The second law of thermodynamics and a theory of the origin of life itself

I have in all my time of reading science, and science news, never quite experienced the absolute abstraction of objectivity, as I did this morning. For the first time I found myself emotional, and even partially conflicted, upon reading about Professor Jeremy England, and his approach to explaining the physics of the origin of life.

Professor Jeremy England and his work on A New Physics Theory of Life.

The question of the origin of life, and the origin of selection and evolution, has plagued me for extended periods of time, since I first prepared a paper on evolution as an undergraduate. I have also recently wrote a partially coherent bit about the second law of thermodynamics and biology, which was a subtle attempt at making a connection between the quantum world and biology.

The origin of evolution

It has long been assumed and argued that the origin of the first complex molecules, capable of self replication was the result of a unique set of conditions (primordial soup), and a few strokes of luck (lighting or similar) in conditions thought to prevail on earth around 3.5 billion years ago. This summary explanation accounts for the formation of the majority of amino acids from inorganic precursors, resulting in what is commonly referred to as the primordial soup followed by the “spontaneous” assembly of these components into complex, self replication units, and ultimately, systems of self replicating units. As soon as any of these units can exert some influence on its replication probability, natural selection kicks in and life becomes inevitable.

Where there has been very little investigation from evolutionary biologists, is where the discipline of evolution transitions away from biology and chemistry and enters the realm of quantum physics. The fundamental question about evolution is no longer how complex life forms can evolve from simpler life forms, but rather, how do these first life forms come into existence, and more importantly, why? This raises the question of life itself, and has been addressed by some of history’s most influential figures. Schrödinger himself wrote on this topic.

Selection at quantum level

Now however, Professor England has succeeded in publishing a coherent theoretical model of the origin of life, that relies not on small probabilities and luck, but the notion that the second law of thermodynamics provides the framework that increases the probability of the existence of life. This model does not assume life to be a fortuitous result of “just the right” conditions, but proposes that life is an inevitable result of the same fundamental forces that causes your coffee to cool down.

If my understanding of their thesis, and my intuition serves accurate, then life will result necessarily because the selection between combinations of particles, and their ability to facilitate the distribution of energy, i.e. the second law of thermodynamics. Seemingly complex arrangements of matter at a molecular level, serves to increase the gradient between the various organizational states of energy, and in this manner, the arrangements that are more efficient at distributing energy, become more numerous, as they have a greater probability of existing than alternative arrangements. Selection at quantum level one is tempted to say.

There is more to this argument, as this the spontaneous assembly of complexity is not so uncommon in modern times as you would imagine. Snowflakes have seemingly complex molecular arrangements that cannot be explained unless the probability of their particular [complex] molecular assembly is not overwhelmingly favoured. If snowflakes assemble in complex formation all around the world every day, then it is not a stretch to imaging that there is a fundamental similarity between this and the formation of complex chemical arrangements, such as those required for the existence of life. An example of this is the high probability of the organization of lipid membranes in water into bilayer structures, that are itself a fundamental requirement for the existence of life.

Phospholipid bilayer assembly in water.

The future is exciting

The concept of selection is an enormously powerful concept, and one fundamental to explaining the complexity and diversity of life. However, there is reason to be excited, as the physics of the origin of life, may hold yet more answers about the everyday workings of life. If this model can be extended to include and make room for selection at molecular and quantum level, then we will go a far way to explaining and understanding a whole lot more about ourselves, life in general, and the possibility of life elsewhere in the universe.

Sugar! The devil that prayer is not saving you from

Early warning

Sugar addiction has been correlated with the increase in per capita consumption of sugar and other high-glycemic-index compounds such as corn syrup and selected starches. The USA per capita soft-drink consumption has increased by 500% over the last 50 years. This is bad news for everyone, except shareholders of this lucrative industry.

Addictive substances are generally speaking, either illegal, or regulated. We are not allowed to use morphine for run-of-the-mill headaches, we are not allowed to smoke until we are 18 (or 21), and we are not allowed to consume alcohol before roughly the same age yet, we expose our children to what has been labelled “the most dangerous drug of our time” by a Dutch health official in an official health communication. It goes by thy name Sugar. But more generally, glycemic carbohydrates.

The threat of massively increased morbidity due to the ever-increasing health challenges associated with obesity is thoroughly publicized in international media, and I believe warrants an assumption that requires little validation. (Read into that my laziness in providing an exaggerated list of supporting scientific literature on the topic, but I assure you that it does exist)

Sugar has, on numerous occasions, and not just recently, been associated with increased incidences of obesity, diabetes mellitus, cardiovascular disease, stroke and these components have been correlated with one another in various elaborate combinations, very extensively and thoroughly. Little doubt remains that glycemic sugar is one of the major, if not the major, causes of health complications in modern society.

Add to that, the fact that the underlying mechanism of sugar addiction mimics that of opioid addiction. That is right. Being addicted to sugar is like being addicted to heroin light, but the worst thing really, is that most of us remain unaware of this fact, and attribute the problem to ill discipline.

Binge eating and sugar addiction

In a well cited study by Avena, Rada and Hoebel on the topic of sugar addiction, the authors succeeded in producing a relevant animal model of binge eating and sugar dependence.

They would subject rats to food deprivation for 12 hours, followed by 4 hour normal circadian driven activity and then 12 hour access to ordinary rat food and a sugar solution. Both were made available simultaneously.

After one month, it was found that the behaviour of these animals mimicked that of drug seeking behaviour. These animals would exhibit the following behaviours:

  • Increasingly over consuming the sugary solution – Bingeing
  • Opiate like withdrawal
  • Craving
  • Locomotor and consumatory cross sensitization of sugar and drug abuse. (Simulates drug dependence at a neurological level)

After one month, the rats were addicted to sugar, and they were bingeing on every occasion that they gained access to sugar.

The neurological mechanism of sugar addiction

A well known characteristic of drug use is the cause of repeated, intermittent increases in extracellular dopamine in a brain region responsible for behaviour reinforcement, called the Nucleus Accumbens (NAc). This characteristic is shared by large, intermittent doses of sugar (and other equally palatable treats), albeit to a lesser magnitude than exhibited by drugs of abuse.

The increased intermittent release of dopamine over time, causes changes in dopamine receptor expression/availability in the NAc, which relates to the development of tolerance similar to drug addiction, and withdrawal in the event of abstinence. Decreased dopamine release in the NAc and increased acetylcholine release from neurons in the NAc in the event of abstinence, is the cause of the majority of withdrawal symptoms, and very closely mimics the mechanism whereby which opiates cause withdrawal symptoms.

The theory proposed from the paper of the authors above states that intermittent, excessive intake of sugar, can have dopaminergic and cholinergic effects that is similar in mechanism, but smaller in magnitude, than opiate addiction. Simply stated, sugar is addictive in the same way heroine is addictive, just not as potent.

The physiological consequence of sugar addiction

Different sugars have different effects on blood glucose levels, blood insulin response, satiety response (feeling of not being hungry), and ultimately, energy and weight homeostasis.

The capacity of carbohydrate to reduce hunger is directly correlated with the rate at which your blood glucose level rises. The higher the glycemic index (GI) of the carbohydrate you are consuming, the higher the satiety peak will be, but the shorter the effect will last, and vice versa for low GI carbohydrates. This is why a sugary treat provides greater satisfaction for hunger and/or cravings than does meat or raw oatmeal. This is the reason why children have to forced to eat their vegetables before they are allowed to have pudding.

The best example of the addictive properties of sugar can be seen when compared to the habits of a smoker. After a meal, a smoker is very rarely too “full” to enjoy a cigarette. It is because the nicotine in that cigarette provides an addictive stimulus that is not replaced by his dinner. In a similar manner, people always seem the have a little extra space for desert after dinner, and it is simply because, more meat, more vegetables will not supply the addictive stimulus that sugar can. You are no longer hungry, yet you crave a very particular high calorie nutrient. Isn’t that strange?

The solution?

There are many short term solutions to losing weight, but odds are small that you have been one of the lucky minority who have succeeded in losing weight and keeping it off. I say lucky, because those who have succeeded where others have failed, were the ones, who in all likelihood gave up their sugary binge habits for good but failed to realize the significant impact of the absence or restriction of sugar in their diet.

In a key-note address by Professor Timothy Noakes in this very topic, he made mention of a number individuals who have given up carbohydrates in their diet. A resounding agreement by a number of subjects who had written to Prof Noakes, expressing gratitude, exclaimed that they have lost weight, but most importantly, eating significantly smaller volumes of food, but being less hungry. How can that be?

Eating less, but being less hungry, means that you are no longer consuming high calorie nutrients for that craving that you aim to satisfy, but you have allowed yourself to recalibrate, in order to realise the difference between hunger, and cravings. It is made immensely difficult by the fact that sugar craving sensations, present almost identically to the sensation of hunger, and the indulgence in sugary sins, provides a feeling of satiety in the same way as many other food nutrients do. Or not quite, but hopefully you get the idea.

The cause of the problem is hiding in plain sight, but the significant realization that is yet to dawn upon the larger global health community, is that the problem to the addictive pandemic is hiding in the staple diet of modern society.

One last thought

The significance of the addiction is frequently underplayed to a large extent. The level to which one could rationalize against giving up an addictive substance has power beyond your imagination. If you get a cold feeling when you imagine never ever again consuming chocolate, or sweets of any kind, bread from your favourite bakery, cake, pizza, pasta, fruit juice, McDonald’s, ice cream, sugar in your tea… If you find yourself rationalizing that you will not go through life without enjoying any of a number of those, you have only just begun to experience the power of addiction. You need none of those to enjoy life from nutritional perspective. In fact, the less of those you enjoy, the more life you will end up enjoying.

Selected references:

[1] Nicole M Avena, Pedro Rada, and Bartley G Hoebel. Evidence for sugar
addiction: behavioral and neurochemical effects of intermittent, exces-
sive sugar intake. Neuroscience & Biobehavioral Reviews, 32(1):20–39,
[2] Wendy Foulds Mathes, Kimberly A Brownley, Xiaofei Mo, and Cyn-
thia M Bulik. The biology of binge eating. Appetite, 52(3):545–553,
[3] David Benton. The plausibility of sugar addiction and its role in obesity
and eating disorders. Clinical Nutrition, 29(3):288–303, 2010.
[4] David IG Wilson and Eric M Bowman. Nucleus accumbens neurons in
the rat exhibit differential activity to conditioned reinforcers and primary
reinforcers within a second-order schedule of saccharin reinforcement.
European Journal of Neuroscience, 20(10):2777–2788, 2004.
[5] G Terence Wilson. Eating disorders and addiction. Drugs & Society,
15(1-2):87–101, 2000.
[6] G Harvey Anderson and Dianne Woodend. Effect of glycemic car-
bohydrates on short-term satiety and food intake. Nutrition reviews,
61(s5):S17–S26, 2003.
[7] MP St-Onge, F Rubiano, WF DeNino, A Jones Jr, D Greenfield,
PW Ferguson, S Akrabawi, and SB Heymsfield. Added thermogenic
and satiety effects of a mixed nutrient vs a sugar-only beverage. Inter-
national journal of obesity, 28(2):248–253, 2004.

How the second law of thermodymics pervades all of biology

How biology is failing biology

I have spent a vast selection of my personal and professional time wondering about the one-dimensional representation of biological information and processes. I have also concluded that the representation of biological processes lacks very far behind other disciplines, such as engineering and computer science.

The notion is by no means novel, but after having read this article “Can a biologist fix a radio?—Or, what I learned while studying apoptosis“, it seemed as though the author had shared thoughts I had long harboured myself, albeit more articulately than I could likely have mustered.

The author of the above article uses the notion of fixing a broken radio to compare the diverging solutions that the disciplines of biology and engineering would likely employ. What fascinated me most, was the humour, but more importantly, clarity, with which he showcased the inefficiencies in the biologist’s evaluation of biological phenomena. I might add at this point, that being a biologist myself, I think it is okay for me to make this statement.

Biology is taught in one, or at most, two dimensions. Those of you who have been fortunate enough to pick up a biochemistry textbook in the last few decades, have been greeted by this, or similar, idyllic representation of a biological process:

Cleavage at carboxyl end of hydrophobic amino acid, phenylalanine.

Cleavage at carboxyl end of hydrophobic amino acid, phenylalanine, by the enzyme chymotrypsin.

Though in principle, for teaching purposes, this is not wrong, nor is it wrong in any general sense. What I find particularly disconcerting is the implication of certainty that this action takes place at molecular level. Well it does. But not for all 100% percent of molecules present in any solution.

Agreeably, you might be thinking, enough with the ambiguity! Get to the point already!

Law of mass action and chemistry

Equilibrium chemistry is the study of the ratio at which products and reactants exist in a particular chemical solution, when that solution has reached equilibrium.

Law of mass action in equilibrium chemistry.

Law of mass action in equilibrium chemistry.

The law of mass action is the mathematical model concerned with understanding the likelihood that products would form, given an initial concentration of reactants. In the figure above, the ratio at which these components exist in solution after sufficient time has been allowed, is termed the equilibrium constant.

The effect therefore, of any compound, be it medicinal, nutritional, or hormonal, has a very strange road by which it affects the physiological equilibrium that is central to all of life. It is in fact the capacity to regulate this equilibrium, with enzymes and the separation of reactants from one another by subcellular compartmentation, that allows life to exist at all.

The biochemical reactions similar to the first figure is what you are used to seeing, and it is as one dimensional as saying that the presence of glucose in ones blood, increased the concentration of insulin, and therefore increases the absorption of glucose into the muscle/adipose tissue. Strictly speaking of course, this is not wrong, as this is just the 2nd grader summary of what really occurs.

In reality of course, the process still abides by the law of mass action and more fundamentally, the second law of thermodynamics. The nature of equilibrium chemistry above makes the reality of the simple blood glucose statement above, seem a very complicated process indeed. Indeed it is the proverbial equivalent of herding water.

The process above is more closely simulated by the diagram below.

The control of reactants allows the exploitating of the second law of thermodynamics to sustain differential cellular equilibrium.

The control of reactants allows the exploiting of the second law of thermodynamics to sustain differential cellular equilibrium.

The second law of thermodynamics

The second law of thermodynamics states that all isolated systems are evolving towards a state of equilibrium (state of maximum entropy, or disorganized energy). It also states that the entropy of an isolated systems will spontaneously evolve towards a stable thermodynamic equilibrium.

Essentially, this means that if a cell, or subcellular compartment is irreversibly separated from its external environment, it will cease to live. It will reach thermodynamic equilibrium, and the only energy fluxes that occur will be the loss of heat energy. It is the continuous, and gradual shift in chemical equilibrium from extraneous sources that allows for the rate of energy flux to be larger than 0 (dE/dt > 0).

The impact

Ever wondered why there seem to be and infinite number diverging apparent solutions to common ailments? Antioxidants for the prevention of cardiovascular disease, low fat diet to reduce the risk of cardiovascular disease, increase exercise to reduce risk of cardiovascular disease. It is not a topic of discussion whether E=mc², is most appropriate law to use when the goal is building a nuclear reactor. Yet, in order to lose weight for example, there must be almost as many diets than there are individuals who are, at this very moment, trying to loose weight.

Why? It is because biology is poorly understood. The workings of biology is represented with visual flow diagrams, but because biology is dynamic in nature, the effects of the changes induced by the actions that modelled are not taken into account. The predictions that serve as foundations of biology, and therefore nutritional sciences, pharmaceutical sciences, and modern medicine, are based on assumed mechanisms and are therefore fundamentally flawed.

A solution to this problem?

The language of biology is not equipped to deal with this issue, but mathematics is. Calculus presents us with the ideas, philosophy and tools with which to analyse changes in equilibrium chemistry, with which to ultimately understand the magnitude of the impact that any one component can have on human physiology.

Should the flow diagrams in biology be replaced by systems of differential equations, perhaps we could envision a biological research platform, where different results can be integrated with one another and mechanisms are not assumed for the sake of supporting correlation, and the inference of causality not committing the cardinal sin of statistically unwarranted extrapolation.

Coding the weasel

I recently took up reading yet another of Richard Dawkins’ works on evolutionary biology, “The Blind Watchmaker”, something I have neglected since I reread “The extended phenotype”. This lead me to thinking about, and eventually programming a version, of the much famed “weasel program”. It has endured as much scrutiny as it has received praise, but it is such and eloquent example of the principles of natural selection, that I felt compelled to explore it once more.

The extended phenotype is my personal favorite book of all time, and I struggle to see it being toppled from my favorites podium any time soon. I like it so much, not only for its unrivaled insights into evolutionary biology, or it’s unique and paraphrased invocation of game theory in explaining evolution in terms of strategies, but the philosophical framework it presents for thinking about any topic with a completely novel perspective.

The Blind Watchmaker however, surprised me with the insights it presented (having expected little, in order to avoid disappointment after “The Extended Phenotype”), and for me it came at exactly the right time, as I recently began to dabble in a little light mathematical modeling and computer programming.

Within the first half of the book, Richard Dawkins invokes his computer programming skills to showcase the beautifully basic principles, by which natural selection can assemble complex structures from un-complex components. In addition to that, he eludes to the subjective nature of complexity, a matter which set me to a catatonic state of introspective reasoning for some undefined stretch of time.

Among his examples was the, seemingly popular, example of evolution of a sentence from the individual components that is assembled from, its letters. The program is called the weasel program, as it stems from a quote in a William Shakespeare play, reading “Methinks it is like a weasel”.

The program starts by selecting 28 random characters from the alphabet. The sentence is copied, each position in the sentence copied with a certain chance of mutation to any one of the remaining 25 letters of the alphabet and the “space”. Before a copy is made, the program checks the sentence for its accuracy in resembling the target sentence, but it is checked letter by letter. If a letter in the sentence at position is identical to the letter in position x in the target sentence, it becomes immune to mutation and is “locked” in that position.

I wrote, a simple little python script that does exactly what is described above. I subsequently wrote a not so simple version of in R, to satisfy my curiosity as to “how to”.

With this I look the liberty of using both uppercase ad lowercase letters to form a library of 53 characters, including the “space”. This was the result for the locked example.

Locked example of evolution of the sentence to it target sequence.

Locked example of evolution of the sentence to its target sequence.

This result was obtained using a 100% mutation rate when the letter in position is not identical to the corresponding position in the target sentence.

Thereafter, I was pondering, as any scientist would at this point, that if the target sequence was defined in advance did we really witness the assembly of something complex from simple sub-units? I would like to point out at this point, that fundamentally, the principle is still illustrated, but not to the satisfaction of many out there.

I then took to programming an unlocked example, again in R, as I was more familiar with the matrix notation in R than I was in python at that stage. R is not as friendly with string manipulation as python is, but every problem has a solution.

The program is structured to have the following properties:

  • A sentence of a “target” length of characters is generated randomly from the library of 53 characters. The target sentence can consist of any sequence of letters.
  • For this example, it consisted of the sentence: “Methinks It Is Like a Weasel”, printed with the capitals in place.
  • The target sentence the produces 5 copies of itself, one letter at a time, with each letter having a 5% chance of incorporating a random character from the character library.
  • The 5 sentences or “progeny” are each evaluated for the fraction to which it resembles the target sentence.
  • The “progeny” with the highest resemblance to the target sequence, is chosen as the new parent and the cycle is repeated.

This is the result:

Mutation of random characters to target sequence.

Unlocked example of evolution of the sentence to it target sequence.

Interesting observations from this results it that the correct sequence evolves (over many more generations than for the locked example) with selection coefficients attributed to the progeny of each generation, completely arbitrarily. We chose to allocate the selection coefficient that allows for evolution to the target sequence, but by allocating the lowest selection coefficient to the progeny with highest resemblance, we could probably evolve an opposite sentence to our target, whatever that would look like.

The validity of this coding approach is open for debate, should there be any resistance, but it was written according to the example algorithm on the bottom of the wiki/Weasel_program page.

I found it to be an immensely educational to program these codes, and I will pursue the next phase of recreational programming to evaluate how to manipulate the selection coefficients with respect to the environment in which any sentence finds itself, relative to the frequencies of rival sentences, along the lines of game theory, if it is conceivable to code such an example. I hope it is not a bridge too far.

On the evolution of immortality

The average human lifespan has significantly increased in the last couple of hundred years, prompting suspicion of a potential evolutionary trend towards living longer.

I have before heard the argument, that human interference in the natural progression of disease and disability is affecting the “Darwinian, survival of the fittest”, and consequently is likely to influence evolution in the favor of a genetically ‘weaker’ human species. That argument has merit only when predicated on the inaccurate assumption that the individual or group (population) is the fundamental unit of selection. [Dawkins, 1976; Dawkins, 1982]

Can we however reasonably expect our descendants to keep getting older every generation, or is there likely to be an upper limit for maximum age for humans?

To postulate an answer to the question at hand, we will have to delve into the technicalities regarding the evolution of longevity, though I suspect that my (possibly feeble) attempt at a thought experiment, might only answer questions to which we already know the answers.

First, I would like to suggest that we define the term longevity for its use herein, as the length of time that extends beyond reproductive age, as a proportion of total life expectancy, or lifespan, used interchangeably with ‘length of time beyond reproductive age’.

Is it likely that genes ‘for’ longevity will have an increased selection coefficient compared to their rival allele(s)?

For there to be an increase in life-expectancy, due to selection in favor of an increased longevity proportion, we have to assume for the purpose of this argument, that average time to reproduction remains constant, in order to isolate for the selection coefficient regarding a ‘longevity’ gene/allele. We also assume the existence of an allele that confers some sort of increased lifespan due to increased longevity (increased proportion of life-expectancy after reproduction).

Selection pressure that would favor the propagation of a gene ‘for’ increased longevity, is linked to the phenotypic effect that this gene is likely to have on the propagation of copies of itself into future generations. The presence of an allele ‘for’ longevity, should in principle favor the increase of such an allele in future populations, at the expense of its rival.

Since we have stated that the average age of reproduction is not affected, and this gene is strictly for increased lifespan beyond reproductive age, we can safely assume that the gene ‘for’ longevity has no direct influence over copies of itself being present in its progeny. The only way by which such a gene can increase the inclusive fitness of copies of itself, is by insuring an increased survival probability of such a gene (and therefore individuals who carry a copy of this gene) in future generations. If there is more time after reproduction in which the principle investment of energy goes to ensuring survival of progeny, then such a gene will benefit from an increased longevity fraction. If energy is no longer invested in reproduction, then it makes evolutionary sense to invest energy in ensuring the survival of offspring, which carries copies of the genes of its parents.

Selection in favor of a gene ‘for’ longevity will have a higher selection coefficient than its rival allele, all other things being equal.

However, it is safe to assume that there is an evolutionary stable state for longevity, based on costs of developing such a trait. In principle, if there were no increased costs associated, then organisms would tend to evolve to gain immortality. But lifespan after reproduction is likely to be optimized for ‘minimum time beyond reproduction required to insure survival of copies of genes into the next generation’. This is necessarily bound to reproductive age. A gene ‘for’ longevity will increase the probability of its survival, if it can insure that its progeny survives until reproductive age. It will thereafter have exactly half the benefit if it can can assist grandchildren of itself to reach reproductive age. Whatever arbitrary value of inclusive fitness a gene ‘for’ longevity can have, will be halved in each subsequent generation, reducing the evolutionary benefit of survival after reproductive age, with the passing of each generation.

The chance that his children will contain this ‘increased longevity’ gene is ½, and that for his grandchildren is only ¼. The value of a parent assisting his grandchildren to survive is only half the value for that of his own children. A gene ‘for’ longevity will gain double the advantage of assistance, if both its parents and grandparents are assisting it in reaching sexual maturity, and has therefore twice the (arbitrary) fitness value for surviving into the next generation, compared to its rival alleles which incur no such advantage. From the offspring point of view, it might seem beneficial to survive for parents to survive for long periods of time after reproduction.

However, the advantages of increased longevity is balanced by the costs of diverting resources away from reproduction, in order to increase lifespan thereafter. Off the top of my head, it would require the evolution of better policing systems, genetically speaking, to ward of age related diseases (cancer, Alzheimer’s etc.). It would also require the co-evolution of better copying fidelity for somatic cell genes. Resources for reaching maximal physical health at reproductive age would have to be diverted to ensure better mechanical tenacity at advanced age. We can stop here, by assuming the list is very incomplete, and whatever other factors that need be considered, will add to the burden of costs. We can also assume that costs will also increase rapidly with time, whereas benefit will decrease radically with each passing generation.

What then if we assume, that there is an established equilibrium for longevity, governed by the average reproduction age? This has already been shown to be the case, both in previous research and for reasons mentioned in the above argument. It has been described more accurately here.

Would an increased average time to reproduction lead to an increase in lifespan? Would the artificial selection pressure induced by humans, reserving the capacity to procreate until much later than the average, lead to an increased average reproductive age, and therefore increased lifespan?

At first glance, the argument above would suggest that increased average reproductive age would indeed lead to increased longevity. Though I would like to get into the details of selection governing such a potential increase, this communication is already at its limits with respect to readability due to my ramblings over technicalities.

I will simply state, that, artificial selection for ‘increased age of reproduction’, is required to have an increased propagation potential (selection coefficient), compared to shorter reproductive cycles, for such an allele to stabilize itself in a population. Waiting longer to have children in this instance would have to increase the number of descendants from longer reproductive cycles, relative to the number of those produced from shorter reproduction intervals. This has associated with it a number of costs, such as increased resource requirements to reach reproductive age. It has been suggested for this reason, that life-expectancy is negatively correlated with reproductive age.

I would like to add another component to this line of thought. The Constructal Law. Recently published in this here article, is a mathematical model, describing the correlation between, body size, distance traveled during a lifetime and off course life-expectancy. Whether, reproductive cycles and life-expectancy is a product of organism size, or organism size is a product of either one, or a combination, of the aforementioned components, remains a discussion best reserved for a future opportunity.

The Constructal Law essentially states that, the larger a moving body, the longer its lifespan and distance traveled during its life. If my logic serves correct at this juncture, then increased life-expectancy will be associated with increased average human size, though I am certain that we have speciated our way to within the current limits of our (human) body size distribution, very long ago.

If you are wondering whether there is a reasonable chance that humans will one day live to exceed 100 years on average, then the answer should be no.

And if and you might be still be inclined to answer yes, then the following is something to consider. If such a genetic mutation does happen to occur, one that causes a change in the very roots of embryology, one that will increase body size, increase time to reproduction and therefore increase life-span, it is likely that they would not be referred to as humans (by our current criteria), as a result of speciation. It would be the evolutionary equivalent of primates having predicted that humans would evolve a more intelligent descendant from an ancient common ancestor. What the latter paradoxical statement is really implying, is that, if this were to occur, current modern humans would probably only be the common ancestor for that line of evolution.

On cheating. A scientific perspective.

The very recent past has not been kind to one of history’s most celebrated sporting achievers. Lance Armstrong faces defamation of a legacy that has recorded no less than seven Tour De France titles and a winning bout with cancer. Though I should probably say, seven ‘top of the podium’ finishes, as the US Ant-doping Agency (USADA) has stripped him of those official victories. (Not the cancer one.)

Lance Armstrong has since refused to contest the doping charges, forfeiting his rights to all awards and prizes, citing a depleted emotional capacity to sustain the battle.

Whether or not Lance Armstrong is a dirty doper, is not the main inquiry of this communication. Though I find it extremely interesting that such a retrospective inquiry has any merit at all.

The nature of professional sport, which is analogous to saying, the nature of nature, is to succeed with maximum advantage whilst incurring minimum cost. It is no surprise that doping has any place in professional sport.

Professional sport can very easily be viewed as an isolated system, within which, greatest advantage is gained by a strategy that will out propagate its rivals for success, and compete well in an environment that has a high frequency of the same strategy [Maynard-Smith, 1982; Dawkins, 1976]. This system does not encourage anti-doping, as much as it serves the purpose of a rigid framework, that drives the selection between winning strategies, that include a factor of doping. In fact, the arms race between anti-doping agencies and dopers in professional sport, has become a well debated topic.

What has me particularly disconcerted, is the lack of responsibility that the USADA are willing to claim for the role in this mess. In designing artificial upper limits of fairness, the system enforces the selection of strategies that will approach an asymptote of the allowable. What is worse still, is that this limit of fairness applies only to doping (and gender and technique), which exists as an extension of nutrition. Everything else is allowed in limitless quantities; training, sleeping, genetic advantage, historical advantage, etc. Where they choose to draw the doping line with respect to nutrition is arbitrary, yet the fact that an upper limit exists, is all that is important for now. I might add, that anti-doping organizations have both the spirit of fairness, and the athletes best interests at heart. In principle.

If the nutritional component of race preparation can be viewed as a continuum of nutritional strategies, with mash and veggies being on the right (correct) side of the upper limit and steroids on the other, then strategies that approximate the upper limit of fairness has a maximum advantage. This strategy is very likely the predominant one in professional sport, as most athletes that compete at this level, are at the upper limits of genetic capacity, physical training etc. for humans. Since nutrition offers an additive contribution to most attributes of a physical nature, there would be a strong general trend towards maximizing its effect.

Anti-doping agencies create regulations, that at the outset, seek to govern fairness. This is the driving force behind the arms race between catching dopers, and doping to the maximum, without getting caught. Doping to the maximum without getting caught, is the strategy that allows for greatest advantage, all other things being equal.

 Lance Armstrong is a product of an environment that selects for the most effective strategies, one which is governed by limits, enforced by the arms race between doping and anti-doping. Whether or not Lance has slipped through the cracks of a previously inadequate system of policing, is unimportant. The fact that there are allegations of this nature, should prompt an introspective inquiry for the USADA more than it should a retrospective hunt for ‘fairness’, at the expense of the competitor.

If Lance had an unfair advantage during his reign of success, it necessarily means that equal such opportunity existed for each of his competitors. If he had both cheated and bribed his way to success, it can be ascribed to a corrupt system that allowed blatantly ‘unfair’ competition, which renders its purpose null and void.

Cheating within the upper limits of legal is not moral failure from an athlete’s perspective. No sir. It is failure from a governing perspective.

The Scientific Discipline

Wherever there exists ambition to exceed, there is an accompanying potential for failure, directly proportional to the level of difficulty associated with completion of such a challenge. As Sam Harris in his stimulating read, “The Moral Landscape” proposed, there exists two definite extremes of the human condition, which he termed ‘the good life’ and ‘the bad life’, which are connected by a continuum (the subjective association of) ‘good’ and ‘bad’ components. Theoretically speaking, and forgive me for paraphrasing, all individuals aspire to the good life, whatever his/her subjective interpretation of that good life is.

I do find it ironic however, that rationally minded individuals (whom, as a scientist, I pride myself in thinking I am surrounded by) can be so abducted from the rationality of scientific inquiry when posed with aspirations of a personal nature. One individual can produce the most phenomenal research covering years, and even decades, yet struggle to maintain something as simple as a diet for the duration of one week.

Having recently re-read “The Extended Phenotype” by Richard Dawkins, I have come to the conclusion that there is as a matter of fact, another side to the Necker cube. All of us are posed with challenges that at times, seems too large for the aspirations of even the most disciplined amongst ourselves. It is along the lines of the philosophical, and scientifically feasible, model discussed in “The Extended Phenotype”, that I had decided to restructure the way in which I am to approach specific personal challenges.

In life, you are provided with variables and constants. Constants, I like to think of as all things which I have no ability or capacity to control, even though they do not produce repeatable output, yet can still be regarded as constantly beyond your control. For instance; as a lecturer, you accept as a constant, that all undergraduate students, are trying to succeed in passing, by doing the minimum required effort. Therefore, low cost to benefit ratio. Along the lines of evolutionary biology, positive selection of any trait, is a product of the cost of evolving that trait, relative to the benefit such a trait would produce, associated with the direct milieu that trait finds itself in. In short, students are lazy because the system incentivizes laziness.

Now, I am not here to solve the riddle of student education, for that extends far beyond both my expertise and capabilities. I am however proposing a variation on the outlook of student laziness, or more importantly, lack of achievement in our personal lives.

What if discipline is not (always) a product of motivation, strong will and endurance, but simply an unavoidable byproduct of a system that incentivizes success, relative to a perception that is conducive to success in that particular environment? What if, instead of working up the energy and motivation to maintain your diet/exercise routine, you could take a step back, and design for yourself a system, in which you are most likely to succeed? (Though I have had some success with this approach in my personal life, I am hardly specialist on these subject matter.)

For everything that is propagated into the next generation, there exists a fundamental selection, if represented by competing versions of the same component. Richard Dawkins proposed the meme theory of selection as far back as 1974, in his book, “The Selfish Gene”. In accordance with this proposal, I would like to set forth the following parameters for an example of an exercise routine.

When propositioned with a choice of either performing a component of your exercise routine, or let’s say, watching television, you are presented with alternatives for use of a unit of time, each measured by arbitrary values of fitness, related to cost and benefit. What these units of fitness is, although measured arbitrarily, is not irrelevant, as the extent thereof will serve as the basis for selection. Which of these activities one is likely to pursue, and is likely to pursue for the remainder of, perhaps a calendar week, is linked to the selection coefficient for each activity. So we satisfy the criteria of evolution by selection, in producing alternative components from which to select.

The second criteria for evolution by selection, is propagation into the next generation. If we imagine any specific activity chosen at the beginning of a week, as an arbitrary commitment to a line of evolution, then initial selection of either activity should in principle serve as the higher probability decision for all subsequent choices for those activities. This of course, if the popular “I’ll start next week” attitude is anything to go by. It also assumes for the third factor governing selection in favor of either as an activity, discussed hereafter.

The probability of propagation of any component (perception/meme) into the next generation, is subject to selection coefficients of each alternative, within the conditions in which it finds itself. Therefore, if becoming overweight and unfit is the milieu in which either choice, exercise vs television, finds itself, then going outdoors for a jog is very incompatible with achieving that aim. In addition to the global milieu, there exists interactions with other components (activities) that influences the selection coefficients for each one of our proposed alternatives. Watching television likely has a selectional advantage over exercise, if the food of choice is McDonald’s and the choice of drink is a sugary soft drink. As Richard Dawkins brilliantly proposed, some memes (genes) have a higher probability for selection in favor of, when present in a mix of memes that will positively influence its propagation.

This third component is where I would like to make a distinction between constants and variables in this model of selection between activities, if there can be such a thing. If we consider the first two components as constants, therefore in any conventional system (which is likely to be the majority), selection in favor of watching television has a higher inclusive fitness than does exercise, for the reasons mentioned above, then the third component can be considered a variable. If we can succeed in designing a system where healthy eating and exercise has a higher selectional advantage than the alternative, then it should proceed naturally to make decisions that include the latter. If running a marathon is the global objective, then all selection pressures should on average favor the activity which is most conducive to achieving the objective. i.e. Exercise. And being a scientist, the following should be generally true. If we require 8, then 4 + 3 will not suffice.

There is no reason not to see the obvious analogies with the psychology of motivation and discipline, yet seeing that my training is limited to biology and my experience limited to introspection, this rational approach has served me well. I’ll leave with this thought: For every individual that fails, there exists a system that allows him to fail.

Brontosaurus Dolly: Feasibility of dinosaur cloning?

In response to an off topic question, posed during a research methodology lecture, I was humbled by the response of one logically minded undergraduate.

Can we clone a dinosaur? Not as far as I know, but apparently the internet knows more. An Australian billionaire by the name of Clive palmer, has hinted at the possibility of funding research for the purpose of cloning a dinosaur. First of all, we would have to look at a long list of factors governing its feasibility. Initial impressions would suggest that eccentric billionaire, Clive Palmer, is posing a challenge, laced with more humor than sincere ambition. The reality of live dinosaurs should in my mind, present a slightly larger public fascination than even the sensational athletic prowess on display at the recently concluded London Olympics.

Then a student responded, that they have indeed succeeded in cloning a dinosaur, which according to a bit of research, is postulated by some individual, to have occurred at the University of Florida. At first glance, it seemed to be too good to be true, and this opinion has since prevailed.

This publication seems at odds with the research publications and news from the University of Florida’s homepage. I find it strange, that they would have failed to be the first ones to make public this discovery, especially considering the funding (and inadvertent criticism) they would be privy to. But the apparently online-presence-deprived Dr. Norman Trudell, Biology Professor at UF, has neglected several important aspects considering the potential cloning of dinosaurs, and as it may happen, even more recently extinct species, of which he have near complete DNA databases.

But let us steer away from the breaking news of cloned dinosaurs and get into the challenges of feasibility surrounding the cloning of an extinct species.

Is Clive Palmer wasting his time and money? More importantly, is he potentially monopolizing resources that can best be allocated to disciplines related to more pressing public concerns, such as those of cancer and HIV?

The cloning of previous organisms such as the immortally famous (now deceased), Dolly, required some key elements, that is currently in short supply, with respect to dinosaurs. Dolly was cloned using a technique called nuclear transfer, where the nucleus of a somatic cell from primary in vitro cell culture, is introduced to an enucleated oocyte. The oocyte containing a full diploid complement, complete with all associated structural and regulatory protein, is transferred to a surrogate, until it reaches terminal gestational development.

From what I could gather, modern research has not yet produced a complete DNA sequence from any species that has retired from existence during ancient times, which includes many who have gone extinct far more recently than did the dinosaurs. With extensive biological and physiochemical DNA damage that far exceeds 60 million years, I have very little doubt that the scientific community might be expecting the recovery of an intact dinosaur genome any time soon and since we are only just beginning to understand the cellular physiology of extinct animals, the synthesis of a viable genome is as yet, probably even less likely.

According an article published by Nature (Ancient Biomolecules in Quaternary peleocology), we are seeing significant technological advances that increases the rate at which ancient DNA and other biomolecules can be analyzed, yet the National Center for Biotechnology Information (NCBI), does not mention any entry of DNA sequences that is related to the Apatosaurus (Dinosaur postulated to have been cloned).

Even if – with the advances made hitherto – we are capable of extracting sufficient quantities of DNA from paleontological specimens to obtain a complete DNA sequence of some prehistoric species, we would still be very far away from understanding the organization and nuclear morphology of ancient chromatin. I would think that this would make any attempts at cloning redundant. Even if, by some means, assembly of a complete and viable sequence (comparative to that taken from somatic cells in Dolly’s case) could be theoretically feasible (perhaps in cell culture of cells from a species with a close phylogenetic association), there would exist but still, a vast number of challenges in ‘interspecies’ nuclear transfer. There is no telling what difficulties such imperfect chromatin organization could produce, let alone the compatibility, or probable incompatibility of genes and gene products of donor DNA, with cellular components of the oocyte, that has had a hundred million odd years to evolve.

The question remains though, if there should be a public denouncement of this sort of frivolous allocation of resources, to the likes of unrealistic ambition, even if privately funded? This researcher remains a skeptic as to it feasibility, yet I firmly encourage any private funding that will, no doubt, result in the advancement of technologies that could in the future be applied for numerous ambitions, other than frivolity.

In reality, we are unlikely to see this research endeavor materialize to anything more than debated fantasy. Even if Clive Palmer is pursuing this avenue of research merely to satisfy personal curiosity, it may still inadvertently lead to the development of a technology, or even technique, that could justify such expenditure many times over. In any case though, he will be contributing to the advancement of science, or at least propagating some humor in a scientific community, that at times, seems much deprived thereof.