November 26, 2007

The Problem of Heroism

While you wait for me to shake off my post-Thanksgiving lethargy and complete the next MIT biology commentary, I submit this article for your consideration.

It is on the "problem" of heroism, and these excerpts get to the point of the article (which is longish):

Twenty minutes after the crash, the sun was going down, and no one had been able to reach the six survivors. They were doomed...until suddenly, miraculously, a rescue chopper came whisking across the darkening sky. It dropped a life ring right into the hands of one of the survivors and plucked him from the water. Then things turned really strange.

The next person to receive the ring handed it over to someone else. The chopper lofted her to safety, then wheeled back.

The man gave away the ring again.

And again.

He even gave it away when he knew it was his last chance to live. He must have known, because when the chopper thundered back seconds later, he was gone. The man in the water had vanished beneath the ice.

Who was he? But far more perplexing: Why was he? Why would anyone put the lives of strangers ahead of his own? He couldn't even see the faces of the people he was saving, because they were on the opposite side of the wreckage, yet he made a sacrifice for them that their best friends might have refused.

. . .

Even Charles Darwin, that human decoder ring of bizarre behavior, found the idea of saving a stranger's life to be a total head-scratcher.

"He who was ready to sacrifice his life, as many a savage has been, rather than betray his comrades, would often leave no offspring to inherit his noble nature," observed Darwin, who consequently couldn't figure out how to crowbar heroism into his survival-of-the-fittest theory.

Die for your own kids? Perfectly logical. According to Darwin, your only reason to exist is to pass your genes along to the next generation. But to die for a rival's kids? It seems totally counterproductive. No matter how many virile, healthy heroes you bore, it would take just one selfish bastard with a hearty sex drive to spoil the whole species. Selfish Bastard's kids would thrive and multiply, while SuperDad's kids would eventually follow their father's example and sacrifice themselves into extinction.

Even if evolutionists can propose a story to explain how such an altruistic streak could have survived in the gene pool, despite its most dominant carriers' untimely demise, they are still left to explain why we also seem to have an equally strong selfish streak. I do not think I am overplaying my hand here to say that such behavior is a problem for naturalism, which entails that all instincts must be part of the biological programming, whereas seemingly conflicting noble and fallen natures is perfectly consistent with biblical Christianity.


November 14, 2007

MIT Biology Class - Reading Between the Lines (3)

Lecture Note:

Many physical characteristics, like eye and hair color, are the direct result of having certain dominant genes. However, there are some genes that may be dominant in an individual yet do not manifest themselves except under certain conditions. I believe that a predisposition to heart disease and diabetes were mentioned as examples, where lifestyle choices can be the deciding factor in appearance.

My thoughts:

My thought here is more social commentary rather than evolution related.

Let's say that researchers did manage to find the elusive "gay gene." There is good reason to think that such a gene would not have a determinative effect, like those for eye color, but would merely provide a susceptibility to the condition. Indeed, this must be the case, since identical twin studies demonstrate that more than 50 percent of homosexual twins have heterosexual siblings. Compare this with 100% parity between twins (as far as I know) for things like eye and hair color. If this condition were actually genetically caused, then twins would always be either both or neither homosexual.

If we would then compare the "gay gene" with the "heart disease gene" we would come to a problematic conclusion. That is because if we think about the actual onset of heart disease, we generally find that it is accompanied by poor diet and exercise. That is to say, the predisposition for heart disease may only manifest itself under adverse conditions. It can clearly be said to be a "bad" thing, in that it is a case of the normal operation of the body gone wrong. In such cases, the related gene is not actually a new and distinct gene from what other healthy persons have; it is due to an alteration (mutation) of an existing gene that serves a valuable purpose.

All this is to say that finding a "gay gene" would not have the desired effect of making homosexuality into a "natural" human variation, like male/female, blonde/brunet, and white/black. At worse, it could be seen as a deleterious mutation of a right-functioning gene (and in Darwinian terms, a non-breeding gene-bearer is clearly at a disadvantage). At best, it is only a gene that may result in homosexuality under certain conditions — conditions which may even be characterized as "unfavorable," meaning something has gone wrong. And any condition which may only be influenced by other factors is a condition which might also be avoided or, perish the thought, reversed. I know, this is all politically incorrect science. But it is a fiction that science is the exclusive domain of white-coated priests of impartiality and truth. Which leads to my next topic.

Lecture Note:

One of the professors recounted several cases of major scientific breakthroughs, some of which were well ahead of their times, that were met with indifference and even rejection by contemporary peers. An example would be the discovery that chromosomes are involved in heredity.

My thoughts:

When I was a young man I had a rather starry-eyed view of science. I imagined that scientists were primarily concerned with truth at all costs and that science dealt with objective concerns that were insulated from the more biased realms of values and religion. I believed that new, paradigm shattering discoveries were welcomed with excitement and that progress was the mutual goal of all. And then I grew up.

Scientists are human, too, and prone to the same biases and mistakes that people make in every other area of life. In fact, there are some ways in which the sciences present unique opportunities for bias. Pet theories must be proved out and ferociously defended if one has hopes for a Nobel Prize. Valuable grants must be courted by way of politically expedient research agendas. Fraternal orthodoxies must be carefully negotiated if one expects to publish in the best journals. I have heard it said that most Nobel laureates had great difficulty getting their original theses past peer reviews and had to publish privately or in minor journals.

But the most troubling (and often most denied) of all are the metaphysical biases that inhibit some ideas from consideration on principle alone. No one is immune to the influence of personal convictions, and some theories have greater ramifications for those convictions than others. The acceptance of big bang theory is one recent example in which personal bias was at work against the mounting evidence and growing consensus in its favor. As Sir Arthur Eddington wrote in 1931, "The notion of a beginning is repugnant to me ... I simply do not believe that the present order of things started off with a bang. ... The expanding Universe is preposterous ... incredible ... it leaves me cold." And more recently, Phillip Morrison of MIT said in a BBC film on cosmology, "I find it hard to accept the Big Bang theory; I would like to reject it."

While atheists have found creative ways to shrug off the implications of a "creation" event, the stakes for a rejection of naturalistic evolution are perhaps even higher; for if nature has not shaped us, then exactly who has? Let me just end here by quoting Harvard geneticist and evolutionary biologist, Richard Lewontin, who publicly summarized the materialistic (and his) bias better than I could ever hope to.

Our willingness to accept scientific claims that are against common sense is the key to an understanding of the real struggle between science and the supernatural. We take the side of science in spite of the patent absurdity of some of its constructs, in spite of its failure to fulfill many of its extravagant promises of health and life, in spite of the tolerance of the scientific community for unsubstantiated just-so stories, because we have a prior commitment, a commitment to materialism. It is not that the methods and institutions of science somehow compel us to accept a material explanation of the phenomenal world, but, on the contrary, that we are forced by our a priori adherence to material causes to create an apparatus of investigation and a set of concepts that produce material explanations, no matter how counter-intuitive, no matter how mystifying to the uninitiated. Moreover, that materialism is absolute, for we cannot allow a Divine Foot in the door.

If Intelligent Design is indeed the cause of biochemistry, then we shall never know it so long as the gatekeepers of "science," like Lewontin, stand guard to insure that only pre-approved ideas are admitted for consideration.

Labels: ,

November 05, 2007

MIT Biology Class - Reading Between the Lines (2)

(Part 2 in a series)

Lecture Note:

Many proteins that are made by the cell are destined for use outside of the cell. This includes not only those protein assemblies that will serve needs on the outer cell wall (e.g., sensors), but also those which are not even meant for use by the cell that produced them. Particularly, in multi-cellular creatures, proteins are made that are meant to communicate with, or provide services to, other parts of the organism. Examples would be digestive enzymes, hormones, and neurotransmitters. The cell wall is designed to keep the bad out and the good in. Consequently, for each item slated for external use there must be a discriminating mechanism to allow or transport it outside of the cell.

My thoughts:

Let's assume for a moment that we are an organism composed of cells, which has managed a spectacular mutation that codes for a new protein that would be a boon to our survival. Now our cells are busily generating said protein. But we've got a problem: no matter how much of an advantage this protein would give us over our peers, it will do us absolutely no good if it cannot get a hall pass to leave the cell and go to work just where it is needed. In fact, while it waited generation after generation for such a pass (i.e., a new cell portal, or an existing portal change) it would actually be a detriment to us, since its construction would consume valuable resources. Worse, without simultaneously evolving the accompanying regulatory mechanisms our cells — perhaps every one of them — would be busily manufacturing these proteins without end. This is highly reminiscent of viruses, which hijack the machinery of the cell (by inserting their own genes into the DNA) in order to make continual copies of themselves. They do so until they fill the cell and it bursts.

Lecture Note:

Proteins are the workhorses and building materials of the cell. They consist of long (polypeptide) chains of amino acids, which are then folded into intricate shapes fitted to serve specific tasks. The average polypeptide chain is about 150 amino acids in length, and some are well over 3000 in length. Each amino acid could be one out of a variety 20 different amino acids that are used by all living systems. The folding occurs due to various chemical and electrical attractions and repulsions that exist between different parts of the chain, and the final folded form is dependent upon the exact arrangement of amino acids in this chain. The possible arrangements of a polypeptide chain of 150 amino acids in length is 20 to the 150th power (20^150). The enormity of possible configurations for proteins makes computer simulations of protein folding a monumental task. At this time, even with our best supercomputers, it is impossible to predict what the 3D structure of any given polypeptide chain will be from merely knowing the arrangement of the individual amino acids that make up the chain.

My thoughts:

Let me start by driving something home. As I mentioned, the possible arrangements of amino acids in an average protein is 20^150. That roughly equates to 1 with 195 zeros after it! (Remember this 196 digit number for later.) For comparison, the number of atoms in the entire universe is "only" about 1 with 80 zeros after it. Since DNA contains the instructions for these proteins, and DNA instructions are supposedly acquired by way of mutations, this means that coming up with a functional protein is a matter of statistical probabilities. Even if we had an unused stretch of gene-space to work with, and we confined all mutations to just this region of DNA, and we had every generation of every organism that had ever existed on earth pumping out mutations, we would never arrive at any of the perfectly functional proteins that you could name in the average cell.

Not so fast, the skeptic may say. Calculating odds like this is only applicable if we have a hand in mind before we draw the cards. There may be any number of arrangements that could make some kind of useful protein. Life may simply consist of collections of random poker hands. While this might be a good objection in principle, it runs aground for a couple of reasons.

The laws of physics constrain the kinds of functional systems that are available for use in the cell, and the cell itself, once framed out, further constrains its own options. Many features of life (including proteins) in creatures that are widely divergent from one another are similar if not identical in form, and these features are claimed to have been evolved independent of each other (convergent evolution). This suggests that there are certain best or right ways to accomplish certain tasks. And the fact that most life shares many proteins in common, and the most complex life has only 10's of thousands of genes, means that we may have a rather small target set to compare against the astronomical alternate possibilities. Assuming a high estimate of 100 million species on earth, and making a generous assumption that 10,000 genes in every species is unique, this means we get to knock 12 zeros off of our 196 digit number. A statistical drop in the bucket.

Additionally, in systems that are composed of multiple proteins, the design of the proteins is tightly constrained by the other proteins in the system. For instance, if I have a "bolt" protein, and chance is expected to complete the set, only some form of a "nut' protein will do. This all means that for at least some evolutionary outcomes to obtain, there will be certain predefined poker hands that chance must deal.

The skeptic may again object by questioning whether or not all amino acids in the protein are absolutely necessary to form the functional structure. This would be a good objection, because some regions are merely filler and/or connective in nature; and in some cases even functional amino acids may be replaced by another amino acid with similar properties. While this may certainly lessen the odds, it does not ultimately bring them into the realm of the plausible.

Let's be generous and say that only 40 of the amino acids are important to our average protein. Let's further compound our generosity by saying that there are two different amino acids that could work at each point for our essential 40, i.e., 1 in 10 odds rather than 1 in 20. So now our odds of arriving at any specified "average" protein is 10^40. While certainly a better number than 10^195, it is still no help, since this number actually exceeds or equals the estimated number of organisms that have lived on our planet in all of history!

But let's not stop here. Let me up the ante by revisiting one of my earlier generous allowances. Mutations do not confine themselves to, or target, specific genes; mutations are just blind errors that occur in the process that copies the entire DNA package in preparation for cell division. Now, the DNA replication machinery is very efficient, but it does make the occasional mistake. In fact, we are now far enough along in the genetic sciences that we can say that the average mutation rate is about one nucleotide (a "point mutation") out of every 100 million. Since there are 4 possible nucleotides for any given point, this means our odds of arriving at any specified mutation is 1 in 400 million. And because the instruction for a particular amino acid is made up of groups of 3 nucleotides (a "codon"), and because several nucleotide arrangements can code for each of the amino acids, this means that we often need 2 nucleotide changes to get from one amino acid to another. This compounds our odds of getting just one meaningful (and possibly beneficial) change to 1 in 160 quadrillion, i.e., 16 followed by 16 zeros.

While this may be attainable by a large bacterial population in a matter of decades, it is a profound problem for less numerous and slowly reproducing creatures like mammals. For example, the human evolutionary line supposedly diverged from the chimpanzee line around 5 million years ago. Let me be as generous as possible here. If we were to take 10 million years, assume a continuous population of 100 million primates, and allow each to breed by age 10, then we are talking about only 100 trillion mutation candidates, i.e., 1 followed by 14 zeros. (Note: you do not multiply these three values to arrive at this number.) That's 3 orders of magnitude fewer events than what is needed to match the odds for getting just a 2-point mutation! We're talking about the odds for changing just a single amino acid here, and surely there would need to have been thousands of events at least this significant to get from primate to modern human. To go to just 3 specified nucleotide changes, which might get us 2 new amino acids (assuming one of the two needs only a single nucleotide change), we bump our odds up to approximately the total number of mammals that have ever existed on earth!

Another possible objection occurs to me at this point, which is certainly answerable, but I have gone on too long already. I will address it if comes up in comments.

I hope my readers have been able to follow my science, reasoning, and statistic, since I believe I'm addressing an issue that is absolutely devastating to evolutionary theory. In the face of such staggering improbabilities, evolution advocates seem to lean upon their presupposition that evolution is just a "fact," and, consequently, there must be some statistically viable mechanism to drive change that is as yet undiscovered. In my mind it is a case of "evolution of the gaps" thinking. This is not simply a matter of ironing out the details of a theory; this is foundational to the mechanism that is the supposed driver of the evolutionary process (or at least half of it). If one cannot say how something happened, and that it is within the realm of chance, then how can one say that it happened?

Labels: ,

Pensees - Wordpress