Evolution Page

Are Multiple Mechanisms for Evolution Possible?

Central Dogma vs LaMarckian Evolution

Now for some completely wild speculations about two aspects of basic BIology, consistent with some BioImaging® and acupuncture results we have seen clinically, that suggest that the conventional "central dogma" although true, may not be the complete story. Perhaps, yet another level of embedded "semi-teleological" self-determination intelligence can be found deep in our cells and genes. Research is needed.

Heredity is considered to be a one way transcription street from the DNA that has survived long enough to reproduce, to RNA acting as the copy machine, leading to the production of a protein. Proteins are the structural elements or the enzyme catylysts that allow us to have a shape that can move quickly vs. glacially. Evolution is considered to only proceed on the "germ line" via sexual reproduction (for those organisms limited to this method).

What if a biofeedback loops exist such that environmental impacts on proteins are captured and worker designed improvements are recommended, like on the old "Saturn shop floor", in "molecular productivity circles" that work their way up the hierarchal management chain of command. From protein to RNA to DNA, the reverse of normal DNA transcription. If such a heretical reversed information flow takes place, another route of hereditary change and correction might be possible.

This is a modified Lamarckian evolutionary view. If true, it opens many therapeutic possibilities. But theories are cheap. Is there any data to support a reemergence of a previously discounted theory? To date, only one anomalous laboratory study (report below in box) and some anecdotal clinical evidence from a number of patients supports this notion.

An E coli strain, without a gene for the lactase enzyme, was fed only indigestible lactose. In this experiment, a few individual e coli bacteria seems to have managed to achieve an intelligent self-directed DNA modification of the best candidate gene they had. The bacteria choose to try various genetic engineering modifications on a gene that coded for an glycolytic enzyme closest to what the environment required they have, an enzyme that previously could breakdown other similar sugars, but not lactose. The bacteria that succeeded in this engineering project survived to form a the new lactase capable colony.

Of course single-celled organisms are amazingly sophisticated biochemists. The little beasties are amazingly flexible and can trade appropriate pieces of their DNA to other beasties that need them, kind of like the post-Napster file sharing on the WWW. But if no one has the song...how do you record, rather, __cord it, if no individual has a copy?

One simple suggestion is that an existing low-affinity enzyme, that could break down lactose in a pinch, was expressed in high numbers. This may prove to be the true explanation that preserves the "central" one-way dogma of biology. Yet it remains an anomaly. Ignoring anomalies is bad science, it's also very typical science and very human. The pay-off if it is true might be substantial. Retro-viruses show that at least half of the 2-way street may be paved.

A rapid, focused identification of, and self-directed mutation of a genes, even when it has no "good" gene to use as a template, seems almost like a cellularly conscious attempt to improve genes for the demands of the environment. In the case above, Cairn et al placed bacteria without the ability to eat lactose sugar were put in a culture media where lactose was all they had to eat. Some survived. This was not the usual case of natural selection where a few bacteria with a pre-existing gene for making a lactase enzyme are selected for, with death of all those without the necessary lactase gene. Cairn controlled for, and eliminated from the gene pool, any individual bacteria capable of making a lactase enzyme. This would, otherwise, be the typical explanations of the results of the experiment. In this case, it seems a de novo creation of a new gene might have occurred, perhaps by a focused modification of an existing related gene. This tinkering of an existing gene so that it could perform a new function to allow the survival of that individual bacteria is new old idea. They then passed on that new learning, that creative solution to their progeny. If you are familiar with Darwinian evolution and Lamarckian Evolution, this looks a lot more Lamarckian than Darwinian.

Neo-Darwinian research is voluminous and convincing. This single possible exception does not refute Darwin, but raises the possibility that both might be true. Occam's razor, looking for the simplest explanation and throwing out the more complex, may be OK for physics but biology goes in for flamboyant redundant complex systems. Because it happens in bacteria doesn't mean it happens in humans, but remember that two different ancient symbiotic bacteria are the original source of all animal cells, including our own.

Reverse transcriptase was independently discovered in 1970 by David Baltimore and Howard Temin. Since its discovery, reverse transcriptase has been associated with eukaryotes and prokaryotes along with retroviruses, retrotransposons, hepadnaviruses, retrons, and even humans. Although Cairn, as I do here, raised the possibility that an environment to DNA flow of information might have occurred with reverse transcriptase mediating, Patricia Foster (http://jb.asm.org/cgi/reprint/174/6/1711.pdf) notes that the K12 -lac strain of e coli, used in many of these experiments, lacks reverse transcriptase.

Foster's detailed article suggests several alternative explanations, consistent with Darwinianism. Replication of Cairn's work has uncovered older work showing that non-dividing bacteria can produce mutations and if the non-dividing rate of mutation was increased 10 fold, by such mechanisms as slowed repairase function, this might account for the apparent sudden arrival of directed selection. Nonetheless, the ability to increase mutation overall rates is a version of directed selection, though much less exploitable clinically than the gene focused selection suggested by Cairns.

The job of reverse transcriptase in all retroviruses is to synthesize double-stranded DNA from the retrovirus' own single-stranded RNA genome.  This DNA double helix is then integrated into the host cell's chromosomes as a provirus. Transcription then leads to copies of the viral RNA genome, from which the virus's own proteins and enzymes are formed. New viral particles then bud from the membrane of the cell.  Thus, reverse transcriptase is essential for viral replication, becoming an important target for drugs against AIDS.

Retroviruses are considered to be "escaped" RNA that is part of our normal cellular machinery, but had to make it on it's own. They did, much to our misfortune. However, these normally occurring cellular reverse transcribing molecules, retrotransposons, retrons, have a physiological role to play...does that role include emergency reconfiguration of our hard disk--the DNA?

The existence of DNA repairase and polymerase also raise the possibility that our DNA is, in certain cases, a writable CD-RW, not just read only CD-R. The increasing realization of the importance of the "junk" DNA as critical regulatory areas that make complex choices on how to influence expression and the complex relationship of associated nuclear proteins and DNA make the possibility of intelligent DNA plasticity vs. fixed genetic determinism imaginable.

Freeman J. Dyson, a mathematical physicist better known as one of the architects of quantum electrodynamics, took a mid-career detour into theoretical biology that resulted in a thin volume titled Origins of Life. in this link Dyson, a famous physicist, looked at the possibility of a symbiosis of two critical components of life, a nucleic acid based replicating biochemistry and a structural protein based biochemistry that later became linked and specialized. He considered that these two forms of life have different evolutionary imperatives and for one, LaMarckian may have been common, particularly in the early stages of life's evolution.

LaMarckian thought also lives on electronically. Computer scientists use this kind of evolution as an algorithm to find solutions in complex systems in an attempt to model how life works, e.g., how various locomotion strategies, 2 legs, 4 legs, crawling, etc. developed.


2nd Dogma: Activation of DNA Repairase by Acupuncture or Consciousness

Except for the Y chromosome you have 2 versions of each gene. 1 version on the chromosome mom contributed and 1 on dad's chromosome. You can have 2 good genes, 1 good 1 bad, or 2 bad. (Bad is an oversimplification. Non-optimal for the current environment would be closer to accurate in most cases. But sometimes they are really just bad and non-functional.) If 1 of these chromosomes has a good wild type gene and 1 a bad, this is called a heterozygous polymorphism. In this case the 1 good gene makes up for the bad gene unless the system has been overstressed.

Perhaps, the better gene can be preferentially expressed?

But can a treatment improve the pathway if both copies are marginal or even dysfunctional bad genes? This is called a homozygous polymorphism. This problem seems much more difficult theoretically.

The notion of a DNA targeting and repair intelligence in living systems is consistent with well established systems of DNA repair systems. If we can use acupuncture to access and activate this kind of intelligent attempt at self-repair of genes then many things become possible.

We have some limited clinical evidence that suggests that the amazing possibility of self-directed gene splicing might be operating in this new acupuncture technique. We have seen a number of people who process folic acid slowly and require many thousands of micrograms of folic acid to use mass concentration to attempt to push a sluggish MTHFR enzyme to better efficiency by increasing the concentration of the substrates it must work on. Or if the enzyme is completely inactive you have to give a form of reduced folate that bypasses this gene and it's enzyme. Interestingly, in patients with the genetically poor versions of the gene and its sluggish enzyme the acupuncture treatment seems to improve ability to reduce folic acid. Perhaps we are just improving other related pathways, not the genetically compromised ones, but it is interesting.

Genetic screening for this folic acid problem is not a bad idea. If not addressed it can significantly increase the risk of cardiovascular disease, colon and breast cancer and depression. A good research project would be to take those who are genetically homozygous for the slow MTHFR enzyme and to use the biochemical correction acupuncture treatment. Then follow related markers like homocysteine and even repeat the genetic testing to see if the gene profile has changed, which would be unexpected, to say the least.

But the idea of cells de-differentiating into adult stem cells used to be heretical too. Dogmas are both very useful but when enshrined can create a fossilized technology. Questioning authority, while usually respecting it, is what a good scientist strives for. We used to have a minor assumption, a little dogma, that differentiation was a one way street. RO Becker proved that de-differentiation does happen. He really should have gotten a Nobel prize for that and his other work on regeneration. We now know that DC biocurrents, ions and chemical trophic factors can all induce dedifferentiation.

So if the need for folic acid is reduced does that mean that the gene repair mechanism is being accessed and the gene improved? Not necessarily. But if so is does raise the possibility we have a built-in self-directed intelligent mutation and splicing program, probably using an unknown class of messenger proteins, in conversation with a retro-virus type of protein which would have to link up with polymerase and repairase and be directed to the best candidate genes? It is a lot to have gone unnoticed, but not impossible. And if these are homozygous genetic polymorphism (mutations) then what is the healthy gene template for a more efficient enzyme? What is the intelligent biofeedback mechanism that tracks whether the mutation works, and if not, to go back to the drawing table? These are very exciting questions in Knowledge Based Medicine that are unlikely to be even considered in Industrial medicine.

The Mineral Vitamin Page has more on this subject.

From Wikipedia:

While Lamarckism has been discredited as an evolutionary influence for larger lifeforms, some scientists controversially argue that it can be observed among single celled organisms [2] . Whether such mutations are directed or not also remains a point of contention.

In 1988 John Cairns at the Radcliffe Infirmary in Oxford , England and a group of other scientists renewed the Lamarckian controversy (which by then had been a dead debate for many years) [3] . The group took a mutated strain of E. coli that was unable to consume the sugar lactose and placed it in an environment where lactose was the only food source. They observed over time that mutations occurred within the colony at a rate that suggested the bacteria were overcoming their handicap by altering their own genes. Cairns, among others, dubbed the process adaptive mutagenesis .

If bacteria that had overcome their own inability to consume lactose passed on this "learned" trait to future generations, it could be argued as a form of Lamarckism; though Cairns later chose to distance himself from such a position. [4] . More typically, it might be viewed as a form of ontogenic evolution .

There has been some research into Lamarckism and prions . A group of researchers, for example, discovered that in yeast cells containing a specific prion protein Sup35, the yeast were able to gain new genetic material , some of which gave them new abilities such as resistance to a particular herbicide . When the researchers mated the yeast cells with cells not containing the prion, the trait reappeared in some of the resulting offspring , indicating that some information indeed was passed down, though whether or not the information is genetic is debatable: trace prion amounts in the cells may be passed to their offspring, giving the appearance of a new genetic trait where there is none. [5]

Finally, there is growing evidence that cells can activate low-fidelity DNA polymerases in times of stress to induce mutations. While this does not directly confer advantage to the organism on the organismal level, it makes sense at the gene-evolution level. While the acquisition of new genetic traits is random, and selection remains Darwinian, the active process of identifying the necessity to mutate is considered to be Lamarckian.

Other voices in the controversy:

Donald G. MacPhee 1 and Mark Ambrose 1


School of Microbiology, La Trobe University, 3083 Bundoora, Victoria, Australia

Received: 16 February 1995   Accepted: 19 April 1995  

Abstract   Several investigators have recently reported that significant numbers of appropriately adapted mutants can be induced in bacterial and yeast strains by exposing stationary phase cells to specific environmental challenges. The resulting mutants are said to be both selection-induced and demonstrably non-random in origin; if this interpretation is correct, it is in direct conflict with the conventional neo-Darwinian view, which is that spontaneous mutants are truly random in origin and arise without the intervention of any overtly adaptive forces. We believe that there are alternative ways of accounting for the appearance of many (and probably all) of the additional mutants which proponents of the adaptive mutation theory claim are observed only after they applied the appropriate selective pressure. Having reviewed the available evidence, we consider that most (if not all) of the sorts of mutants which are said to have been induced following exposure of stationary-phase cells to intense selective pressure are equally likely to have been generated during the operation of certain well-known, conventional (and essentially random) cellular DNA repair processes. Evidence in support of our view can be found in the mainstream literature on the origins of spontaneous mutations. We also note that some of the molecular models which have recently been proposed to explain the production of selection-induced mutations preferentially (or even only) in genes of adaptive significance may turn out to be of considerable interest in their own right, even although the mutants whose origins they were intended to explain may turn out to have arisen in a manner which is totally independent of the conditions used for their selection.

Key words   adapti

Michael C. White, Daniel B. Marin, Deborah V. Brazeal and William H. Friedman

Abstract   There has been much debate in the managementliterature between neo-Darwinists (who believe in thenatural selection of populations of organizations) andadaptationists (who contend that changes in organization structure and behavior occur in response to theenvironment). The general thesis of neo-Darwinism isthat species are blindly selected for survival by theenvironment. The latest empirical support for the dominant neo-Darwinism perspective adopted bymost biologists is based primarily on the experimentsconducted by Salvador Luria who claims to haveconclusively demonstrated that genes mutate randomly.Recently, however, biologists have re-examined Luria sresearch methods and, after replications of hisexperiments, now question some aspects of the validityof his results. Moreover, there is now new researchwhich provides support for the earlier adaptationistposition, namely, the existence of evolutionary driversand directors existing within self-organizing systems.Of particular importance to the present study is the experimental indication thatself-organizing systems play a conscious role in theirown evolution. We propose that similar mechanisms orprocesses operate in organizational adaptation, thuspointing toward a theoretical modification ofneo-Darwinism that embraces both adaptation and naturalselection in a general, unified theory.