As the reviews of professor Behe’s new book Darwin Devolves continue, many who participate in the discussions on many blogs or websites may have noticed the seeming paradox involving high fat, high cholesterol diet and heart disease issues… Dr. Behe devoted a good portion of his book to the issue of the devolution of the polar bear, which supposedly evolved, or rather devolved according to Behe, to tolerate the drastic switch from the dietary habits of its ancestors some 400 000 years ago…This particular issue I’m planning to cover in one the upcoming OPs…
This OP is more of an introduction to the fat/cholesterol/heart disease issue that while it seems complicated at the first glance, it really isn’t…
Some members on TSZ have already alluded to this issue, so I will cover just the very fundamentals:
- cholesterol is a fatty substance produced by the liver (about 80%)
- only 20% of cholesterol enters the bloodstream via diet
- if more cholesterol is consumed, the liver slows down its production
- cholesterol is essential to life as cell membranes require it (among others)
- if cholesterol is not produced in sufficient amount by the liver the organism dies
- people who consume little cholesterol still develop heat disease, including atherosclerosis–the fatty deposits of cholesterol (and other, like calcium) in arteries
- people with low blood cholesterol levels develop heart disease;
patients with advanced heart failure often have low cholesterol, which is associated with a poor prognosis for survival
If people and many animals who consume little cholesterol develop heart disease, one might also ask whether people who consume a lot of fat and cholesterol are at the same risk…
The simplest answer is no.
That’s why the issue of high fat and cholesterol consumption diets in humans with low rates of heart disease have been labeled as the cholesterol paradox, because, from at least one point of view, it just doesn’t make sense…
As the side point, the great majority of Cell article Behe explores in his book Darwin Devolves is based on the assumption that high fat, high cholesterol diet causes heart disease (arteriosclerosis) therefore the polar bear must have evolved the adaptation to eat seal blubber and have no atherosclerosis…
Behe just plays along and simply exposes the assumptions that if polar bear evolved to eat high fat, high cholesterol diet, it has done so by breaking or blunting gene functions…This will be covered in the upcoming OP…
Why cholesterol paradox?
Because there are many groups of people (not as many anymore) all over the world that seem to be the exception to the assumed rule that high fat, high cholesterol diet cases heart disease, like atherosclerosis…Some of them are called hunter-gatherers but others, like Canadian Inuit, could be called seal blubber eaters, just like the lowly poplar bear at issue between evolutionists and ID…
Inuit eating seal blubber
If there are exceptions or paradoxes to the rule among those groups of people, are they due to adaptive mutations, just like it has been claimed in the Cell article that Behe explored regarding polar bears?
Or, is there another possible explanation?
You tell me… 😉
DNA_Jock,
You are an idiot, Jock!
This is the original paper based on which Liu and other authors of the Cell paper established that polar bears’ cholesterol levels are extreme:
Ormbostad I. Relationships Between Persistent Organic Pollutants (POPs) and Plasma Clinical-Chemical Parameters in Polar Bears (Ursus maritimus) Svalbard, Norway: 2012. pp. 1–73.
https://www.google.com/url?sa=t&source=web&rct=j&url=https://core.ac.uk/download/pdf/30875800.pdf&ved=2ahUKEwi2y7qWk5zhAhUMyYMKHeZPCekQFjACegQIAxAB&usg=AOvVaw2ypY6hvL6e4NF-mylAPoWC
Download the PDF and let me know how the evidence works either in your own words or Ormbostad’s. Go ahead! Shock me! 😉
Oj, don’t forget!
From Liu in Cell
“Due to a lack of appropriate functional studies of polar bears, we were unable to directly identify causal variants. Nevertheless, we assessed the impact of polar bear–specific substitutions on human proteins for top-20 genes under positive selection by computational predictions: a large proportion (c. 50%) of mutations were predicted to be functionally damaging”
It’s a hell of the thing… 🤣
My mistake — Ormbostad’s was not a Ph.D. thesis, but rather a Master’s thesis. So I’m an idiot, apparently.
🙂
The paragraph from Liu that you quote here is the one that Behe mis-understood, and then went and, hilariously, based a whole chapter of his book on. The readout from PolyPhen-2 is either “benign”, or “possibly damaging” or “probably damaging”. PolyPhen-2 does not report “beneficial”.
Since you seem unwilling (or unable? …) to put numbers on polar bear cholesterol, I will help you out:
Total cholesterol averaged 8mM in the Spring and 8.6mM in the Autumn. That’s elevated (50 – 60% above ULN for a fasting human) but not quite as elevated as the HDL levels were: 2.8 – 3mM is 70% – 85% higher than human’s ULN.
I calculate their non-HDL cholesterol at ~197mg/dL, that’s right at ULN for a fasting human. Your doctor will tell you to cut back on the ice cream, but if you’re still this high in six months’ time, he’ll start you on a statin. Although given a chol/HDL ratio of 2.8, which is near the low end of the standard range (2 – 5) , your doctor might not bother. Given the differences in lifestyle between polar bears and humans, I’m not sure I would really call that “extreme”, and Ormbostad did note a little something that might be messing with his cholesterol data.
I met your challenge.
So, gonna explain how to calculate RMST and HR?
Of course he isn’t. He’s going to copy-paste some irrelevant nonsense and then liberally spray his post with pointless emojis. That’s all he’s capable of.
Excusez-moi?
Have you even looked closely at the original paper as I told you to?
The paper didn’t even focus on cholesterol and definitely not on the “killer LDL”…
They were focused on some kind of contamination…
My question is:
Why would the Cell authors use this paper as the reference for the high cholesterol levels in bears and the ApoB transport fast evolution, if the reference paper didn’t even list LDL?
Can you see my problem?
Can you explain it, Jock?
Good point!
The disrespect is mutual… 😉
I have a feeling that the so called “cholesterol paradox” is going to cause some problems (not for me, I hope), especially the Cell paper regarding “the polar bear speedy evolution”…
It’s funny how a sceptical eye about evolution makes one spot nonsense so quickly …
The first time I looked at the paper, I’d sensed that something was wrong…
Not only that, the cholesterol paradox and hair pigmentation happened to be my favorite subjects other than cancer prevention of course …
Whatta coincidence! 😉
Well, given that I am quoting data from the paper and calculations based on those data, I think it should be obvious to anyone who has read the paper that I…
Oh
Never mind.
Well, d’oh. The title is “Relationships Between Environmental and Biological Variables, Plasma
Clinical-Chemical Parameters and Persistent Organic Pollutants (POPs) in Polar Bears (Ursus maritimus) from Svalbard, Norway” So anyone who had read the title would know that.
[spit-take]
Huh?
So you did a text search of the paper and decided that it didn’t mention LDL or cholesterol?
ROFLMAO
Yes, yes I can.
Not within the rules, I can’t.
😉
Lol
How was the killer bear LDL cholesterol measured, Jock??
You said I was right about the bears’ cholesterol levels. Would you like a link? You asked me if I informed Behe about it… What made you to change your mind, Jock ???
Oh dear, J-Mac. Ormbostad did not measure LDL cholesterol; no-one with even a passing familiarity with cholesterol would expect them to.
For those of you trying to follow along at home, anytime someone makes a statement about the effect of LDL as a risk factor in cardiovascular disease, they are not talking about measured LDL. Since 1972, they are talking about calculated (Friedewald) LDL-C, which was a dramatic improvement since it avoided the use of a preparative ultra-centrifuge. All the big CV risk studies that showed that LDL was bad for you used calculated LDL, not measured LDL.
What people measure is TOTAL cholesterol, cholesterol in HDL (so-called “good” cholesterol), and triglycerides.
To figure out how much LDL-C you have, you take TOTAL cholesterol* and subtract the HDL-C* and subtract an estimation of the cholesterol tied up in triglycerides*.
That’s the Friedewald equation.
To figure out your “ratio”, you divide the TOTAL-C* by the HDL-C* value.
So when a paper (e.g. Ormbostad) reports out the three values that everyone measures (marked with asterisks above), it is assumed that grown-ups are able to recognize that they have provided all the information needed to derive the level of LDL-C, and the ratio, which are the first two things considered as risk factors.
It’s especially gob-smacking when the same paper provides, in Appendix B, an idiot’s guide to how the three measurements were performed.
I had assumed that J-Mac was at least familiar with the terminology, if not the research.
I have, yet again, over-estimated him.
What made you change you mind about me being right about the high cholesterol level in bears, dear Jock???
Do you think you can remove that comment of yours?.
Go ahead! I would love it!
So, you are full of it?
Thank you Jock! You are really full of it!’
Obviously you have the power to remove the embarrassing to you comments and pretend that you are … whatever…
For those who are following it: Jock_DNA has become a born-again evolutionary citizen who decided to defend evolution instead of nailing Behe for basing his book on garbage evolutionary science…
I had predicted it, so let’s see how Jock pretends that his comment that Behe was wrong about the Polar Bears’ cholesterol levels now is turned around and supports his nonsense.. It is quite amazing….lol
Over to you Jock_DNA lol
BTW: Please don’t forget to tell us why and how you changed your mind about polar bears’ having extreme cholesterol levels … Remember??? lol
J-Mac,
You cannot read ass-hole. So stop pretending. Go get an education first. Spend at least four or five years learning to actually read, then, if you achieve such an unthinkable feat, you can come back and apologize for your current stupidity.
“What I cannot create, I do not understand”-Richard Feynman
Seems Entropy can do the other way around… 😉