Are You Smarter Than a Reptile?

                                                              William B. Miller, Jr. M.D.

Are you smarter than a reptile? In many respects, you certainly are. After all, no reptile is going to read this article. However, our clearly superior intellectual abilities for certain skills has seduced us towards a dismissive attitude towards the surprisingly deep and broad range of analytical gifts of our companion creatures. A growing body of research now indicates that other animals of all sizes and varieties are highly intelligent problem solvers within their own realms. After all, their cognitive skills have enabled them to successfully survive for eons and that may not necessarily prove to be true of we humans. Consider termites. They are strikingly social animals and have constructed elaborate societies for 200 million years. They engage in a primitive sort of agriculture, farming varieties of fungus for food. As individuals, they demonstrate remarkable intelligence and an even more surprising group intelligence that enables complicated feats of soil engineering in a diverse range of environments. Within their complex societal structure, termites divide labor between varied types of specialized workers, for example, infant care, manual labor, reproduction or soldiers for the defense of the colony. All of this proceeds via highly evolved and complex patterns of communication and signaling.Individual bees are intelligent and can even solve problems that are mathematically based. For example, they effectively decide the Traveling Salesman dilemma of optimizing the most efficient route to visit large numbers of locations in a single day. Bees communicate in a rich symbolic non-verbal language that enables them to transmit abstract concepts to others such as the location of particular flowers over large distances based on angles of the sun. They even seem to understand some rudimentary concepts of medical care utilizing medications within their hives. For example, honeybees colonies have been demonstrated to self medicate with plant resin to combat fungal infections. What about ants. They’re no slouches. They can navigate long distances to find food and can communicate its location to others with facility. As individuals, they can seek family members, memorize multiple alternate locations and can integrate a large number sources of information. They are even altruistic and will help other ants in distress. Modern research is teaching that intelligence is not directly linked to brain volume. All sizes can be demonstrate high intelligence. Birds have small brains but are terrific problem solvers. They are highly cooperative and exhibit a wide range of highly intelligent behaviors. For example, they use vocal learning. Their songs are a complex language. Did you realize that they give lifelong names to their young? They are even known to mourn the loss of others. Birds also have a gyroscopic sense of geography and can store seeds in thousands of places that they can remember. Can we do that? Perhaps you suppose that only humans are capable of understanding analogies. However, crows can use analogies to solve higher order tasks. They understand sharing, can use rudimentary arithmetic and can invent meanings for words. Cockatoos can solve puzzles with at least 5 steps. They can even keep time to music.So perhaps lizards aren’t smart. How unfair if you think so. Lizards are social animals with rich societies and hierarchies. They can bond, recognize family members, and care for children. Some iguanas demonstrate counting abilities and can rapidly learn techniques that they haven’t seen in the wild.Might fish be intellectually impaired? In fact, fish lead complex social lives and are highly intelligent. Predator fish species can cooperate together and even with other species by utilizing head motions and posturing to cooperate to capture elusive prey. They understand concepts of negotiated agreements of partnership and, just like humans, sometimes cheat. In a comparison of the intellectual capacity of primates and fish, who do you think should win? In a food test comparing fish with monkeys, chimpanzees and orangutans, it was the fish that proved more adept at learning the advantages of certain patterns of food choices and were faster at it. And individual fish have personalities. Timid ones stay timid and aggressive ones remain bold. They also demonstrate individually distinguishable levels of curiosity and social ability. Fish can play, have excellent memories and perform complex courtship rituals. And Tusk fish even use tools to open shells for food, an act of intellect which used to be considered as exclusive to humans but is now known to be widely distributed among species. Certainly then, we must be much smarter than microbes. However, if intelligence is construed as using information to solve problems to successfully reproduce and survive in hostile environments, then they might be considered among the most intelligent. Some bacterial strains and even some viruses have survived essentially unchanged in any significant manner for hundreds of millions of years, in part this by using elaborate signaling patterns for communication among themselves and others. So what might we make of this widely distributed world wide intelligence than had been previously understood? First, our intelligence might be of a unique kind, but it is not the only intelligence of consequence on this planet. Ours is just different and suited to the types of problems that we need to solve. We have vastly underestimated the intelligence, feelings and complexity of the inner lives of our companion creatures on this planet. The implications are profound for our relationship towards them and our stewardship of the planet we share. Additionally, the ubiquity of refined intelligence requires a thorough re-examination of our evolutionary narrative. Intelligence exists at every scope and scale underscores every aspect of evolutionary development. This emerging understanding teaches us that all cognitive ability starts at the cellular level. All complex creatures must in turn be viewed as integrated collections of intelligent cells,……..vast collaboratives of cellular intelligence, …. we in our human package, and they in theirs. Our form of collective intelligence may be privileged compared to others, but it is not different in its essence. As a species, we would do well to grasp this vital truth.

Dr. Bill Miller

The outbreak of Ebola will not be the last global epidemic. I recently was interviewed by Jeanine Prezioso of Reuters concerning this subject. The original article appeared here — http://blogs.reuters.com/global-markets-forum/2014/10/23/ebola-will-not-be-the-last-global-epidemic-time-to-hit-the-reset-button-on-how-we-treat-it-physician/.

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Ebola will not be the last global epidemic. It is, however, the first to spread as we hop on planes, rely on oil and chocolate from far flung locales and blindly lean on modern medicine’s ability to control and kill the very pathogens that live among us.

Now is the time to hit the reset button on our approach to viral outbreaks. While it’s taken health agencies, drug makers and the public-at-large time to wake up to the current spread of the deadly virus in Africa, there’s no time like the present to prepare for the next outbreak, Dr. Bill Miller, a physician and author of “The Microcosm Within: Evolution and Extinction in the Hologenome” said in an interview on Thursday.

A hologenome is essentially an organism’s sum of its parts, a combination of its cells and all the microbes (bacteria and viruses) that live within it. It’s the bacteria in your gut that helps your body break down food and the cold virus that makes you sick.

Ebola is just another microbe in a long list of those that seek to destroy its host, Miller says. His theories are a challenge to die-hard Darwinists, who, in turn, have challenged him. He has studied the intersection between immunology and infectious disease and says “our evolutionary narrative is different from Darwinian natural selection alone.”

Ebola, meanwhile, is thinning out the population in three West African nations. The U.N. World Health Organization’s (WHO) latest figures on Wednesday showed at least 4,877 people out of 9,936 confirmed cases have died in the outbreak in Liberia, Sierra Leone and Guinea. By many accounts those numbers may be conservative.

“The the single most important element of our health and success as individuals and species is how we cope with infectious diseases,” Miller told the Global Markets Forum. “Quarantine and isolation are really the only tools we have to deal with a pathogen such as Ebola since there is no generally available treatment other than supportive care and no vaccine.”

A lack of trained and available doctors to treat the infected at the virus’s epicenter and contain it is a big issue. Healthcare workers in contact with patients who have the virus run a higher risk of catching it. A doctor who returned to New York after treating Ebola-infected patients in Guinea was rushed to the hospital on Thursday with symptoms of the virus and tested positive for it later in the day.

Thomas Eric Duncan, who was visiting the U.S. from Liberia last month, was diagnosed with the virus in Dallas, Texas, and died earlier this month. A small outbreak in Nigeria was contained and a nurse in Spain was cured of the virus. The U.S. imposed screenings at major airports and six people who recently arrived to Connecticut from West Africa have been placed under quarantine.

Ebola is not known to spread in an airborne manner between humans, Miller said. It is “never impossible but very unlikely”. Miller’s recommendations for containing the outbreak are not far off from the protocols health and government officials have already put in place, i.e. setting up a team of infectious disease experts to assess individual cases. Also on hand should be a “core of highly trained individuals to come into any discrete area,” he said.

Miller called on researchers to speed up the study of the patterns of the disease and to streamline vaccine research. Big pharmaceutical companies are in the process of developing vaccines but want protection from legal entanglements. On Friday, the WHO said it expects to have 200,000 doses of Ebola vaccine available by the middle of next year.

“In the end, it is likely the big drug makers will be the ones that come out ahead. They have the budgets to do the expensive research, and they can buy any of the small ones that are initial leaders that succeed despite the odds,” he said.

All epidemics eventually burn out, Miller added.

“One day, this Ebola outbreak will just be a notation in the history books. And likely not nearly the most consequential, that is unless we exercise some foresight and this becomes that moment when a global partnership in common stewardship and joint need eventuates and we go forward with a very much improved international system.”

What produces biological complexity, novelty or impels the origin of species? When examined through all available contemporary evidence, the expression of novel phenotype and metabolic function emerges from processes other than natural selection and fitness as they have been traditionally assessed.

To best understand this issue, it is useful to closely consider a facet that is often overlooked in general discussions of evolutionary development. The case for natural selection dominating in evolutionary development can only be sustained if it is concomitantly presumed that variation is only random. In the circumstance in which organic variation is simply random, then abundant changes to a reproductive entity can be consistent with a path that builds alternative organic outcomes. Yet, even in this particular case, there would be no necessity for increasing complexity or useful novelty, since a random mechanism might just as easily go off in any direction. The barriers are obvious. Hence, an entire assembly of addenda to natural selection theory such as sexual selection mechanisms has been advanced to try to rescue Darwinism from this conundrum.

Once it is perceived that evolution is not entirely random and perhaps not even fundamentally so, then the centrality of natural selection is displaced. Clearly, if evolution is subject to any non-random agency, it is that explicit process that becomes the proximate force and dominant agency in evolution and supplants natural selection. It really is that simple. A direct choice is required; random or not? If evolution is non-random to any extent, then natural selection is simply a participatory agency within a more encompassing process.

Hologenomic evolution theory asserts that evolution is subject to both random and non-random forces. The non-random aspects relate to the activity of cells that are aware within their scope and scale. This faculty energizes cellular and genetic engineering as a non-random set of complex reactions to environmental influences through cell-cell interactions. These relationships build in intricate layers of both genetic and non-genic interchange, thereby enacting complexity and novel solutions to environmental stresses through collaborative, cooperative and competitive cellular networks.  Speciation emanates from these same cellular interchanges as immunological events that separate one set of cellular networks from another. Immunology ultimately governs all cellular relationships and it is these immunological factors that separate differing cellular ecologies from one another from which new species can emerge.

Natural selection acts precisely at the initiation of novel cellular expression from inter-cellular processes and genetic interchanges. At that moment, natural selection acts implacably to assure that only the ‘fit enough to survive’ do so. Importantly though, it acts specifically at the immunological level first, and the phenotypic level after. After all, reproduction is itself an immunological event and all inter-cellular exchanges are governed by immunological rules.

Thus, natural selection does not drive speciation, complexity or novelty. It acts instead as a filter of biologic outcomes as new species aggregates emerge through both random and non-random cellular interactions.  It also acts to maintain any species once present in its attempt to successfully react to an ever-changing environment by encouraging the expression of phenotypic variety from within an underlying capacious genome. All complex organisms are expressions of this coordinated cellular activity. It is innate cellular awareness that enables complex networks of co-linked and collaborative cellular ecologies. Hologenomic organisms are their product. All complex organisms on this planet are hologenomes. There are no exceptions. There are non-random reasons for it.

Darwinism has always been bedeviled by same sex attraction. Evidence indicates that this trait is genetically rooted. Yet, if same sex attraction remains eternally common, how can it still resist being expunged by natural selection? Few traits can be regarded as more likely to govern reproductive frequency than same sex attraction. However, it is certainly known that this trait is widely distributed in the animal kingdom exhibited by mammals, fish, lizards, birds and insects. For humans, Richard Dawkins struggles to make sense of this within Darwinism. He offers three potential answers.

The ‘gay uncle’ theory

He proposes that a homosexual male in a hunter-gather society would be
preferentially entrusted to watch over the children of non-homosexual men. That
individual would then have protected and nurtured children any of whom might have
had a genetic predisposition to same sex attraction. In this manner, the genetic trait is
shielded and passed on. However, if the homosexual male is not himself reproducing in
this theory, the trait clearly still yields a selective disadvantage for homosexual
individuals.

The ‘lull the suspicions’ theory

In this instance, the homosexual male was entrusted by heterosexual men to be
a safe choice to stay home with women while the dominant heterosexual males went
off to hunt or fight. So according to Dawkins, this is a stealthy ploy whereby
homosexual or bisexual men gain surreptitious sexual access to women, mate with
them and pass on their genes. Not only is this fanciful on any thoughtful consideration,
but also makes the larger unfounded assumption that homosexual men are conditionally
attracted to women and further, are innately less aggressive than heterosexual men and
thereby less ‘manly’. Further, it makes the unwarranted assumption that bisexuality and
homosexuality are in some manner necessarily united.

The ‘social construct’ theory

Dawkins proposes that a ‘gay’ gene expresses itself differently under different
social circumstances. For example, a gay gene might be more expressed in urban than
rural environments. So, in accordance with this theory, the expression of same sex
tendency relates to social construct and environmental factors. Although it is clear that
epigenetic factors do definitively matter in evolution, a study from Vietnam in 2008
compared the differences in prevalence and practices of homosexual men in urban and
rural areas. This study concluded that there was a measurable difference in the
frequency of same sex intercourse but no change in the number of individuals engaged
in that activity. There is therefore no objective evidence to support this theory. Indeed,
if someone were inclined to agree, then inadvertent justification would be lent to those
who feel that same sex attraction can be mediated by intervention. Certainly, it would
be supposed that this is the opposite of Dawkins’ intent.

Instead, it would be reasonable to look elsewhere beyond natural selection theory to
explain same sex attraction. This is an exact power of hologenomic evolution theory. In
the hologenome, same sex attraction is assumed to be a conserved core process just as
many others are known to be. In the cellular world from which we are all descended,
asexual reproduction is commonplace. Some animals are unisexual. For example, all
rotifers are female, and there are other examples in the animal kingdom of unisexual
reproduction. So within hologenomic evolution theory, the continued incidence of same
sex attraction is simply an example of the dominant cellular imperative to preserve
what has always occurred. A trait exhibited as an essential element of our cellular
ancestors is brought forward through time and exhibits its effects within organisms as
they are eventually constituted. This is a scientifically realistic mechanism to explain
the persistence of same sex attraction. None of Dawkins’ theories based on natural
selection plausibly do so.

The Ebola Outbreak and Global Epidemics

The agitating Ebola outbreak has captured headlines. There are some who undoubtedly assume that this kind of epidemic is unusual. However, epidemic disease has always been a part of our biological system. Pandemics or the form of infectious disease that can spread across a continent or even the entire world are ancient processes too.

As the Ebola outbreak demonstrates, we humans have an extensive acquaintance with global epidemics and pandemics. Many of these infectious diseases occurred long before the modern era with its current ease of global travel or any concerns about a changing climate. Our written record of epidemics can be traced as far back as the Ten Plagues of Egypt which devastated livestock and humans. This experience is chronicled in Exodus 9:9, “ It will become fine dust over the whole land of Egypt, and festering boils will break out on men and animals throughout the land”. In the First Book of Samuel in the Old Testament, there is a vivid description of a lethal outbreak of ‘groin tumours’ in the Philistines, which was noted to occur in the presence of rats. This is possibly an early description of bubonic plague or tularemia associated with rodents. In the Middle Ages, there are extensive and graphic descriptions of the pandemic spread of bubonic plague in Europe and Asia that occurred in successive waves.

In more recent history, during the First World War in the fall of 1918, influenza ravaged populations worldwide accounting for an estimated 20-40 million deaths. It moved with astounding speed and at such a pace that more American troops died of influenza than in battle. Although there had been mild outbreaks of influenza in the spring of 1918, few deaths had occurred. However, within a short interval, a new strain of influenza virus emerged that was incredibly lethal. Uncontrollable hemorrhage into the lungs often lead to death within hours of the onset of symptoms. This pandemic was so sudden and unprecedented, and it exerted its worldwide effect with such fury, that a state of panic and chaos was experienced by many communities across the globe. Fatalities were not confined to the very young, elderly and infirm as is the typical distribution for influenza. Instead, it disproportionately attacked young adults and the previously healthy. This reversed the normal pattern of mortality so that its impact on the infrastructure of society had critical socioeconomic reverberations.

Now Ebola has raised global alarm. Although the spread of Ebola does not appear to follow the same mode of transmission as influenza, there are certain commonalities among any of the diseases that are currently considered to have the potential for world wide spread. Both influenza and Ebola are zoonoses, just like the viruses that spread HIV, SARS (Severe Acute Respiratory Syndrome), MERS (Middle East Respiratory Syndrome), or West Nile Virus. A zoonosis is an infection spread from one species to another, from animals to man or from man to another animal. The majority of human pathogens are zoonotic and nearly all the emerging diseases are caused by zoonotic pathogens.

Our human activities are crucial to its incidence and spread. We interact with other animals by hunting across a broad range and consuming a great variety of other species for food. We are eager travelers and keep diverse pets that often accompany us as we wander. Modern technology has dramatically changed our speed and ability to travel the globe and even inhabit inhospitable climates. Consequently, we may inadvertently introduce a new pest to a pristine environment. We, as humans, are not merely the victims of disease but an important carrier of an immense amount of microbial life and may inadvertently introduce novel pathogens to other animals through our actions.

As a result, relatively obscure diseases are now being granted a larger global range. Once a new disease emerges outside of its prior range, our cultural traditions can have a crucial impact on its dissemination. Societies can react idiosyncratically to vaccination programs, have long standing burial rituals, or access to vastly different health resources. Stigmatization of the ill, traditional health practices in some cultures, handling of wastes and secretions, perceptions of individual rights, or acceptance of an imperative to quarantine can widely differ between cultures.

Despite such disparities, the current Ebola outbreak renders a unique opportunity. Disease recognizes no boundaries of class distinction, ethnicity, language, race, or religion. If properly understood, this tragic epidemic is a gateway to a crucial international dialogue. A global action plan should be swiftly formulated and implemented based on our experiences with this current tragedy.

What might such actions be?

There are existing health agencies with crucial expertise that can be strengthened, such as the World Health Organization, the National Institutes of Health or Centers for Disease Control. Heightened worldwide coordination of similar agencies is imperative and funding must be significantly increased.

A dedicated team of recognized international experts should be formed as a ready response team in preparation for the next outbreak since there will always be another.
Resources and research must be devoted to studying the patterns of communicable disease and improving assessment tools. The search for vaccines and other cures must be markedly accelerated.

New methods to restrict populations of mosquitoes, tics, other insect vectors or rodents must be extensively implemented on a global scale. These inexpensive measures would have an immediate and consequential impact on worldwide disease burden.

A global effort to educate leaders and populations about infectious disease control and precautions must be started immediately. Overcoming cultural impediments will take time and patient instruction.
It is certainly realistic to ask where the money for such programs will come from and how might such cooperation be organized?

Our world wide discussions about climate change offers one model. Expensive responses to that peril are urged but it is uncertain whether any such measures will realistically affect climate trends. However, no matter the cause of a changing climate or its time line, its ultimate effect on our own human experience will be most dramatically experienced by a changing pattern of infectious disease. Even now, there are currently observable examples. There has been a notable shift in distribution of malaria in Africa and Asia and a northward migration of West Nile Virus in the US. Previously rare infections apart from Ebola are extending beyond their prior endemic zones. A serious viral infection, Chikungunya, was once confined to a small area of Africa. It had previously spread to Europe and Asia but now for the first time surfacing in the Caribbean and the continental US.

Zoonotic diseases are ever occurring. Some are relatively harmless; yet, others may intermittently and unpredictably spread with such ferocity that unprepared and inadequate health systems will surely be overwhelmed. A prompt coordinated redirection of a significant proportion of our limited resources for climate remediation towards infectious disease research and interdiction is our best response to this Ebola experience. It is now time for all of us to rethink our place in the global village and embrace appropriate priorities and reciprocal responsibilities through common need.

The Hygiene Hypotheses and Causes of Allergies

I was young once. Now, I am a boomer. When I was growing up, I never knew any child with a food allergy. Allergies of any kind seemed rare. Yet now, allergic concerns are frequently encountered? Just a few weeks ago, I was on a flight from Phoenix to Philadelphia. Shortly after the flight began, the flight attendant announced that no nut snacks would be passed out with in-flight drink service since there was a passenger on the plane with a peanut allergy. After I got over my shock that there might have been any snack at all, I reflected with surprise on the notion that the allergy of this person was so severe that any peanuts anywhere in the cabin was a threat. I had come into contact with thousands of children while growing up both as classmates and friends and I had never ever seen any allergic reactions. We all ate the same foods and there were no dietary rules. What is happening? What is different? After all, just think of it,…. how many boomers ever had a friend with a gluten allergy?

The answer to this apparent disconnect may lie in the emerging science of the hologenome and our contemporary fastidious cleanliness. Current research has suggested that the surge of allergic symptoms is related to our attempt to distance ourselves from our ubiquitous microbial companions. This has been dubbed the “hygiene hypothesis.” In theory, as we seek to protect our young from dirt and disease, we are inadvertently causing an imbalance in our vital exposure to microbial companions that are imperative for our optimal health. New research is showing that we live in an exquisitely intimate association with a vast collection of microbial life. This partnership can directly affect our response to allergens. There is epidemiological evidence that supports this new perspective. Some studies strongly suggest that immunological diseases such as asthma and autoimmune diseases are less common in countries considered to be underdeveloped compared to wealthier nations. Interestingly, this same pattern sees to also hold for a variety of other chronic illnesses.

These microbial partnerships are essential to our metabolism, reproduction, longevity, and well being. This is now known as the new science of the hologenome. The concept of the hologenome re-envisions all organisms as a deeply interlinked complex partnerships between the cells that make us ourselves and our indispensable microbial partners. This has lead to a concept called the ‘old friends hypothesis’. As proposed in 2003, this theory asserts that there needs to be a requisite exposure to a variety of diverse microbes with which we were associated during our evolutionary journey. Therefore, our metabolism is dependent upon certain microbes, as ‘old friends’, and they have become absolutely necessary for our optimal immunological development.

In our zeal to protect against harmful infections, we have inadvertently shielded our children from the typical exposure to a diverse array of microbial life that had characterized all prior generations. The consequence of this exclusion from these vital exposures is experienced as a significant increase in allergic reactions such as hay fever, food intolerance and asthma. In theory then, a substantial increase in the incidence of allergy is a result of this restricted exposure to the microbial domain. All of these problems are thought to be an expression of a decrease in immune tolerance related to a significant change in how our children encounter the environment compared to previous generations.

It currently appears that allergic reactions of all sorts may be directly related to the inadvertent exclusion of critical microbes that co-evolved with us and are required for our personal microbial and cellular ecological balance. Medical practitioners are learning that our health depends on this striking balance of microbial forces. For example, recent research suggests that infants that are not fully exposed to an extensive group of microbes have a less diverse gut microbiome ( microbial species in the gut) and are at increased risk of allergies and asthma. A recent Canadian study provided evidence that exposure to pets and a large number of siblings influenced the early development of gut microbial community of an infant. Less exposure was directly implicated in the subsequent development of allergic disease.
Some scientists believe that the lack of exposure of children to the normal distribution of microbial interchanges can have additional implications. Research studies suggest a potential association between this generational change in childhood experience and the increasing incidence of chronic diseases beyond asthma, food allergies or allergic rhinitis. Many immune centered diseases are potential related to this dynamic such as diabetes, multiple sclerosis, some cancers and even psychological entities such as depression or autism.

What then is an appropriate response to these concerns? Actually nothing special at all. If your child has been vaccinated, simply be willing to let your child share in reasonable unrestricted play with other children and share toys. And also, just let them roll in the dirt with a pet.

Homosexuality and Epigenetics

It is now well established that same sex attraction is not volitional. In The Microcosm Within, the incompatibility of any adequate theory for the persistence of homosexuality within the standard Darwinian construct of natural selection is fully discussed. The evidence points to same sex attraction as a genetic event representing the conservation of an original cellular capacity for self-reproduction brought forward over time as a conserved core process and expressed throughout the animal kingdom as same sex attraction.

More recently, there has been consideration that same sex attraction might be under epigenetic influences. A relationship between epigenetics and homosexuality have been cued from a 2012 study that proposed an experimental model in which epigenetic markers relate to same sex orientation.  This theory was offered as an explanation for some interesting well known observations; the tendency for homosexuality to run in families, the fact that only 20% of identical twins express same sex attraction, and the fact that no ‘homosexuality’ gene has ever been identified. 

The proposal of the research scientists in that study is that epigenetic markers are shaped by androgen signaling and become a factor in gonad development thereby molding sexual orientation. In effect, the underlying genes are modified by epigenetic factors based on the differential experience of the fetus to the stress of maternal hormonal levels. These markers can then be transferred to successive generations accounting for the familial tendency. It is not merely the absolute level of the androgen signals that might matter, but the underlying sensitivity of the developing cells to these signals. This might differ from individual to individual based on genetic architecture or there may be an inherent difference between males and females. The effects of these transmitted epi-marks need not be specific to the gonads, instead affecting areas of the brain, so that there is no difference in the gonads themselves. 

Not everyone feels that this type of theorizing is particularly important since it is clear that same sex attraction is simply part of the human condition and our inherent variability. Yet, this sort of investigation and speculation does serve to emphasize that same sex attraction, what ever its causes, is not subject to the simple rules of natural selection that underpins Darwinism. Further too, if such a trait with its consequential impact on reproduction escapes natural selection, then a theory of evolution as impelled by natural selection needs to be reexamined. 

Epigenetics and Chromatin

Chromatin represents the combination of both the DNA and proteins in a cell nucleus. This combined material can assume specific configurations. This chromatin architecture is currently viewed as having a critical role in controlling gene expression and DNA replication. The primary protein elements of chromatin, or histones, compact DNA and assist in mitosis. Epigenetic changes occur by complex interactions between environmental influences and the underlying protein structure and DNA of a genome, which can alter the configuration of chromatin or change how segments interact in their three-dimensional environment. Examples include DNA methylation and alternations to chromatin architecture through histone modification. It is believed that most epigenetic modifications to underlying DNA sequences, either through promotion of genetic expression or silencing of genetic sequences proceeds through alterations in chromatin architecture.

In general, it is currently considered that epigenetic changes to a genome are less stably heritable than base genetic heritability. That is, if a genetic change occurs to the underlying genetic code it is more likely to be stably transmitted to future generations than epigenetic changes, termed epialleles. These latter modifications are thought to be generally unstable. In addition, the fidelity of transfer if it occurs may not lead to exactly the same degree of genetic expression in a further population, termed variable penetrance. So the genetic expression potentiated by the epigenetic change may still persist, but be lessened or the new trait may entirely disappear in future generations. The process that appears to account for this is that most epigenetic changes are believed to act by modification of underlying chromatin architecture rather than the intrinsic DNA base sequences within that complex assembly. It has even been postulated that the protein histone elements of chromatin may even constitute its own form of code that offer cues and instructions for gene regulation and could then account for differing states of genetic expression and activity.

Yet, according to William Kelly at Emery University in a recent article on transgenerational epigenetics, some things are clear. Complex and overlapping epigenetic mechanisms build changes in chromatin architecture that are heritable. These changes can guide genetic expression in germline cells, and then guide chromatin architecture in the zygote. There is an “initiating event” that triggers these epigenetic processes. Some further maintenance mechanism assures that this altered genetic expression and activity is maintained through successive rounds of replication and reproduction. Further, there appears to be some ability to discriminate at the germline as to which epigenetic processes persist and which are expunged. All of these mechanisms are fully compatible with hologenomic evolution theory, as explored in The Microcosm Within. Importantly, such new scientific findings critically undermine the simplified paradigms of conventional of the Modern Synthesis and its unfaltering allegiance to unfettered natural selection and random genetic mutation.

Epigenetics and Cancer

New research is demonstrating that the etiology of cancer is complex. Epigenetic modifications of the genomes of cancer cells appear to be quite important. These are changes that do not necessarily reflect the exact DNA sequences within a cell, but alter, by various means, the expression of the underlying code. It is increasingly apparent that epigenetic modification may be as important as genetic mutation in the transformation of a normal cell to a cancer cell. This does not change the fact that many cancers are induced by infectious disease which itself can be considered an epigenetic variable. 

Such epigenetic mechanisms are being successfully defined. These include DNA methylation, arguably the most researched marker, by which the methylation profile can be linked to tumorigenesis as promoters of unlicensed cell reproduction. Alternatively, hypermethylated DNA zones can result in consequential gene silencing, which is considered itself to be a form of carcinogenic epigenetic mutation. It is also theorized that hypomethylation in parts of a genome can lead to chromosomal instability and the activation of transposable elements which can increase cancer risk or directly induce it. 

Recent studies have implicated an epigenetic signature that can predict whether a woman may develop breast cancer, even without those BRCA gene mutations that are typically considered a prime risk factor. An epigenetic signature in women with a mutated BRCA-1 gene has been linked to increased cancer risk and lower survival rates in a study conducted at the University College of London. 

Interestingly, a new epigenetic therapy designed to treat cancer by regulating gene expression has been cleared for Phase I trials. A recent clinical trial of a small molecule inhibitor drug of a particular class of proteins helps to control gene expression. This epigenetic control mechanism has shown initial promise in the treatment of refractory carcinomas. As the researchers note, the success of this initial trial, albeit limited, points the way for other investigational epigenetic cancer therapies. Thus, our emerging understanding of epigenetics if offering profound clues to both the causes of cancer and its cure.