Biology is typically known as a science without laws. There is evolutionary theory, of course, but it’s quite complex and looks different depending on what level you are looking at it; nothing like Newton’s Force = mass * acceleration. Biology does have quite a few “rules” though, such as Cope’s rule, which states that “population lineages tend to increase in body size over evolutionary time,” but there, of course, always exceptions to the rule. The existence or non-existence of laws in biology (and specifically, evolution) is a large matter of debate in philosophy of biology and I am certainly not qualified to discuss it (especially because I haven’t read much about it!).
Back in September, I wrote a blog post about the work of philosopher Robert Brandon which claimed that genetic drift is actually biology’s first law – analogous to Newton’s first law of motion, inertia. If you want more details, read the post or the footnote.*
So imagine my surprise when I found Robert Brandon had co-authored a new book (2010) with Daniel McShea titled Biology’s First Law: The Tendency for Diversity & Complexity to Increase in Evolutionary Systems. That doesn’t sound like what Brandon had written about at all and in the very same year! And well, it isn’t, although it shares some essential features. Perhaps the most essential shared feature is that both drift-as-first-law and this law is that they describe change as the default state which doesn’t exactly line up with Newton’s first law of inertia which describes stasis as the default state. However, both biological first laws and the first law of motion tell us what happens when nothing acts upon or constrains the subject of interest, i.e., they are *zero-force* laws.
So what McShea and Brandon’s zero-force evolutionary law (ZFEL)? The language is written accessibly enough to just quote them outright:
ZFEL (general formulation): In any evolutionary system in which there is variation and heredity, there is a tendency for diversity and complexity to increase, one that is always present but may be opposed or augmented by natural selection, other forces, or constraints acting on diversity or complexity (4).
“ZFEL (special formulation): In any evolutionary system in which there is variation and heredity, in the absence of natural selection, other forces, and constraints acting ond iversity or complexity, diversity and complexity will increase on average (3).
What they are saying is that increasing diversity and increasing complexity is what we should expect out of any evolutionary system. Two of biology’s “great sources of wonder,” diversity and complexity , are expected by default. Complexity is typically seen as a result of natural selection, but this is an unnecessary assumption; complexity *can* be the result of natural selection, but not always so. McShea and Brandon do save adaptation, the third great wonder, for natural selection to explain, however.
The simplest analogy of the law the authors employ is a white picket fence. The fence begins as a uniform sequence of white planks. Over time, however, the individual pickets accrue changes, such as warping, holes, and mold, making this sequence of pickets more complex and more diverse than it originally. There was external or teleological reason for the accumulating complexity and diversity; it’s just a natural tendency – it just happens. Similarly, biological systems tend to become more complex and diverse. Take a genome sequence, for example: independent point mutations accrue throughout the sequence and each mutation causes increasing diversity and complexity. Selection didn’t create the complexity – it just happened as a result of the imperfect copying process.
The rest of this review will examine problems I had with the book before reading and discuss how the authors satisfied my initial complaints.
The problem of complexity.
When I first read the subtitle, “The Tendency for Diversity & Complexity to Increase in Evolutionary Systems,” I was skeptical. Complexity talk frequently veers toward focusing exclusively on animals, and usually ends up anthropocentric – I’m a die-hard anti-anthropocentrist – but McShea and Brandon avoid this issue altogether with how they establish and interpret Biology’s First Law.
We typically say humans are more complex than bacteria because instead of one cell, we have billions, and those billions of cells constantly signal each other and are tightly integrated; even a single organ, like the brain, is considered more complex than a bacterium. McShea and Brandon point out how muddied this concept is: how do we quantify it? How do we restrict ourselves to a precise definition? And most importantly (to me), how do we avoid our zoo- and anthropocentric perceptions?
The authors spectacularly avoid what they call “colloquial complexity” – what we normally mean when we say complexity – in favor of “pure complexity,” a measure of “number of part types” and “differentiation among parts.” In this sense, a mammalian spine is more complex than a fish spine because there are different kinds of mammalian vertebrae (cervical, thoracic, etc.). The key, however, is that pure complexity is “level-relative.” Just because a mammalian spine is more complex than a fish spine doesn’t mean a mammal is more complex than a fish. Because pure complexity doesn’t scale up hierarchies, comparing two organs to two organisms (or taxonomic classes) doesn’t work. So to get back to the bacteria/human question, we need to compare a bacterial cell to a human cell (not the human organism). That’s how the complexity question actually becomes fascinating, especially because the answer is not quite so clear.
The roles of natural selection and function.
A another problematic aspect of colloquial complexity is that it usually gets tied up with function, and with function comes natural selection which further muddies the complexity concept. A trait may be seen as more complex if it specializes in some specific function and does it well, like the eye or the brain, and this function is usually assumed to be designed by natural selection. McShea and Brandon believe the entangling of these concepts is what causes so much confusion over complexity and think has prevented the study of complexity in biology to truly take off.
The authors again disentangle the mess with the “pure complexity” concept. The definition of pure complexity being “number of part types” or “degree of differentiation among parts” precludes any notion of function or selection. Under this framwork, one can (hopefully) study complexity without assuming it was the result of natural selection.
It is crucial to note that McShea and Brandon don’t think selection doesn’t explain complexity. There are certainly times when selection favors a more complex trait over another, but selection can also act against complexity. Their first law states that there is an omnipresent tendency to become more complex and diverse, but, again as the law states, this tendency “may be opposed or augmented by natural selection, other forces, or constraints.” Biology’s First Law and natural selection are separate laws and can act concurrently or against each other.
In addition, the law keeps open “an open empirical question the importance of natural selection as a force in evolutionary change” and that “the zero-force condition [gives] us a neutral background against which to see selection in action,” just like inertia does for the study of gravity (103-104). So when it comes to selection and adaptation, McShea and Brandon’s First Law potentially allows a clearer framework with which to study them. Not only is this good philosophy, it’s good science!
Isn’t this more like the Second Law of Thermodynamics?
In discussions of complexity, entropy often makes an appearance (or maybe it’s just me), because there is an assumption that complexity = order (like the eye)… or is it that complexity = disorder (like the human genome)? Complexity honestly seems to fit both and this is one of the reasons McShea and Brandon avoid invoking the Second Law – it’s messy when we take a law of physics and try to apply it to biology (110).
Furthermore, and more interestingly, McShea and Brandon argue that the ZFEL reduces to probability theory which is ultimately more general than entropy so why reduce to only the Second Law (110)?
What about Brandon’s 2010 paper (book chapter) that argued genetic drift is the first law?
[What follows is my attempt at an explanation of some ideas I didn't fully comprehend. If anyone wishes to correct me here, please do so!]
As I noted above, I previously blogged Brandon’s work arguing that drift is actually biology’s zero-force law and not Hardy-Weinberg equilibrium. Why the change?
To McShea and Brandon, while drift is not the ZFEL, it is still a component of the ZFEL. Populations or part types drift independently of and randomly in respect to each other; drift is a measure of how far a subject deviates from the rest – it’s specific to the subject. The ZFEL, on the other hand, measures the variance among these populations, a higher order phenomenon. Drift among the populations increases the variance – just what the ZFEL says will happen (93-84).
I’m not sure why Brandon makes the switch from drift to complexity/diversity but I think there is one crucial aspect that makes the newly formulated ZFEL more compelling and useful. Genetic drift is a part of population genetics which analyzes a specific aspect of evolution: allele frequencies. Thus it is difficult to apply drift-as-ZFEL to any other level of biological hierarchy, such as part types.** Their current ZFEL is applicable to all levels of biology, not just allele frequencies but also the complexity of vertebrate spines and cell structures or the diversity of arthropods and songbirds. So while the new formulation isn’t as immediately appealing to me – the Newtonian analogy of population genetics is tight and illustrative – I think it may be more useful and powerful.
An interesting historical note.
As is being made clearer with every blog post, I have a keen interest in the history of evolutionary thought, and thankfully, the authors note some historical antecedents.
McShea and Brandon argue that their historical ancestor is Herbert Spencer who had a concept of the “instability of the homogeneous” (5) and wrote that “evolution is a change from an indefinite, incoherent, homogeneity to a definite, coherent, heterogeneity, through continuous differentiations and integrations” (152), which appear alternative statements of the ZFEL: there is a tendency of the “homogeneous” to become more “heterogeneous.”
Furthermore, the ZFEL can almost be construed as a revival of orthogenesis (126-127). Orthogenesis is the idea that there is some internal driving force in the evolution of life in some direction. It was rightly discredited in the early 20th century but what else is the ZFEL but an innate tendency not subject to local environments and present adaptation? The ZFEL “acts independently of selection and potentially in opposition to it” (127) but unlike orthogenesis (as it was conceived), the ZFEL will not always overpower selection. So the ZFEL can be seen as a revival of internalism (or at least not-ecological-externalism) in the same tradition as orthogenesis.
As a book, Biology’s First Law is succint, coming in at about 150 pages. The authors write in an accessible style and typically make sure to clarify their views. If you are interested in an alternative view of how evolution and the biological world work, I recommend this highly. It will hopefully serve as a basis for further research in the nature of diversity and complexity – topics that have troubled us for centuries and will certainly do so for centuries to come. According to McShea and Brandon, though, we can count on more of each.
* Briefly, Brandon’s argument is that within the framework of evolutionary theory as a “theory of forces,” in which allele frequencies are pushed up and down as objects in a Newtonian analog, genetic drift does not constitute a force because it doesn’t have a predictable direction; instead, it is in the background. He points out that Hardy-Weinberg equilibrium cannot be a “zero-force” law (i.e., inertia is a zero-force law because it describes an object with no forces acting upon it) as is typically argued because one of its restrictions is that a population must be of infinite size to exclude the effects of drift… but how many populations are of infinite size? Brandon argues that drift is always present in any population and thus describes the default state of any population, i.e., “a population at equilibrium will tend to drift from that equilibrium unless acted upon by an evolutionary force.”
** McShea and Brandon argue that drift can be applied at different levels (like selection may apply to groups) but as stated earlier, I didn’t fully understand this section or its applicability (96-97).