*1 AMENDMENT* AMENDMENT: It’s been pointed out to me by @F0Xit (on RUclips) that the researchers (Study 246) should have done a Bonferroni correction on the data. For those not into statistics, if researchers perform multiple comparisons (group A vs group B), it’s common practice in statistics to perform some form of correction, because the risk of detecting an effect that isn’t truly there increases with more comparisons made. A Bonferroni correction drastically cuts down on that risk, which is why many statisticians argue for its use. If a Bonferroni correction were applied to all the data (19 comparisons), the true p-value to meet would be 0.00263 (much lower than the typical 0.05 and what I reported in the study). However, I met with a statistician here at my medical school to discuss the topic, and he argued this would be the incorrect use of a correction, because some of the measures are independent of one another. Technically, he argued none of the comparisons should have a correction applied to them, but he mentioned he could see an argument for some of the measures being corrected (6-9 of them in Table 2). So, if we assume a middle ground and a correction is applied to 9 comparisons, the p-value wanted would have to be below 0.00556. If no corrections are applied, the results are as presented (based on a p-value of 0.05). In the end, even with the most strict option (option 1), some of the effects are still significant. More are significant in the middle option, and obviously all the ones I reported are significant in the uncorrected option. Thank you to “@F0Xit” - I learned something from the comment (below), and although I wasn’t a stranger to statistical corrections, I’ll be on the lookout in 2 sample tests just as I do in multi-sample tests. “None of these measures are significant. When you have so many comparisons you need to correct the p-values. This is done with Bonferroni and with so many comparisons you should divide 0.05 by the number of comparisons (you have 19 observables in the first two tables, therefore is 0.05/19= 0.002). Bonferroni is a quite strict corrector, you may want to use Holm-Bonferroni. This study is statistically quite weak. Although, it may be useful for future meta-analyses. Note: I do medical statistics for a job.”
If you have 19 comparisons and only one of them shows a positive effect, then the p-value should be 0.00263. However, if multiple comparisons show a positive effect while none show a negative effect, the the p-value can be increased again.
HIIT. Most ischaemic events (heart attacks and stokes) occur when a plaque bursts and the outpouring of goo causes a large blood clot which then affects the heart or brain. You have to be careful starting HIIT as this additional pressure can cause plaques to burst and cause an ischaemic event. This happened to a well known BBC presenter in the UK who suffered a stroke trying HIIT.
are you implying that if we've had a bypass (ie lots of plaque), then we shouldn't be doing any HIIT? HIIT is the best way to build collateral arteries
If you had bypass, then stenosis as a result, possibly tied into bad artery. What are my choices, what testing can i do. I never had a heart attack. Im completely lost.
@@bradkeenan4428 If you have narrowed arteries from atherosclerosis then you may have had angina pains or your doctors found calcification in your Coronary arteries. If narrowing is severe then your doctors may choose to operate without you having had a heart attack. Any thought of HIIT must be discussed with your doctor.
Very interesting information! I think another thing to look at would be nattokinase supplementation. There are a couple studies that show pretty dramatic plaque reduction, but the dose had to be high enough.
The vast majority of supplements to reduce LDL and apoB have been found to be pretty much useless. Plant stanols or sterols can reduce it by 5% but a simple 5mg Rosuvastatin give you 39% reduction. nattokinase supplement unless from tested scientifically verified trial should be avoided. The famous SPORTS trial showed supplements are generally useless for LDL reduction
I'm taking 12,000 Fibrinolytic Units of nattokinase every day on an empty stomach and have never had any stomach upset. Food will deactivate the Nattokinase, so it's important to take it away from food. @@thomasmuller1850
On another note: soon new CT photon counting high resolution scanner will be able to reveal intima borders of coronary vessels, information that was previously visible only via OCT wich is highly invasive. No study as of today could compare CT and OCT conclusively because of low resolution. When more data will be available we may be able to see regression in atherosclerosis and potentially retargeting cure and habits of the observed patient.
Sorry, I’m late to the video. Just finished reading the book “The Clot Thickens” by Dr Malcolm Kendrick, any comments on his theories? My motivation, I’m recovering from a heart attack a month ago…
Kendrick has long denied the role of (LDL) cholesterol in cardiovascular disease and used confounded epidemiological studies to support his arguments. He ignored clinical trials and genetic studies as well as those epidemiological studies which refuted his claims. I haven't bothered reading his latest book but I suspect it is more off the same. Try reading an alternative viewpoint before deciding which way to go. For example, Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. It's free to read.
What about vitamin K2 supplementation (MK7) ? Some MD s claim that supplementing with K2 decreases calcification inside the arteries. I've been taking vitamin K2 together with vitamin D3 for years now but I'm not convinced that it has any effect on existing calcification.
Calcification has a protective funktion preventing plaques from ruptoring. I do not know if we want that. Vitamin K is also a factor in blood clotting, and if you have arteriosclerosis, you want to prevent clotting, not promote it. Vitamin K is also an antidote for heparin blood thinners. I'm sceptic
Fascinating, I lowered my LDL 50 points in six months by upping my fiber intake, taking plant sterols, cutting out cheese and butter replaced with olive oil/ cod liver oil / black seed oil/ flaxseed oil, eating 600 calories in vegetables daily, and intermittent fasting ( not eating after 2 pm) ( also I always exercise daily so that didn’t have any effect). I’m skinny so everyone said my high cholesterol was genetics, but I proved that by following a different diet than the rest of the family and taking plant sterols I could lower my cardiovascular risk. 😅Also wanted to add that when increasing fiber intake it’s really important to up water intake if you don’t want wrinkles. 😅 I would love to see analysis on any studies on plant sterols and intermittent fasting for atherosclerosis.
Nick Norwitz lower his LDL by 75% with 12 oreo cookies in 2 weeks, he went from 420 to 111 by adding carbs back to his diet. Hes on carnivore or low carb diet.
@@beautylover8138 What are your cholesterol numbers LDL HDL and triglycerides? Before and after ? Do you have family CVD history ? What was your diet before ?
@@manojlogulic4234 Unfortunately his conclusions are BS. He is a hyper responder which is a tiny fraction of people. For the vast majority of people they should NOT eat Oreos(common sense would tell us that). They should follow a Med diet, exercise and if their LDL and apoB are high take a statin. The fact he is on carnivore diet or claims that means he is to be discounted.
@@supernova1976 I improved my LDL cholesterol from 136 to 100, dropping 36 points and shifting from high to normal. Initially, I didn't fast before the test, resulting in an LDL of 125 after a diet change and starting plant sterols. Three weeks later, it was 125, and after five months, including a trip to Ireland where I indulged but balanced it with vegetables and continued plant sterols, it dropped to 100. Even after eating Popeyes the night before my last test, my levels were normal. That was three months ago, and my cholesterol might be even lower now, despite the occasional half cookie. I struggle to maintain weight with a high fiber intake (25-28g daily), requiring 14 cups of fluid to avoid wrinkles and keep up with intermittent fasting and gym routines. My HDL rose from 52 to 61, and triglycerides fell from 120 to 83. Previously, my diet was heavy on cheese, protein shakes, pizza, and buttered popcorn. Despite a family history of high cholesterol (but low blood pressure), I was unaware of the 25g daily fiber recommendation and its impact on skin health until recently. Adjusting my fluid intake restored my skin. Sharing this in case it helps anyone!
Anti plaque stack: Fast 1-3 days a week (free) burpees + jog/run 4 days a week (free) niacin - flushing kind daily (super cheap) vitamin k2 daily (super cheap) psyllium husk daily (cheap) Magnesium daily (cheap if oxide, moderate cost if better form) Add-ons to the stack: Weight training 2-3 days a week (moderate price) Creatine (moderate) Protein (expensive)
This was an excellent presentation on the topic and worth the time to view it. It's a complex topic, you covered the key aspects people need to know to get a fuller understanding of the process of CVD.
If I understand you correctly, reducing the burden of LDL particles passing through the endothelial layer is very important. And the way to do this you say is by lowering LDL-C or even better ApoB. This makes perfect sens to me. But if I understand you correctly,.. the only (significant) way to achieve this is by reducing LDL-C / ApoB. This I find confusing. Because I would think that there are more ways to achieve this, and perhaps to such an extend that the LDL-C/ApoB level becomes less important. Maintaining a health glycogalyx (lowering glucose levels, quit smoking), reducing low-level systemic inflammation, lowering blood pressure, etc. all reduce the "permeability" of the endothelial layer. Especially when all these things are achieved through non-medical interventions. (I believe that non-medical interventions have much stronger effects than what can be achieved with medications) Exercise, as you have shown, has a plaque reducing effect. Exercise is a non-medical intervention that improves all of those goals I mentioned. All of those can be achieved through dietary interventions. Is there a specific reason you didn't mention these? Or were they simply not part of the studies that you went through? Are there even studies that look at these factors in relation to dietary interventions?
This was so interesting! It looks like many presenters on youTube over simplify what cardiovascular disease is & how it's caused; it's the first time I've seen something detailed enough to help me figure out why cardiovascular disease is such a common problem in my family. I've been plant-based for 6 years and am fairly fit (not overweight). I wonder if my dietary choices are going to be helpful. I'm 71.
check out nutritionfacts. He claims heart disease is reversible with a plant based diet. Its always good to have lots of sources of info since this stuff is complex. @locutia7
Plant based doesn't say that much. For example a lot of vegans eat a lot of sugar, and they can still be called "plant based". And the problem with that is that insulin resistance is involved in all of the metabolic chronic diseases.
Diet is an important part of the equation but sedentary behaviour and pollution also increase cardiovascular disease risk (so do cigarette smoking and alcohol consumption ... and marijuana use). Controlling blood pressure is also important. I understand that 'plant based' works if it contains lots of whole fresh fruits and vegetables, whole grains etc but very few processed foods (plant based or not).
I strongly suggest reading The Clot Thickens by Dr Malcolm Kendrick. A very convincing alternative hypothesis regarding the etiology of CVD backed by a mass of references.
I also strongly recommend reading or viewing content from Dr. Malcolm Kendrick. Atherosclerosis is a disease first and foremost of chronic inflammation and repeated thrombosis brought on by metabolic dysfunction.
@@patrickweisser3185 Dr Kendrick has written 4 books to date and I recommend all of them for different viewpoint of different aspects of health and health systems.
@@patrickweisser3185does he say if eating a low inflammatory diet and fasting helps reverse at all or nah ? If it's from chronic inflammation you'd think that would help
Or Dr. Ernest Curtis's (a cardiologist) "The Cholesterol Delusion" which demonstrates the low quality and outright manipulation of the original studies that led to current medical thinking. Three of the studies are included in appendices so that the reader can see for themselves what he explains in the book.
I did it, Nattokinase and pine bark extract once a day on an empty stomach Of course your diet should be somewhat healthy Anyway this took me 18 months, had PAD
In 1997 3 Doctors wrote a book The Arginine Solution Nobel Prize Beseech proving Arginine dissolved the plaque in the arteries. Helped me a lot .I have family history of Atherosclerosis. I have none.
I'm a bit torn with this, as vitamin-C prevents calcification of plaques. That is not good at all. Calcification is a secutity measure of the body to prevent plaques from rupturing. Plaques are more dangerous if soft, as they can rupture, clot and travel to heart, lungs or brain causing infarction. Statins for example increase calcification, seen in the CAC score, stabilizing plaque and decreasing risk. What interests me is the lip(a), as we do not really have a current way how to lower it - meds are still in development. If this would be an option for individuals having that elevated through genetics, maybe they could lower their risk to those without this predisposition. So much for the carnivores: I can't hear the claim anymore, that they do not need so much vitamin C, as they do not have symptoms of scurvy... They do not get that surviving does not mean no deficency or negative effects. I'll make sure to eat my fruit and veggies to get enough for prevention of several chronic diseases.
@@stellasternchen good post , people see what they want to see . Same for these "miracle' drugs to clean up cells. Yet the body knows how to do autophagy , so senescence is not to be lightly mucked around with - just do the hard work ( HIIT or intense exercise and let the body do its job) , until better understanding comes . As for the topics at hand - if there was an easy method we would know about it . Plagues of any type are hard to remove even with direct access , teeth , bathroom walls etc , when given time to embed . They are incredibly tough and can survive extremes in nature . Given that doing the things outlined here is generally enough , to continue to live healthy - ie no more growth , then if keep strength , VO2 max , chance of a problem outside an acute infection/inflammation /over exertion/dehydration /chemical or electrolyte imbalance . Drug addicts probably survive some bad scares ( eg too much meth ) solely due to young heart - not sure a 60 year old wants a heart going crazy at 200 bps
Good conventional info but what these studies don't address is: why are we one of the few species that develop plaques?; why do the plaques only occur in arteries just outside the heart and not in veins or elsewhere in the body?
6:57 “if the level of LDL is too high, LDL gets stuck.” You gloss over this statement without showing data that confirms controlling LDL levels prevents this mechanism from occurring. This is the key statement supporting the widespread use of Statins.
HIIT group had average LDL 2.1mmol/L +/- 0.7. This places them exactly at the threshold of plaque reversal (lowered Atheroma volume) due to low enough LDL according to some other study. This means some participants were above, some were below. It means it makes it very hard to know if any changes in plaque were because of low enough LDL of some participants or was it because of HIIT.
@@adamjackson713 it's not. We can use epidemiology to establish a cause-effect relationship. Smoking, environmental carcinogens, and others. But it's not epidemiology only: - trials of LDL-lowering drugs, - Mendelian randomization trials - animal models So, you can't have a single "study" that proves everything, but rather pieces of evidence from the hundreds of studies. The same logic is used by AIDS denialists to "disprove" the HIV-AIDS link. No single study proves that casual relationships, but still the general overwhelming consensus that HIV causes AIDS.
Have you done (or will you do) any videos specifically regarding the potential benefits of garlic for cardiovascular health? I see others claiming garlic (specifically alacin) has shown some benefit in reducing plaque burden. I’m cautiously optimistic that could be true, but I’d love to see some study data to confirm or deny that claim and you seem like the kind of chap to fairly and rationally investigate such a claim.
Can I suggest that you bring in the glycocalyx and also the fact that diabetes dramatically increases the risk of CVD. If it is all explained by LDL, why does hyperglycemia and diabetes have such a dramatic effect? Everyone accepts that diabetes causes major vascular problems in the periphery, so why doesn’t it also cause problems in the coronary arteries? Another important question is why does arthrosclerosis only occur in high-pressure, high turbulent areas of the coronary arteries? Why does it never occur on the venous side?
@@miltonhondrakis2431 so how is LDL and shear stress connected? Shear stress damages the glycocalyx particularly if it is thinned out by hyperglycemia.
It does happen on the venous side but less common. The biggest factor is high blood pressure and the location of the arteries because arteries branch and are often curved or arched. This is where it happenes
Manganese daily up to 5mg even better in combination with selenium preferably selenocysteine and on top Hesperidin methyl chalcone. A maximal prevention trio
You mentioned that you want a thick covering of fibrosis to prevent a rupture of sorts. So what about the use of proteolytic enzymes like Nattokinase? Can that potentially do more harm than good for someone with existing CVD?
They affect the clotting cascade, which plays a role, but the ECM release is mediated by the fibroblasts, not the platelets (although the platelets also play a role in atherosclerosis, just through a different mechanism).
All I know is i vastly increased my overall activity and exercise while changing nothing about diet or medications (because diet and medication changes were something my doctors and I had adjusted the previous year) and in the six months of increased exercise my cholesterol numbers were all vastly improved. Our next experiment is taking me off avortastatin for 6 months to see if I can continue to get more muscle mass with less pain (muscle pain is a potential side effect from statins that I feel was interfering with exercise) We check blood every 6 months and make a decision on what to adjust or change next. Over the past 3years I've lost 160 pounds(starting from 500) while slowly being able to stop taking various medications. We started with diet and lifestyle choices and then expanded to body building for muscle gains. Hopefully I can lose another 100 pounds over the next year and then see where I am and what needs to be the next target goal.
Dude. This is a beautiful explanation! Watching all of the out-of-control layers and buildups is just freaking me out even more and reminding me to keep to my good habits. Seriously, thank you!
Heart disease is the number one killer of people today and cancer is number two. Being over weight is the number one factor leading to an early death. People who are over weight have higher risks for high blood pressure, heart disease, diabetes and cancer. Even children today have signs of artery disease. Fast foods and sugary drinks have long term consequences. There is an obesity epidemic today where over 60% of the population is overweight or obese. What is common today and "NORMAL" is not healthy. The average person today is not healthy and is taking medications. Heart attacks were once only common in people over 65. Today people in their 40 are having heart attacks. Add more plants and vegetables to your diet and less junk and overly processed foods
Dr. Esselstyn debunked his own book. The artery image from the Esselstyn book is from his colleague Dr. Joe Crowe a general surgeon who at age 44 had a heart attack even though he was slim, a non smoker, not a diabetic, no high blood pressure and had low total cholesterol of 156 mg/dL. So Esselstyn debunked himself because Crowe had all the metrics for preventing heart disease but could not explain why it happened. He changed the Crowe diet to less animal foods but if animal foods caused the problem why did they not raise his cholesterol level high like Esselstyn says they will.
LDL of 2.1mmol/L was the threshold when there was negative % plaque volume change observed in some study, unfortunately I only took a screenshot of the graph/results so it doesn't show study link/name. Largest reduction was with 1.1mmol/L which seems to be very low, even 2.1 seems to be very low number.
Great topic, thanks for covering the #1 cause of death in the world. Are Dr. Esselstyn and Dr. Ornish correct when they claim a Whole Food Plant Based Diet, salt oil and sugar free, can reverse arterial plaque? What about high intensity interval training? Like high water pressure flushing out the plaque through intense vigorous exercise…
Considering that statins is the all time highest selling drug and can lower ldl makes you wonder why not only CAD is still the top killer but .... also on the rise. Maybe its because loweing ldl has no effect on CAD mortality outcomes? and that there are other factors inducing atherosclerosis.
Statins weren't commercially available until the late 1980's, yet coronary heart disease (CHD) mortality rates had been dramatically declining since the late 1960's (due to public health campaigns to reduce CHD risks: reduce smoking, reduce hypertension, diet - to reduce cholesterol, hypertension etc, increase exercise, etc). CHD mortality rates continued to dramatically drop after statins were introduced, but slowing down in the 2000's, plateaued about 2007, then started a gradual increase from about 2013. Only good news - premature CHD mortality rates (younger than 65yrs) are still much lower today than in the 60's, and earlier.
This was excellent! If I were to request anything from your channel, it would be that you present some analysis on soluble versus non-soluble, fiber intake, especially as it impacts those with heart disease. Keep up the good work.
If you are looking for new material to cover. There was a study done on the effects of nattokinase, that showed reduction in arterial placque. I would love to hear your opinion on that study as well. There may have been some bias, I really don't know, but the only bias I could imaging, is soy bean farmers, manufacturers that produce nattokinase... This was a great video, and I appreciate you pulling back, to keep the information understandable for all.
@@Physionic I'm not even sure what a DOI number is, but I will certainly see whatever information I can find on the study. I'd really be interested to see if you can make a mechanistic correlation to the supposed outcomes.
I've heard about Apo B for a few years but never really knew what it was until recently. From what I read it seems to be a sum of all the LDL particles and is probably a better risk predictor than LDL-C because it includes VLDL. having listened to Dave explain his Lipid Energy Model and having had high TG and VLDL it's an easy to understand concept why it's a better risk predictor. But I think the reason that HIIT didn't have much effect in the data is because of diet. Exercise burns glucose and fat but if you continue to eat in a way that puts in more sugar and fat then you're not making much of a difference.
So do I. Nattokinase, Serrapeptase, and Lumberkinase all work in a similar fashion and the three can work together synergistically, but most of the research to date has been done on Nattokinase.
It's been on my radar. Unfortunately, those lengthier videos take me about 2-3 weeks of research, a few days for notes for the video and recording, and another week of illustrations and video editing, so it's an expensive process. I may still cover it, however.
Seed oil toxicity ....Hm, those oils have shown in RCT's as LA veterans to lower cardiovascular events. A low carb doctor, right? I have nothing against low carb diets, was on one myself with a good experience and can reccomend it to reach certain goals, fight diabetes or prediabetes etc. But I do not understand this constantly need of those diet gurus to claim the opposite of what the sum of evidence shows. I do not understand this obsession with saturated fat. High fat does not mean high saturated fat. I know, because I did make sure when I was low carb dieting to eat mostly unsaturated fat. If you exclude a good source of unsaturated fat as those frying oils does make it more difficult and you end up with butter, palm oil, lard or even worse, coconut oil.
Paul's video is based on 'The Clot Thickens' by Dr. Malcolm Kendrick who has developed the Clot Theory of plaque formation. The book presents significant analysis supporting this theory. It seems to explain the creation of plaques better than the current "burrowing" theory. Since the Clot Theory deviates from current theory supporting statins, Dr. Kendrick has been blackballed by the medical community.
@@markhapner8499 Hmm, aspirin for arteriosclerosis has been tried. This drug blocks Cox1, and thus the synthesis of clotting factors. It did more harm then benefit.
@@markhapner8499 Hmm, aspirin for arteriosclerosis has been tried. This drug blocks Cox1, and thus the synthesis of clotting factors. It did more harm then benefit.
Excellent information. I want to know why my cardiologist hasn’t informed me on any of this? All I get is go on a Statin and or Repatha plus put a Stent in. No lifestyle change conversation at all. I have a high CAC score but no symptoms and can workout very hard 2 hours a day plus 30 minute sauna 6 days a week. 58 YOM 69” 155lbs
Serrapeptase inhibits vascular inflammation, seems important. Mechanistic studies demonstrated that SRP significantly inhibited the LPS-induced production of proinflammatory cytokines such as IL-2, IL-1, IL-6, and TNF-α in aortic tissue. Furthermore, it also inhibited LPS-induced oxidative stress in the aortas of mice, whereas the expression and activity of monocyte chemoattractant protein-1 (MCP-1) decreased after SRP treatment. In conclusion, SRP has the ability to reduce LPS-induced vascular inflammation and damage by modulating MCP-1.
Serrapeptase inhibits vascular inflammation, seems important. Mechanistic studies demonstrated that SRP significantly inhibited the LPS-induced production of proinflammatory cytokines such as IL-2, IL-1, IL-6, and TNF-α in aortic tissue. Furthermore, it also inhibited LPS-induced oxidative stress in the aortas of mice, whereas the expression and activity of monocyte chemoattractant protein-1 (MCP-1) decreased after SRP treatment. In conclusion, SRP has the ability to reduce LPS-induced vascular inflammation and damage by modulating MCP-1.
I'm so impressed, thank you! I put this video down in my notes for your detailed description of the whole course of atherosclerosis at the cellular and molecular level, then the summary of processes to regress plaque, then your great bullet points at the end on lifestyle changes. It's like a reference for January 2024 state-of-the-art in atherosclerosis and lifestyle treatment! Thanks. (I was diagnosed with CAD after CAC 586, 97th pct, Sept 2023; I'm hunting data to strongly suggest lifestyle changes so I can stop the disease, regress plaque, and avoid PCI and bypass if possible)
Sugar fast food alcohol tobacco. Give up all. 1.2 million IU’s of Serrapeptase at minimum. Start at 240 iu. And slowly build up to HIIT Heavy bag boxing drills. I went from emphysema to the FITTEST boxer in a gym. Ventim before boxing. At 54 I could maintain 170bpm! 72 pinches in 10 seconds. You must log your ABSOLUTE MACIMIM SPEED. And begin HIIT Boxing at That speed… till you drop. Start with a drum beat BPM If unfit perhaps two punches per beat at 65 70 bpm hip hop works well.
There are a lot of recent studies, which have shown surprising and amazing results with daily Manganese intakes reversing Arteriosclerosis. Take Manganese daily up to 10 mg even better in combination with selenium preferably selenocysteine and on top Hesperidin methyl chalcone. A maximal prevention trio
@@jesincov a well balanced combination with Niacin further significantly reduces cardiovascular risks, where by ,balanced‘ it means niacin taken together with TGM (Trimethylglycine) in accordance to your individual methylisation capacity. If someone is an under-methylisator (the majority of people are!) it is mandatory to combine niacin with TMG, if you want to protect your liver of negative effects of niacin. If you are not an under-methylisator TMG still isn’t harmful at all. So it seems reasonable for everyone taking higher doses of Niacin to always add TMG. Then this combination together with Manganese, Selenium (preferably Selenocysteine) and Hesperidine Methyl Chalcone is probably the best plaque remover combination available certainly much more effective than any statins and, if you follow the advice to combine niacin with TMG, without any negative side effects
The Dr. LINUS PAULING protocol works! I started on it way back some 15 years ago as my alternative to conventional med interventions. However, I noticed the see-saw effect of reverting increased BP by taking Vitamin D3 K2 MK7, lots of anti oxidants and anti inflammatory food. Also avoided processed and ultra processed foods, seed oils. Many of my friends who did the same thing were able to get pass cardio vascular disease. I am now 77 years old and still healthy
So, after all of this entire, for me confusing,lecture …what I took away from this is there was no help with reversing atherosclerosis! A lot of whatever you call it to say, no proven help. Gee even tho it was interesting, but confusing, I feel like I have no hope. Im Soon to turn 79 and have heart disease and atherosclerosis. Had one surgery on left carotid already and right is just above 50%. I’ve already tried Hit and dozens of other things like just sprints,etc did Keto for 2 1/2 yrs, then Carnivore for last 2 months so I don’t think I can change this terrible atherosclerosis! They may find something, it won’t be in my lifetime, I’m sure. I sure wish you all could just explain these things a bit simpler because it’s to long to just be disappointed in the end! By the way, I’m 4ft11 inches and weigh 97 lbs. so not overweight and no diabetes., and stopped smoking 20 yrs ago after quadruple bypass surgery.
Thank you for your analysis of Atherosclerosis! Can you share your thoughts on the functions of stem cells, the difference between general and specialized stem cells, as well as the action of stem cells when rebuilding the body's broken down cells and tissues. A large part of the population in the Western world is attacked by osteoarthritis after they have passed the age of 60. I assume that part of the cause lies in autoimmune conditions, which develop inflammation, especially in the joints. Autoimmune inflammation is known to attack the body's own cells, and in osteoarthritis, stem cells are prevented from rebuilding the cartilage in the joints. Can you confirm this?
Incredibly clear presentation on arteriosclerosis! Thanks 👍. My understanding is that HIIT did not have an effect on this study. The fact that the control group declined in their metrics is a bit suspicious as they would be expected to stay the same over the course of the study, unless this was an especially sick group of people (in which they need to do the HIIT). Perhaps the duration of the HIIT or it's level of execution was not enough to induce a measured effect. Would be interesting to hear more studies that tried to measure the benefits of exercise (in different forms) on levels of arteriosclerosis.
You are what you eat. Your diet impacts your health. Lower stress, reduce obesity, get enough sleep and more exercise are key to a healthy life. Obesity in children and adults is rising across the world. Fast food and sugary drinks including fruit juices are contributing to the problem of poor health and obesity. Eat a healthy plant based diet and exercise regularly. Reduce or ELIMINATE cows milk, eggs, cheese and meat. Eat more salad greens, beans, fruit and vegetables. Eliminate fast food, snacks like cookies, cakes, chips, and sugary drinks and juices. Every adult and child should own a bicycle and ride it regularly. Regular exercise will help you sleep better. Yoga is a great stress reducer. Obesity is all too common today. Get off the couch. Get off the phone, ipad or video game. A variety of stretching and other exercises help with increased mobility. Ride to work, ride to school, ride for fun. Every city should be a bicycle city. Speak up for bicycles in your community
9:52 “you can have a perfect healthy endothelium, and if you have high levels of LDL, then that LDL can cross through the cell itself (endothelial cell, endothelial cell to cell boundaries etc.)”. Please cite where you get this information from, thank you.
And why does LDL levels need to be high for that to happen? The veins see same levels of LDL, yet at those reduced pressures and more laminar flow this does not happen. Free cholesterol crystals found in plaques are not present in the bloodstream, but are contained in the structure s of damaged red blood cells. Damage to the protective glycocalyx layer readily allows damage to the endothelial cells, and hence clotting is instigated. Many things end up in the plaques and clots that were not part of the original damage. Whether arterial endothelial damage occurs by mechanical, chemical, or stress induced hormones, etc such damage is a prerequisite for plaque and clotting. Actually, lipoproteins carry much more than fats and cholesterol,.... lipoproteins are simply the vehicle of transport having coatings of different nutrients, antioxidants, and hormones that are delivered to sites of damage to remove inflammation, calcifications, and bloated foam cells that have outlived usefulness but refuse to die. Properly coated, the lipoproteins are constantly maintaining the state of repair. Lacking these coatings of CoQ10, Vit k1, k2, Vit D, Vit C, or lack of Magnesium and other minerals the repair process slowly grinds to a stop and atherosclerosis ensues vigorously as calcium solidifies to attempt walling off the damage and exposure to the bloodstream.
@@cattleprods911 From my post...."mechanical, chemical, or stress induced hormones, etc ". The mechanical damage is largely due to high pressure causing non laminar flow and the contact of blood cells and any other cells or molecules in circulation. In sickle cell anemia the blood cells are sickle shaped (pointy ended) and those afflicted die very young from massive atherosclerosis and calcification. Our veins being subjected to lower pressure and having more laminar flow almost never develop plaques like arteries do, unless surgeons use this vein in a bypass where it serves as an artery (CABG). Those grafts plug up in 6-8 years or so. Another type of damage is chemical, as when smoking cigarettes. The new under the tongue camera can detect this damage within seconds of smoking and dead endothelium cells are found in the bloodstream. Sugar also induces chemical damage because of glycation. Diabetics mostly die of heart disease. Also, an imbalance of hormones like cortisol caused by emotional stress can wreak havoc on the glycocalyx and the endothelium.
@@cattleprods911 I forgot to include bacteria as a damager of endothelium glycocalyx. Basically that is what happens in sepsis as bacteria runs rampant destroying the glycocalyx all over the body causing multiple organ failures.. The under the tongue camera is used to check the condition of sepsis patients.
I just listened to Prekure- prevention, with doctor Paul Mason, Decoding Atherosclerosis, and I think there's some compeling finding, going back to the 60's that high LDL is not the issue. Plant steriods may be a part of the puzzel.Thanks for your analysis ,so the average person can make wise decisions.
I'm a member in your physionics group and was looking for this report in the Mighty app, but I want able to find it. Can you give me some guidance on where I might find it?
Both the control and HIIT groups had quite low total and low density cholesterol .. ldlc = 2.1 (mmol/dl) [*36] == 75(ish) mg/dl … most post mi would be delighted with an ldlc of 75mg/dl. Even their total cholesterol was low (3.1*36) == 100(ish) mg/dl. ApoB … also low …. For “overweight” people they had amazingly low total etc
@@Physionic Table 1 on the footer lists High Potency Statins - which would explain the amazing low LDLC/ApoB for "overweight" people. Is this study more the effect of exercise in conjunction with high potency statins ?
My ldl is 3.44 mmol/l = 133 mg/dl. I want to bring it down with 200 mg Nattokinase and 1200 mg red yeast rise powder after the first meal/day. Is this a good idea? I'm 70 years old male, 62 kilos.
Some additions: Keto diet (already kind of specified) The following supplements, but not at the same time: Mg supplement Vitamin K2 - MK7 (only 1 every 3 days) Sunshine or d3 supplement Nattokinase - breaks up fibring - caution: blood thinner warning Chanca Piedra - loosen calcium deposits - blood thinner warning Inositol and as mentioned, exercise.
No mention of extended fasting and autophagy? I am a sample size of one, but I have reversed my severe arteriosclerosis in 3 months. The before and after MRIs are incredible.
@@jfdomega7938 It was roughly a semi-extreme keto diet: 1. Replaced butter with olive and avocado oils, 2. Zero sugar, not even fruits, 3. Zero rice/bread/pasta - basically only vegetables. But the important part is the extended fasting: At least one 3-day or 4-day fast per week. Often 5 days of fasting per week. And 1 or 2 meals only in non-fasting days. My only indulgence (limited) Cheese!
Nic, How certain are you of the accuracy of the model of the development of arterial plaque? Specifically, if it's just a question of LDL from consumption of saturated fats, why has the incidence of arterial plaque increased so dramatically over the last 60 years?
Yes and saturated fat consumption has also come down over that 60 years but the incidence of CAD has risen. The only good news is that modern medicine can keep us alive better after an event.
@@shauna996 But what has risen over that 60 years is consumption of seed oils and processed foods, and, of course, the $billions in profit from advertised pharmaceuticals to treat the symptoms. Hmmm
Yes this exactly, plus a lot of sugar in all the fat free foods to make them not taste like cardboard. The producers of corn syrup and the pharmaceutical companies make for a very profitable team.@@neuromax3766
How about MCT's and coconut oil? As I seem to remember seeing studies that these had a positive effect?? Though both are triglycerides, is it the case that some triglycerides are more equal than others??
Cholesterol has been found in plaques, and is generally attributed to LDL but I have never seen studies showing Apo B being present. However, I have heard of studies showing that Apo A has been found in plaques, pointing to Lp(a) being the source of the cholesterol. As I mentioned below, if you consider endothelial damage and clotting, it is known that Lp(a) is involved in the arterial damage clotting process, so, this hypothesis carries much greater weight in my mind. Research in this area seems to be lax, as there is no pharmaceutical solution to Lp(a) values.
How would + charged APOB particles "randomly escape" the plaque after electrostatically binding to the - charged proteoglycan that's created by migratory-secretory smooth muscle cells in the sub-endothelial space??? I believe it is more likely they are actively removed by immune function as inflammation and excess oxidative stress are resolved.
Certainly a possibility, Tim. I think the mechanisms aren’t as clear. We do know that aggregation of LDL can change its affinity to proteoglycans. Additionally, changes to the ApoB structure change the affinity (there’s a 10 amino acid sequence that is known to canonically link ApoB to proteoglycans). There’s probably other factors I’m not familiar with, as well. But, it wouldn’t surprise me if it had to be through some active resolution like immune cell clearance.
Regarding "general solutions": Very recently we have seen that lean healthy fit people can have both high HDL (good) and high LDL (bad) with low triglycerides (good). They are called LMHR phenotypes - Lean Mass Hyper Responders. Does it mean that reducing LDL is still part of the solution above ? Is there proof of a causal link between high LDL and cardio events, or do we have only associative hypotheses. Selective data from selective studies are mostly useless.
Multiple clinical trials have shown that lowering LDL levels by diet, lifestyle changes or drugs significantly reduces the rate of major adverse cardiovascular events (fatal and nonfatal heart attacks and strokes, and the need for revscularisation surgery). They have convinced the worldwide scientific and medical professions that high LDL is a causal risk factor for CVD. It's not the only one of course but it is undoubtedly a causal risk factor.
I'm just a normie on the Internet who got a bit more serious about health fairly recently (~6 months ago). I've learned a lot of actionable basics during this time but this is the first time I've seen an actual in-depth (from my PoV) illustration of the atherosclerotic process. Amazing stuff, thank you for this and looking forward to seeing even more content like this!
@@stevegcqI haven't watched the video but what do you think is the correct point of view? I can tell you I am reversing my CAC with the Linus Pauling Heart Protocol 200 points down from 660 in 20 months. Even with LDL at 124 and HDL at 36.
@stevegcq This guy here is about standard medicine pretty much Dr. Ken is a step well above. And what I have done is a major step above Dr. Ken. My CAC was 660 and after 20 months it was 458. Not many people achieve this. I did it following the advice of Dr. Thomas Levy, cardiologist author of "Stop America's #1 Killer" Proof that the Origin of All Coronary Heart Disease is Clearly Reversible Arterial Scurvy. I suspect at my 3 year anniversary of my 660 score that if I did another CAC it would be down by 50% to 330 or even less....imagine that....my score is reversing as fast as it progressed.....
I got stuck on the formation of atheromas I could not get beyond it because it seems so wrong. If ldl simply passes between the cells, even if you can explain the mechanism as -/+ attraction how is that 1. it does not happen all over the body 2. Does not happen in veins 3. ldl needs to be high, surely the presence alone of ldl is sufficient 4. Other things do not just simply pass through the tight junctures between the cells, why are we not constantly bleeding out? Added to which, it is well documented that people with 'normal' and lower than normal levels of ldl also suffer atherosclerosis at the same rate as those with high. Even if you want to explain that ldl sticks to endothelium, it still doesn't explain points 1, 2 or 3. You can go ahead and blame apopb but considering this is the backbone so to speak of all lipoproteins it ends up being the same argument. ldl really isn't even a significant component of plaques, cholesterol crystals wrapped in macrophages yes. So does the ldl pass behind the cell, drop of the cholesterol and the return to the blood stream? Considering the body makes ldl why would the body make an excess? Why would millions of years of biological development create a mechanism so flawed? Sorry .... not buying it.
I answered a lot of those questions in another comment on this video, I'll refer you there. I'd also need a study reference for this claim "Added to which, it is well documented that people with 'normal' and lower than normal levels of ldl also suffer atherosclerosis at the same rate as those with high." It is true that ApoB is not the only factor for heart disease, but I've repeated myself over and over on that. It is a factor, but not the sole factor. I'd still be interested in seeing a study on low vs high LDL and no heart disease difference, if you can post one (the DOI number, please, links get deleted sometimes on RUclips).
The first thing I should mention is the glycocalyx and its role in protecting vascular permeability. Highlights can be found on wiki here: /wiki/Glycocalyx#In_vascular_endothelial_tissue This alone calls into question ANYTHING passing through the endothelium never mind only ldl *A search for this:* "Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines" will give you a pubmed article -> /19081406/ /releases/2009/01/090112130653
@@PhysionicOk so I posted the message twice, once with links once without. So obviously youtube is an A$$. I guess all that is left to say is glycocalyx and lean mass hyper-responders with ldl levels up to 600 and no increased plaque risk.
First off, thank you. Second, these studies don't surprise me - there are many confounding variables that even the researchers acknowledge. For example, the first study cited was looking at people who had a cardiovascular event across over 500 hospitals. It's a cohort based study (meaning, they simply compare one group against another at a single time point, generally), and that's notable, because they can't control for who was on lipid lowering drugs and who wasn't, between each group. So, for example, about 12% of people with very low LDL still ended up in the hospital for CVD, but it's entirely possible most of those individuals were using lipid lowering drugs to achieve that 70mg/dL, implying they were in poor health before they were put on a lipid lowering drug. Of course, one could argue that the fact that the drug didn't prevent their CVD is proof LDL isn't a factor, but that is not what this study can show, and other analyses show the exact opposite when compared against the correct control (people who are not on a lipid lowering drug, or put on a placebo) - implying that lipid lowering drugs are effective relative to people in the same health condition at the start who choose not to fix their lipid levels. Also, over 50% of the people in the above analysis had hypertension and they were, on average, overweight. None of those were controlled for in the analysis, and no respected scientist or clinician wouldn't agree that being overfat and having high blood pressure are also independent risk factors. No one is claiming LDL is the only risk factor, just that it contributes causally to atherosclerosis progression, much like blood pressure does, as one example. Oh, and you forgot the rest of that conclusion... "In a large cohort of patients hospitalized with CAD, almost half have admission LDL levels
@@Physionic I was aware but it is irrelevant. When do they stop lowering? When ldl is zero? Its an absurd premise. ldl lowering is about selling a drug which isn't working. A recent study on lmhr (on ketogenic diets) has shown that despite ldl levels four to six times higher than normal (yes, 400 to 600), show no sign of increased plaque when compared to similarly healthy individuals of nominal weight on standard diets. Atherosclerosis is a response to damage to the endothelium.
Thanks for your analysis, Nic. Sounds like the kind of study that would never be published it a company had funded it. Un fortunately, my guess is that there are so many confounding issues there that were not controlled. Also, from a personal experience view point - if you don't change the diet, a little HIIT isn't going to cure you.
Nicholas high LDL do not cause atherosclerosis. Just because LDL is at the scene of the crime does not make it causative. The question is why was the lipid oxidized? It was oxidized because mitochondria oxidized the lipid when in a state of producing reactive oxygen species in excess of the cell’s antioxidants. You need to understand how transient receptor potential channels play critical parts in the atherosclerotic process, how too much TRPV1 stimulates too much ROS in mitochondria, that TRPV4 causes monocytes to change into M1 inflammatory macrophages, become phagocytic and engulf oxLDL. TRPV4 also increases monocyte chemoattractant protein-1 and with piezo -1 a pressure sensor stimulate lp(a) that attaches to apoB. ApoB alone is not an issue it only transports LDL. You need to understand what underlying process leads to the stimulation of TRPV4 and piezo-1. What causes too much TRPV1 ? Insulin causes too much TRPV1. TRPV1 causes hyponatremia and hypoosmolality that stimulates TRPV1 an osmosensor and piezo-1 a pressure sensor. In the end look at the transcriptome of atherosclerosis it includes TRPV4 and klf-4: ck out this article: 2020 article Stem Cell Pluripotency Genes Klf4 and Oct4 Regulate Complex SMC Phenotypic Changes Critical in Late-Stage Atherosclerotic Lesion Pathogenesis The article explains the phenotypic switch and the VSMCs incognito. The problem with your narrative is the complete omission of TRP channel physiology/pathophysiology. I reversed my atherosclerosis and bone mineral density loss by reversing TRP physiology by stopping a drug that upregulates TRPV1 and TRPV4 called oxcarbazepine and consuming the low carb diet that drastically reduces glp-1. Glp-1 stimulates its receptor glp-1R a g protein coupled receptor (GPCR) that: Lowers the threshold of TRPV1 and TRPV4! The glp-1 receptor agonists (GLP-1RA) work by lowering the threshold of TRPV1 and TRPA1 in the hypothalamus. I bet you didn’t know this. Do you see the relationship here with high carb/sugar diabetes and atherosclerosis? TRP channels are the link to understanding the disease process. Diabetes causes hyperinsulinemia and now you see the reason all DM cases get heart disease.
you say "jump on over to the physionic insiders", biut you don't say how. i'm already an insider, but the only related links here are for joining, not for getting the full video.
Nick I wanna give you interesting case study about myself. I started 1 mg of finasteride and I am on 120 mg testosterone a week. I have been on the testosterone for years now. And finasteride for 2 weeks. After two weeks my HDL went from 6 to 50. I am a high dht converter and I found this to be very interesting
Could you some day research Dr. Chafee promoting carnivore lifestyle vs. prof. Sinclair vegan lifestyle? It's quite impossible to choose if sciences 180° oppose each other. Dr. Chauffee also says LDL is no issue etc... What is true?
I tend to believe Dr. Chafee more. But Bryan Johnson is vegan? Except his collagen intake.. I think vegan vs carnivore is the biggest misunderstanding in medical science right now. And how to compare early humans, primates
Sure, I can do that. Unfortunately, most of these people tell you one side of the story and don’t introduce you to data that conflicts (which they then should explain). It’s frustrating for me, as I’m sure it is for you.
Instead of following gurus with agendas on RUclips, why not read reports by panels of world class scientists eg 'Diet, nutrition and the prevention of chronic diseases: report of a joint WHO/FAO expert consultation;', 'Diet, activity and cancer' by the World Cancer Research Fund, the Canadian Dietary Guidelines etc.
I think the major issue with LDL is when it is damaged. Like{small dense} LDL. it can become oxidized, glycated or otherwise inflamed. Someone posits that the liver receptors won't recognize them anymore. But it requires another factor - decimated glycocalyx -to enter the endothelium. Just my working hypothesis. All the more reason for me to avoid constant carbs.
![Taurine: Aging Backwards? [Study 193 Analysis]](http://i.ytimg.com/vi/PNJpM0ac0GU/mqdefault.jpg)
![Does Nattokinase improve Heart Disease? [Study 269-276 Analysis]](/img/1.gif)
*1 AMENDMENT*
AMENDMENT: It’s been pointed out to me by @F0Xit (on RUclips) that the researchers (Study 246) should have done a Bonferroni correction on the data. For those not into statistics, if researchers perform multiple comparisons (group A vs group B), it’s common practice in statistics to perform some form of correction, because the risk of detecting an effect that isn’t truly there increases with more comparisons made. A Bonferroni correction drastically cuts down on that risk, which is why many statisticians argue for its use. If a Bonferroni correction were applied to all the data (19 comparisons), the true p-value to meet would be 0.00263 (much lower than the typical 0.05 and what I reported in the study).
However, I met with a statistician here at my medical school to discuss the topic, and he argued this would be the incorrect use of a correction, because some of the measures are independent of one another. Technically, he argued none of the comparisons should have a correction applied to them, but he mentioned he could see an argument for some of the measures being corrected (6-9 of them in Table 2). So, if we assume a middle ground and a correction is applied to 9 comparisons, the p-value wanted would have to be below 0.00556.
If no corrections are applied, the results are as presented (based on a p-value of 0.05).
In the end, even with the most strict option (option 1), some of the effects are still significant. More are significant in the middle option, and obviously all the ones I reported are significant in the uncorrected option.
Thank you to “@F0Xit” - I learned something from the comment (below), and although I wasn’t a stranger to statistical corrections, I’ll be on the lookout in 2 sample tests just as I do in multi-sample tests.
“None of these measures are significant. When you have so many comparisons you need to correct the p-values.
This is done with Bonferroni and with so many comparisons you should divide 0.05 by the number of comparisons (you have 19 observables in the first two tables, therefore is 0.05/19= 0.002).
Bonferroni is a quite strict corrector, you may want to use Holm-Bonferroni. This study is statistically quite weak. Although, it may be useful for future meta-analyses.
Note: I do medical statistics for a job.”
I just helped someone with statistics class and this stuff is fascinating but can be mentally taxing.
If you have 19 comparisons and only one of them shows a positive effect, then the p-value should be 0.00263. However, if multiple comparisons show a positive effect while none show a negative effect, the the p-value can be increased again.
Out of the 9 measures in table 2, 5 of them have a desirable effect with p
chlorine dioxide can reverse this
Thanks for your thorough look into suggestions made by peers and/or from your audience
HIIT. Most ischaemic events (heart attacks and stokes) occur when a plaque bursts and the outpouring of goo causes a large blood clot which then affects the heart or brain. You have to be careful starting HIIT as this additional pressure can cause plaques to burst and cause an ischaemic event. This happened to a well known BBC presenter in the UK who suffered a stroke trying HIIT.
are you implying that if we've had a bypass (ie lots of plaque), then we shouldn't be doing any HIIT? HIIT is the best way to build collateral arteries
@@johnhurt888 Not saying that you shouldn't. Just be careful. Certainly discuss with your doctor.
@@peterholt4806what is hiit please
If you had bypass, then stenosis as a result, possibly tied into bad artery. What are my choices, what testing can i do. I never had a heart attack. Im completely lost.
@@bradkeenan4428 If you have narrowed arteries from atherosclerosis then you may have had angina pains or your doctors found calcification in your Coronary arteries. If narrowing is severe then your doctors may choose to operate without you having had a heart attack. Any thought of HIIT must be discussed with your doctor.
Very interesting information! I think another thing to look at would be nattokinase supplementation. There are a couple studies that show pretty dramatic plaque reduction, but the dose had to be high enough.
Is there any way to become more tolerant for higher doses? The studies mention 6.000 IU, meanwhile some people vomit with only 2.000 IU.
The vast majority of supplements to reduce LDL and apoB have been found to be pretty much useless. Plant stanols or sterols can reduce it by 5% but a simple 5mg Rosuvastatin give you 39% reduction. nattokinase supplement unless from tested scientifically verified trial should be avoided. The famous SPORTS trial showed supplements are generally useless for LDL reduction
Nattokinase is scary. If it really works it's likely that it would destabilize plaque.
I'm taking 12,000 Fibrinolytic Units of nattokinase every day on an empty stomach and have never had any stomach upset. Food will deactivate the Nattokinase, so it's important to take it away from food. @@thomasmuller1850
Oh and my dosage is based on this study: www.ncbi.nlm.nih.gov/pmc/articles/PMC9441630/@@thomasmuller1850
On another note: soon new CT photon counting high resolution scanner will be able to reveal intima borders of coronary vessels, information that was previously visible only via OCT wich is highly invasive. No study as of today could compare CT and OCT conclusively because of low resolution. When more data will be available we may be able to see regression in atherosclerosis and potentially retargeting cure and habits of the observed patient.
That sounds amazing
Sorry, I’m late to the video. Just finished reading the book “The Clot Thickens” by Dr Malcolm Kendrick, any comments on his theories? My motivation, I’m recovering from a heart attack a month ago…
Kendrick has long denied the role of (LDL) cholesterol in cardiovascular disease and used confounded epidemiological studies to support his arguments. He ignored clinical trials and genetic studies as well as those epidemiological studies which refuted his claims. I haven't bothered reading his latest book but I suspect it is more off the same. Try reading an alternative viewpoint before deciding which way to go. For example, Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. It's free to read.
Diabetes by far is the biggest risk factors for heart disease, high blood sugar damage the arterial lining.
Yes, this!
Inflammation is also a contributor.
Read a book called "The Clot Thickens". An excellent book on the subject.
What about vitamin K2 supplementation (MK7) ? Some MD s claim that supplementing with K2 decreases calcification inside the arteries. I've been taking vitamin K2 together with vitamin D3 for years now but I'm not convinced that it has any effect on existing calcification.
I don’t know. I would need to look into it. I can do that.
@@Physionicplease do
@@Physionic yes please.
@@Physionic EDTA
Is supposed to be even better
then k2 ( mk7 )
Calcification has a protective funktion preventing plaques from ruptoring. I do not know if we want that. Vitamin K is also a factor in blood clotting, and if you have arteriosclerosis, you want to prevent clotting, not promote it. Vitamin K is also an antidote for heparin blood thinners. I'm sceptic
Fascinating, I lowered my LDL 50 points in six months by upping my fiber intake, taking plant sterols, cutting out cheese and butter replaced with olive oil/ cod liver oil / black seed oil/ flaxseed oil, eating 600 calories in vegetables daily, and intermittent fasting ( not eating after 2 pm) ( also I always exercise daily so that didn’t have any effect). I’m skinny so everyone said my high cholesterol was genetics, but I proved that by following a different diet than the rest of the family and taking plant sterols I could lower my cardiovascular risk. 😅Also wanted to add that when increasing fiber intake it’s really important to up water intake if you don’t want wrinkles. 😅 I would love to see analysis on any studies on plant sterols and intermittent fasting for atherosclerosis.
Nick Norwitz lower his LDL by 75% with 12 oreo cookies in 2 weeks, he went from 420 to 111 by adding carbs back to his diet. Hes on carnivore or low carb diet.
@@manojlogulic4234 well that’s the one thing I can’t give up 🙃- my cookies, but I at least wait til the end of my eating period to go for it!
@@beautylover8138 What are your cholesterol numbers LDL HDL and triglycerides? Before and after ? Do you have family CVD history ? What was your diet before ?
@@manojlogulic4234 Unfortunately his conclusions are BS. He is a hyper responder which is a tiny fraction of people. For the vast majority of people they should NOT eat Oreos(common sense would tell us that). They should follow a Med diet, exercise and if their LDL and apoB are high take a statin. The fact he is on carnivore diet or claims that means he is to be discounted.
@@supernova1976 I improved my LDL cholesterol from 136 to 100, dropping 36 points and shifting from high to normal. Initially, I didn't fast before the test, resulting in an LDL of 125 after a diet change and starting plant sterols. Three weeks later, it was 125, and after five months, including a trip to Ireland where I indulged but balanced it with vegetables and continued plant sterols, it dropped to 100. Even after eating Popeyes the night before my last test, my levels were normal. That was three months ago, and my cholesterol might be even lower now, despite the occasional half cookie. I struggle to maintain weight with a high fiber intake (25-28g daily), requiring 14 cups of fluid to avoid wrinkles and keep up with intermittent fasting and gym routines. My HDL rose from 52 to 61, and triglycerides fell from 120 to 83. Previously, my diet was heavy on cheese, protein shakes, pizza, and buttered popcorn. Despite a family history of high cholesterol (but low blood pressure), I was unaware of the 25g daily fiber recommendation and its impact on skin health until recently. Adjusting my fluid intake restored my skin. Sharing this in case it helps anyone!
Anti plaque stack:
Fast 1-3 days a week (free)
burpees + jog/run 4 days a week (free)
niacin - flushing kind daily (super cheap)
vitamin k2 daily (super cheap)
psyllium husk daily (cheap)
Magnesium daily (cheap if oxide, moderate cost if better form)
Add-ons to the stack:
Weight training 2-3 days a week (moderate price)
Creatine (moderate)
Protein (expensive)
What about vitamine D and omega 3?
Developers be stackin everything 😂
Berberine?
Fasting 1-3 days a week? Hmmm...
@@NThunderMy cardiologist has me on Berberine
This was an excellent presentation on the topic and worth the time to view it. It's a complex topic, you covered the key aspects people need to know to get a fuller understanding of the process of CVD.
Nope, but my explanation ... censored.
If I understand you correctly, reducing the burden of LDL particles passing through the endothelial layer is very important. And the way to do this you say is by lowering LDL-C or even better ApoB.
This makes perfect sens to me. But if I understand you correctly,.. the only (significant) way to achieve this is by reducing LDL-C / ApoB.
This I find confusing. Because I would think that there are more ways to achieve this, and perhaps to such an extend that the LDL-C/ApoB level becomes less important.
Maintaining a health glycogalyx (lowering glucose levels, quit smoking), reducing low-level systemic inflammation, lowering blood pressure, etc. all reduce the "permeability" of the endothelial layer.
Especially when all these things are achieved through non-medical interventions. (I believe that non-medical interventions have much stronger effects than what can be achieved with medications)
Exercise, as you have shown, has a plaque reducing effect. Exercise is a non-medical intervention that improves all of those goals I mentioned. All of those can be achieved through dietary interventions. Is there a specific reason you didn't mention these? Or were they simply not part of the studies that you went through? Are there even studies that look at these factors in relation to dietary interventions?
This was so interesting! It looks like many presenters on youTube over simplify what cardiovascular disease is & how it's caused; it's the first time I've seen something detailed enough to help me figure out why cardiovascular disease is such a common problem in my family. I've been plant-based for 6 years and am fairly fit (not overweight). I wonder if my dietary choices are going to be helpful. I'm 71.
check out nutritionfacts. He claims heart disease is reversible with a plant based diet. Its always good to have lots of sources of info since this stuff is complex. @locutia7
Nick does a great job, doesn’t he?
Yes. Since switched to a plant based diet, then you're good
Plant based doesn't say that much. For example a lot of vegans eat a lot of sugar, and they can still be called "plant based". And the problem with that is that insulin resistance is involved in all of the metabolic chronic diseases.
Diet is an important part of the equation but sedentary behaviour and pollution also increase cardiovascular disease risk (so do cigarette smoking and alcohol consumption ... and marijuana use). Controlling blood pressure is also important. I understand that 'plant based' works if it contains lots of whole fresh fruits and vegetables, whole grains etc but very few processed foods (plant based or not).
I strongly suggest reading The Clot Thickens by Dr Malcolm Kendrick. A very convincing alternative hypothesis regarding the etiology of CVD backed by a mass of references.
I also strongly recommend reading or viewing content from Dr. Malcolm Kendrick. Atherosclerosis is a disease first and foremost of chronic inflammation and repeated thrombosis brought on by metabolic dysfunction.
@@patrickweisser3185 Dr Kendrick has written 4 books to date and I recommend all of them for different viewpoint of different aspects of health and health systems.
Yep yep yep. Pay attention here people.
@@patrickweisser3185does he say if eating a low inflammatory diet and fasting helps reverse at all or nah ? If it's from chronic inflammation you'd think that would help
Or Dr. Ernest Curtis's (a cardiologist) "The Cholesterol Delusion" which demonstrates the low quality and outright manipulation of the original studies that led to current medical thinking. Three of the studies are included in appendices so that the reader can see for themselves what he explains in the book.
Can fasting help?
Couldn't hurt.
I did it, Nattokinase and pine bark extract once a day on an empty stomach
Of course your diet should be somewhat healthy
Anyway this took me 18 months, had PAD
You are providing outstanding content. Thank you for service to the public.
In 1997 3 Doctors wrote a book
The Arginine Solution
Nobel Prize Beseech proving Arginine dissolved the plaque in the arteries. Helped me a lot .I have family history of Atherosclerosis. I have none.
Remember us at a million subs brother. Always loved your channel, dating almost all the way back from it’s conception
Nothing will change. Thank you. :)
Thank you for your service!
Thanks for stopping by :)
The Linus Pauling method - vitamin C + lysine could be worth covering - if you haven't done so.
So underrated. The issue is, there isn't many studies done on it because it makes no one money so there isn't much to show.
@@Always_there99 That is the Pauling Protocol. Its reported, but no studies really done on the protocol itself.
What about the study using 2400mg of aged garlic? Pretty significant improvements.
I'm a bit torn with this, as vitamin-C prevents calcification of plaques. That is not good at all. Calcification is a secutity measure of the body to prevent plaques from rupturing. Plaques are more dangerous if soft, as they can rupture, clot and travel to heart, lungs or brain causing infarction. Statins for example increase calcification, seen in the CAC score, stabilizing plaque and decreasing risk.
What interests me is the lip(a), as we do not really have a current way how to lower it - meds are still in development. If this would be an option for individuals having that elevated through genetics, maybe they could lower their risk to those without this predisposition.
So much for the carnivores: I can't hear the claim anymore, that they do not need so much vitamin C, as they do not have symptoms of scurvy... They do not get that surviving does not mean no deficency or negative effects. I'll make sure to eat my fruit and veggies to get enough for prevention of several chronic diseases.
@@stellasternchen good post , people see what they want to see . Same for these "miracle' drugs to clean up cells. Yet the body knows how to do autophagy , so senescence is not to be lightly mucked around with - just do the hard work ( HIIT or intense exercise and let the body do its job) , until better understanding comes . As for the topics at hand - if there was an easy method we would know about it . Plagues of any type are hard to remove even with direct access , teeth , bathroom walls etc , when given time to embed . They are incredibly tough and can survive extremes in nature . Given that doing the things outlined here is generally enough , to continue to live healthy - ie no more growth , then if keep strength , VO2 max , chance of a problem outside an acute infection/inflammation /over exertion/dehydration /chemical or electrolyte imbalance . Drug addicts probably survive some bad scares ( eg too much meth ) solely due to young heart - not sure a 60 year old wants a heart going crazy at 200 bps
Good conventional info but what these studies don't address is: why are we one of the few species that develop plaques?; why do the plaques only occur in arteries just outside the heart and not in veins or elsewhere in the body?
6:57 “if the level of LDL is too high, LDL gets stuck.” You gloss over this statement without showing data that confirms controlling LDL levels prevents this mechanism from occurring. This is the key statement supporting the widespread use of Statins.
HIIT group had average LDL 2.1mmol/L +/- 0.7. This places them exactly at the threshold of plaque reversal (lowered Atheroma volume) due to low enough LDL according to some other study. This means some participants were above, some were below. It means it makes it very hard to know if any changes in plaque were because of low enough LDL of some participants or was it because of HIIT.
Where is the study that shows LDL causing plaques ?
@@garyroach8624 where is the study that shows we need oxigen?
When babies are born they need to take a breath to continue living, that aside the lower the LDL the higher all cause mortality. @@YuraL88
@@YuraL88 strawman argument. Just because one correlation is actually due to causation doesn't mean that other correlations are as well.
@@adamjackson713 it's not. We can use epidemiology to establish a cause-effect relationship. Smoking, environmental carcinogens, and others.
But it's not epidemiology only:
- trials of LDL-lowering drugs,
- Mendelian randomization trials
- animal models
So, you can't have a single "study" that proves everything, but rather pieces of evidence from the hundreds of studies.
The same logic is used by AIDS denialists to "disprove" the HIV-AIDS link. No single study proves that casual relationships, but still the general overwhelming consensus that HIV causes AIDS.
Have you done (or will you do) any videos specifically regarding the potential benefits of garlic for cardiovascular health? I see others claiming garlic (specifically alacin) has shown some benefit in reducing plaque burden. I’m cautiously optimistic that could be true, but I’d love to see some study data to confirm or deny that claim and you seem like the kind of chap to fairly and rationally investigate such a claim.
Can I suggest that you bring in the glycocalyx and also the fact that diabetes dramatically increases the risk of CVD. If it is all explained by LDL, why does hyperglycemia and diabetes have such a dramatic effect? Everyone accepts that diabetes causes major vascular problems in the periphery, so why doesn’t it also cause problems in the coronary arteries? Another important question is why does arthrosclerosis only occur in high-pressure, high turbulent areas of the coronary arteries? Why does it never occur on the venous side?
Because ldl numbers aren't the cause, they are a side effect. And there's other factors that also effect it.
@@Vincent_Beers you are talking bullshit.
Look up "shear" rate in the blood and you will get your answer about high pressure coronary arteries.
@@miltonhondrakis2431 so how is LDL and shear stress connected? Shear stress damages the glycocalyx particularly if it is thinned out by hyperglycemia.
It does happen on the venous side but less common. The biggest factor is high blood pressure and the location of the arteries because arteries branch and are often curved or arched. This is where it happenes
Supplements, other than Omega3s, were not taken into consideration in this study. What supplements may help in reducing arterial sclerosis?
Manganese daily up to 5mg even better in combination with selenium preferably selenocysteine and on top Hesperidin methyl chalcone. A maximal prevention trio
Im a cardiovascular tech and this has been a great listen
Sharp thinking, and you are always looking for the right statistic and conclusion..clever scientist !
You mentioned that you want a thick covering of fibrosis to prevent a rupture of sorts. So what about the use of proteolytic enzymes like Nattokinase? Can that potentially do more harm than good for someone with existing CVD?
They affect the clotting cascade, which plays a role, but the ECM release is mediated by the fibroblasts, not the platelets (although the platelets also play a role in atherosclerosis, just through a different mechanism).
Nattokinase
Berberine
Niacin
Thanks for your service! 😊 Could you please do a video on NATTOKINASE, serrapeptase and lumpkinase?¿?¿?¿¿
🙏🏼❤️
All I know is i vastly increased my overall activity and exercise while changing nothing about diet or medications (because diet and medication changes were something my doctors and I had adjusted the previous year) and in the six months of increased exercise my cholesterol numbers were all vastly improved.
Our next experiment is taking me off avortastatin for 6 months to see if I can continue to get more muscle mass with less pain (muscle pain is a potential side effect from statins that I feel was interfering with exercise)
We check blood every 6 months and make a decision on what to adjust or change next.
Over the past 3years I've lost 160 pounds(starting from 500) while slowly being able to stop taking various medications. We started with diet and lifestyle choices and then expanded to body building for muscle gains.
Hopefully I can lose another 100 pounds over the next year and then see where I am and what needs to be the next target goal.
Congrats on that 160lb. Finding a way to love exercise is crucial. Good luck on that next 100lb.
Will be passing your email summary on this one on to a few since I’m in the mid 50s group. Thx Nic.
Look for it next week
Dude. This is a beautiful explanation! Watching all of the out-of-control layers and buildups is just freaking me out even more and reminding me to keep to my good habits. Seriously, thank you!
Glad you liked it! Thanks!
kenberryMD
This was great. Thanks
How would you do a double blind HIIT Trial?? Would the participants not know that they were doing high intensity interval training???
Heart disease is the number one killer of people today and cancer is number two.
Being over weight is the number one factor leading to an early death.
People who are over weight have higher risks for high blood pressure, heart disease, diabetes and cancer.
Even children today have signs of artery disease. Fast foods and sugary drinks have long term consequences.
There is an obesity epidemic today where over 60% of the population is overweight or obese.
What is common today and "NORMAL" is not healthy. The average person today is not healthy and is taking medications.
Heart attacks were once only common in people over 65. Today people in their 40 are having heart attacks.
Add more plants and vegetables to your diet and less junk and overly processed foods
Dr. Esselstyn debunked his own book. The artery image from the Esselstyn book is from his colleague Dr. Joe Crowe a general surgeon who at age 44 had a heart attack even though he was slim, a non smoker, not a diabetic, no high blood pressure and had low total cholesterol of 156 mg/dL. So Esselstyn debunked himself because Crowe had all the metrics for preventing heart disease but could not explain why it happened. He changed the Crowe diet to less animal foods but if animal foods caused the problem why did they not raise his cholesterol level high like Esselstyn says they will.
LDL of 2.1mmol/L was the threshold when there was negative % plaque volume change observed in some study, unfortunately I only took a screenshot of the graph/results so it doesn't show study link/name. Largest reduction was with 1.1mmol/L which seems to be very low, even 2.1 seems to be very low number.
Can you make a video about the proper human diet in your opinion?. Or just what you eat daily. I know that topic is controversial.
I'd also be interested.
Carnivore
Great topic, thanks for covering the #1 cause of death in the world. Are Dr. Esselstyn and Dr. Ornish correct when they claim a Whole Food Plant Based Diet, salt oil and sugar free, can reverse arterial plaque? What about high intensity interval training? Like high water pressure flushing out the plaque through intense vigorous exercise…
Considering that statins is the all time highest selling drug and can lower ldl makes you wonder why not only CAD is still the top killer but .... also on the rise. Maybe its because loweing ldl has no effect on CAD mortality outcomes? and that there are other factors inducing atherosclerosis.
Statins weren't commercially available until the late 1980's, yet coronary heart disease (CHD) mortality rates had been dramatically declining since the late 1960's (due to public health campaigns to reduce CHD risks: reduce smoking, reduce hypertension, diet - to reduce cholesterol, hypertension etc, increase exercise, etc). CHD mortality rates continued to dramatically drop after statins were introduced, but slowing down in the 2000's, plateaued about 2007, then started a gradual increase from about 2013.
Only good news - premature CHD mortality rates (younger than 65yrs) are still much lower today than in the 60's, and earlier.
I wonder if th day is more likely linked to a reducing in smokers more than anything else. But so many variables...
This was excellent! If I were to request anything from your channel, it would be that you present some analysis on soluble versus non-soluble, fiber intake, especially as it impacts those with heart disease. Keep up the good work.
Definitely can do - thanks
If you are looking for new material to cover. There was a study done on the effects of nattokinase, that showed reduction in arterial placque. I would love to hear your opinion on that study as well. There may have been some bias, I really don't know, but the only bias I could imaging, is soy bean farmers, manufacturers that produce nattokinase... This was a great video, and I appreciate you pulling back, to keep the information understandable for all.
Could you send me the DOI number of the study? I’d be happy to cover it.
@@Physionic I'm not even sure what a DOI number is, but I will certainly see whatever information I can find on the study. I'd really be interested to see if you can make a mechanistic correlation to the supposed outcomes.
@@Physionic pubmed.ncbi.nlm.nih.gov/36072877/
Thank you
@@Physionic This is what I have found. I am not sure if that is exactly what you need to find the study
I've heard about Apo B for a few years but never really knew what it was until recently. From what I read it seems to be a sum of all the LDL particles and is probably a better risk predictor than LDL-C because it includes VLDL. having listened to Dave explain his Lipid Energy Model and having had high TG and VLDL it's an easy to understand concept why it's a better risk predictor. But I think the reason that HIIT didn't have much effect in the data is because of diet. Exercise burns glucose and fat but if you continue to eat in a way that puts in more sugar and fat then you're not making much of a difference.
Take high dose Nattokinase and you will see the difference in plaque reduction
As a supplement or food? Is there any evidence behind your statement?
@dragosxtc1901 supplement and there are many trials but most on animals though and I personally seeing results
This channel is a fucking goldmine
What about the effects of vitamin K-2 (mk4/mk7) in atherosclerosis?
Sounds like the study needed to be longer, the statistically insignificant values were trending in each marker consistently.
I wish there was a study like this for Serrapeptase.
So do I. Nattokinase, Serrapeptase, and Lumberkinase all work in a similar fashion and the three can work together synergistically, but most of the research to date has been done on Nattokinase.
Would love to hear your thoughts on a video lecture by doctor Paul Mason Decoding Atherosclerosis: The clotting theory and seed oil toxicity
It's been on my radar. Unfortunately, those lengthier videos take me about 2-3 weeks of research, a few days for notes for the video and recording, and another week of illustrations and video editing, so it's an expensive process. I may still cover it, however.
Seed oil toxicity ....Hm, those oils have shown in RCT's as LA veterans to lower cardiovascular events. A low carb doctor, right? I have nothing against low carb diets, was on one myself with a good experience and can reccomend it to reach certain goals, fight diabetes or prediabetes etc. But I do not understand this constantly need of those diet gurus to claim the opposite of what the sum of evidence shows. I do not understand this obsession with saturated fat. High fat does not mean high saturated fat. I know, because I did make sure when I was low carb dieting to eat mostly unsaturated fat. If you exclude a good source of unsaturated fat as those frying oils does make it more difficult and you end up with butter, palm oil, lard or even worse, coconut oil.
Paul's video is based on 'The Clot Thickens' by Dr. Malcolm Kendrick who has developed the Clot Theory of plaque formation. The book presents significant analysis supporting this theory. It seems to explain the creation of plaques better than the current "burrowing" theory. Since the Clot Theory deviates from current theory supporting statins, Dr. Kendrick has been blackballed by the medical community.
@@markhapner8499 Hmm, aspirin for arteriosclerosis has been tried. This drug blocks Cox1, and thus the synthesis of clotting factors.
It did more harm then benefit.
@@markhapner8499 Hmm, aspirin for arteriosclerosis has been tried. This drug blocks Cox1, and thus the synthesis of clotting factors.
It did more harm then benefit.
Excellent information. I want to know why my cardiologist hasn’t informed me on any of this? All I get is go on a Statin and or Repatha plus put a Stent in. No lifestyle change conversation at all. I have a high CAC score but no symptoms and can workout very hard 2 hours a day plus 30 minute sauna 6 days a week. 58 YOM 69” 155lbs
My cynical opinion of cardiologist like yours is, there’s no money to be made in stopping the progression of your disease.
Super Interesting! Thanks for sharing. I suspect carnivores will not take kindly to this video,,and anecdotally greatly disagree. Just saying.
Vitamin K2-7?
it is hard for me to belive that when sobmody loses 30kg, evryhitng shrinks bur arteriar plack does not ;).
Serrapeptase inhibits vascular inflammation, seems important.
Mechanistic studies demonstrated that SRP significantly inhibited the LPS-induced production of proinflammatory cytokines such as IL-2, IL-1, IL-6, and TNF-α in aortic tissue.
Furthermore, it also inhibited LPS-induced oxidative stress in the aortas of mice, whereas the expression and activity of monocyte chemoattractant protein-1 (MCP-1) decreased after SRP treatment. In conclusion, SRP has the ability to reduce LPS-induced vascular inflammation and damage by modulating MCP-1.
Serrapeptase inhibits vascular inflammation, seems important.
Mechanistic studies demonstrated that SRP significantly inhibited the LPS-induced production of proinflammatory cytokines such as IL-2, IL-1, IL-6, and TNF-α in aortic tissue.
Furthermore, it also inhibited LPS-induced oxidative stress in the aortas of mice, whereas the expression and activity of monocyte chemoattractant protein-1 (MCP-1) decreased after SRP treatment. In conclusion, SRP has the ability to reduce LPS-induced vascular inflammation and damage by modulating MCP-1.
I'm so impressed, thank you! I put this video down in my notes for your detailed description of the whole course of atherosclerosis at the cellular and molecular level, then the summary of processes to regress plaque, then your great bullet points at the end on lifestyle changes. It's like a reference for January 2024 state-of-the-art in atherosclerosis and lifestyle treatment! Thanks. (I was diagnosed with CAD after CAC 586, 97th pct, Sept 2023; I'm hunting data to strongly suggest lifestyle changes so I can stop the disease, regress plaque, and avoid PCI and bypass if possible)
Sugar fast food alcohol tobacco.
Give up all.
1.2 million IU’s of Serrapeptase at minimum.
Start at 240 iu.
And slowly build up to HIIT Heavy bag boxing drills.
I went from emphysema to the FITTEST boxer in a gym.
Ventim before boxing.
At 54 I could maintain 170bpm!
72 pinches in 10 seconds.
You must log your ABSOLUTE MACIMIM SPEED.
And begin HIIT Boxing at That speed… till you drop.
Start with a drum beat BPM If unfit perhaps two punches per beat at 65 70 bpm hip hop works well.
I understand that autophagy can also reduce plaque... What say you?
Thanks. Another very helpful video was full of very important information. 👍🏽💯🔥
There are a lot of recent studies, which have shown surprising and amazing results with daily Manganese intakes reversing Arteriosclerosis.
Take Manganese daily up to 10 mg even better in combination with selenium preferably selenocysteine and on top Hesperidin methyl chalcone. A maximal prevention trio
Easy to get in diet - 3 tbsp wheat germ and some oats and almond butter gets you 7mg/day plus beta-glucans and spermidine as a bonus!
@@jpintero6330 you won’t get 1 mg manganese by your recommended diet, which however is quite good for other reasons
I’d like this to be true as I love hibiscus tea. I’ve often worried about excessive manganese
@@jesincov a well balanced combination with Niacin further significantly reduces cardiovascular risks, where by ,balanced‘ it means niacin taken together with TGM (Trimethylglycine) in accordance to your individual methylisation capacity. If someone is an under-methylisator (the majority of people are!) it is mandatory to combine niacin with TMG, if you want to protect your liver of negative effects of niacin. If you are not an under-methylisator TMG still isn’t harmful at all. So it seems reasonable for everyone taking higher doses of Niacin to always add TMG.
Then this combination together with Manganese, Selenium (preferably Selenocysteine) and Hesperidine Methyl Chalcone is probably the best plaque remover combination available certainly much more effective than any statins and, if you follow the advice to combine niacin with TMG, without any negative side effects
The Dr. LINUS PAULING protocol works! I started on it way back some 15 years ago as my alternative to conventional med interventions. However, I noticed the see-saw effect of reverting increased BP by taking Vitamin D3 K2 MK7, lots of anti oxidants and anti inflammatory food. Also avoided processed and ultra processed foods, seed oils.
Many of my friends who did the same thing were able to get pass cardio vascular disease.
I am now 77 years old and still healthy
I regressed my CAC Score from 102.9 to 32.01 in 18 months
Crestor Ezetimibe Nattokinase and other supplements
I wonder how daily consumption of baked goods made with manufactured plant fats affects atherosclerosis/heart?
Does he ever mention insulin resistance or ldl particle size?
So, after all of this entire, for me confusing,lecture …what I took away from this is there was no help with reversing atherosclerosis! A lot of whatever you call it to say, no proven help. Gee even tho it was interesting, but confusing, I feel like I have no hope. Im Soon to turn 79 and have heart disease and atherosclerosis. Had one surgery on left carotid already and right is just above 50%. I’ve already tried Hit and dozens of other things like just sprints,etc did Keto for 2 1/2 yrs, then Carnivore for last 2 months so I don’t think I can change this terrible atherosclerosis! They may find something, it won’t be in my lifetime, I’m sure. I sure wish you all could just explain these things a bit simpler because it’s to long to just be disappointed in the end! By the way, I’m 4ft11 inches and weigh 97 lbs. so not overweight and no diabetes., and stopped smoking 20 yrs ago after quadruple bypass surgery.
Wow! Great information! Thank you!! 👏🏼👏🏼👏🏼
Thank you for your analysis of Atherosclerosis!
Can you share your thoughts on the functions of stem cells, the difference between general and specialized stem cells, as well as the action of stem cells when rebuilding the body's broken down cells and tissues. A large part of the population in the Western world is attacked by osteoarthritis after they have passed the age of 60. I assume that part of the cause lies in autoimmune conditions, which develop inflammation, especially in the joints. Autoimmune inflammation is known to attack the body's own cells, and in osteoarthritis, stem cells are prevented from rebuilding the cartilage in the joints. Can you confirm this?
Incredibly clear presentation on arteriosclerosis! Thanks 👍. My understanding is that HIIT did not have an effect on this study. The fact that the control group declined in their metrics is a bit suspicious as they would be expected to stay the same over the course of the study, unless this was an especially sick group of people (in which they need to do the HIIT). Perhaps the duration of the HIIT or it's level of execution was not enough to induce a measured effect. Would be interesting to hear more studies that tried to measure the benefits of exercise (in different forms) on levels of arteriosclerosis.
Are donations to physionics tax deductible? Is physioncs a 501(c)3 corporation?
You are what you eat. Your diet impacts your health.
Lower stress, reduce obesity, get enough sleep and more exercise are key to a healthy life.
Obesity in children and adults is rising across the world.
Fast food and sugary drinks including fruit juices are contributing to the problem of poor health and obesity.
Eat a healthy plant based diet and exercise regularly.
Reduce or ELIMINATE cows milk, eggs, cheese and meat. Eat more salad greens, beans, fruit and vegetables. Eliminate fast food, snacks like cookies, cakes, chips, and sugary drinks and juices.
Every adult and child should own a bicycle and ride it regularly.
Regular exercise will help you sleep better. Yoga is a great stress reducer.
Obesity is all too common today. Get off the couch. Get off the phone, ipad or video game.
A variety of stretching and other exercises help with increased mobility.
Ride to work, ride to school, ride for fun.
Every city should be a bicycle city.
Speak up for bicycles in your community
9:52 “you can have a perfect healthy endothelium, and if you have high levels of LDL, then that LDL can cross through the cell itself (endothelial cell, endothelial cell to cell boundaries etc.)”. Please cite where you get this information from, thank you.
exactly my question
And why does LDL levels need to be high for that to happen? The veins see same levels of LDL, yet at those reduced pressures and more laminar flow this does not happen. Free cholesterol crystals found in plaques are not present in the bloodstream, but are contained in the structure s of damaged red blood cells. Damage to the protective glycocalyx layer readily allows damage to the endothelial cells, and hence clotting is instigated. Many things end up in the plaques and clots that were not part of the original damage. Whether arterial endothelial damage occurs by mechanical, chemical, or stress induced hormones, etc such damage is a prerequisite for plaque and clotting. Actually, lipoproteins carry much more than fats and cholesterol,.... lipoproteins are simply the vehicle of transport having coatings of different nutrients, antioxidants, and hormones that are delivered to sites of damage to remove inflammation, calcifications, and bloated foam cells that have outlived usefulness but refuse to die. Properly coated, the lipoproteins are constantly maintaining the state of repair. Lacking these coatings of CoQ10, Vit k1, k2, Vit D, Vit C, or lack of Magnesium and other minerals the repair process slowly grinds to a stop and atherosclerosis ensues vigorously as calcium solidifies to attempt walling off the damage and exposure to the bloodstream.
@@mozit6 what damages the glycocalyx?
@@cattleprods911 From my post...."mechanical, chemical, or stress induced hormones, etc ". The mechanical damage is largely due to high pressure causing non laminar flow and the contact of blood cells and any other cells or molecules in circulation. In sickle cell anemia the blood cells are sickle shaped (pointy ended) and those afflicted die very young from massive atherosclerosis and calcification. Our veins being subjected to lower pressure and having more laminar flow almost never develop plaques like arteries do, unless surgeons use this vein in a bypass where it serves as an artery (CABG). Those grafts plug up in 6-8 years or so. Another type of damage is chemical, as when smoking cigarettes. The new under the tongue camera can detect this damage within seconds of smoking and dead endothelium cells are found in the bloodstream. Sugar also induces chemical damage because of glycation. Diabetics mostly die of heart disease. Also, an imbalance of hormones like cortisol caused by emotional stress can wreak havoc on the glycocalyx and the endothelium.
@@cattleprods911 I forgot to include bacteria as a damager of endothelium glycocalyx. Basically that is what happens in sepsis as bacteria runs rampant destroying the glycocalyx all over the body causing multiple organ failures.. The under the tongue camera is used to check the condition of sepsis patients.
You don't distinguish between soft plaque and stab;e plaque. Stable plaque is not reducible.
Does taking statins (low dose) help reduce the foam cells? Or just that inflammatory signals are damped?
I just listened to Prekure- prevention, with doctor Paul Mason, Decoding Atherosclerosis, and I think there's some compeling finding, going back to the 60's that high LDL is not the issue. Plant steriods may be a part of the puzzel.Thanks for your analysis ,so the average person can make wise decisions.
I'm a member in your physionics group and was looking for this report in the Mighty app, but I want able to find it. Can you give me some guidance on where I might find it?
do you think that Vit K2 has a significant role in atheroma/endovascular calcium regression?
Both the control and HIIT groups had quite low total and low density cholesterol .. ldlc = 2.1 (mmol/dl) [*36] == 75(ish) mg/dl … most post mi would be delighted with an ldlc of 75mg/dl. Even their total cholesterol was low (3.1*36) == 100(ish) mg/dl. ApoB … also low …. For “overweight” people they had amazingly low total etc
Great point
@@Physionic Table 1 on the footer lists High Potency Statins - which would explain the amazing low LDLC/ApoB for "overweight" people. Is this study more the effect of exercise in conjunction with high potency statins ?
My ldl is 3.44 mmol/l = 133 mg/dl. I want to bring it down with 200 mg Nattokinase and 1200 mg red yeast rise powder after the first meal/day. Is this a good idea?
I'm 70 years old male, 62 kilos.
Imagine if you created a tweaked LDL that somehow forced LDL out of the pockets.
Some additions:
Keto diet (already kind of specified)
The following supplements, but not at the same time:
Mg supplement
Vitamin K2 - MK7 (only 1 every 3 days)
Sunshine or d3 supplement
Nattokinase - breaks up fibring - caution: blood thinner warning
Chanca Piedra - loosen calcium deposits - blood thinner warning
Inositol
and as mentioned, exercise.
Doc, thanks, I am so happy that you have not flagged alcohol as a reason, so I am going to the bar for scotch. See you there. Cheers..
No mention of extended fasting and autophagy? I am a sample size of one, but I have reversed my severe arteriosclerosis in 3 months. The before and after MRIs are incredible.
hi there. what are you eating if you could please tell me. thanks in advance.
@@jfdomega7938 It was roughly a semi-extreme keto diet: 1. Replaced butter with olive and avocado oils, 2. Zero sugar, not even fruits, 3. Zero rice/bread/pasta - basically only vegetables.
But the important part is the extended fasting: At least one 3-day or 4-day fast per week. Often 5 days of fasting per week. And 1 or 2 meals only in non-fasting days.
My only indulgence (limited) Cheese!
Nic, How certain are you of the accuracy of the model of the development of arterial plaque? Specifically, if it's just a question of LDL from consumption of saturated fats, why has the incidence of arterial plaque increased so dramatically over the last 60 years?
Yes and saturated fat consumption has also come down over that 60 years but the incidence of CAD has risen. The only good news is that modern medicine can keep us alive better after an event.
@@shauna996 But what has risen over that 60 years is consumption of seed oils and processed foods, and, of course, the $billions in profit from advertised pharmaceuticals to treat the symptoms. Hmmm
@@neuromax3766 We are in agreement.
Yes this exactly, plus a lot of sugar in all the fat free foods to make them not taste like cardboard. The producers of corn syrup and the pharmaceutical companies make for a very profitable team.@@neuromax3766
@@shauna996 They want you alive, just sick as hell. Nobody wants to lose a customer.
How about MCT's and coconut oil? As I seem to remember seeing studies that these had a positive effect?? Though both are triglycerides, is it the case that some triglycerides are more equal than others??
Cholesterol has been found in plaques, and is generally attributed to LDL but I have never seen studies showing Apo B being present. However, I have heard of studies showing that Apo A has been found in plaques, pointing to Lp(a) being the source of the cholesterol. As I mentioned below, if you consider endothelial damage and clotting, it is known that Lp(a) is involved in the arterial damage clotting process, so, this hypothesis carries much greater weight in my mind. Research in this area seems to be lax, as there is no pharmaceutical solution to Lp(a) values.
AboB-100 is found in IDL, LDL, VLDL, and Lp(a).
How would + charged APOB particles "randomly escape" the plaque after electrostatically binding to the - charged proteoglycan that's created by migratory-secretory smooth muscle cells in the sub-endothelial space??? I believe it is more likely they are actively removed by immune function as inflammation and excess oxidative stress are resolved.
Certainly a possibility, Tim. I think the mechanisms aren’t as clear. We do know that aggregation of LDL can change its affinity to proteoglycans. Additionally, changes to the ApoB structure change the affinity (there’s a 10 amino acid sequence that is known to canonically link ApoB to proteoglycans). There’s probably other factors I’m not familiar with, as well. But, it wouldn’t surprise me if it had to be through some active resolution like immune cell clearance.
Regarding "general solutions": Very recently we have seen that lean healthy fit people can have both high HDL (good) and high LDL (bad) with low triglycerides (good). They are called LMHR phenotypes - Lean Mass Hyper Responders. Does it mean that reducing LDL is still part of the solution above ? Is there proof of a causal link between high LDL and cardio events, or do we have only associative hypotheses. Selective data from selective studies are mostly useless.
Multiple clinical trials have shown that lowering LDL levels by diet, lifestyle changes or drugs significantly reduces the rate of major adverse cardiovascular events (fatal and nonfatal heart attacks and strokes, and the need for revscularisation surgery). They have convinced the worldwide scientific and medical professions that high LDL is a causal risk factor for CVD. It's not the only one of course but it is undoubtedly a causal risk factor.
Best video on RUclips. Thank you.
EDTA
I'm just a normie on the Internet who got a bit more serious about health fairly recently (~6 months ago). I've learned a lot of actionable basics during this time but this is the first time I've seen an actual in-depth (from my PoV) illustration of the atherosclerotic process. Amazing stuff, thank you for this and looking forward to seeing even more content like this!
Except the content is wrong
How is it wrong
@@stevegcqI haven't watched the video but what do you think is the correct point of view?
I can tell you I am reversing my CAC with the Linus Pauling Heart Protocol 200 points down from 660 in 20 months. Even with LDL at 124 and HDL at 36.
@@SET12DSP10 letters, first three, 'ken', second three, 'ber', third three letters, 'rey', the last two letters are, 'MD'.
@stevegcq This guy here is about standard medicine pretty much Dr. Ken is a step well above. And what I have done is a major step above Dr. Ken. My CAC was 660 and after 20 months it was 458. Not many people achieve this. I did it following the advice of Dr. Thomas Levy, cardiologist author of "Stop America's #1 Killer" Proof that the Origin of All Coronary Heart Disease is Clearly Reversible Arterial Scurvy. I suspect at my 3 year anniversary of my 660 score that if I did another CAC it would be down by 50% to 330 or even less....imagine that....my score is reversing as fast as it progressed.....
@physionic would you please check out this protocol that involves plaquix natokainase k2 d3 magnesium and serropeptase
And a new supplement called cavadex
I got stuck on the formation of atheromas I could not get beyond it because it seems so wrong. If ldl simply passes between the cells, even if you can explain the mechanism as -/+ attraction how is that 1. it does not happen all over the body 2. Does not happen in veins 3. ldl needs to be high, surely the presence alone of ldl is sufficient 4. Other things do not just simply pass through the tight junctures between the cells, why are we not constantly bleeding out? Added to which, it is well documented that people with 'normal' and lower than normal levels of ldl also suffer atherosclerosis at the same rate as those with high.
Even if you want to explain that ldl sticks to endothelium, it still doesn't explain points 1, 2 or 3.
You can go ahead and blame apopb but considering this is the backbone so to speak of all lipoproteins it ends up being the same argument. ldl really isn't even a significant component of plaques, cholesterol crystals wrapped in macrophages yes. So does the ldl pass behind the cell, drop of the cholesterol and the return to the blood stream?
Considering the body makes ldl why would the body make an excess? Why would millions of years of biological development create a mechanism so flawed? Sorry .... not buying it.
I answered a lot of those questions in another comment on this video, I'll refer you there. I'd also need a study reference for this claim "Added to which, it is well documented that people with 'normal' and lower than normal levels of ldl also suffer atherosclerosis at the same rate as those with high."
It is true that ApoB is not the only factor for heart disease, but I've repeated myself over and over on that. It is a factor, but not the sole factor. I'd still be interested in seeing a study on low vs high LDL and no heart disease difference, if you can post one (the DOI number, please, links get deleted sometimes on RUclips).
The first thing I should mention is the glycocalyx and its role in protecting vascular permeability. Highlights can be found on wiki here:
/wiki/Glycocalyx#In_vascular_endothelial_tissue
This alone calls into question ANYTHING passing through the endothelium never mind only ldl
*A search for this:*
"Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines"
will give you a pubmed article -> /19081406/
/releases/2009/01/090112130653
@@PhysionicOk so I posted the message twice, once with links once without. So obviously youtube is an A$$.
I guess all that is left to say is glycocalyx and lean mass hyper-responders with ldl levels up to 600 and no increased plaque risk.
First off, thank you.
Second, these studies don't surprise me - there are many confounding variables that even the researchers acknowledge. For example, the first study cited was looking at people who had a cardiovascular event across over 500 hospitals. It's a cohort based study (meaning, they simply compare one group against another at a single time point, generally), and that's notable, because they can't control for who was on lipid lowering drugs and who wasn't, between each group. So, for example, about 12% of people with very low LDL still ended up in the hospital for CVD, but it's entirely possible most of those individuals were using lipid lowering drugs to achieve that 70mg/dL, implying they were in poor health before they were put on a lipid lowering drug. Of course, one could argue that the fact that the drug didn't prevent their CVD is proof LDL isn't a factor, but that is not what this study can show, and other analyses show the exact opposite when compared against the correct control (people who are not on a lipid lowering drug, or put on a placebo) - implying that lipid lowering drugs are effective relative to people in the same health condition at the start who choose not to fix their lipid levels. Also, over 50% of the people in the above analysis had hypertension and they were, on average, overweight. None of those were controlled for in the analysis, and no respected scientist or clinician wouldn't agree that being overfat and having high blood pressure are also independent risk factors. No one is claiming LDL is the only risk factor, just that it contributes causally to atherosclerosis progression, much like blood pressure does, as one example.
Oh, and you forgot the rest of that conclusion... "In a large cohort of patients hospitalized with CAD, almost half have admission LDL levels
@@Physionic
I was aware but it is irrelevant. When do they stop lowering? When ldl is zero? Its an absurd premise. ldl lowering is about selling a drug which isn't working.
A recent study on lmhr (on ketogenic diets) has shown that despite ldl levels four to six times higher than normal (yes, 400 to 600), show no sign of increased plaque when compared to similarly healthy individuals of nominal weight on standard diets.
Atherosclerosis is a response to damage to the endothelium.
Any research about adding Serrapeptase to this?
Really good information. Thanks
Thanks for your analysis, Nic. Sounds like the kind of study that would never be published it a company had funded it. Un fortunately, my guess is that there are so many confounding issues there that were not controlled. Also, from a personal experience view point - if you don't change the diet, a little HIIT isn't going to cure you.
Nicholas high LDL do not cause atherosclerosis. Just because LDL is at the scene of the crime does not make it causative. The question is why was the lipid oxidized? It was oxidized because mitochondria oxidized the lipid when in a state of producing reactive oxygen species in excess of the cell’s antioxidants.
You need to understand how transient receptor potential channels play critical parts in the atherosclerotic process, how too much TRPV1 stimulates too much ROS in mitochondria, that TRPV4 causes monocytes to change into M1 inflammatory macrophages, become phagocytic and engulf oxLDL. TRPV4 also increases monocyte chemoattractant protein-1 and with piezo -1 a pressure sensor stimulate lp(a) that attaches to apoB. ApoB alone is not an issue it only transports LDL. You need to understand what underlying process leads to the stimulation of TRPV4 and piezo-1. What causes too much TRPV1 ?
Insulin causes too much TRPV1. TRPV1 causes hyponatremia and hypoosmolality that stimulates TRPV1 an osmosensor and piezo-1 a pressure sensor.
In the end look at the transcriptome of atherosclerosis it includes TRPV4 and klf-4: ck out this article:
2020 article
Stem Cell Pluripotency Genes Klf4 and Oct4 Regulate Complex SMC Phenotypic Changes Critical in Late-Stage Atherosclerotic Lesion Pathogenesis
The article explains the phenotypic switch and the VSMCs incognito.
The problem with your narrative is the complete omission of TRP channel physiology/pathophysiology.
I reversed my atherosclerosis and bone mineral density loss by reversing TRP physiology by stopping a drug that upregulates TRPV1 and TRPV4 called oxcarbazepine and consuming the low carb diet that drastically reduces glp-1. Glp-1 stimulates its receptor glp-1R a g protein coupled receptor (GPCR) that:
Lowers the threshold of TRPV1 and TRPV4!
The glp-1 receptor agonists (GLP-1RA) work by lowering the threshold of TRPV1 and TRPA1 in the hypothalamus. I bet you didn’t know this.
Do you see the relationship here with high carb/sugar diabetes and atherosclerosis?
TRP channels are the link to understanding the disease process.
Diabetes causes hyperinsulinemia and now you see the reason all DM cases get heart disease.
Wow. Thank you for that explanation.
you say "jump on over to the physionic insiders", biut you don't say how. i'm already an insider, but the only related links here are for joining, not for getting the full video.
If you’re an insider, just log in and head to the Study Analyses tab. The full video is there.
The same links for joining will let you sign in.
Subbed, glad I found you. Love studies, thanks.
Nick I wanna give you interesting case study about myself. I started 1 mg of finasteride and I am on 120 mg testosterone a week. I have been on the testosterone for years now. And finasteride for 2 weeks. After two weeks my HDL went from 6 to 50. I am a high dht converter and I found this to be very interesting
Yes, by diet and lifestyle, but it is a bit complicated.
My arteries hurt when watching (and I was the one doing the watching)
Could you some day research Dr. Chafee promoting carnivore lifestyle vs. prof. Sinclair vegan lifestyle? It's quite impossible to choose if sciences 180° oppose each other. Dr. Chauffee also says LDL is no issue etc... What is true?
The sugar is our problem.
We can't handle consuming high carbohydrates 24/7/365.
It destroys our glycocalyx.
I tend to believe Dr. Chafee more. But Bryan Johnson is vegan? Except his collagen intake.. I think vegan vs carnivore is the biggest misunderstanding in medical science right now. And how to compare early humans, primates
Sure, I can do that. Unfortunately, most of these people tell you one side of the story and don’t introduce you to data that conflicts (which they then should explain). It’s frustrating for me, as I’m sure it is for you.
Instead of following gurus with agendas on RUclips, why not read reports by panels of world class scientists eg 'Diet, nutrition and the prevention of chronic diseases: report of a joint WHO/FAO expert consultation;', 'Diet, activity and cancer' by the World Cancer Research Fund, the Canadian Dietary Guidelines etc.
I think the major issue with LDL is when it is damaged. Like{small dense} LDL. it can become oxidized, glycated or otherwise inflamed. Someone posits that the liver receptors won't recognize them anymore. But it requires another factor - decimated glycocalyx -to enter the endothelium. Just my working hypothesis. All the more reason for me to avoid constant carbs.