has to be different factors involved now I understand because he is a lipidologist.
we have a video coming to try to explain the individual variability but it's the same with every risk factor. many smokers don't get lung cancer. genetics always matters. risk factors work probabilistically
great thanks I really want to know about the mitochondria. The disfunction that drugs cause
weight loss by lowering visceral fat, fatty liver, bad cooking oils and processed carbs will do wonders to IS and triglycerides and ldl for everybody and anybody with IR
All the attempts to boil down the confluence of factors into a simple narrative tend to avoid the one simple narrative that seems universally true. It is incredibly bad for you to be overweight.
24:35 It's A-PO-b.....
....
[sry had to say it]
My first guess without watching is that you can have heart disease without insulin resistance.
I was view number 777!
I was view number 681, I just finished the video.
The more single ingredient carbs and less fat and oil you eat, the less insulin resistance and heart disease.
Excellent discussion. Speaking for myself, there's interest in furthering this discussion. In my case once you've gone beyond risk and the damage is done (EF 20-25%): does any of this matter?; Can EF be improved?? or only maintained preserving what little you got?
I don't get this debate. Anyone who gets hung up on insisting HOMA-IR is the end all an be all for good health and LDL/APOB is unimportant must have psychological issues. No rational doctor is going to ignore either insulin resistance or high cholesterol in their patients. Regular exercise and a healthy calorie restricted low saturated fat, high fiber semi vegetarian/vegetarian/vegan diet and a statin or other suitable cholesterol lowering drug will help anyone and everyone. Haven't we known this for many decades?
I'm with you. Lowering ApoB is always good, as long as the means by which you lower don't have side effects which counteract whatever good the lowering does - personally I'm on atorvastatin 10mg/d because my LDL is very high, but I happen to tolerate statins well. Not everyone does. But yes, lowering ApoB is an unalloyed good. Becoming insulin sensitive is harder for me. Lifestyle adjustments do nothing for my insulin resistance (and nothing for my ApoB), I excercise extensively, have a very good diet etc., so I'm wondering what medication might work - metformin didn't work for me, and besides metformin has unacceptable side effects of abolishing the benefits of exercise. The worst thing is how poorly equipped most doctors are to handle all of this - my PCP has been pretty useless wrt. my insulin situation, sent me to a doctor who handles diabetics (I'm pre-diabetic) and that guy was useless too. Unfortunately, in many respects medicine is still in the middle ages.
People that are insulin sensitive aren't getting heart disease. Failure to define IR in this video.
I don’t know what dr you are seeing, but in my 70 year experience, no dr has ever bothered to look at insulin resistance and they certainly don’t test for APOb which many dr won’t do even if you ask for it. They only look at LDL and do a fasting glucose test that is useless in predicting IR as your pancreas will increase insulin output to correct the glucose level. More Recently A1C is a better test for overall glucose control, but still doesn’t test for high insulin.
I was vegetarian from 2010 to 2019 with normal cholesterol every year until 2020 and then last year my brother who is 3 years younger than me had a heart attack. He’s fit and walks 5 miles a day and not overweight, but tested pre-diabetic. So I had Calcium ct scan done and results were over 1000. And I had no clue. And this had to have been developing for the last 15-20 years, when again my cholesterol was normal and ate very little saturated fat.
Short answer, It’s complicated