Evidences for Evolution: The Heart and Circulatory System of Vertebrates

Darrel FalkDavid Kerk
On July 12, 2010

In one of our previous essays we made the prediction that if evolution is true, and ancestral species do give rise to descendant species by a process of “descent with modification,” then we should be able to find fossil transitional forms which display body characteristics clearly showing evidence of this process. Out of many possible examples, we then examined one specific instance (evolution of whales) where this expectation has been resoundingly confirmed. The process of fossilization, however, is overwhelmingly biased toward hard mineralized body parts (bones and shells) – traces of soft body parts are very rarely preserved. But if evolution is true, then each of us should retain, in our own bodies, “buried fossils” in the form of the soft tissue of our organs, which show evidence of descent with modification. In this and the following essay we will examine the human heart, and the great arterial vessels which emerge from it. We will see that in those structures is the clear record of an evolutionary process.1

Let’s start by recalling some aspects of the human heart with which you are probably familiar. The human heart (like that of all mammals) has four pumping chambers – two atria (which receive blood coming into the heart) and two ventricles (which receive blood from the atria, then pump it out to other destinations). Furthermore, functionally the human heart works by using two pumping “circuits,” one served by each side of the heart (a set of one atrium and one ventricle), which work in parallel. The right side of the heart receives “spent” blood from the body and pumps it to the lungs. The left side of the heart receives “fresh” blood from the lungs, then pumps that to the rest of the body (Figure 1).2 There is a set of large vessels (arteries) which leave the heart, and are vital in carrying blood to the appointed destinations.

How do the human heart and this set of great vessels develop? One might think that the most straightforward way to do this would be for a mass of primitive tissue to hollow out into a tiny four-chambered structure with the appropriate connections, then progressively enlarge them as the entire embryonic and fetal body grows. However this is far from the case. Instead there is an intricate (at first sight perhaps bizarre) set of stages and transformations which are shown in Figure 2.3

Figure 2: Early stages of human heart development

The first stage is the formation of an elongated tube with thickened walls. This occurs near the beginning of the fourth week. Blood comes in at one end, passes successively through several structures to the other end, then it is pumped out. Note that there is only a single atrium, which receives the blood from the body and a single ventricle which sends the blood on its journey out of the heart. A couple of days later this tube-heart twists so that it becomes more compact in shape. Near the end of Week 4, the two structures at each end (the sinus venosus and the bulbus cordis) become absorbed into the atrium and ventricle, respectively.

Figure 3: Human Heart Just before its division into four distinct chambers (41 days)

Eventually, at the end of Week 6, the single atrium and single ventricle become divided by a partition, forming the final four chambered configuration we are familiar with. Figure 34,5 shows an internal view of the human heart as it nears completion of the constrictions that lead to four chambers.

Note at this point that the end that receives blood (the atria) has shifted to the top (the head end), while the sections that deliver blood to the body (the ventricles) have shifted to the bottom, just the reverse of the way that things had been earlier.

This set of transformations is altogether remarkable, and not at all what we would expect to be necessary to form a human heart and its major arteries. It is, however, even more amazing when we consider the fact that this process resembles in essential ways the process of development in all other animals with backbones (vertebrates). For example, the “tube heart” stage we described above for the early human heart corresponds closely to the early structure of the heart as a fish develops (Figure 4).6

There is thus only one atrium and one ventricle in the mature fish heart. In amphibians, such a “tube heart” stage also occurs in development, along with a very specific folding that also occurs in the fish. But now in addition, the single atrium becomes divided into two. The ventricle, however, remains as a single chamber. In reptiles, the same sequence of changes again occurs (with the same looping that characterizes the fish heart), but now in addition to the atria being divided, there is some division of the ventricle into two (variable in different types of reptiles, but complete in crocodiles, for example).

Thus the human heart at its different stages of development resembles closely that of fish, amphibians, and reptiles during some stage of their development. Are these just isolated “factoids” or can we account for them in some more meaningful way?

If we reconsider the development of the heart, this time in an evolutionary context, then all of this suddenly and dramatically makes sense. If evolution is true, then fish were the first vertebrates that appeared in the history of life. Indeed, fossil evidence indicates that fish predominated about 400 million years ago, which has sometimes been called the “Age of Fishes.” If evolution is true, then amphibians appeared later (fossil evidence shows this began about 400 million years ago), and reptiles appeared still later (around 300 million years ago based on fossils). Furthermore, if evolution is true, each major vertebrate group evolved through “descent with modification” from a pre-existing group. Thus amphibians evolved from fish, reptiles from amphibians, and mammals from reptiles. Thus if evolution is true, and all of this is so, then we might expect that as a member of a later group of organisms develops before birth, it would use aspects of the “developmental program” (i.e. the “instructions”) that were already in place for its ancestral organism. Why reinvent the wheel and develop a complex structure from scratch when it is possible to modify a previous structure to suit instead? When viewed in this light, it becomes quite sensible that the human heart passes through stages during its development which would be similar to those seen in a fish, amphibian, and reptile.

What about the set of arteries leaving the heart? There is a set of six paired arteries that are formed (each pair has a left and a right component), connected by a vessel on the belly side of the body (called the aortic sac in humans) and a pair of longitudinal vessels on the back side (each called a dorsal aorta). Figure 5 at right shows an idealized representation of the six arches.

Figure 6below shows them as they actually exist at about six weeks into human development. The six paired vessels are not all present at the same time. The first two pairs at the head end appear first, followed by the last several, which appear in sequence moving toward the hind end of the body. The first two have disappeared by the time the last ones become prominent. In humans the fifth pair are either rudimentary or do not appear at all, depending on the individual.

It turns out that the third, fourth, and sixth pairs of vessels are particularly important. The third pair forms the carotid arteries which supply the head. The fourth artery on right side withers away, but the artery on the left side is important in forming part of the aorta, which is the main artery leaving the finished heart. The sixth artery on the right side also withers, but the one on the left side is important in the circulation of blood to the lungs (Figure 7).8,9

Why do the blood vessels emanating from the human heart develop in such a strange way? Why six arches, especially when some subsequently disintegrate? As we all remember, fish have gills to allow them to exchange gases while living in water. The gills develop from a set of structures called the “branchial arches” (“branchial” means gill). Most fish have six arches at some point in their development, each one containing a blood supply, muscle, cartilage and nerve. Each arch is supplied by an artery called a branchial arch artery, and there are initially six of them, arranged from the head back toward the tail. The heart is on the belly side of the body, and sends blood forward toward the branchial arches. The blood then passes through the six pairs of arch arteries, and collects in paired dorsal aortae on the other side, finally to go to the rest of the body. At first, in the embryonic fish, these arteries simply carry blood through this region (there is no gas exchange yet). In fact, the first two branchial arches and their arteries are diverted to support the development of structures in the head. As the fish matures, slits break through around each of the remaining arches, allowing the flow of water, and the vasculature of arches 3,4,5, and 6 form the functional gills, which then persist throughout life. The heart now sends blood first toward the gills, through them, and finally away from them, through the mature branchial arch artery vasculature (Figure 8).10,11

In an amphibian like a frog a process very similar to fish development occurs. Very early on, the branchial arch arteries merely carry blood through the arches, prior to the development of the gills. Then during the tadpole stage the gill vasculature develops from these arch arteries, and the gills become functional. Finally, as the mature frog develops, the arch arteries are again modified to supply the needs of a land-dwelling animal. The arteries of the 3rd arch supply the head and neck, those of the 4th arch supply the rest of the body, and those of the 6th arch supply circulation to the lungs (Figure 8). In reptiles, there is never any functional gill apparatus. Yet a similar set of branchial arch arteries develops, and supplies various body regions using the same arch arteries as in amphibians (Figure 8). We introduced the mammalian pattern earlier in this essay (see also Figure 8). Thus at each stage the successor vertebrate type, during its development, will reproduce structures much like those of its series of ancestor organisms during their own early development. This is comprehensible only if evolution is “adding new features on top of old.”

In the human, sometimes the set of paired transitional arteries which appear during development before their later transformation are called “aortic arch arteries,”12,13 since they join a ventral to a dorsal aorta. However, they are often called the “branchial arch arteries” to emphasize their evolutionary origins. They are a classic example of the retention of a structure which has lost its ancestral function (i.e. supplying blood vessels to functional gills) but is retained exclusively to be used as a building block for a more recently evolved structure. This is precisely how we would expect evolution to work.

Let’s summarize, and be very clear about what we have just observed. The structural characteristics of the heart and great arterial vessels amongst living vertebrates do not merely possess surface similarities. Two crucial points need to be emphasized here. First, the retention of “aortic arch arteries” (or “branchial arch arteries”) in non-aquatic vertebrates serves no respiratory function. They are merely connecting pipes. Their sole purpose is to be used as building blocks to construct modified circulatory elements which function in the species which possess them. But remember, in principle, such “building blocks” might have been constructed in any manner whatsoever. The fact that all living vertebrates retain a set of six arch arteries during their development is strong evidence that they have inherited this pattern of development from a common ancestor, one which did use these arteries to develop functional respiratory structures (i.e. gills).

Second, given a set of six arch arteries, there is no logical or structural reason why the 3rd artery must contribute to the carotid circulation, the 4th artery must supply blood to the body, and the 6th artery must contribute to the circulation to the lungs. Why not use different arch arteries for different final structures in various vertebrates? The conclusion is inescapable—successor organisms have inherited a set of instructions for development from ancestral organisms, and are not free to deviate readily from it. Rather, since evolution is a historical process, it is a necessity that the descendant organisms follow the same general pattern of development used by their ancestors.

Previously, we discussed how, if evolution is true, we would expect that the embryonic development of complex structures such as the heart and its great vessels would proceed through a process of “adding new features on top of old.” Rather than each type of organism possessing a “direct development” where a particular complex structure is produced in the most straightforward way imaginable, things are interestingly complex. Within the embryo, development occurs in a rather roundabout way and includes intermediate stages from previous ancestral organisms. If biologists are interpreting this correctly, then we would expect that descendant species are building upon the genetic instructions of their ancestors. Gradually, through the eons of time, species alter these instructions enabling them to make new models of old “equipment.” So, just as we see structural evidence for “adding new features on top of old” so also we would expect to see genetic evidence of the same phenomenon.

The total collection of an organism’s genes (the genome) is, in essence, the instruction book on how to build its body. Furthermore, one can think of the instruction book as having chapters—like a “how-to-build-the-heart” chapter. If we investigated the genes which are important in making a heart, the genes used in today’s organisms would be an elaboration of an old “how-to-to-build-a-heart” chapter from an early version of the instruction book, a chapter that has been under continual revision for hundreds of millions of years. We would be able to make predictions about what sort of traces would remain from those much earlier heart chapters, and we would be able to determine whether predicted traces really exist. In essence what we would predict is this: we would expect to see evidence for certain “old” genes still in use in a similar manner today compared to what would have been the case in the early days of heart “manufacture.” Just as the structure of the heart of mammalian embryos goes through stages where the developing heart almost certainly resembles the old heart of ancient organisms (see our previous post), so we would expect to see certain “old” genes still in use as the cells in the developing embryo “read” the heart chapter of the instruction book and proceed to assemble into a heart.

But what would be an example of an “old” gene, and how would it be possible to recognize one when we saw it? That’s our task, and we’ll begin it by reflecting on an old song.

I could stay young and chipper
And I’d lock it with a zipper,
If I only had a heart.

Who doesn’t remember this ditty from the classic film “The Wizard of Oz”? It’s the Tinman’s song, of course. What has this got to do with the development of the heart? Well, sometimes scientists can manifest a quirky sense of humor. Some years ago a gene was found in the fruit fly Drosophila which is very important in the development of the heart. If that gene is mutated, no heart develops. So the gene was named “tinman” because the poor mutant fly larva were constructed, just like the beloved character from the movie, without a heart.1

What sort of a gene is tinman? In essence, tinman is a master gene. It, like most genes, provides the instructions on how to make a protein. However, the protein product (named TINMAN) of the tinman gene is special. When produced in an embryo, TINMAN is able to activate the reading of other genes which carry the instructions on how to make a heart. Cells that receive the TINMAN signal start to follow the heart-making program and, as the process continues, the little embryo makes a heart.

The fruit fly heart is simple. It is little more than a muscular tube, but it has little valves called ostia through which body fluid can seep into the central core of the tube. By constricting, the heart pumps the fluid that accumulates inside of it by a process known as peristalsis. Peristalsis is a moving wave which constricts the tube at one end and then pushes the fluid forward just like you do with a tube of tooth paste. The moving constriction drives the fluid forward so that it leaves the open head end via the heart’s aorta ensuring ongoing circulation of the internal fluid in the insect’s body. This very simple heart is not unlike the human heart at its very earliest stage of embryonic development.

So how does the TINMAN protein cause embryonic cells to make a heart? The answer is pretty simple. In essence, the TINMAN protein just turns on a switch. As you sat down at your computer earlier today, you probably used your index finger to push the on-switch, correct? That’s what the TINMAN protein does. Just as your index finger opens up a series of circuits in your computer that eventually constructs an image on the monitor, TINMAN does the same in the Drosophila embryo. It turns a switch from “off” to “on.”

Let’s carry this analogy between the switch on your computer and the TINMAN switch in embryos further. Let’s say that as your computer begins to age you update it regularly. Maybe, the monitor starts to get out-of-date, for example, and you decide you want a new model, one with a nice wide screen. So you change the monitor. The old switch still works though and you still turn your computer on by pressing the button with your index finger. Let’s say that another year goes by and you want a new wireless keyboard, so you substitute that. The next year, it’s time for a new hard-drive so you add that as well. Indeed, as the years go by you find you’ve changed almost everything except the housing for the switch. Because you’ve built your computer bit by bit, it now bears very little resemblance to your old computer—it has evolved—but the switch is still the same and it still works with your index finger. It’s not a toggle switch; it’s not a foot switch nor is it a voice switch. It is still the same index finger switch and it works just fine.

Analogies are never perfect, but that one might help clarify an important point about the TINMAN switch for heart development. Let’s make a prediction about what would happen in the history of making new varieties of hearts if evolution is true. Evolution of the heart, by definition proceeds by making gradual single step changes to a pre-existing heart design. If ever the TINMAN switch was broken, what would happen to the organism? No heart, correct? Organisms with a broken switch would die. End of the lineage, correct? Would you expect a major overhaul in the switch, like changing it from a push-button to a voice-activated switch in a single step? No. If evolution were true, you would expect the switch to stay pretty much the same over the years. In some lineages, the switch might come to activate increasingly complex circuits, as increasingly sophisticated hearts are built to sustain increasingly complex bodies, but the initial “make-a-heart” switch ought, most likely, to remain a TINMAN switch. It does one thing (turns on a circuit), does that one thing well, so why change it?

We want to emphasize that it is very clear that any switch will do. Embryos have hundreds of switches each activating a particular embryonic circuit. The reason that we would expect switches to be conserved is not because one variety of switch works better than another, it is, quite simply, historical: once a switch is put in place, it is exceedingly unlikely that it will be changed.

So in the fruit fly, that which controls the “make-a-heart” switch is TINMAN. What controls the same switch in other organisms? The zebra fish is a little aquarium fish which produces transparent embryos. This transparency trait makes it the embryologist’s dream organism and thereby it has been widely studied. Fish, like fruit flies, have a heart. We talked about the structure of the fish heart in our last post. What controls the “make a heart” switch in zebra fish? You guessed it. Out of the hundreds of proteins that operate various switches in fish embryos, the one which controls the “make-a-heart” switch is almost the same as the fruit fly, TINMAN. In fact, when one puts one of the several zebra fish versions of TINMAN into mutant fruitfly embryos which lack their own TINMAN, one of the zebra fish versions will throw the switch, and cause the mutant embryo to produce a heart.2 Zebra fish and fruit flies have been on separate lineages for over 500 million years, however each, despite hundreds of possible switches, still retain a switch that can only be activated by a variety of the TINMAN protein. So do other organisms like frogs and mammals have this same switch operated in the same way? Yes, all tested vertebrates, including humans make their heart in response to the TINMAN signal. It has changed a little more in mammals so the mammalian varieties are not interchangeable with the fruit fly’s TINMAN, but it is still the same gene which makes almost the same protein.

This is exactly what one would expect if evolution is true and it is one of a host of verifications for the fact that creation occurs through gradual modification of pre-existing organisms. Any switch would do if organisms were being created from scratch. A switch is a switch is a switch. All that is needed is to start the “make-a-heart” program. If evolution is true, one would expect that frequently the same switch would be used down through the eons of time. Furthermore, one would predict there would, through time, be some slight mutational modifications. This is exactly what we find, and we find the same exact sort of pattern for the other switches which activate the embryonic construction of other body structures, like the eye, the limbs, and the vertebra for example.

Five hundred and fifty million years ago the hearts of the entire animal world were simple tubular hearts, something that still characterizes heart development at the early embryonic stages in animals today. However, as time went by in certain lineages the hearts became increasingly sophisticated. As they became more sophisticated, new switches for the add-ons were put into place. In our next post, we’ll look at some of the new switches and explore some predictions we can make about them as well.


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About the Authors

  • Darrel Falk

    Darrel Falk

    Darrel Falk is the author of Coming to Peace with Science: Bridging the Worlds Between Faith and Biology and co-author of The Fool and the Heretic: How Two Scientists Moved Beyond Labels to a Christian Dialogue about Creation and Evolution.  He speaks frequently on the relationship between science and faith at universities and seminaries. From 2009 to 2012, he served as president of BioLogos. Under his leadership, the BioLogos website and daily blog grew to thousands of readers and hundreds of authors, the Biology by the Sea workshop trained Christian biology teachers, and private workshops in New York were a forum for conversation and worship with top evangelical leaders. As president, he brought BioLogos into conversation with Southern Baptist leaders and with Reasons to Believe, and today he continues to be a key member of those dialogues. Falk received his B.Sc. (with Honors) from Simon Fraser University, and earned his Ph.D. from the University of Alberta. He did postdoctoral work at The University of British Columbia and the University of California, Irvine before accepting a faculty position at Syracuse University in New York. Darrel’s early research focused on Drosophila molecular and developmental genetics with funding from the National Institutes of Health and the National Science Foundation. In 1988 he transitioned into Christian higher education in the biology department at Point Loma Nazarene University in San Diego, where he is now Emeritus Professor of Biology. He is a member of the American Association for the Advancement of Science, the Genetics Society of America, and the American Scientific Affiliation.  
  • David Kerk

    David Kerk

    David Kerk is Professor of Biology, Emeritus, at Point Loma Nazarene University. Dr. Kerk obtained his PhD in Anatomy at UCLA and is currently involved in bioinformatics research at the University of Calgary. He resides on Vancouver Island, in Parksville, B.C. Canada.