A rather odd reference diagram talking about diabetes and from Diabetes Wellness Australia.
But that diagram bears no resemblance to the actual video/podcast which was about cholesterol as you described from somebody looking totally unrelated to that organisation.
Anyway, I listened to all that and I was not impressed. All sorts of misinformation IMHO. I shan’t go into detail, but my recommendation is to beware of the information in here.
Really? Curious what information you thought was different/wrong? Perhaps we heard something different from each other. Kind of surprised. 1) fat does not cause CVD 2) high ldl does not cause CVD 3). Sugar causes CVD, and not everyone needs to be on a statin 4) LP little A is involved in plaque (same as Kendrick). Deposition. 4) diet and exercise best to reduce risk. 5) genetics counts (more than I think it does , but …). You think some of those are incorrect?
I can’t remember the details, and I was not taking notes as I listened to this. Your points 1-3 are right, and I was OK with what was being said while those points were made. But in the last half it seemed to get into a number of beliefs that I disagreed with. I will listen again and detail those out. Quite possible that I misunderstood what he was saying, so I will listen again and see if I feel the same.
OK, I listened again, and my memory was correct. For the record here are the issues that I have with what was said. BTW, always happy to be wrong and be edjumacated if my understanding of things is wrong. I 100% realise that I have a credibility gap issue here… uneducated me vs a cardiologist. But I still think I am right and he is wrong.
I didn’t quite make the quarter century. But I think that’s enough. Yes, there was some sense in this video, but I reckon an even greater load of nonsense that should be called out. Just because someone has a title of Dr does not make them right.
McQueen, Alec McQueen, my main takeaway from this is that on #7 you blurred bollox. I didn’t know that was an actual “bad” word. Thought it was just something like utter nonsense.
Live and learn.
It’s Britslang for testicles, but it can mean both bullsh1t, or screwed up. Bullocks, on the other had, are castrated bulls (steers, in the US). 
Robin is right. In Brit parlance, bollox means rubbish, utter nonsense. Derivation is unclear, but my introduction to the word was during my young adult life when I was an avid Viz reader. The word bollox was used a lot! Especially by a character called Roger Mellie the Man on the Telly.
I think it derived from the similar word bollocks, which means testicles. Bollox is semi-rude. Not the kind of word I would use in a church!
While we’re unpacking Britslang … I see the definition of “sod off” is “go away.” Is it really? I always thought it was the brit-quivalent of f*** off which, in US slang, doesn’t literally mean go away, it means leave me alone / get away from me / stop talking to me (or maybe even, go **** yourself), you’re a jerk.
Not sure that is right… I used to be a Brit for 30 years but now living in Australia.
Sod off does mean go away. Again, it is semi-rude, not what you would say to your aging aunt! But this is the kind of word that the BBC would use in a comedy program.
But f*ck off also means go away, but is 10 times ruder for obvious reasons. I don’t think there is any connotation in the phrase that is literal ie go and fornicate. It is just about the strongest and rudest way to say go away.
Well, good on you for noticing a lot of tidbits that are most likely incorrect. I guess I was mostly listening to the main messages, but upon reading your thoughts, I can see a lot of issues that one could argue as incorrect. In general I agree with most of your concerns, even though many are opinion, and i suspect some of the language is less precise for the generic listener.
I will only note that AFAIK, HDL does reverse transport lipids from all over, including within plaques I believe.
Michael
Good stuff, and agree with your summation. And yes, lots of opinions on both sides. End of the day (having read Kendrick’s Doctoring Data), that’s pretty much all anybody has got. Firm truth is very rare in these arenas, and Kendrick warns against believing anything as absolute truth. I like his summary that he categorises everything in 3 buckets: probable, possible, unlikely. Nothing is definitively ruled in or out.
Your point about HDL transporting lipids is interesting… is that the same as “sucking fat out of the arteries”. That is the language he used, and I don’t think that is the same as HDL transporting lipids.
Thanks for provoking some interesting thinking for me. I 100% acknowledge that some of my opinions above will be wrong. I wonder if the good doctor would be as humble.
I know that some people believe this, but I’ve seen other argue this is bullocks. I don’t know what to believe, especially because if you have high HDL you most likely have low trigs. To me, this means what you’re eating more important than HDL. Too many variables.
Not to mention that sometimes high HDL associates with high atherosclerosis:
But I still think scientifically. If there are a group of people with high LDL who are the same age, they should all have about the same level of atherosclerosis (assuming LDL was about constant over time). If not, LDL is unlikely to be causal.
Kendrick is definitely a statin denier. I looked at some of the studies he sometimes states a few years ago, and for the most part, as I recall, they were observational in nature and really not worth the paper they are written on. But he does have his followers.
Interesting paper, of course efficiency does not dispute function. I wonder if HDL are at all involved in the process when statins reduce soft plaque within arteries, or is there is a different effect from statins that reduces/removes trapped cholesterol and proteins from plaque. Still a lot of details to learn/clarify despite my constant learning.
What we do know (from radio-labeled food studies) is that “triglycerides” are dietary carbohydrate packaged into chylomicrons for storage in adipose tissue, and “high-density lipoprotein” transports fatty acids from the adipose to where they are needed. All lipoproteins also transport cholesterol around for cells that need more than they can make on their own, so it’s obviously the cholesterol that kills us. 
But what the ratio of triglycerides to HDL really tells us is whether we are eating in a way likely to promote cardiovascular disease, or in a way that is likely to avoid it.
Absolutely! He is a prominent member of the International Network of Cholesterol Sceptics (THINCS). For the record, even THINCS membes agree that statins do lower cholesterol. They also appear to have an anti-inflammatory effect that can be beneficial for cardiovascular patients. However, what the THINCS people maintain is that cholesterol has no causal role whatsoever in atherosclerosis.
Their position, which makes a lot of sense to me, is that there are factors that cause tears in arterial walls. In a person on a healthy diet (not the diet recommended by the authorities, which is damaging), the repair mechanisms can keep up with the damage without producing arterial plaque. Once the rate of damage increases, however, plaques form to help stabilise and repair the damage, and cholesterol appears in the plaques as part of this process. But its presence in plaques does not mean it caused the plaques, any more than the presence of fire engines at a building fire means they caused the fire.
My understanding is that statins lower serum cholesterol so that it won’t seep into arterial walls and cause plaques. Since cholesterol doesn’t seep into arterial walls, and since plaques form in response to blood clots formed in response to damage to arterial walls, and cholesterol doesn’t cause that damage, the logic that statins help by lowering serum cholesterol is faulty.
More evidence from Dr Paul Mason. Blood oxidative stress causes blood clots, which is the cause of CVD. Interestingly he calls out oxidised LDL (small dense) as a potential oxidative stressor. But what causes the LDL molecule to become oxidised?
My opinion on HDL is that the main reason higher HDL is (mainly) related to better outcomes is because it’s part of the trigs/HDL marker, and higher HDL typically (though there are exceptions) means better nutrition or exercise (though my HDL never changed with exercise). I doubt the theory about reverse transport is true. I think whatever protects your endothelium will be a benefit, and lower trigs/higher HDL protects the endothelium because you’re not killing the endothelium with high glucose. Like this for instance:
I know people also think PUFAs are bad, but I haven’t looked into that as much. Particularly because if LDL isn’t bad, I have a hard time believing oxidized LDL (or small, dense LDL) is bad.
I feel the same way, but Dr. Mason’s explanation of the mechanism (or proposed mechanism) of how oxidised LDL can damage the glycocalyx does make sense.
