The cholesterol paradox

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:

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

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…
😉

Polar bear eating seal blubber

94 thoughts on “The cholesterol paradox

  1. DNA_Jock: But the polar bears have elevated plasma cholesterol. So they cannot have reduced ApoB function per Behe’s logic.

    😉

    What’s authors’ of the original paper in Cell conclusion regarding the effects of mutations in ApoB, which Swamidass also supports?
    Can you quote it and explain?

    BTW: Did you watch the webinar, especially at 1:44.00?
    It’s all there… 😉

  2. J-Mac: Cell paper that the ApoB mutations improved the clearance of LDL cholesterol, if the same paper clearly says that polar bears cholesterol levels are extreme?
    Someone is not being truthful… If cholesterol levels in polar bears are extremely high, how could the clearance of cholesterol be improved by the beneficial mutations?

    You’re confused.

    You first need to find out what the ApoB gene actually does, and then you need to find out what the polar bear ApoB mutations do. Whether polar bears have high levels of LDL cholesterol and low levels of heart disease is besides the point.

    The point is that the mutations are beneficial, fixed by natural selection. And that Behe thinks they somehow degrade the function of the ApoB in some way.

    Do they? Are the ApoB mutations in polar bears reducing the function of the ApoB gene? To know that we need to know all the things ApoB do. ApoB is involved in more than merely affecting blood cholesterol levels, as it is also involved in all kinds of blood fat transport.

    While polar bear cholesterol levels might be very high, it is entirely possible the polar bear beneficial mutations in the ApoB gene actually increase the overall fat transport capacity, which would make sense given the high fat contents of polar bear diets.

    It is even possible some of those mutations increase fat transport capacity overall, while also degrading the LDL clearance. It’s a multifunctional gene and it’s entirely possible there are tradeoff functions at work, where increasing one function substantially which has a high fitness advantage, will come with a reduced function in another capacity with a much lower fitness cost(if any).

    You have not even BEGUN to do the kind of work you hold in abiding faith will vindicate Behe.

  3. Rumraket: You first need to find out what the ApoB gene actually does, and then you need to find out what the polar bear ApoB mutations do. Whether polar bears have high levels of LDL cholesterol and low levels of heart disease is besides the point.

    Besides the point?! Boy!!!
    Speaking of someone being confused… 😉
    Jock! Your customer… lol

  4. Another fact to consider here is that LDL cholesterol is actually involved in fat transport too. And fat molecules in the bloodstream are actually carried by cholesterol molecules. So for a bear eating extreme amounts of fat, it will have high cholesterol simply because those molecules are synthesized so as to carry the fat around in the bloodstream.

    Mutations in the ApoB gene might actually increase the fat transport and clearance capacity, even tough bears still have extremely high blood cholesterol, simply because the bears eat so much fat.

    There is no reason to think the ApoB mutations increasing fat transport and clearance should cause polar bears to have lower levels of blood cholesterol compared to brown bears when polar bears still eat much, much more fat than brown bears.

    If the clearance and transport capacity of the gene is increased by 15% (say), but polar bears eat (say) 300% more fat than brown bears, they are still going to have higher blood cholesterol than brown bears, even though they are also better at dealing with it.

    You get it now?

  5. J-Mac: Besides that point?! Boy!
    Speaking of someone being confused…
    Jock! Your customer… lol

    As usual you have nothing to say but to drool and whinge. Responding to you IS like responding to Robert Beyers.

  6. J-Mac is equating high serum cholesterol with reduced fitness. That’s a mistake.
    Behe equates diet-induced hypercholesterolemia with reduced fitness; slightly better, but still a bridge too far.
    Atherosclerosis is caused by plaque deposition.
    The irony being that we know Behe is wrong about the effect of reduced ApoB function in the mouse (Huang is right and Farese is wrong: it leads to male sterility, amongst other things).
    As Rumraket correctly notes, anyone who talks about the effect of those polar bear mutations in ApoB is speculating. A little bit of speculation is the reward you earn for putting in the work, like Liu et al did.

  7. DNA_Jock: J-Mac is equating high serum cholesterol with reduced fitness

    I do? I didn’t know that…😉
    Stop misrepresenting my views and embarrassing yourself at the same time…😂

  8. DNA_Jock: As Rumraket correctly notes, anyone who talks about the effect of those polar bear mutations in ApoB is speculating. A little bit of speculation is the reward you earn for putting in the work, like Liu et al did.

    You’ve changed your mind, again?
    I’m not speculating one bit… I know…😉

  9. No, but I did hear Michael Brown explain to Mark Bretscher why he does not eat egg yolks.
    Can you figure out why, J-Mac?
    😉

  10. DNA_Jock:
    No, but I did hear Michael Brown explain to Mark Bretscher why he does not eat egg yolks.
    Can you figure out why, J-Mac?
    😉

    He doesn’t? Too bad… I eat 2-5 eggs almost every day… My buddy eats at least 8 eggs or more… as he is on full keto and hates cooking…Can you make a prediction regarding our cholesterol levels? 😉

    Tip. Gregg’s one type of cholesterol carrier protein was either extremely low or extremely high as it was not detected by the test… The test needed to be repeated several times…Can you guess which one it was and whether it was high or low?🤗

  11. DNA_Jock: J-Mac is equating high serum cholesterol with reduced fitness

    If you wanna play the game, be specific! High or low serum cholesterol levels in relation to fitness?

  12. Rumraket: Mutations in the ApoB gene might actually increase the fat transport and clearance capacity, even tough bears still have extremely high blood cholesterol, simply because the bears eat so much fat.

    Read this again and again and then try to figure it out why I don’t feel like responding to such nonsense… Can you? 😭

  13. Rumraket: You have not even BEGUN to do the kind of work you hold in abiding faith will vindicate Behe.

    😂
    How about this: We test it by analyzing the cholesterol levels in brown bears eating high fat diet in Alaska without the “beneficial mutations” in ApoB protein.
    What is your prediction? 😉

    I might not be aware that I disagree with Behe on more than one issue…I think he knows by now what they are…😉

  14. It is already challenging to take anything you write seriously, please don’t make it harder than it already is.

  15. Rumraket:
    It is already challenging to take anything you write seriously, please don’t make it harder than it already is.

    Why should I take your speculative evolutionary science seriosly? Because you really wish it were true? That’s not science! Not to me…

  16. J-Mac: He doesn’t? Too bad… I eat 2-5 eggs almost every day… My buddy eats at least 8 eggs or more… as he is on full keto and hates cooking…Can you make a prediction regarding our cholesterol levels?

    Tell us more, age, family history, ratio of “ good “ and “bad”. What else do you eat?

  17. J-Mac: How about this: We test it by analyzing the cholesterol levels in brown bears eating high fat diet in Alaska without the “beneficial mutations” in ApoB protein.
    What is your prediction? 😉

    My prediction is that J-Mac chasing disgruntled brown bears to take blood samples will be even more amusing to watch than him chasing chickens.

  18. My prediction is that brown bears in Alaska will be highly polymorphic.
    Here’s the research proposal:
    Pick a tractable experimental animal (one where you can actually take sequential fasting blood samples), probably the dog, but the silver fox might be fun…
    Replace it’s ApoB gene with the putative ancestral bear one (could default to the panda, I guess).
    Research the cholesterol levels, diet-induced hypercholesterolemia and susceptibility to atherosclerosis and CHD in these animals for a variety of diets.
    Introduce each of the five ApoB mutations that were fixed in the polar bear. Do all 32 possible alleles.
    Research the cholesterol levels, diet-induced hypercholesterolemia and susceptibility to atherosclerosis and CHD for each of the 528 possible genotypes for a variety of diets.
    You’ve got a lot of work ahead of you, J-Mac. Maybe your kids can help.

  19. DNA_Jock:
    My prediction is that brown bears in Alaska will be highly polymorphic.
    Here’s the research proposal:
    Pick a tractable experimental animal (one where you can actually take sequential fasting blood samples), probably the dog, but the silver fox might be fun…
    Replace it’s ApoB gene with the putative ancestral bear one (could default to the panda, I guess).
    Research the cholesterol levels, diet-induced hypercholesterolemia and susceptibility to atherosclerosis and CHD in these animals for a variety of diets.
    Introduce each of the five ApoB mutations that were fixed in the polar bear. Do all 32 possible alleles.
    Research the cholesterol levels, diet-induced hypercholesterolemia and susceptibility to atherosclerosis and CHD for each of the 528 possible genotypes for a variety of diets.
    You’ve got a lot of work ahead of you, J-Mac. Maybe your kids can help.

    Well J-nut is fond of declaring that he’s got “contacts” that can “fund” these experiments.

  20. DNA_Jock: My prediction is that brown bears in Alaska will be highly polymorphic.

    No way?! Really?! 😉 That is hell of the thin, you know… 😉

  21. DNA_Jock:
    My prediction is that brown bears in Alaska will be highly polymorphic.
    Here’s the research proposal:
    Pick a tractable experimental animal (one where you can actually take sequential fasting blood samples), probably the dog, but the silver fox might be fun…
    Replace it’s ApoB gene with the putative ancestral bear one (could default to the panda, I guess).
    Research the cholesterol levels, diet-induced hypercholesterolemia and susceptibility to atherosclerosis and CHD in these animals for a variety of diets.
    Introduce each of the five ApoB mutations that were fixed in the polar bear. Do all 32 possible alleles.
    Research the cholesterol levels, diet-induced hypercholesterolemia and susceptibility to atherosclerosis and CHD for each of the 528 possible genotypes for a variety of diets.
    You’ve got a lot of work ahead of you, J-Mac. Maybe your kids can help.

    We have already established that you’ve forgotten how to research the pubmed…
    Now you have confirmed that you can’t google…
    It took me 30 seconds to find this:

    Brown bears (Ursus arctos) seem resistant to atherosclerosis despite highly elevated plasma lipids during hibernation and active state.

    https://www.ncbi.nlm.nih.gov/pubmed/22686205

    Give me one more reason why I should respond to your further comments?
    Why should I waste my time?

  22. Rumraket: Well J-nut is fond of declaring that he’s got “contacts” that can “fund” these experiments.

    I do…but why bother? 😉

    Bears not bothered by diet high in saturated fats
    Grizzlies show no clinical signs of disease following short-term consumption of saturated fats but scientists question long-term health

    https://www.sciencedaily.com/releases/2017/10/171030084745.htm

    I want focus on the new evolutionary theory with evidence gaps. No evidence for evolution? No problem. Maybe God guided it… 😉

  23. J-Mac: Maybe God guided it

    Guided what? Evolution? But you just said there was no evidence for it.

    Your position is as confused as I’m sure your children are.

  24. Robert Byers: The bible says man is given 70 years, 80 with health. It doesn’t mention diet.

    Actually, Byers made me think and can anyone guess?

    Does the bible recommend eating fat, or prohibits it? 😉

  25. OMagain: Your actual level of commitment to the truth is thus revealed.

    Your actual level of commitment to cherry picking in order to distort the truth is thus revealed…

  26. Further to testing the idea of whether J-Mac has any clue what he is talking about
    I was so entertained by Dr. Malcolm Kendrick’s use of the restricted mean survival time (RMST) statistic to quantify the benefit of statin therapy, so I did a “back of the cigarette packet” calculation of my own. Let’s see if fanboy J-Mac understands the stats…
    His 15.6 day to 17 day reduction in RMST seen in the HPS and 4S studies implies that there is a roughly 0.5% per annum absolute mortality effect.
    Sounds kinda lame ass, am I right?
    But it isn’t:
    0.5% p.a. absolute risk reduction would lead to an average lifetime benefit of 3.9 years for a 40-year-old man, 4.5 years for a woman.
    The graph below (life curve for a 40-yo woman with or without an extra 0.5% mortality) shows why RMST is the wrong metric.
    Pop quiz for J-Mac:
    1. Describe in your own words how to calculate the RMST after five years from this graph.
    2. Describe in your own words how to calculate the Hazard Ratio after five years from this graph.
    E4typo 45 should read 40

  27. Let’s review the conversation, J-Mac.
    Behe has claimed that the five mutations that fixed during the evolution of the polar bear from the common ancestor with brown bears (specifically N716K,D749E, D2623N,T3920P, and L4418H) are mostly deleterious; that is, the polar bear evolved via a process of “blunting or breaking” gene functions.
    Basically, he reached this conclusion because he mis-interpreted the meaning of the analysis in Liu et al 2014, in particular the application of the human-developed PolyPhen-2 algorithm to Bear genes. Only when the 3 Musketeers pointed out his errors did Behe realize his mistake; that’s when he latched onto Farese et al 1995. Farese et al made a disruption in the mouse ApoB gene and showed that (when homozygous) the mutation was embryonic lethal but the heterozygote, weirdly, showed a resistance to diet-induced hypercholesterolemia – suggesting (to Behe, at least) that reduced ApoB function could be adaptive for animals on a high fat diet. This is the entirety of his data to support his contention that the mutations in ApoB are “blunting or breaking”, and that they support the thesis of his book.
    Suspiciously, this Farese reference is cited in the Wikipedia page on ApoB. This, combined with the fact that it is WRONG, leads me to suspect that Behe’s citing of Farese was a post-hoc rationalization. But I could be wrong about that, and it’s not important right now.
    What is important is the fact that Huang et al 1995 (J Clin Invest. 96: 2152-2161) actually did the knock-out properly and found that the heterzygote led to male sterility, amongst other problems. As I noted, “That’s not going to be adaptive”.
    After much teasing, you finally reveal that your ‘killer’ argument is the claim that Liu et al’s statement

    We suggest that the shift to a diet consisting predominantly of fatty acids in polar bears induced adaptive changes in APOB, which enabled the species to cope with high fatty acid intake by contributing to the effective clearance of cholesterol from the blood.

    is not well supported.
    Well, to the extent that you have a fair criticism here, it goes double for Behe’s claims.
    Your “support” for the “killer” nature of your position consists of noting that polar bears have elevated plasma cholesterol levels. “Extreme”, even.
    Various posters have pointed out that this is a total non-sequitur, including (most recently, and most enjoyably) the poster J-Mac, who has cited a paper showing that Brown bears are resistant to atherosclerosis despite having high plasma cholesterol.
    (It’s not just the level of LDL, it’s where it goes, apparently. ApoB does a bunch of things. That deep-sixes your simplistic argument. If you were capable of thinking this through, you would understand that the nature of the role of ApoB in controlling plasma cholesterol and the roles of ApoB in preventing atherosclerosis is entirely peripheral to the issue of whether ApoB in polar bears has evolved or “devolved”.)
    I’ve even been trying to gently guide you to look at the LDL receptor (egg yolks and Nobel Laureates), which (unlike ApoB) IS involved in human cardiovascular disease. As are a bunch of other factors, like Lp(a) levels and PCSK9, too. It is very complicated.
    On the other hand, you missed the bit about Brown Bears hibernating, apparently. Awkward. (There’s actually a rather cute, if contorted, argument to be made here in Behe’s defense. Let’s see if any of you guys is smart enough to spot it.)
    Behe’s argument hinges on the effect of the specific mutations that fixed in the polar bear. No amount of mis-reading of the effect of HMG-CoA reductase inhibitors by loopy British PCPs (see above) will support that argument.

    You are not fooling anyone. Not even the creationists.
    I am quite confident that you are unable to comprehend the primary literature; you have given us no reason to think otherwise. You are painting your cause in a very poor light.

  28. J-Mac: Bears not bothered by diet high in saturated fats
    Grizzlies show no clinical signs of disease following short-term consumption of saturated fats but scientists question long-term health

    You keep thinking this is a question merely of the propensity of heart disease in bears. There are more factors at work here. Fat metabolism, transport, and storage, just to name a few. And these all have to be viewed in the context of the life-history evolution and development of polar bears and their ancestors.

    It is difficult to overstate how much you have yet to grasp. I can only repeat myself: You have not even begun the kind of work it would require to parse out the biochemical or phenotypic effects of these mutations on the function the ApoB gene.

  29. J-Mac: Your actual level of commitment to cherry picking in order to distort the truth is thus revealed…

    In what sense? What have I cherry picked? What is the full meaning of my quotation in it’s full context? What have I distorted? What is the truth?

    I don’t expect you do answer this question, in a very real sense it’s purely rhetorical.

  30. J-Mac: Thank you Einstein!

    If there is no evidence for it, how can there be gaps in that evidence?

    J-Mac: I want focus on the new evolutionary theory with evidence gaps. No evidence for evolution? No problem. Maybe God guided it…

    Do you think god guided evolution? If so, which god? And how do you know?

  31. J-Mac: I want focus on the new evolutionary theory with evidence gaps.

    It’s “I want to focus”. Don’t you read what you write?

    Actually, never mind…

  32. DNA_Jock:
    Let’s review the conversation, J-Mac.
    Behe has claimed that the five mutations that fixed during the evolution of the polar bear from the common ancestor with brown bears (specifically N716K,D749E, D2623N,T3920P, and L4418H) are mostly deleterious; that is, the polar bear evolved via a process of “blunting or breaking” gene functions.
    Basically, he reached this conclusion because he mis-interpreted the meaning of the analysis in Liu et al 2014, in particular the application of the human-developed PolyPhen-2 algorithm to Bear genes. Only when the 3 Musketeers pointed out his errors did Behe realize his mistake; that’s when he latched onto Farese et al 1995. Farese et al made a disruption in the mouse ApoB gene and showed that (when homozygous) the mutation was embryonic lethal but the heterozygote, weirdly, showed a resistance to diet-induced hypercholesterolemia – suggesting (to Behe, at least) that reduced ApoB function could be adaptive for animals on a high fat diet. This is the entirety of his data to support his contention that the mutations in ApoB are “blunting or breaking”, and that they support the thesis of his book.
    Suspiciously, this Farese reference is cited in the Wikipedia page on ApoB. This, combined with the fact that it is WRONG, leads me to suspect that Behe’s citing of Farese was a post-hoc rationalization. But I could be wrong about that, and it’s not important right now.
    What is important is the fact that Huang et al 1995 (J Clin Invest. 96: 2152-2161) actually did the knock-out properly and found that the heterzygote led to male sterility, amongst other problems. As I noted, “That’s not going to be adaptive”.
    After much teasing, you finally reveal that your ‘killer’ argument is the claim that Liu et al’s statement

    is not well supported.
    Well, to the extent that you have a fair criticism here, it goes double for Behe’s claims.
    Your “support” for the “killer” nature of your position consists of noting that polar bears have elevated plasma cholesterol levels. “Extreme”, even.
    Various posters have pointed out that this is a total non-sequitur, including (most recently, and most enjoyably) the poster J-Mac, who has cited a paper showing that Brown bears are resistant to atherosclerosis despite having high plasma cholesterol.
    (It’s not just the level of LDL, it’s where it goes, apparently. ApoB does a bunch of things. That deep-sixes your simplistic argument. If you were capable of thinking this through, you would understand that the nature of the role of ApoB in controlling plasma cholesterol and the roles of ApoB in preventing atherosclerosis is entirely peripheral to the issue of whether ApoB in polar bears has evolved or “devolved”.)
    I’ve even been trying to gently guide you to look at the LDL receptor (egg yolks and Nobel Laureates), which (unlike ApoB) IS involved in human cardiovascular disease. As are a bunch of other factors, like Lp(a) levels and PCSK9, too. It is very complicated.
    On the other hand, you missed the bit about Brown Bears hibernating, apparently. Awkward. (There’s actually a rather cute, if contorted, argument to be made here in Behe’s defense. Let’s see if any of you guys is smart enough to spot it.)
    Behe’s argument hinges on the effect of the specific mutations that fixed in the polar bear. No amount of mis-reading of the effect of HMG-CoA reductase inhibitors by loopy British PCPs (see above) will support that argument.

    You are not fooling anyone. Not even the creationists.
    I am quite confident that you are unable to comprehend the primary literature; you have given us no reason to think otherwise. You are painting your cause in a very poor light.

    This is BS Jock… lol

    You set yourself up… Well I had… but you fell for it… 😉

    Someone once told me:
    “Do not let emotion to distort your judgment!”

    If you really paid close attention to all the hints I have given you, you may have figured out the trap I was setting up right from the beginning…

    You should have paid closer attention to one aspect of my Darwin Devolves review, where I clearly stated that I don’t agree with Behe on few things and that his views are often based on not “sound science”… 😉

  33. J-Mac: If you really paid close attention to all the hints I have given you, you may have figured it out the trap I was setting up right from the beginning…

    This seems to be the sock gnome argument.
    1. You didn’t pay attention
    2. ?
    3. I’m right.

    You need to give more attention to point 2.

  34. Alan Fox: This seems to be the sock gnome argument.
    1. You didn’t pay attention
    2. ?
    3. I’m right.

    You need to give more attention to point 2.

    I realize that Alan Fox and DNA Jock are too ignorant to figure out what I’m implying…So, yes, I’m suggesting that the famous 2014 Cell article was an evolutionary bluff…
    Yes, I have evidence and DNA Joke has seen most of it…he is just to ignorant to acknowledge it…

  35. Aw, don’t be so coy, J-Mac. We’re quivering in anticipation. Do tell us how you’ve overturned evolution!
    Although, I would appreciate a pledge of faith:
    1. Describe in your own words how to calculate the RMST after five years from the graph above.
    2. Describe in your own words how to calculate the Hazard Ratio after five years from the graph above.
    It’s basic stats for anyone who can read the clinical literature.
    Right now, you appear uncannily like a complete bullshitter. Just a friendly heads-up.
    😉

  36. DNA_Jock:
    Aw, don’t be so coy, J-Mac. We’re quivering in anticipation. Do tell us how you’ve overturned evolution!
    Although, I would appreciate a pledge of faith:
    1. Describe in your own words how to calculate the RMST after five years from the graph above.
    2. Describe in your own words how to calculate the Hazard Ratio after five years from the graph above.
    It’s basic stats for anyone who can read the clinical literature.
    Right now, you appear uncannily like a complete bullshitter. Just a friendly heads-up.
    😉

    Here is my, or rather your, first problem:

    “You are right, J-Mac!
    The observation that polar bears have elevated plasma cholesterol completely refutes Behe’s argument re APOB.

    http://theskepticalzone.com/wp/the-cholesterol-paradox/comment-page-1/#comment-250087

    I hope you understand my concern about your credibility first…
    I don’t need to overturn anything… It does it by itself… 😉

  37. All hat, no cattle.
    According to Behe, polar bears have suffered a “blunting or breaking” of their ApoB gene. When challenged to explain how he can tell the difference between an “increase” in ApoB function and a “decrease” in ApoB function, Behe (on multiple occasions) hauls out the observation (Farese) that mice with a 50% reduction in ApoB function (the heterzygous null) have reduced plasma cholesterol levels.
    Therefore, according to Behe, polar bears’ elevated cholesterol must be a sign of elevated ApoB activity, thereby refuting his thesis.
    Not to worry, he has both his facts and his logic wrong.

    N.B. In my view, each of the phrases in quotes represents an incoherent concept. As a biochemist, Behe ought to know better.

    Now it’s your turn, J-Mac
    1. Describe in your own words how to calculate the RMST after five years from the graph above.
    2. Describe in your own words how to calculate the Hazard Ratio after five years from the graph above.

Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.