Bill Nye vs. Ken Ham

What you think is just a new tasty recipe is really rat poison.

BigThink.com writes:All humans have a gene for a protein called Apolipoprotein AI, which is part of the system that transports cholesterol through the bloodstream. Apo-AI is one of the HDLs, already known to be beneficial because they remove cholesterol from artery walls. But a small community in Italy is known to have a mutant version of this protein, named Apolipoprotein AI-Milano, or Apo-AIM for short. Apo-AIM is even more effective than Apo-AI at removing cholesterol from cells and dissolving arterial plaques, and additionally functions as an antioxidant, preventing some of the damage from inflammation that normally occurs in arteriosclerosis. People with the Apo-AIM gene have significantly lower levels of risk than the general population for heart attack and stroke, and pharmaceutical companies are looking into marketing an artificial version of the protein as a cardioprotective drug.

Wikipedia writes:Apolipoprotein A-I is a protein that in humans is encoded by the APOA1 gene.[1][2] It has a specific role in lipid metabolism.Apolipoprotein A-I is the major protein component of high density lipoprotein (HDL) in plasma...As a major component of the high-density lipoprotein complex (protective "fat removal" particles), apo A-I helps to clear fats, including cholesterol, from white blood cells within artery walls, making the WBCs less likely to become fat overloaded, transform into foam cells, die and contribute to progressive atheroma. Five of nine men found to carry a mutation (E164X) who were at least 35 years of age had developed premature coronary artery disease. One of four mutants of apo A-I is present in roughly 0.3% of the Japanese population, but is found 6% of those with low HDL cholesterol levels.ApoA-1 Milano is a naturally occurring mutant of apo A-I, found in a few families in Limone sul Garda, Italy, and, by genetic + church record family tree detective work, traced to a single individual in the 14th century. Described in 1980, it was the first known molecular abnormality of apolipoproteins.[8] Paradoxically, carriers of this mutation have very low HDL-C (HDL-Cholesterol) levels, but no increase in the risk of heart disease, often living to age 100 or older. This unusual observation was what lead Italian investigators to track down what was going on and lead to the discovery of apo A-I Milano (the city, Milano, ~160 KM away, in which the researcher's lab was located). Biochemically, apo A-I contains an extra cysteine bridge, causing it to exist as a homodimer or as a heterodimer with apo A-II. However, the enhanced cardioprotective activity of this mutant (which likely depends on fat & cholesterol efflux) cannot easily be replicated by other cysteine mutants.Recombinant apo A-I Milano dimers formulated into liposomes can reduce atheromas in animal models by up to 30%.[10] Apo A-I Milano has also been shown in small clinical trials to have a statistically significant effect in reducing (reversing) plaque build-up on arterial walls.

"AIMilano apoprotein identification of the complete kindred and evidence of a dominant genetic transmission" Research Report writes:The AlMilano apoprotein variant is associated with a marked reduction of high density lipoprotein (HDL) cholesterol levels and with increased triglyceridemia. In spite of the low HDL-cholesterol (HDLCh), carriers do not generally show clinical signs of atherosclerosis. The biochemical disorder is linked to a molecular change in apoprotein Al, that is, an arg -- cys substitution in the 173 position, thus allowing the formation of AIMilano-AIMilano dimers and AIMilano-AII complexes. The origin of the variant gene has been located in Limone sul Garda, a small community in Northern Italy (about 1,000 individuals). This community has a genetic, biochemical, and clinical individuality,
consequent to its isolation up to a few years ago; the citizens show highly uniform alimentary habits and elevated consanguinity.The complete population of the small village was sampled, and, by the use of an analytical isoelectric focusing technique for the detection of the mutant, a total of 33 living carriers, ranging in age from 2 to 81 yrs, were identified. Analysis of the genealogic tree of the complete family groups showed that the apoprotein (apo) AIMilano is transmitted as an autosomal dominant trait, all carriers coming from a single mating couple, living in the eighteenth century. The carriers are heterozygous for the apoprotein variant.

How do you know it was a mutation and not simply a normally occurring but rare allele that happens to be possessed by the people identified?

How do you know it was a mutation and not simply a normally occurring but rare allele that happens to be possessed by the people identified?

"Why Mutants Might Save My Life" ABC News 13 Oct 2013 http://abcnews.go.com/Health/mutants-save-life/story?id=20720645 writes:His name is Giovanni Pomarelli from the small Italian Mountain village of Limone sur Garda. He and his descendants have something you and I don't havea specific set of mutant genes...Giovanni's descendants (about 35) have a much different destiny. They have a rare, unknown until recently, genetic protection against clogged arteries. Many of his family, I hear, eat whatever they want. Some smoke and I'll bet don't even know the recommendations of the American Heart Association. To make it all the more amazing they have bad numbers.hardly any "good" cholesterol or HDL. What they do have is something scientists call the ApoA-Milano protein. It's not normal. There's a spot in that wonderful protein DNA double helix (spot 173) that should be occupied by something called cysteine. Arginine is there instead. It's a mutant.I've had several conversations with the experts hoping to be able to explain how this all works. I'll save you. They don't know exactly how it all works. The best explanation is the Pomarelli family has their own kind of good cholesterol. It prevents the bad stuff from hanging out in the blood vessels.Scientists have figured out how to create the ApoA Milano protein. It was tried out in animals, folks in Italy and finally here in the United States. It's as close as they come to an arterial rotor-rooter--Drano for the Heart, to borrow a Time Magazine headline. Forty seven lucky patients finished the U.S. study in just six weeks. In that short amount of time this relentless disease went into reverse. Their arteries were measurably cleaner. The normally conservative scientific community described the results as "dramatic" and "surprising." "We were pretty stunned that in a six-week period of time we could see a significant reduction in the burden of plaque," says study leader Dr. Stephen Nissen. "It showed us the disease was far more malleable, more amenable to very rapid changes than we would have ever guessed."

"Why Mutants Might Save My Life" ABC News 13 Oct 2013 http://abcnews.go.com/Health/mutants-save-life/story?id=20720645 writes:There's a spot in that wonderful protein DNA double helix (spot 173) that should be occupied by something called cysteine. Arginine is there instead.

"Drug removes arterial plaque in surprising clinical trial" Baltimore Sun writes:A small clinical trial has shown for the first time that it is possible to use drugs to remove plaque from clogged arteries, a finding that could lead to radically new ways to treat heart disease, the No. 1 killer in the United States.Infusions of a genetically engineered mutant form of high-density lipoprotein, the so-called good cholesterol, over a five-week period were shown to reduce plaque volume in patients suffering from chest pain."This is an extraordinary and unprecedented finding," said Dr. Steven E. Nissen of the Cleveland Clinic Foundation, who led the study reported in today's issue of The Journal of the American Medical Association.Current therapies targeting cholesterol use a family of drugs called statins to reduce levels of low-density lipoproteins, the "bad cholesterol."Increasing good cholesterol, or HDL, is not only substantially more effective at reducing plaque, but also appears to change its composition, stabilizing it so that chunks are less likely to break off and cause heart attacks or strokes.Surgical alternatives for eliminating blockages include angioplasty (in which a balloon is used to smash the plaque flat) and coronary artery bypass surgery. Both treat only small blockages, however, while the new approach works throughout the body."The results of this study are surprising to even the most optimistic supporters of the concept of targeting HDL as a therapy for atherosclerosis," wrote Dr. Daniel J. Rader of the University of Pennsylvania School of Medicine in an editorial in the same issue. He suggested that HDL-targeted therapies could be one of the most important clinical developments of the next two decades.And researchers owe it all to a young man named Giovanni Pomarelli, who was born in the small northern Italian village of Limone sur Garda in 1780. Although he didn't know it, he was born with a genetic mutation that proved highly beneficial.Two centuries later, a team led by Dr. Cesare Sirtori of the University of Milan discovered that about 40 residents of Limone had unusually low levels of HDL but were nonetheless exceptionally healthy. Even though they ate poor diets and most of them smoked, their arteries were largely free of cholesterol deposits. Their one common ancestor was Pomarelli.Sirtori found that they carried a mutant gene that served as the blueprint for a protein called apolipoprotein A-1, or ApoA-1, a key component of HDL. Those with this mutant form, called ApoA-1 Milano, have HDL that is apparently unusually aggressive at removing LDL from the circulation. In essence, the mutant HDL seemed to protect its bearer from heart disease.This speculation was confirmed during the 1990s in an elegant set of animal experiments by Dr. P.K. Shah of the Cedars-Sinai Medical Center in Los Angeles. Shah found that infusions of a synthetically produced ApoA-1 Milano in a complex with phospholipids could block the buildup of plaque in the arteries of mice and rabbits with high cholesterol and could even repair damage that had already been done, actually causing plaque to shrink.The mutant HDL also changed the composition of the remaining plaque, removing triglycerides and inflammatory cytokines, thereby making the plaque more stable and less likely to fragment.Nissen and his colleagues decided to test this approach in humans, even though they were skeptical that it would work."It seemed improbable, but it appeared the drug had the potential to cull plaque out of arteries in weeks, not years," he said. "We thought it was a long shot, not even a 1-in-10,000 chance, but it did work. We were rather pleased, but very surprised."They enrolled 57 patients with acute coronary syndrome, all of whom suffered chest pains, had high levels of cholesterol and suffered partial artery blockages that were not yet severe enough to require angioplasty or bypasses; 47 completed the study.Thirty-six of the patients received weekly infusions of the synthetic mutant HDL - produced by Esperion Therapeutics Inc. of Ann Arbor, Mich. - for five weeks and 11 received a placebo. The size of their atherosclerotic plaques was measured before and after the treatment using an ultrasound probe that fit inside the artery.They reported that the volume of plaque was reduced by an average of 4.2 percent in those receiving the treatment, while the volume increased slightly in those receiving the placebo. Although that seems a small decrease, it is actually much larger than that achieved with any other technique, Nissen said.With the statin drugs, "reversal of plaque is rare and, even when it occurs, it takes many months to years to see regression," Shah said. The new results "provide proof of the concept that HDL-based therapy has the potential to rapidly and favorably change human atherosclerotic plaques."Nissen said the speed with which results were observed "tells us something very important about the biology of heart disease: that it is a dynamic process that can be reversed rapidly."Researchers already knew that lowering LDL was an important way of fighting heart disease."Now we know that raising HDL is a really important therapeutic target," Nissen said. "If we can find a way to both lower LDL and raise HDL, we have a real chance to make a huge impact on millions of patients with coronary heart disease."The next step is a much larger trial to determine whether the therapy reduces the incidence of heart attacks and strokes. Nissen and others have begun planning such a trial, but it is not clear who will pay for it, he said.Now that his group has proved that HDL manipulation can be clinically useful, Nissen said, "There is going to be a frenzy of activity to understand what happened, why it worked, and how we can do this for the most patients at the least cost."

In any case the occasional fluke of a beneficial mutation is no proof that mutations are normally beneficial at all.

I'll grant that it's possible for a rare mutation to occur like this, but I also don't see why that original person didn't simply have a rarely occurring allele that was yes an "original part of the human genome."

Why couldn't this one person have simply inherited it and passed it on.

What makes it HAVE to be a mutation?

Such a protective function by the way I'd expect to have been part of the original genome because people were so much more healthy in Noah's time, though very likely lost in the Flood bottleneck or through deleterious mutations later. Perhaps mutations sometimes reinstate a formerly lost sequence. just a thought.

In any case the occasional fluke of a beneficial mutation is no proof that mutations are normally beneficial at all.

Have you ever thought whether you actually might be doing a disservice to your co-religiosistas with your complete and utter lack of a) honesty and b) ability to accept that scientists are doing their work well and without preconceived motives?If faith is so weak that it can only survive on distortion, lying and general doshonesty, what does it tell about that faith?

I am actually a Christian and Bible believer but I also see the reality of scientific fact. Though in the past I have had my ups and downs spiritually so to speak (I was once was more of a deist/agnostic). Faith, however is a small subsector of religious people who believe that science and their Christian faith cannot co-exist. I am one of many who does not believe that.

Me writes:You said that it is only a minority that denies science but isn't it actually so that 40 percent of Americans believe that everything was created in 6 literal days according to Gilgamesh

Epic of Gilgamesh writes:So the goddess conceived an image in her
mind, and it was of the stuff of Anu of the firmament. She dipped her
hands in water and pinched off clay, she let it fall in the wilderness, and
noble Enkidu was created.

marc9000 writes:The ultimate rub is actually much of the general public's conclusion about who is being more honest. Just because Nye "indicated" that something can change his view doesn't automatically mean it's the truth. Evidence indicates that evolutionists are just as closed-minded as Christians about their beliefs, despite their assertions about their open-mindedness. There is a difference between assertions and actual demonstrations.

Bill Nye's honesty further comes into question because of one his main assertions, his main recap about the whole science versus creationism debate - that young people's secular scientific education in the U.S. is so very important in keeping the U.S. from falling behind other countries when it comes to new innovations and discoveries. History should tell him that when new innovations and discoveries are made anywhere in the world, the entire world benefits.

That he is so adamant about promoting secularism and downplaying Christianity makes one wonder if he has other interests besides promoting science. A search of his political beliefs reveals the answer - he's a flaming liberal! A big contributor to Democrat candidates campaigns, including Obama's. No wonder he's big on secular science "education", the phrase "endowed by our creator with certain unalienable rights" probably really bothers him.

Now a dozen posters here will sputter with rage at me, but just remember, it's not my fault that not everyone completely trusts scientism/atheism.

True, when someone somewhere invents something then the whole can buy it,

Bill Nye's (extremely obvious) point is that a country's quality of life depends upon its ability to compete with the rest of the world, and education is key to a country's competitiveness. The greater a county's flow of innovation the greater its wealth.

I think we already knew you feel threatened by science, secularism and liberalism.