The ID Report

by Denyse O'Leary
ARN correspondent

Both explained by Dr. Jeff Schwartz.

The easiest way to understand the difference between the mind and the brain is - the brain is a piece of biological matter (protoplasm) in your skull. That's the brain. It's a thing; you can hold it in your hand. The mind is your experiences, and especially for scientific purposes your attention and attention focusing capacity so they aspect and the way in which you focus attention on your experiences.

Also just up at The Mindful Hack

Social psychology: "Only the lonely"? Yes, abstract concepts can generate physical sensations - for better or worse

Near death experiences: Large project to study up to 1500 cases - possible new insights into relation between mind and brain

Evolutionary psychology: Do people see faces in cars?

Spirituality: A conventional sad tale does not transform into a spiritual memoir just because God is hat tipped

Toronto-based Canadian journalist Denyse O'Leary (www.designorchance.com) is the author of the multiple award-winning By Design or by Chance? (Augsburg Fortress 2004), an overview of the intelligent design controversy. She was named CBA Canada's Recommended Author of the Year in 2005 and is co-author, with Montreal neuroscientist Mario Beauregard, of The Spiritual Brain: A neuroscientist's case for the existence of the soul (Harper 2007).

By Robert Deyes
ARN Correspondent

Two studies in immunology published early in 2008 attracted much media coverage because of the elegant way in which the organisms under study had defied each others immune defense and attack responses. The first came from a group at Stanford headed by Charles Hanifin that reported on how Garter snakes had developed 'super-immunity' against a deadly variety of newt (Ref 1). So deadly in fact that Hanifin claims these newts to be the most dangerous amphibians on the planet. It turns out that the secret behind the Garter snake's success resides in a single mutation in a gene that encodes for a cellular receptor called TTX (Ref 1). The mutation, which causes a loss of function (Ref 2), is enough to take the strength out of the newt's lethal toxin (Ref 1). This case has been touted as a prime example of an 'evolutionary arms race' in which the Garter snake has emerged victorious. Perhaps not so dramatic but equally impressive was Munich Immunologist Thomas Miethke's demonstration of how certain strains of bacteria manufacture duplicate forms of human proteins that allow them to avoid detection by the body's immune system (Ref 3). In a functional immune response, specialized cells in our bodies are able to identify invading microbes by using cell-surface receptors that bind to foreign proteins (Ref 3). And yet certain bacteria such as Salmonella are able to inactivate this response by using molecular decoys that 'jam up' immune cells (Ref 3).

The question that naturally arises from both these studies is whether or not one can claim that herein lies the fodder from which immunity supposedly evolved? Can we simply assume that an evolutionary arms race could eventually give rise to the molecular orchestration so visible in, say, the mammalian immune system? A brief examination of the literature reveals significant challenges for the evolutionary picture. Much has been learned in recent years regarding how the various parts of our immune system work together towards the common goal of fighting off invaders. One aspect of the immune response uses the henchmen of the immune defense- our antibodies- to recognize the enormous repertoire of shapes (epitopes in technical jargon) that exist throughout nature (Ref 4, p.14). Stuart Kauffman was absolutely correct when he described the enormous number of possible shapes that these antibodies can latch onto (Ref 4, p.14). Indeed for more than 20 years, many immunologists puzzled over this enormous shape 'repertoire'- a repertoire so large that we now know that as many as a million antibody molecules can be made by combining the different subunits that make up the antibody (Ref 5, p.851).

It is now known that antibodies are not simply floating haphazardly around in the body waiting for an invader to strike but rather are produced by specialized cells called B cells (Ref 5, pp.834-835). Each B cell produces only one specific antibody and carries it on its surface. By recognizing foreign molecules B cells are triggered to proliferate, the result being of course a predominance of B cells that recognize the invading aggressor (Ref 5, p.837). These B cells then secrete their antibodies into the blood stream thereby making the response against the invading aggressor that much more effective (Ref 5, p.838). Foreign antigens are subsequently internalized within cells, chopped up into smaller pieces and presented on the outer cellular surface by a protein complex called the Major Histocompatibility Complex (MHC) (Ref 5, p.881). One recent paper described the diversity of MHC proteins and their role in maintaining immunity in amphibians (Ref 6). This 'fusion' of antigens and the MHC is further recognized by other specialized cells called T lymphocytes- the foot soldiers of the body's own defenses. Molecular messengers called Interleukins signal the T cell to further grow and divide while B cells manufacture more copies of their specific antibodies (Ref 5, p.987).

Antibodies by themselves do not destroy or even harm their targeted aggressors. They are simply signals that mark the spot upon which subsequent reactions act so as to finish the job. Like the action scenes of Hollywood in which enemies are destroyed by explosive-carrying carts that follow tracking devices underneath cars, the antibody provides a signal with which molecular attack complexes can find their target. These complexes form part of the Complement System which, as the name suggests, a system that 'complements' the initial antibody response (Ref 7, p.1031). The proteins of the complement system form a battering ram of sorts that punctures holes into the outer cell membrane of an invading cell destroying it in the process (Ref 7, p.1031). There are a total of 20 different complement proteins all of which are produced in the liver and remain inactive until called into action either by the immune response (the classical pathway) or through recognition of sugar molecules called polysaccharides on the outer surface of the invading cell (the alternative pathway (Ref 7, pp.1032-1034). These complement proteins act cooperatively and in a highly specified order in so far as the binding of one complement protein at the correct place is essential for the binding of the next.

With the eventual demise of the foreign invading cell, the complement system provides a truly masterful mechanism for killing foreign invaders, with each part playing a role in the invader's demise. While not every protein in the complement system is essential (Ref 7, pp.1035-1036), the question that arises is how an integrated immune response that targets foreign bodies while leaving its own cells intact might possibly have evolved? It becomes clear as one considers the complexity of not only the complement system but also the repertoire of antibodies available to the immune response that the origin of such systems severely challenges the idea of a step-by-step evolutionary construction. As science writer Rodney Phillips wrote,

"nearly 150 years after the publication of the Origin of the Species, we are still laboring to understand evolution and selection in many biological systems" (Ref 8).

Of course there should not be total despair for those who wish to stick to the Darwinian framework; for it is easy to see where natural selection may be the driving force that 'improves' the body's defenses in response to selective pressures. Such pressures are seen today in the plethora of methods devised by microorganisms for escaping the body's immune surveillance. Some viruses for example are able to minimize the amount of antigen that they produce while other viruses such as HIV can insert their DNA into the body's own DNA and vary their own proteins so as to avoid the body's so called immunological 'memory' (Ref 8). The malaria parasite is equally evasive. By invading only red blood cells, the malaria parasite avoids the presentation of its own proteins to the cell surface by the Major Histocompatibility Complex (MHC) since these cells do not produce an important class of MHC proteins (Ref 8).

From such examples, it is easy to envisage how slight successive improvements in the immune response might one day help to keep these invading aggressors at bay (Ref 8). Such Darwinian 'triumphs' are not what are being contended here. What is being contended is the promulgation of this rather limited view of natural selection to its more 'globally-encompassing' extension- after all, it is one thing to ascribe successive slight improvements to the powers of natural selection and an entirely different thing altogether to propose that natural selection is the means by which complex systems such as those involved in the immune response have been constructed from scratch. Modern day neo-Darwinists would of course disagree and, rather like the mythological Atlas of Greek legend, would prefer to place the entirety of evolution on the shoulders of natural selection. But where do we begin in our efforts to cobble together the various components of the immune system? Moreover, with the potential recognition of the body's own cells how do we prevent the immune system from becoming more of a liability than a selective advantage? The lack of causal specificity is one of Dembski's core arguments against those who claim that we have a viable proposition for how complex intracellular and extracellular systems evolved. Causal specificity was what Benjamin Franklin exemplified in one much-celebrated quote,

"For want of a nail, the shoe was lost; for want of the shoe, the horse was lost, and for want of the horse the rider was lost" (Ref 4, p.113).

Within such a chain of events, we see causal specificity leading us to an eventual explanation of why the rider finally perished. We should expect the same standards of causality in biology and the origin of complex molecular systems. "Without specificity," Dembski writes, "one has no empirical justification for affirming that a transformation can be effected" (Ref 9, p.242). Without causal specificity we cannot claim to know how the immune system arose through natural processes.

References And Notes
1. Phil McKenna (2008), Toxic newts lose war against 'super-immune' snakes, NewScientist, 11th March, 2008, http://www.newscientist.com/article/dn13438-toxic-newts-lose-war-against-superimmune-snakes.html

2. A key point about the loss of function mutation in the TTX receptor is that no additional genetic sequences (and therefore no additional information) have been added to the ttx gene. In his book Not By Chance, Lee Spetner notes how for the grand sweep of evolution to occur, information has to be built up.

3. Mitch Leslie (2008), Score One for the Microbes, ScienceNOW Daily News, 10 March 2008, http://sciencenow.sciencemag.org/cgi/content/full/2008/310/1

4. Stuart Kauffman (2000), Investigations, Published by Oxford University Press, New York

5. James Watson, Nancy Hopkins, Jeffrey Roberts, Joan Argetsinger, Steitz, Alan Weiner (1988), Molecular Biology of the Gene, Benjamin Cummings Publishing Company, Menlow Park, California

6. Helmholtz Center For Environmental Research (2008) New findings on immune system in amphibians, Press release from June 19th, 2008, http://www.ufz.de/index.php?en=16938

7. Bruce Alberts, Dennis Bray, Julian Lewis Martin Raff, Keith Roberts, James D Watson (1989), Molecular Biology of the Cell, Published by Garland Publishing Inc, New York, 2nd Ed

8. Rodney Phillips (2002), Immunology Taught by Darwin, Nature Immunology Volume 3, pp.987-989

9. William Dembski (2002), No Free Lunch: Why Specified Complexity Cannot Be Purchased without Intelligence, Rowman & Littlefield Publishers, Inc Lanham, Maryland