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The quintessential work of Charles Darwin, On the Origin of Species, wasn’t first among evolutionary theories

Evolutionary Theories and Charles Darwin On the Origin of Species
When most individuals think about evolutionary theories, Charles Darwin’s On the Origin of Species often comes first to mind. His insightful analysis of evolution through natural selection and descent by gradual modification has dominated our debate since his publication of On the Origin of Species in 1859. However, multiple alternatives continue to be debated 
  and there were theories of evolution before his time. Among these was a one advanced by Jean-Baptiste Lamarck in the early nineteenth century. He proposed that individuals can gain or lose capacities based on their advantageous use or lack of use. Therefore, individuals can inherit features from their ancestors based on their pattern of use. Examples that are often presented include giraffes stretching their necks to reach leaves thus imparting slightly longer necks to their offspring. In this way, it was contended that changes in the environment can yield gradual changes in individual organisms based on that pattern of their respective use or disuse of capacities.

Another theory, Uniformitarianism, was propounded by Charles Lyell between 1830 and 1833. He asserted that the laws of nature are constant and immutable over time and space and that such laws could be identified and would account for evolution.

New theories abounded after Darwin, too. In 1893 William Haacke and the zoologist Theodor Eimer espoused Orthogenesis. They generally conceived of evolution as moving forward in a straight line and held to a regular course by non-random forces that are internal to the structure of organisms. These internal factors essentially propel an organism forward developmentally and selection is limited in scope.

The Vitalists in the early 20th Century proposed that evolution was driven by the fact that living organisms are fundamentally different from inanimate ones as they are imbued with an intrinsic ‘vital spark’ or energy. This was not a new idea and, in fact, it was an ancient doctrine that had been believed by many great scientists including Louis Pasteur. However, this concept was eclipsed by the rediscovery in 1900, by Hugo De Vries and Carl Correns, of the critical work previously done by Gregor Mendel, an Austrian friar and scientist who is considered the father of classical genetics. He had discovered by working with garden peas that the result of a cross between peas of different colors was not only a blend, but also yielded offspring of both separate colors in predictable ratios. He conceived of the concept of heredity units, which he called “factors” and were later called genes.

The rediscovery of Mendel’s work in genetics led to a variety of new proposals and theories and a division in perspective that this reverberates today. One school of theory favored viewing evolutionary development as primarily proceeding by large mutations or jumps, called Saltationism. Another opposing school, the Biometric school, advocated that variation was continuous and gradual in most organisms and favored a mathematical and statistical approach. Both were attempting to unite Darwinism with genetics and it is this latter approach that is embodied in what is termed the Modern Evolutionary Synthesis or current Neo-Darwinism.

The development of population genetics as the study of genetic variation and gene distribution in populations under the influence of natural selection was pioneered by Fisher, Haldane, and Wright. Their work was fundamental in establishing many of the underlying principles of Neo-Darwinism. The Williams Revolution of the mid 1960s shifted thinking from population genetics models to natural selection via kin selection. In this model, the gene is the fundamental unit of self-preservation either by acting to protect and preserve itself or closely related genes. This was expanded by Richard Dawkins who popularized the concept of the “selfish gene,” a gene centered view of evolution with selection acting on the genes themselves and not only on organisms or populations. In this view, we are just genetic vessels or carriers.
Contemporaneous to Dawkins, the concept of endosymbiosis was widely popularized by Lynn Margulis in the 1970s although it had been proposed decades earlier. The underlying theme of ‘endosymbiotic theory’ as formulated as early as the late 1960s was that the evolution of eukaryotic cells (cells with complex structures enclosed by membranes) over millions of years was enacted by the interdependence and cooperative existence of multiple prokaryotic organisms engulfing and incorporating one another. Although originally dismissed as a fringe concept, it is now recognized as the key method by which some organelles have arisen.

More recently, Eugene Rosenberg and Ilana Zilber-Rosenberg presented research advancing the concept that the object of natural selection on genomes is not solely on the individual and its central genome but on the combination of a ‘host’ organism and the entire symbiotic community with which it is associated. From this concept of the hologenome, originally conceived by Richard Jefferson, an entirely robust and alternative narrative of evolution can be offered, Hologenomic Evolution Theory. In this theory, evolutionary development builds upon cellular interactions governed by immunological rules. Natural selection remains an important factor but is displaced from its central role.

Spread of Infectious Disease a Consequence of Climate Change

Spread of Infectious Disease a Consequence of Climate Change
This article originally appeared at

The single most pressing consequence of climate change, whether global or localized, will be in the shifting patterns and spread of infectious disease. Substantial alterations in temperature and humidity can directly relate to the distribution and 
virulence of many microbial pathogens, no matter the underlying cause. This correlates with the rich complexity and diversity of all ecologies in which pathogens thrive. So shifts in the distribution of vegetation, the dispersal and range of animal predators or their prey, or distortions in the variety, concentration or specific strains of vectoring insects or other disease-carrying organisms can all influence the transmission of pathogens or their relative abundance.

Many researchers believe that this effect can be currently observed. For example, malaria[1] spreading to the highlands in Africa and the northward spread of West Nile Virus[2] in the United States has been linked to the changing distribution of disease-carrying mosquitoes relating to climate change. So, too, have shifts in the spread of dengue fever[3] in endemic areas.

A wide range of diseases are zoonotic in etiology so a shifting climate may enhance the likelihood of that cross-transmission or its virulence. There is evidence for just this type of consequential shifting pattern. Ecological variation has been ongoing over earth’s history, and that of man’s time on earth. Humans have been both victims of pathogens and carriers. For example, the loss of the North American large mammals like the woolly mammoth and saber-toothed tiger has been correlated by some researchers to a phenomenon termed hyperdisease[4]. In that instance, humans as carriers or our traveling companions, such as hunting dogs or domesticated animals, are thought to have introduced new pathogens or more virulent ones to an unprepared environment.

How then should this affect our global response to climate issues? It must begin with increasing awareness among climate scientists and physicians. However, there should also be a redirection of scant available resources from unproved expensive projects of carbon capture and sequestration to productive research studying the patterns of communicable disease. This might mean evaluating and implementing better means of mosquito, tic, and rat control; sharpening our tracking of current patterns of communicable diseases; and aggressive research into improved prevention or therapies. All would yield substantial benefits with certainty, whether a shifting climate is consequential now or in the future.
–Bill Miller, MD

1.    Bouma MJ, van der Kaay HJ. The El Niño Southern Oscillation and the historic malaria epidemics on the Indian subcontinent and Sri Lanka: An early warning system for future epidemics? Trop Med Int Health 1996;1:86-96.
2.    Morin CW, Comrie AC. Regional and seasonal response of a West Nile virus vector to climate change. Proc Natl Acad Sci USA 2013;110:15620-15625.
3.    Hales S, de Wet Neil, Maindonald J, et al. Potential effect of population and climate changes on global distribution of dengue fever: An empirical model. Lancet 2002;360:830-834.
4.    MacPhee RDE, Marx PA. Lightning strikes twice: Blitzkrieg, hyperdisease, and global explanations of the late quaternary catastrophic extinctions. American Museum of Natural History. Accessed 13 June 2014.


Extinctions and Pathogenesis

A recent article in LiveScience proclaims that ‘Microbes may have caused Earth’s biggest extinction’. The findings are part of a new study in the Proceedings of the National Academy of Science, ‘Methanogenic burst in the end-Permian carbon cycle’. The authors believe that there was a rapid burst of microbial activity triggered by massive volcanism in the end-Permian period that released enormous amounts of methane into the atmosphere.

A cataclysmic extinction event resulted 252 million years ago that is estimated to have killed as much as 90% of life on the planet over the course of approximately 20,000 years.Their conclusions are based on recent research suggesting that a surge of carbon dioxide levels in the atmosphere dates to the end-Permian extinction occurring in the same geologic interval as unusually large volcanic eruptions. The authors offer that the rapidity of the rise of atmospheric carbon dioxide and linked decreased oxygen levels imply a biologic origin for these climatic shifts. Their contention is that this extinction event is directly related to a horizontal transfer of genetic material from a cellulolytic bacterium to a unicellular microbe capable of producing methane and promoting the efficient degradation of organic carbon. This genetic transfer resulted in the expansion of a novel microbial metabolic pathway accelerating the metabolism of acetate as a major growth substrate in methane production. Basically, methane producing microbes, the last common ancestor of Methanosarcina, enabled the rapid conversion of carbon dioxide by other microbes that in turn diminished oxygen in the atmosphere. As a result of these rapid deviations, life across a wide spectrum was extirpated.

Furthermore, it is known that the metabolic activity of methanogenic microbes is limited by the
availability of nickel. The researchers analysed nickel deposits in South China sediments identifying a significant increase in nickel concentrations just before the end-Permian extinction, also presumed due to volcanic action. This catalysed the acceleration of the methanogenic disruption of the carbon cycle and contributed to acidification of the oceans and marine anoxia accounting then for the fact that 70% of marine life was also extinguished. Furthermore, they note that “anaerobic methane oxidation may have increased sulfide levels, possibly resulting in a toxic release of hydrogen sulfide to the atmosphere, causing extinctions on land.”

Certainly, any research that implicates microbial activity as a proximate cause of extinctions is welcomed when all complex organic life is understood to be hologenomic in nature. Yet, it is striking that a prejudice remains among scientists in paleontology, earth and planetary research and atmospheric sciences to disregard direct microbial pathogenesis in their considerations for causes for extinction. For example, Douglas Erwin in his excellent book, ‘Extinction’, from 2006, discusses possible causes of mass extinctions at length including extraterrestrial impacts, climatic aftermath of massive volcanic flood basalts in Siberia, climate change, glaciation and climatic cooling, oxygen depletion, and a Murder on the Orient Express hypothesis suggesting multiple interactions of a variety of these factors. But there is no mention of infection, parasitism, or epidemic pathogenesis. Even now with this report, …. microbes are implicated, certainly. But the described microbial effect is indirect and atmospheric and not related to infectious pathogenesis. Certainly, this is odd when considered within the framework of our own existence in which infectious pathogenic assault governs our lives, from conception to death.

Of course, this scientific blind spot is related to unfamiliarity with infectious pathogenesis in most fields of study rather than from the absence of abundant examples that would demonstrate the power of episodic epidemic disease to decimate populations. Even now, there are readily observable examples of the effectiveness of pathogenesis in initiating or accelerating extinction events. For example, Chytridomycosis is devastating amphibian populations worldwide and 120 species have vanished since 1980. Importantly, this is occurring in relatively pristine environments as well as those deemed environmentally challenged. Bee populations in multiple regions are in critical decline from colony collapse disorder. The culprit is a pathogenic virus, DWV, due to infestation with Varroa destuctor mite. This has spread from Asia across the entire world over the past 50 years. In the plant world, a soil fungus, Fusarium oxysporum, has been identified as the causative agent in Panama disease, an affliction that attacks the roots of banana plants and causes a widespread devastating wilt that is not contained by known fungicides. It need not take 20,000 years when the operative agent is anefficient predator, which is exactly what any pathogenic microbe is. Importantly, infectious pathogenesis is an agency in which wide effects are expected since pathogenic vectors can be spread by movement of carrier organisms, wind, or waves. It is time to accede that a common and readily observable phenomenon capable of undergoing episodic periods of distinctive amplification could
afflict a wide spectrum of species in concert rather isolated populations as is observed today. After all, this kind of cyclicity is the hallmark of all biologic processes.

An important additional component in extinctions is a phenomenon known as the Allee effect. This recognizes that the patterns of response of a population to the stress of disease critically changes when the constituency declines below identifiable index levels. Barriers against infectious virulence are not constant and can dynamically adjust based on population size and communal immunological diversity. This should be a prime lesson for all extinction theorists. Extinction theory cannot be disembodied from a thorough understanding of pathogenesis, the hologenomic nature of all complex organisms, and a willingness to examine the history of our planet based on the immensely broad cycles as they relate to infectious pathogenesis. To do otherwise is fundamentally flawed. Infectious pathogenesis should be the final common denominator of all mass extinctions, no matter which physical factors may accelerate its scope and toll. It alone is omnipresent and ubiquitous on this planet. Only it can account for the idiosyncratic mixture of life extinguished and spared by virtue of episodic waves of assault of novel microbes on populations and species of differing susceptibilities.

There is an inviolable dynamic on our planet. A relentless microbial realm is engaged in a complex immunological competition with the cellular homeostasis of complex holobionts. Unless this interplay is thoroughly considered, there can be no successful explanation for either localized extinctions or those capable of quelling life across our planet. In the final analysis, mass extinctions must encompass and embrace immunological interactions as a final common denominator. After all, is this not the world in which we all dwell?


‘Termite’ Robots Illuminate cellular engineering

Insight into biologic processes can sometimes be gleaned from unexpected sources.Harvard University researchers have designed and programmed a group of tiny robots to mimic the basic building strategies of termites. The robots are equipped with sensors and can assess their surroundings and collaborate through an innovative technique modeled on swarm intelligence.


Lee Hotz in the Wall Street Journal (Feb. 14, 2014) quotes Justin Werfel, a staff scientist at the Wyss Institute for Biologically Inspired Engineering at Harvard University, “Every robot acts independently, but together they will end up building what you want”.

The experiment demonstrated that the robot swarm can build a variety of shaped structures such as castles and pyramids out of foam bricks. Each individual robot can autonomously build staircases to reach the higher levels of these structures. Simple programming rules permit forward, backward, up and down motion. Each robot can also sense the individual bricks that it carries and also the presence of nearby robots. Relatively complex structures can be constructed since the robots are smarter as a group than they are individually, and can recognize and correct some mistakes.

Although the design of this experiment was inspired by termites, the scientists might just as well have done their modeling utilizing cellular dynamics. Individual cells, too, act independently yet collaborate by using their own sensory apparatuses. Cells are aware of their surroundings, their cellular neighbors and even cells at a distance via sophisticated sensing and communication mechanism. These robots were programmed to follow very limited rules that allowed them to “respond to conditions around them and to each other.” 

Cells are easily capable of the same range of responses. Indeed, the rules for cells, just as for real termites, are not exclusively straightforward nor as limited as in this experiment. Their awareness is much more sophisticated and extends beyond their immediate surroundings. However this experiment, even though limited, demonstrates that collaboration based only upon simple rules and basic sensory awareness can enable complex engineering of structures totally unrelated to the design of the originating individuals units. There need be no organizing principle beyond rudimentary rules of interaction. Therefore, it can be appreciated that in the biologic realm, complexity can be the yield of this sort of uncomplicated collaboration and it is reasonable to assume that natural systems would respond in the same manner. As Steven Johnson has said and this experiment elaborates, “ It is not the network itself that is smart; it’s that the individuals get smarter because they are connected to the network.” This is just as true for cells as it is for termites and humans. 

Indirectly then, the analogous power of natural genetic and cellular engineering by genetic aggregates and individual cells with limited awareness to create complex local environments is illustrated. That would be so even if cellular capacities were quite proscribed or comparable to the elementary rules devised by the researchers instead of the vastly broader and deeper capabilities that they possess. Constrained as these robots were, they were still able to build complex structures. Why would we doubt the correlative capacity of aware, linked and co-dependent cells to engineer biological results according to their own preferences, needs and limits? Nor should it be difficult to accept that all complex creatures have evolved and were elaborated by this same process, no different in kind than illustrated by this experiment. 

Collaboration, repeated at every level and at every scale, represents the fundamental process by which all the current biologic endpoints on this planet have been reached ………as hologenomic organisms. Every complex creature on this planet is one. There are no exceptions. Nor could there be if the fundamental pattern of evolutionary development is based on collaborative biological engineering across a broad spectrum of cells, each intent on serving its own aims but capable of working cooperatively to achieve those goals. Indirectly then, this experiment elegantly illuminates the inherent power of natural genetic and cellular engineering in biological processes. Our biological world is based on a system of collaboration and competition through cellular awareness, preference, and intentionality. Even limited as it must be solely to its microscopic scope and scale, its outputs are the wondrous creatures we see all around us.