Dr. Paul Saladino: "Don't worry about elevated Cholesterol."
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- Опубліковано 16 лип 2023
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References:
[1] doi: 10.1146/annurev.micro.55.1.165
[2] doi: 10.4049/jimmunol.1501835
[3] doi:10.1016/j.jacc.2012.09.017
[4] doi: 10.3389/fcvm.2022.860196
[5] doi:10.1001/jama.2015.1206
[6] doi: 10.3390/nu14071503
[7] doi:10.1093/eurheartj/ehv157
Original Video: • Why I don’t worry abou...
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#carnivorediet #carnivore #hearthealth
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Paul Saladino doesn't even eat salad he needs to change his name to Paul Meatareno.🍖🥓
Meatino😂
Or carnerino, maybe 😂
Wouldn't ino translate to little? Paul littlesalad seems more correct. I'm not a linguist and too lazy to google. just a guess.
Meat-I-Yes
He does eat an absolute ton of fruit though
This LDL controversy is what concerns me the most about the carnivore diet. However, the association shown is some studies are always in the range of 00% to 30% max, which is relevant, but not really that high, considering it's only association, not straight forward causality. Also, if carnivore diet manages to reduce body fat massively, normalize blood pressure, soothe inflation, make glicemy super low - among many other benefits, I think it's safe to assume that overall coronary desease risk should go down substantially, even if LDL level is increased.
I never liked vegetables or had a sweet tooth so I’ve been doing carnivore with dairy for 25 years without knowing it was a healthy diet. My family’s genetics have high cholesterol. Mines always high, but I have no plaque in my entire body. I’ve had coronary angiogram and calcium scan 10 years ago and I was good. It’s very important to exercise on the carnivore diet. You have to burn that cholesterol in your blood so it doesn’t cause problems. That’s my logic on it.
Carnivore is not the only diet that can do those things.
You would be wise to be concerned. Carnivores tend to show weak observational studies which are easily confounded, yet never mention the much more powerful and illustrative interventional studies (which make it clear ApoB / LDL is harmful). And while improving other health markers (likely mainly through weight loss) is good, there are plenty of examples of people who are "healthy in all ways except except LDL" who go on to have a premature heart attack or stroke. Maybe check out cardiologist Dr Alo - he talks about this and bit and basically says if you like that way of eating great but if your LDL is too high just make sure you control it (multiple ways of doing it)
@@JoeS97756 But if it does as per many testimonials, it should be celebrated . The other diets can probably do the same but apparently they make autoimmune symptoms worse. Hence, why many prefer the carnivore which seems to have a soothing effect of the system. I really don't think the carnivores are anal about the vegans , it's usually the other way around.
@@JoeS97756Everyone's sensitivity to glucose is different. Going vegan can help with diseases for someone coming from a SAD diet, because they end up consuming less carbs. It's relative. If that doesn't work, going keto is even fewer carbs. Some still may not find satisfaction and moving to zero carbs, or the carnivore diet finally kills off these diseases.
Of course the difference is, veganism is missing over a dozen essential nutrients and is not a long term diet. Red meat is missing precisely nothing.
This is what's wrong with social media, people rant and yell repeatedly the same assertion and somehow claim that makes it true
That's true with mainstream media too.
We need to factcheck almost everything now, no matter where the claims are made.
thanks for your analysis and informative content
Glad to find this scientific based channel! I just subscribed!
Correct me if I'm wrong, but isn't only _oxidized_ LDL (and not standard, healthy molecules of LDL) that actually turns into plaque within arteries' walls? My biggest concern would be with inflammation that helps promote that oxidation.
Amazing content, keep it up!
Great work, thanks for sharing!
I have heard that sugar in the bloodstream can scratch up the walls of the arteries and that scratched surface provides the means by which ldl (sdldl) will adhere to the artery walls. Additionally, calcium at some point becomes encased in the sdldl particles, so there is the hardening ( calcofication) process. Would you care to address this postulation, as well as D3, K2, calcium supplementation, slsl, and elevated triglycerides ?
If you're worried about like glycation then don't eat animals because their fat causes intramyocellular lipids to develop into insulin resistance preventing glucose from entering the cells. Kind of like this video says she much or too little of a good thing can be bad. Glucose is great from Whole plant Foods because fiber helps it enter the bloodstream slower. And whole plant Foods don't cause the insulin resistance.
It's amusing to see a vegan arguing against animal foods in terms of glycation. Without plant foods, glycation of animal foods would be minimal.
@@MarmaladeINFP "Advanced glycation end products (AGEs) are formed when fat- and protein-rich foods are exposed to high temperatures. Some foods that are high in AGEs include:
Meat, especially red meat, Certain cheeses, Fried eggs, Butter, Cream cheese, Margarine, Mayonnaise, Oils, Nuts.
Fried foods and highly processed foods also contain high levels of AGEs. Grilling meat can also cause the formation of AGEs.
Meats high in protein and fat are likely to form AGEs during cooking. Carbohydrate-rich foods such as fruits, vegetables, and whole grains maintain low AGE levels after cooking."
Either way there is no evidence that statins reduce the risk of death from heart disease so what is your point?
That is nonsense. People who have a genetic disorder and produce as a result too much cholesterol die young without statins, have a normal life-span with statins. Your general statement is stupid nonsense.
You can make a good case that doctors prescibe to easily statins instead of checking some aspects better and make than a data based cost-benefit analysis, but thta requires that you pay attention to details.
@@olafkunert3714 I read Dr Aseem Malhotra’s book. He says life expectancy is only increased by three days by taking statins. Take it up with him.
Ps I ignored it and have started taking them again!
@@olafkunert3714and yes , another big debate with more than one side to the story
Outstanding analysis on LDL that even my goldfish mind was able to comprehend. As a fitness trainer focusing on people over 50, this nuanced understanding of LDL was extremely helpful. Thank you Nicolas!
I just passed my entrance celular bio exam and I’m in awe with your content, (I’m a med student) and I aspire to one day do research of my own, thank you for the amazing content!!
Make sure you do a better job then. This guy has been wrong about way too much.
@@thepimptastic2Hey! we are all humans. we are Imperfect.
What has he been wrong about
@@thepimptastic2Can you name something and give your own evidence
It really is worth mentioning at this point that interventions to lower cholesterol have an extremely low effect on absolute risk reduction, in the region of 1.5 - 3%. The only rational I can think of for the use of statins is that at a population level , a 3% decrease in mortality is potentially a lot of people saved. On the individual level , the benefits start to look dubious Vs the potential short and long term side effects.
If you wanted to be rational in your analysis. But rationality wouldn't make statins very profitable.
However, anything less than 5% absolute risk is clinically insignificant and essentially due to chance. So there is no significant evidence that lowering cholesterol is any better than chance.
An important point to this is it means that if lowering cholesterol has virtually zero effect on mortality then cholesterol is not a cause. It's a side effect that just correlates with a yet unknown cause .
@@TheExcellentVideoChannelso we have a good remedy that does nothing... Let's sell it
@@flcpstechnically if the high cholesterol is created by body to fix damaged cells then statins aren't doing nothing, they're stopping the body repair itself aka f'ing people up.
A question I have pertaining to LDL's is concerning the different density species of LDL's. There are different sizes of LDL's and the danger risk is associated ONLY with the lowest density species. But a standard HDL and LDL panel doesn't differentiate between those sub species. I have read that the Larger of the LDL's can make up as much as 80 of the LDL's and they are not a risk factor for CHD. So the statement that a high LDL reading (overall) isn't making that distinction. So the question I have is this: At what percentage of the total LDL reading that is from the Lowest LDL species represents a higher risk for CHD?
This is not correct. All LDL particles are atherogenic. irrespective of size. I understand that the total number of LDL particles provides a better risk estimate.
Thanks for the analysis. Although I'm not technical in this area, I follow and appreciate your input. I recall hearing something about Triglycerides also being a factor, one possibly to be concerned about over LDL, as well. I don't recall where I heard that. Anyway, thanks for the information.
I'm 75 years old and I have high LDL (139). I worked for 52 years and had one sick day back in 1969. Maybe there is something good about having high LDL. I am also Apoe2.
Thanks for your analysis (and the bit with the chairs ... 🙂). With regards to LDL, an you comment on the phenomena related to lean mass hyper-responders? What is the relationship between exercise (in terms of both intensity and volume/ammount of exercise) and LDL? Have you looked at any studies that look at hyper-responders?
There's almost no finished studies on LMHR. There's one (led by Dave Feldman) that is in the process of having data correlated and analyzed. But nothing published. Everyone wants to extrapolate from published studies on LDL-C but LMHR folks are so far outside "normal" range that those studies may not apply. We wait, hope, and do what we do...
I'd like to see a one on one with you and Paul Saladino. I think it would answer a lot of questions.
I imagine Saladino would insist on hosting. I don’t think Physionic’s filter game is up to Saladino’s standards.
Dude looks like an airbrushed cartoon character in that video. 🤭
Great content - thanks Nic :) Would you please also do a piece on statins - are they good or bad for you?
really liked this video, you are the best science based channel ever!
I don't think I'd go that far - there are several great creators in the field, but thank you for the support! :)
@@Physioniclike who?
@@krashanb5767 joining to this question! @Physionic
I ate carnivore for a few years, I ate a high fat keto version I got my cholesterol checked regularly. It stayed low the entire time. Could you go over the "impact' of dietary cholesterol on blood cholesterol?
Are you on keto/carnivore now?
Animal based diet with healthy carbs is good too. I think genetics play a role in cholesterol. You probably workout a lot or burn it off with ketones. I have high cholesterol and no plaque. You have to workout or fast seems to be the key.
"Could you go over the "impact' of dietary cholesterol on blood cholesterol?"
Strawman. In the video high levels of blood cholesterol were dicussed, the origin was not.
The debate here isn't whether too much Cholesterol will kill ya. Too much anything will do that. Question is how much is too much. And is Cholesterol causing your problems or your problems causing the Cholesterol.
Consumption of cholesterol is causing the problem. Ingesting fats from animal products is causing the problem.
Given that cholesterol it endogenously produced in the body, probably the latter.
@@SolveForXphysionic, Attia, and every other well educated individual in the lipid community have come to the conclusion that dietary cholesterol does not increase risk because in most cases it will not increase serum cholesterol. Saturated fat is a different story though, but it’s important to differentiate these.
@@SolveForX How is it that so many of us, including myself, eat tons of animal fat and have perfect blood numbers. Also, I don't exercise a lot either.
@@Dan-gs3kgThat still doesn't mean there's no limit to the quantities of cholesterol and sat fat we should ingest, Nic made that point.
another great video - thank you!
I believe the issue here is not the idea of elevated LDL, but more of the definition of elevated. It seems that as the years go by, the smaller the number that is considered "normal LDL"...
If you consider the factors that make LDL "go bad" then look at the population being used to create the data, it makes sense they push for a lower level.
Essentially LDL follows some form of J or U curve, as do most things.
Where your optimal LDL level lies depends on if it's at risk of glycation or oxodation.
So Saladino's optimal LDL for minimizing risk is likely much higher than an obese diabetic who eats a bunch of processed food.
Well.. most people are metabolically unhealthy, with a diet high in vegetable oils which oxidize easily. This means their optimal LDL for minimal risk is lowered.
This easily explains the data and studies we see, and doesn't disagree as much with Saladino either, though I think his perspective is still a bit too simplified.😮
@@Unsensitive your point makes complete and total sense. Recently, it's made more and more sense for me to then to view the data as part of a system and not as "the" deciding factor of health and longevity. My cardiologist insists on the absolute lowest LDL, even claiming he wants to see it below 40, despite my total cholesterol being 129.
@@Unsensitiveegetable oils are cardioprotective. Various studies show that.😂😂😂. In that way breathing would be unhealthy because you are creating superoxide with every breath you take. Oh, and be careful when eating meat too, because it causes immense oxidative stress during digestion.
@@stellasternchen
I don't disagree that many studies came to that conclusion, but they are biased and incorrect in their understanding of physiology and nutrition. Many are too short to show the harms, which need to be 5+ years in most cases, as these are a long term toxin which are incorporated into your cell membranes.
My anecdotal n=1
Eliminated them from my diet and my arthritis disappeared.
Chronic pain is gone.
My allergies are virtually non existent.
My sun tolerance increased 3-5x and I barely sunburn unprotected if at all.
And lastly, my lifelong asthma, which I had for over 40 years, and was on 2-3 medications plus occasional steroids and antibiotics due to lingering respiratory infections, disappeared. I no longer need any medications.
if you still believe vegetable/seed oils are cardio protective, there's no point in me arguing with you, but you're as ignorant as the diabetes physicians still telling their patients to eat healthy carbs and pump themselves with insulin.
@@stellasternchen Ah yes, Studies shows it's OK so I follow it and accept it like gospel. Are you a journalist? Lmao.
I heard from The Dr. Gundry Podcast that Polyphenols reduce the stickines effect in LDL, and in theory we might rather look on the levels of polyphenols in our food, rather than worry about LDL.
I'm curious what your thoughts would be on this theory?
But polyphenols aren't as profitable as statins. There is the problem.
Thank you for the very well explained VDO. One question though: What LDL-level range would typically be the sweet spot from an overall health perspective?
My lab printouts always give the normal LDL range as 66-100
@@dsmj7389 If you eat Carnivore or Animal Based like Paul Saladino those Numbers are much higher. But then again other numbers are also out of Range. Triglycerides for example are normally lower. So as far sa i know these Numbers are depending on the diet yo take. So this 66-100 represnts the range for a "normal" or "standard american" diet.
I for my part don't think that anyone sees through all the complex mechanisms in our Body.
Meaning.. i don't believe that eating meat or eggs is a risk factor. Those are whole, unprocesed and very bioavailable foods. Why fear such things...?
According to this study published in 2024 the sweet spot is between 100 and 189 mg/dl:
"Is LDL cholesterol associated with long-term mortality among primary prevention adults? A retrospective cohort study from a large healthcare system".
@@dsmj7389 That is too low according to this 2024 study "Is LDL cholesterol associated with long-term mortality among primary prevention adults? A retrospective cohort study from a large healthcare system".
Be aware that what is defined as normal is subject to caution and has been modified several times in order to prescribe statins to more people...
Another issue is that LDL is a calculated value. There are at least 2 types (5?) which can only be determined by direct test, and not all types cause problems. In my opinion, the calculated value should be considered a screening test only, followed up with a confirmatory direct test. And, of course, training for the doctor.
(Yeah, its amazing how many doctors lack training, except perhaps on the golf course.)
that's so true, plus how many different factors may come into play when assessing if an individual with elevated LDL is actually at a health risk
when it comes to doctors, I think it's high time schooling system had finally changed, switching to a more holistic approach - not only teaching how to solve problems with pharmacology but also through lifestyle/diet/environment
Yes there's pattern A which is usually called large and/or fluffy and it's made (as far as what I've read is true) directly by the liver and pattern B which is small and dense and comes from VLDL particles after they've emptied their triglycerides. Some say that pattern A is harmless and others that it's less harmful than pattern B which they all agree that it's more harmful. More pattern B most of the time means bigger lipoprotein number that's why the paradigm shifted to LDL-p or ApoB measurement. There's also LPa which is way more atherogenic than pattern B and people with FH usually have elevated. Another caveat is that while LDL lipoproteins are supposed to get trapped under the endothelium because "they are bigger than the HDL lipoproteins" it's the smaller ones that are more harmful rather than the pattern A particles. And HDL lipoproteins, the ApoA ones, are found to be either protective or completely harmless, depending on who you ask, despite being way smaller than the ApoB lipoproteins. Peter Attia has stated that it's the ApoBs that are atherogenic while the ApoAs are not. Overall there's big ambiguity on that matter with experts like Robert Lustig and Ben Bickman looking at lipids as a secondary measurement with the primary ones being blood glucose and insulin levels (an idea that I personally lean towards most) and others like Peter Attia and Thomas Dayspring who treat lipids as a primary factor for vascular disease.
@@LTJBLTJBInteresting information! Yes, things are more complicated than just "high or low" LDL, and insulin sensitivity should definitely be counted in IMO, as the damage to the endothelial lining of the vasculatory system is amplified pretty quite a lot by the effects of high glucose levels
@@lollsazz And another important factor is that, glucose aside, high levels of insulin are a big risk factor in their own. Kidney disease, hypertension, increased risk for cancer etc, all caused by hyperinsulinemia.
All atherogenic lipoproteins have ApoB and they’re all small enough to get into the arterial walls. Don’t go chasing waterfalls.
I'd be interested to know what you think about his recent discussion with Dr Alo, a cardiologist. Dr Saladino makes some great points as they discuss the subject in detail.
If you are on a keto or carnivore diet or any other diet your LDL will go high just because you need to transfer a lot of fat in your body for Energy. What Saladino usually says is that LDL is only harmfull when the cause of high LDL is insulin resistance or metabolic syndrome. Genetic problems are execeptions not the rule as you made to look
Plenty of people have normal LDL on keto/carnivore
@@defeqel6537 many do and many don't depending on a lot of things. In the beginning there is a spike in LDL and months later when the body gets fat adapted you need less LDL to do the same job
…Then why does LDL skyrocket in some individuals as their BMI decreases below 25 when they may have been only slightly elevated when they were overweight?
@@pacmanfl because what I just said
@@defeqel6537people do keto and carnivore with high range of fat intake
these from low end compared to these on high end can be in totally different situation... not mentioning varying source of their fat in diet...
even amount of omega3 can affect how all the rest results, too low and suddenly what worked well becomes a serious problem
One wildcard in this is whether the studies use measured or calculated LDL. Our blood work results use a Friedewald calculation as it saves money over actually measuring it. I have found that having a good (low) Triglyceride/HDL ratio, say below 1 tends to show a significantly higher calculated level than if using the "Iranian" LDL calculator. My Trig/HDL tends to run around 0.8-0.9 ( a measure of good insulin sensitivity) and my Friedewald LDL calculation tends to run 25-30 higher than the Iranian calculation. Any comments on this?
They use measured in the studies. Usually a variety of measuring techniques, including cholesterol esters and/or particle number by NMR, electrophoresis.
They may use measured in studies, but most people getting tested don’t get measured, unless an NMR test is specifically ordered.
@@1000BabyRage True, but at least some labs, e.g., Quest, offer an LDL-C Direct, and I'd guess that most offer an ApoB which I believe is a useful stand-in for particle number.
Great video, thank you! Insulin resistance and diabetes are precursors to stroke and heart attack. Unfortunately, most docs do not know how to correctly diagnose metabolic issues, which means many people will have an event before they are correctly diagnosed.
So what’s the actionable advice for daily life?
it seems to me as if he has many hypotheses, however I feel that he tried to skip the scientific process for the excitement of a new discovery.
another great video!
To understand what's going on, watch "Dr. David Diamond: Should Low Carbohydrate Diet Guidelines Include Concerns Over LDL Cholesterol?" He explains that it's not the high LDL that is causing the trouble. It's the high *damaged* LDL. In one study in which the damaged LDL were removed, the remaining high LDL had no adverse effect.
And yet the French have high carb diets, they have had riots over price increases and shortages of baguettes. They also are now the longest lived first world nation. At least Monaco which I consider French even if technically an independent principality in France, they also are one of the richest places on the planet. Life expectancy = 89.4 years. You want an odd statistic, the #5 place in the world with the highest number of people over 100 years old is LOMA LINDA in San Bernardino County in California. This is because there is a community of about 9,000 Seventh Day Adventists there and they do not smoke, drink, or eat meat, and take regular exercise. Of course they average 10 years longer life expectancy that the rest of us, but who would want 90 or more years of that?
@@MAtildaMortuaryserver the French do not have high carb diets. In fact, they eat the most saturated fat in Western Europe, primarily from all the delicious cheese they eat. Look it up.
@@MAtildaMortuaryserver I live in the South-West of France. We traditionally eat a lot of fat, including duck and goose fat, as we raise ducks and gooses to make Foie gras. Eating baguettes doesn't necessarily means having a high carb diet.
@@AndreAngelantoniThe French and Italian people eat moderate to high carb diets.
@@spgtenor the French eat more fat than perhaps anyone. That's why it's called The French Paradox.
Love your enthusiasm @5:00 and you're right it is super cool!
Question: what is the reason for exact location of a plaque on endothelial surface of the artery? Why not all over the surface? Why LDL particle has been parked in exact place?
I love your content and willing to pay for more. Question: Can you do a study on the impact of Zone 2 training
On the first point, the argument is aimed at a practicing medical audience where often the paradigm is reducing LDL as low as possible to reduce MIs and CVAs. On the vein issue, he would be referring to SVG stenosis especially compared to LIMA stenosis. The argument towards insulin resistance can't be equated directly as diabetes; though the two occur together often, they don't always occur together and obesity can be an alternate presentation that can explain many of these instances of lack of diabetes.
I believe the researchers tested in the generic trials of those with diabetes 2 because the disease is caused by insulin resistance, specifically in the beta cells of the pancreas usually from fat infiltration disrupting insulin secretion. Ergo, they definitely have insulin resistance.
Although, you are correct that other muscles can have fat infiltration and thus can turn into fat cells causing insulin receptors to retreat into muscle cells.
Wrestling analogies is the perk I like most in Nickolas' videos. Helps a lot to digest science granite.
I would be interested in how the studies bear out the level at which LDL is considered “bad”. Both my parents died in their 90’s and never had LDL below 225 when tested.
You know for a fact that both of them NEVER had LDL below 225? You have a comprehensive history of their lipid panels going back their entire life? If so, I'm impressed, but also, literally means nothing. Risk never guarantees outcome.
Also, to answer your question, "bad" is always quantified in hazard ratios. Either risk to all-cause mortality or risk to a cardiac event. Based on the trials, they'll calculate what the increased or decreased risk is associated with a certain LDL level.
My father too.
Hi - would you know any of their numbers for total and hdl? For me some change over life time - in 20s and 30s total in 130 to 140. Now in 70s is 200 to 220 for total. Maybe change from high hdl amounts around 105 to 115 over past about 10 yrs. In my 20 and 30s doc didnt check my hdl numbers.
I'll bet that your 90 year old parents didn't have a clue about their cholesterol levels. Most people I talk to have no idea what their levels are, especially seniors.
I guess what i tried to say with the previous post is that people with a high LDL often have this from eating a shty diet, and therefor will suffer from CVD more than people with a low LDL who will eat a overal healthier diet. If you get your high LDL from a healthy diet you might not get sick from it at all.
Even before I play the video I’m already appreciating your Zoolander face on the intro graphic, Nic. 😂
Quick question but relates to another one of your presentations : For glycine , cysteine supplementation may one use Mg glycinate instead of glycine ? Txs
This video did not address subgroups, other than the genetic differentiators.
For those without the gene "snips" , there are basically two reasons why people have higher than average LDL particle counts; one is because the Apo-B particles get damaged; they get too oxidized, glycated, or small because of other problems, and the liver fails to recognize and recycle them, so they float aimlessly in the bloodstream, liable to get in trouble including building plaque. The other is that a person's individual metabolism is adapted to using triglycerides as a major fuel source, so more Apo-B particles are put into circulation as VLDL packed with triglycerides, which eventually become a higher number of LDL particles after they've delivered the triglycerides. Such particles, however, are recognized and recycled by the liver.
This video completely ignores the issues of LDL/Apo-B particle size and health, which is the elephant in the room that any honest evaluation of the role of LDL in atherosclerosis should be focusing on.
Perhaps Physionic might take up Dave Feldman's challenge of producing a good study that finds a high risk of atherosclerosis in people with ultra-high LDL but also with low fasting triglycerides and healthy HDL levels. There is a reward of thousands of dollars in the challenge. There is also the fact to consider that in the NHANES database, the 5 most long-lived people had very high LDL by current mainstream standards, and this was not measured in their final days, but was recorded as "high" for many years.
Lumping very different people together based on a single, independent characteristic is not the best way to do science, as it allows false proxies to contaminate the data and conclusions.
The fact is, total LDL count has so little association with atherosclerosis, that many heart risk calculators don't even ask LDL levels; the other factors are just so much more predictive, that many calculators don't bother to ask. I've played with various calculators, some of which do ask for LDL counts, and none of them changed their predictive risk as much when you changed LDL counts, as when you changed other parameters.
The point that many LDL-catastrophe deniers are making is not that there is never an *individual* correlation between LDL counts or particle numbers and atherosclerosis; the point is that there are good or neutral reasons, and clearly bad reasons, why LDL might be elevated. Those which are elevated because of triglyceride delivery in a fat-burning metabolism do not have to worry about LDL if their HDL and triglycerides are healthy. If this is true, then LDL is worthless as a marker for health, and concerns of disease should concentrate on damaged LDL which does not get recycled by the liver, and not all forms of LDL.
Yup this is mind blowing.
Well said.
Take extra niacin to be safe 😉👌
I have thoroughly looked at Dave Feldman's works and, while he is free to experiment upon himself, I would not be a participant. It's like rolling the dice at a craps table.
right on, bro.
I love your videos. You are the "Data'” of the medical video world! Funny and factual. Keep making the fact checking videos!
Thank you!
Well, thank you. One of the things that is glaringly absent from much of the health advice and opinions on social media is the scientific aspect of these things. I don’t mind that people are attempting to make these things easy to understand, but the problem is, if you do not properly interpret the factual data, all you have done is make ignorance easy to accept. That’s not what we need. I don’t really care about the personalities of individuals. Because someone sounds right, or because they are popular and have the right image doesn’t really matter if the information that is being given is inaccurate. We’re not dealing with just one person’s opinion as opposed to another. If we follow the wrong advice, it could be extremely harmful to us physically mentally, etc. So we need to be very careful and very detailed as possible and wise in our evaluation of any and all kinds of information that we are receiving regarding health over social media. That’s why I like what you’re doing and I really hope you continue to keep up the great work..
No doubt, he's nailing it!
@@VeganLinked 🤣🤡🤏
Thanks for this.
Could you please tell me what you think about iodine suplementation? In my country they add it to salt and still almost everyone has thyroid issues... Thank you in advance! Jo from Poland
What I was taught at uni was exactly in the middle of those two points of view. LDL is not what causes any problems to anyone - the problem begins when LDL binds with a sugar molecule. Such a product can no longer be a part of the lipid delivery cycle and ends up dumped on the artery walls, causing all the trouble. You can fight that issue in two ways: lower your LDL, or lower your blood glucose levels. So... the main problem I see is all the blame gets excessively put on a single culprit - although it takes two to tango. From this perspective, you can get away with higher LDL on a keto diet, or you can eat a whole cake if you have low LDL. I would not go for such extremes, though.
are you talking about glycation? do studies back your argument?
@@archascents5157 You mean the difference between LDL and oxidated/glycated LDL for atherosclerosis? That is no secret or guesswork, really. pubmed.ncbi.nlm.nih.gov/18607185/ But the part about "lower your sugar, you will lower the glycation" might not be studied yet at all. I do not know, but who would put any money to such a study?
Glucose attaches to red blood cells when the diet is highly restricted of carbohydrates the red blood cells live longer because there is less insulin in the blood. So A1C can appear higher because the blood cell looks like a sugar ball after a while. But the health improvement in the body is very evident. That is just on example. Not sure if any glycation occurs on LDL. You might want to look up Dr. David Diamond PhD he did a good video with Dr. Shawn Baker. On UA-cam as well.
@@jeffjensen2083 "Glucose attaches to red blood cells" that sounds like glycation
@@archascents5157 Yes that is Glycation it happens to much of the body I believe but I’m not sure if LDL get Glycation it is how the body carries Lipids around in the body while glucose flows in the blood stream. My other point is glucose is essentially treated like at behaves like a poison that the body needs to get rid of as quickly as possible.
Could you please name the researchers that you’re reading in your studies in the videos? It helps promote those researchers and in my opinion thanks them in a way.
Great, great point!
He just made an 1hr 20min video on LDL last month. Check it out.
Researchers are not to be revered over practitioners. There's a Dr. Gundry, with more than 10.000 heart surgeries under his belt who's advocating that he couldn't care less about LDL numbers! I'd take his advice over 1000 studies on the issue. The statins industry is a huge one (just to point one possible unethical confounder for those "findings"). The said cardiologist/surgeon has nothing to gain by pointing out the insignificance of high LDL.
I’m wondering if the question better put forward is, what is high cholesterol, or appropriate cholesterol and what does the body do with the cholesterol it doesn’t need. As I’ve understood the matter, high levels of LDL can be either a matter caused by insulin resistance that breaks down the cycle of regeneration of cholesterol in the liver thus backing up expended cholesterol into the blood stream thus giving us a marker of ill health. There are some on the Carnivore diet however that produce more cholesterol in the liver (exogenous cholesterol seems never to contribute more than 20% to the mix). This cholesterol however is not oxidized in a body free of inflammation. So why would higher elevations of it be considered bad? Are we working with an outmoded concept of what excess is? Great discussion as usual. I’m starting my formal studies on the long path of functional medicine on Thursday the 20th of July. I’m excited. What endless nuance, what a puzzle with infinite pieces. Thanks for this Mr Verhoeven!
What increases LDL cholesterol the most ?
Is it cholesterol intake ?
Or saturated fat intake ?
Appears to be saturated fat intake as per Alan Flanagan when he reviews Ancil Keyes's leading evidence on the Proof with Simon Hill.
An important consideration is any fasting diet also raises LDL. Why? The LDL is an energy transportation molecule. Once you need to transport FATS to energy rather than glucose LDL will elevate to transport this secondary energy system. My doctor was shocked when my yearly check showed a complete change and LDL was elevated. I had lost weight blood glucose down. Triglycerides down. He still wanted to prescribe Statins! I told him as he didn’t have time to do research on new studies in his field I would. Still not taking statins. 😂
Good for you. A crutch isn't doing your body any favors.
@@C_R_O_M________ it's not a crutch, it's the main energy source for endurance athletes, and sports athletes.
Any inflammation, including exercise, also increases LDL, which is what you want. Problem seems to be mostly damaged LDL.
@@Dan-gs3kg I was obviously referring to statins.
It's wonderful how you know so much more about this subject than the global scientific and medical communities.
Re the Mendelian randomisation studies. It works the other way also. Those that genetically have high LDL (familial hypercholesterolemia) have greatly increased heart disease levels (can reduce life expectancy 15-30 years if untreated; even more if the homozygous form). Seems like a pretty straightforward demonstration that LDL is causally implicated ...
Straightforward? Not so sure.
For example, people having a genetic disease resulting in more cholesterol could perfectly have other factors which have some health consequences.
And let's assume that the culprit is not LDL-C but rather the number of damaged LDL particles. People with FH could be simply more at risk because they have, on average, more damaged particles. Does it mean than somebody with high LDL-C but with a very low number of damaged particles would be at risk?
@@Noegzit That idea could be plausible if a single mutation was involved. However FH is caused by mutations in multiple different genes so unlikely they would result in the same phenotype
@@llicit1833
But even if we have different variants a particular group could have a sufficiently more increased risk to make all people with FH look more at risk. There are some FH variants leading to very high plasma cholesterol levels which are not necessarily associated with premature atherosclerosis and mortality. Better read that twice. We also have patients misclassified as having FH. They don't have FH, they have sitosterolaemia with elevated plant sterols and look as if they had FH. And having elevated plant sterols in the blood is not that great.
The fact that there are variants of FH not associated with premature atherosclerosis and mortality tells us that things can be a bit more complicated than we thought.
My yoga teacher has FH, she's 78, she's not on statins and has never been. And yet she's still alive and, of course, teaching yoga. I know it's just an anecdote but it proves that having high levels of LDL-C during your whole life doesn't necessarily kills you by "clogging" your arteries at 50.
For the record I don't think that having more than 500 mg/dl of LDL-C is particularly great for health, I just wanted to pointed out that sometime things are not as "straightforward" as they seem to be or as some people would like they were.
Nicely presented video but I do have a question. Is it possible that ASCVD is simply mechanical or at least mostly mechanical in so far that ASCVD occurs on the pressure side of the vessel it seems the particles are pressed through the epithelial wall in the same way positive pressure osmosis filters work?? I know this sounds overly simplistic but it would help explain why ASCVD progresses more quickly when larger amounts of LDLc floating in the blood i.e the more is likely to be pressed through, that is my theory anyway???.
With all the discussion regarding cholesterol, LDL, HDL etc. would you have any thoughts regarding Malcom Kendrick's book The Great Cholesterol Con? Thanks.
I did not hear VLDL mentioned and how it differs in effect from LDL. Very often VLDL is referred to as simply LDL and this can be very misleading since the two are quite different. Also I did not hear anything about the HDL and the Ratios and those effects on overall health.
The words, "relative vs absolute" made this video well worth watching and heeding. THANK!!! YOU!!! I've had a great amount of frustration over the last couple years, because of the seemingly well informed, and researched based presenters of information on CAD, were contradicting eachother on this particular point. Thanks again. I'm 67, and have a relatively low calcium score for a man my age, BUT, I have one particular coronary artery that is "50-70% occluded." perhaps 50% isn't what I was hoping for, but it's hell of a lot better than 70% Needless to say I am concerned. With family history of CAD, I want to be sure I'm not misinformed. Thus far, instead of a stent, my cardiologist and I have opted for the higher dosis of the cholesterol meds. So.... There it is. scary reality.
Study at 9:50 . The people with the relatively high LDL, what do they eat to get that high LDL. If you eat cookies and get high LDL will you be off the same/worse/better than if you eat actual beneficial food like red meat that raises your LDL to that same level?
Are we doing the right thing by just looking at LDL without asking other questions?
@@stephx9759 Yes we are. HDL is not relevant because in studies where theyve increased HDL, it has had no net effect
What medications did he or she put you on? I'm curious.
@@danyalraza4388 why is it that heart risk calculations use HDL/TG ratios, and not LDL?
@@Dan-gs3kg Where? Anyone still doing that (including labs and sensationalist fad-youtubers in the carnivore/keto space), are using outdated or very selective science.
Basically, HDL & TG are symptomatic of some other issues, such as a large waistline and bad diet, but LDL is actually causative for heart disease. You want to see HDL & TG in the good ranges, but they're just markers of good health, not the cause of good health. Does that make sense?
I know this is a stretch, but could apoB or LDL be used as a treatment for persistent infections?
Would people who have genetically lowered LDL, which we discussed has a myriad of health functions, potentially suffer from other issues (morbidity and even mortality) first before suffering from a cardiovascular issue? I think of the U-shaped curve that pops up in certain health markers and how too low and too high areas of the curve can indicate confounding variables in health.
What about elevated LDL from fasting? Does that increase the risk of heart disease?
No
Since my cancer diagnosis 2 years ago, I developed what my husband considers an obsession with becoming healthy. I read - no, study- everything I can and make use of it in my personal life to that end. Granted, I am a test subject of 1. But here’s what happened to me.
In September 2021, I had surgery for breast cancer followed by radiation therapy. I am 5’3.5” tall and weighed 160 lbs., had insulin resistance with morning fasting BG levels around 102. Blood lipids were in the normal range, though Total cholesterol was a bit over 200. However, there were questions regarding the health of my liver based those lab results.
Fast forward to September 2022. Went for my annual check-up. Cancer hasn’t returned but blood work hasn’t improved, but hasn’t gotten worse either. My weight is now 165, I feel sluggish, and don’t sleep well. My cancer doc is concerned about my BP and fasting glucose. Forgot to mention that my BP was around 143/78. Typical HR was 76-78. My GP insisted I start statins. I complied, though the only lipid out of line was total cholesterol. In November, cholesterol was low enough to be considered normal but I felt even worse. Brain fog, muscle cramps. It was almost as bad as Covid. I was disgusted and determined to do everything I needed to do to get healthy. I started intermittent fasting, got rid of all sugar in my diet, had no more than 1 alcoholic drink per month (at celebrations) then started following a mostly keto diet.
Again fast forward 6.5 months. My weight is now 132. A DXA scan shows visceral fat at 1.8 which is ideal. My RER is 0.71, also great. In addition, I had in-depth labs done - CardioIQ Advanced Lipid Panel and Insulin Resistance Panel with Score. Insulin resistance was gone - Ref Range is Insulin sensitive
Great! I just left a comment about Dr. Gundry, a surgeon and cardiologist with vast experience (more than 10000 surgeries) who says that he couldn't care less about LDL. He proposes monitoring triglycerides and HDL and how the two relate to each other. Look him up. One like him worth more than 10000 papers "proving" anything.
@@RandomGuy-qg9xf lol....random thought from the random guy. look into a mirror random but don't blame the mirror for your ignorance
Weight loss can increase ldl because it is a lipid carrier and keto can increase ldl because you would use fats for energy more. Congrats on the lifestyle bump up!
But the Physionic guy read TONS of HUNDREDS of papers!
My experience exactly! In fact my experience and decision making exactly parallels all that you have written Veronica. The only slight difference is the timeline with my BCA Stage IIB diagnosed Aug 2022. My husband is a surgeon and insisted I stop the Ketogenic diet because my Total cholesterol and LDLs went up when I started the ketogenic diet. Yet my Triglycerides and HDL were still normal. I refused to stop my lifestyle and dietary changes so he insisted I see my Cardiologist. The cardiologist asked if I was considering Statins and I told him that although my husband took them (had 95% blockages in 2 arteries and stents subsequently placed) there was NO way I would take Statins because of all their associated risks. He said so Statins are off the table for you. I replied YES! So he suggested a Calcium Score to see what that showed. Results were ZERO score for all cardiac arteries. He was stunned as I am 69 yo. He said my cardiovascular system was “like a 30 yo!)
So at 5ft 3.5in (161cms) and 115lbs(52.2kgs) doing 6kms power walking a day, alternate days, weights for strength training, no alcohol since Aug 2022 and a strict ketogenic diet I will continue this regimen as it seems to be the way to best manage my future health post Stage II BCA! I will not be worried about a higher Total Cholesterol or higher LDL when there are many more significant factors I need to manage to reduce my risk of cancer recurrence when exercise and diet are such unequivocal factors in reducing risk for recurrence. (For evidence see, Dr Eric Westman, Obesity Specialist, Duke Uni; Dr Christy Kettlering, Radiation Oncologist, NorthWestern; Dr Robert Lustig, Paediatric Endocrinolgist, Prof Uni California; Dr Jason Fung, Nephrologist, Uni Calf and Uni Toronto; Dr Daniel Lieberman, Paleo-anthropologist Prof Harvard; and on and on…)
You bring up some great points. You two should debate. Yes it's a risk factor but I don't see how you explained why it's not causative which is his point.
I read somewhere that overall LDL is not the problem, there are I think two kinds of LDL, small and large and its the small that are harmful and large beneficial (forgive me I am just a 'layman'). However most doctors just do the standard tests and not the comprehensive one. So is there a way of targeting small LDL only? I have familial hypercholesterolaemia and even when my overall levels were normal way back when I was young, my LDL was always higher.. I was on Statins from 2018 - 2022 40mg and lowered to 3 with LDL higher than HDL but in normal range; then I had a heart Scan and my CAC socre is zero, so if LDL causes calcification of arteries why is my score zero? Maybe because when I was young overall scores were in normal range, and when I stopped statins values went through the roof. How long does it take to build up? Maybe take vit K2 to take calcium to bones and not arteries will help? I now have an appointment with cardiology, they put me on urgent cat 1 appointment as they were freaking out about my cholesterol... watch this space for when I see them...
The one thing health UA-cam is lacking is mano a mano debate. People who have guests on their channel always pick people drinking the same Kool-aid. Would love to see an hour debate between you and Paul Saladino, Shawn Baker or.... Peter Attia on areas of disagreement...
Interesting. Most don’t look at cancer rates esp colon and longterm high meat and or animal protein intake. Also studies on effect of IGF1 (certain healthy level -not too high or low) and pesticides/fertilizer etc concentrated/ stored in animal fat.
I think almost all of dieting can be summarized with "Dosage makes the poison".
Great video 🎉
Out of an overall population you can have groups with different characteristics. You can prove that the overall population is overall aided by lower cholesterol. But that doesn't mean that it applies all subsets of the population. For instance, those specifically on Keto diet may not have the same disease or malfunction vectors that those not on Keto diet and there characteristics of the LDL are shaped differently. I believe AI's are going to eventually sort out much of these subset issues and we will get much closer to individualized and specific medicine based on the entirety of an individuals lifestyle. There are a large number of tracking apps are gathering daily information from individuals health decisions and I believe ultimately AI's are going access and sift this data for a huge advance in determining correlations and causations.
It depends on what initial assumptions these AI bots will be initially fed with. The GIGO principle is a very crucial factor in these.
Great video. On the study confirming the LDL as the independent risk factor, was there any risk stratification with inflammatory markers? Or with hypertension?
😊😊😊😊
I did a topical google search, but only looked at the first reference:. It looks on point to me.
"Treatment with statins reduced deaths from coronary heart disease by 28% in men with very high levels of low density lipoprotein (LDL) cholesterol but no other risk factors or signs of heart disease, a 15 year follow-up study has reported in the journal Circulation."
"The authors said that the findings provide the first direct randomised trial evidence to confirm current guidance that patients with LDL above 190 mg/dL should be considered for statin treatment regardless of other risk factors."
Long term study backs statins for patients with high LDL and no other risk factors
BMJ 2017;358:j4171
@@jackbuaer3828 Is the "28%" reduction an absolute reduction or a relative reduction?
@@daisiesushitam984 Relative. Absolute rates were also included below. "Overall, among all subjects initially allocated to pravastatin, CHD death, cardiovascular death, and all-cause mortality were significantly reduced by 22%, 17%, and 12%, respectively (Table 2). Long-term risk of CHD death, cardiovascular death, and all-cause mortality were significantly reduced by 28%, 25%, and 18%, respectively, among those with LDL-C ≥190 mg/dL originally randomly assigned to pravastatin. The absolute reduction in the risk of death at 20 years from CHD, cardiovascular causes, and any cause was at least 2-fold greater among patients with LDL-C ≥190 mg/dL (absolute risk reduction 2.34%, 3.25%, and 5.39%, respectively) in comparison with those with LDL-C
@jackbuaer3828 I don't understand how to determine whether a 2.34% absolute risk reduction is overall that significant in days or years of life saved. Any ideas how that is figured out?
LDL is being referenced without regard for type of LDL. ApoB little particles are dangerous. We need to learn to differentiate the two and recognize risk
This is very interesting to me, on a personal level. Two years ago I was a fit healthy 59 year old with good dietary habits, no overweight, no smoking, very little drinking and no drugs when I had a heart attack completely unexpected. Turns out I have clogged arteries. No one can tell me why. I have zero pre-diabetes, perfect blood sugar levels but higher than average LDL-c. That last one, no one can explain other than 'genetics.'
I am now looking into elevated levels of homocysteine as a possible cause, because 'genetics' doesn't really mean anything. I fortunately didn't suffer any damage to my heart and I am fine for now but I did have a stent placed and I probably need more care, although I feel perfectly fine - but I felt fine the night before the heart attack so...
Your videos have a real life impact on me and I'm sure others, so thank you for this. 👍
I thought particle count (ApoB) was more important then LDL-cholesterol levels.
It is
@@Physionic Yay. I’m learning. ty
Interesting point about LDL and heart attack risk. I'll have to chew on that for a while. Although, I am still staying away from statins given the other risks such as dementia, Parkinson's, muscle aches, fatigue... while I can understand that extremely high LDL could directly harm the endothelial cells as can sickle cells as can a constant barrage of high insulin levels and high blood pressure.... I am still extremely skeptical that reducing LDL's with drugs that have such harmful side effects is the way to go.
There are other lipid lowering medications instead of statins. Ezetemib or psk-9 inhibitors for example.
What about lower cholesterol,but risk for neurodegenerative? My husbands family has “normal” cholesterol, only to spend the last 15 years going downhill with Parkinson’s.
regarding your first rebuttal: shouldnt the same argument be used against exogenous glucose?
Man you read a lot! Well, I think Dr. Saladino also reads a lot. Given he is 45 and he looks remarkably healthy despite his elevated Cholesterol levels. I suspect he is stronger maybe than most people 25. I guess we need to define what is elevated, because what is an accepted reference range maybe defined on an otherwise unhealthy population.
Reading is one thing, practice is the other. You can read all the books in the world but the question is can you be as healthy as Dr. Saladino when you are 45?
👍
A lot of UA-camrs use filters on their cameras which help them look better. Not saying Dr. Saladino does, saying he may. His face looks kind of “plastic” so I believe “filter”. Our presenter here is clearly not using a filter. His face looks real.
😆 You're awesome man! love your wry humor. That accompanied by your clear explanations and quality in depth research is golden. I love that you get into the biochemistry details without over simplification. I come to your channel for facts and i'm enjoying it very much. Thanks.
Much appreciated!
Good Day
I enjoyed this discussion. Could the issue be that not all LDL cholesterol is the same. Logically the smaller LDL sized particles probably represent more damaged or Oxidized LDL. Larger sized LDL particles are probably represent a normal functioning particle and healthier metabolic state. Maybe the actual number of LDL particles is not the issue but the Condition of the LDL particle is more important. This may explain the differing outcomes when LDL association with MI is discussed from 10,000 feet in the studies you put forth. Don't Know - Any Data to support this idea ???
Being a non academic person, my simple understanding is diabetes results in obesity due to diet (sugar and processed carbs) , obesity causes inflammation, oxidation from say seed oils cause damaged LDL which combined with inflammation cause plaque which grows and causes blockages.
Its the LDL size and LDL particle count that matters.
Equilibrium is the key.
Some foods are addictive and triggering and should either be avoided or limited. I've never been addicted to meat and fat but fruit, crackers or anything with a sweet taste is triggering.
I'm not sure why fatty beef is so satisfying and why I can go over 6 hours without any hunger but it does just that.
genetic memory
Fatty beef is statisfying because it's fatty and has protein, both satisfy. Where carbohydrates don't, infact carbohydrates make you want to eat more, and are normally found in abundance at the end of summer. The result is you eat lots of carbs just before winter kicks in, you get fatter and survive winter. The problem is we are no longer are hunter gathers, and carbs are everywhere, and now everyone is diabetic!
How many ways can you damage the endothelial wall? Have you ever seen a scab form where there's no injury? Injury occurs through many different mechanisms. Mechanical, chemical, infection. Clearly, diabetes is not the only way you can damage arteries.
This is excellent! I love your unbiased approach that is based on an analysis of reputable studies. Thanks for the fact checking on potentially harmful claims being made in other other youtube videos
It would be interesting if Dr. Saladino chose to respond to this video, which I found extremely compelling by the way. I’m learning a lot from you. I still think it would be interesting to hear Saladino’s rebuttal, however. ❤
Saladino would mop him up!
@@pharmdog1 Seeing the Physionic channel engage directly with other YT creators such as Saladino would make for powerful viewing.
@@pharmdog1 Yup
Who decides what "normal lab value" is?
@@pharmdog1yep, Saladino is probably better with a mop
Total cholesterol - HDL - LDL = VLDL, if this number is
Interested layman here. The LDL was measured but what were the HDL and TG levels? Surely they provide a wider context?
I like your rebuttal of the (hypo)theses of dr. Saladino. Still I wonder if current guidelines are set correctly. Of course water is healthy, but deadly if we drink 30l/day, but also it is better to drink 3l than 2l. What about the cholesterol? How can we be sure that slightly increased levels are not better than "normal" as we know it? How were the tables creatred? Just my 5 cent for a potentially very insightful and interesting new video topic that we would be happy to hear you commenting on!
low ldl has a higher all cause mortality than high LDL - also see new study of LMHR (LDL 350+ )compared to Miami Health study that showed no difference in plaque buildup over 4 years
I love the way you explain things and your delivery is brilliant. 😊👍
I would love to have someone to talk to about this stuff. I have a developing theory that I can't get any feedback from anyone on, of course everyone I know is not able to understand most of what I say so that doesn't help. lol. Ok. I believe that many conditions are caused by distubences in homeostasis that activate HIF. At first I thought that hypoxia was a requirement but then I learned that HIF is also elevated in inflammation. As you know everything in the body is intricately linked and explaining that would take a while so I willl get to the point. I learned recently that iron is involved in atheroslerosis (high concentrations of iron salts) and I also learned that tissue macrophage polarization can be altered by iron accumulation causing healing disruption. My question is if arteries under pressure are constantly in need of macrophage repair and the macrophages are stuck in this iron overloaded state could they be instrumental to the clotting that happens with atheroslerosis?
How much is too much? I have about 200 to 250 ldl for 50 years and I am now 60 years old.
According to physionic and the medical establishment this would be considered “high”. I recommend before trying to aggressively lower LDL you get a CT angiogram and assess how much plaque burden you have and if you are generating nee plaques.
I think we should take into consideration that the reference ranges for cholesterol have been constantly lowered by the science community in the last 30 years. I remember when I was doing my faculty education the limit for overall cholesterol was 6, now it is 5.
We do have to wonder if this is only due to new emerging studies or something else (and no, I am not a conspiracy theoriest).
True science holds up to any and all questions about the data, the facts, or how the study was conducted, doing so doesn't make you a conspiracy theorist. The problem arises when political interests / corporate greed become entangled with science to the point where people who ask questions are labeled as conspiracy theorists in order to silence them.
@@Deep_DiversPaul sells supplements
@@VeganLinkedpoor Paul against all medical corporations...
no, poor vulnerable people he misleads and poor animals that suffer the most consequences@@flcps
@@Deep_Divers Making wild claims that are constrary to the scientific evidence and then claiming that that evidence has been fabricated by powerful interests to hide the Truth is what defines conspiracy theorists. Not asking questions.
A relative risk reduction of 10% per 5mg/dl LDL seems insane and almost impossible condisering the fact that normal ldl levels would be about 120mg/dl if I remember correctly (see 9:50). Do I understand the numbers correctly? Also, what is the optimal LDL level? If LDL is just one risk factor the graph cannot be completely linear...
The graph on risk versus LDL is parabolic. A better factor to consider is free HDL/TG. Another way to think about it is "How can something that is required for fat transport, and hormone production in the body that bad?"
@@Dan-gs3kgThis is really the point. When he talks about water consumption, he makes de analogy break down, because most of the transporter is generated and recycled by the liver. Water production through metabolism does not compare to what the body does to generate LDL. We drink most of our water. High LDL might be a risk factor when blood biochemistry damages the LDL, i.e. high blood glucose. One of the papers shown actually says “association” in the title, but he skips that, because he wants to insist on causation in such a complex problem. What about the inaction of statins on damaged ldl or the effects on the brain? I grow tired of pseudo science. Some people read papers like they are sacred law. That is not how science works. No one knows what an optimum level of ldl is for every individual, so what is really high or low? The average in a metabolically damaged population?
Optimal LDL is below 70.
@@reason3581 that would mean that a person with 120 mg/dl has an increase of (heart disease) risk of 100%. That seems very much since LDL is just a minor factor and even very high levels of LDL only contribute to
@@Dan-gs3kg Thank you for the answer, but the graph seems to suggest a linear response?
I tested negative for Hypercholesterolemia despite my doctor telling me he wouldn't order the test because I should 'assume I have it'. Blood test showed no evidence of inflammation and calcium test showed no plaque. I eliminated sugar and processed foods from my diet 2 years ago and lost 40 pounds of body fat while otherwise maintaining my physique. I'm probably at 15% body fat. My physician still insists that I take Statins to lower my unacceptably high ldl but I told him 'No thank you'. Will I regret this decision and drop dead from a heart attack? The doctor insinuates that I might, yet my body has never felt better.
great analysis
Great analysis and presented respectfully.
Love the humour thrown in!
I remember reading study that showed little correlation between LDL and CVD after age 55, and another study that showed an inverse correlation between LDL and all-cause mortality (with a high optimum level). "LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature" "Burgess et al., ‘Power, linkage disequilibrium, pleiotropy, canalization and population stratification have all been recognized as potential flaws in the Mendelian randomization approach’"
Reverse causality. Step away from the David Diamond nonsense.
And that impressed you? First of all, if you suffer from certain cancers your cholesterol drops. That doesn't mean low LDL is unhealthy; it means it can be a marker for cancer. Second, some people with high cholesterol dropped dead before age fifty-five. Third, a lot of people who have low cholesterol in the over fifty-five cohort have it because they were diagnosed with cardiovascular disease and are currently taking statins and eating a diet lower in fat than they used to. Once again, the low cholesterol has become a marker of disease (but not a cause of it).
@@profd65 There's a Dr. Gundry, thoracic surgeon and cardiologist, with over 10000 heart operations under his belt who says that he couldn't care less about high LDL. He looks for triglycerides and HDL. He has no (visible) incentives to lie and tons of PRACTICAL experience.That's who I'd trust in this. Not 1000 academic studies of who knows what content within them.
Thank you for citing the article "LDL-C does not cause ....". I have been looking for this:)
People who use associative data to form a scientific conclusion are in the business of pseudoscience and charlatanism. They need to go back to school and understand what the scientific method entails.
Every single LDL study I've ever read has methodological errors and makes bold claims all based on associations. Not to mention the fact that most of them are riddled with statistical errors, that's if they're not statistically insignificant (and most of them are).
The guy who makes these videos needs a degree in statistics too. Because he reads mere associative data and takes it all at face value.
Is it possible that that a diabetes study might differ in outcome than if it were simply insulin resistance? Isn't there a distinction between these two conditions?
Ive noticed a personal trend when my cholesterol levels are low(hdl and ldl), so are my vitamin D levels. High? My vitamin D is perfect generally. Does cholesterol help absorption of vitamin D?
Yes, 7dehydrocholesterol is the skin precursor to vitamin D3 (cholecalciferol)
I'm not taking Dr Saladino's side as many of his arguments are specious, but I do think part of the problems with these studies is that LDL is more complex that just LDL. The nature of the LDL profile (and triglycerides and HDL) in toto need to be taken into account. I enjoy this channel because Physionic does go into direct mechanisms and depth and does find multifactor studies to ferret out conclusions that are informed and closer to truth. I have just dipped my toes(watched 3 or 4) into the Physionic waters and I'm impressed by the thoughtfulness he brings to the casts. As a critical thinker I do note that multifactor health analysis is extremely difficult and prone to many inference errors in a multitude of studies. Physionic sifts and distills a lot of information!
We should always be caution of ANYONE making ABSOLUTE claims.
But, yes, taking all the vaccines WILL DEFINITELY 100% KEEP YOU FROM GETTING COVID19 ;-0)
but we don't get the universal measure of how good studies are available vs the perfect studies proving information we actual want to know.
We get what is available not knowing how far from truth we still are in each topic.
but we still navigate using this partial knowledge
I mean we should navigate keeping in mind there is a degree of unknown that in many cases can be huge unknown that existing studies keep us far from the optimal direction
HDL is only partly valid, since both to low and to high lewels are associate with higher risc for CVD. And the cardioprotective effect is called into question, but that it is only a marker and not caual for decreased risk. So it is not that reliable, looking at the ratios including HDL. Triglycerides need to be taken into account as well. I agree. Non-HDL- cholesterol is taking other lipoproteins into account as well, so I think it's a pretty good thing to look at besides LDL-C.
@@stellasternchen Most People are just going to be concerned that the bag says "Doritos" on it. :-0)
I would also be interested to see the Mendallion randomization results on high ldl with low apoB. I really don’t think that anyone that speaks with authority on the topic believes that LDL is a valid metric independent of how it correlates to other markers such as apoB. It aggravates me that we still talk about LDL as if it is useful for anything other than tracking well with markers that actually cause CVD.
This is fun. Intelligent discourse is fun.