I first encountered chemical and neo-Darwinian evolution as a freshman in high school. Thanks to the authority of my science teacher, I swallowed it — hook, line, and sinker. However, a few years later, while reading about the parts of the eye and ear and how they work together to let us see and hear, in a flash of insight I said to myself “There’s no way this all came from unguided chance. The neo-Darwinists are over-simplifying and over-extrapolating things.” It was at that moment that I became a proponent of intelligent design.

Given that the scientific evidence in the last several decades has been skewing toward ID, I’ve been puzzled as to why most biologists vehemently oppose ID, and why many in the public believe them. That is, until I read Darwin’s Bluff, by Robert Shedinger. He explains not only why Darwin didn’t publish his Unfinished Book but also Darwin’s tendency to be long on imagination and rhetoric and short on authentic humility and accepting of, and appropriately responding to, legitimate criticism. Shedinger writes:

The problem with Darwin’s book is that it failed to provide evidence to support its main point — transmutation of species by natural selection. By dwelling instead on the similarities one can observe between various species “it simply added some new illustration of what was perfectly well known before, but nothing that was in the least fitted to alter the balance of argument or evidence on the question. Mr. Darwin succeeds, so pleasantly and so ingeniously, that many an unwary reader imagines that he is proving his theory. All he is proving is, that if you admit the fundamental principle of his theory, it might possibly work in practice.” The elegance of Darwin’s writing married to exhaustively detailed descriptions of the most minute characteristics of living organisms produced a rhetorical tour de force. Surely someone who observed nature in such exquisite detail knew what he was talking about. While he made arguments, he provided little evidence and essentially proved nothing.

Darwin’s modern-day followers continue to use his method. It, a priori, rules out any possible explanation for the origin and diversity of life other than natural selection acting on variation, and it blinds them to, or makes them purposely omit, any evidence to the contrary — evidence that demands an explanation!

Human Life Is a Hard Problem

In the book I co-authored with Steve Laufmann, Your Designed Body, we showed that to solve all the hard problems the body faces from the laws of nature to survive, it needs several coherent interdependent systems precisely working together. This is Michael Behe’s “irreducible complexity” raised to several orders of magnitude. That’s because to do the job right requires much more than “a purposeful arrangement of parts.” It also requires that each part be made to the right specifications so that when rightly activated they do the right thing(s) to the right degree(s) to keep a specific vital parameter within the right range. This is the Goldilocks principle in action — fine tuning. 

When it comes to human life, as in our human technology, real numbers have objective life-or-death consequences. If a given chemical, like oxygen, carbon dioxide, glucose, potassium, or calcium, or a physiological parameter, like temperature, heart rate, or blood pressure, falls outside a given range, every physician (like every engineer) knows that, unless it’s immediately corrected, malfunction and death are likely to result. There’s no way of getting around this truth! 

As we say in our book:

Hard problems require ingenious solutions. Fortunately for us, ingenious solutions are everywhere in biology — and nowhere more so that in the human body. Life never exists as a formless blob, but instead always exists in an architecturally complex form. Nor, of course, does life exist in the often-fertile imaginations of materialist scientists. Life is found in the real world, and reality has a way of humbling theories that are not grounded in the nitty-gritty details of what life requires. Physicians don’t get to make stuff up. They don’t have the luxury to merely observe how life looks or theorize about its superficial qualities. They need to know how the body really works, how the parts affect each other, and what it takes in practical terms to keep it all working over a (hopefully) long lifetime. Though their mistakes sometimes take longer to discover than those of physicians, engineers also must live in the real world. Engineers design, build, deploy and operate complex systems that do real work in the real world. And it takes yet more work to keep these systems from failing, which is pretty much guaranteed to happen at the least opportune times.

If you’ve never used mental energy to try to solve any one of the hard problems that need to be solved for human life to continue, then how can you appreciate what it took to come up with and apply the solution? Or as Marcos Eberlin put it in his book Foresight, “But if Nobel-caliber intelligence was required to figure out how this existing engineering marvel [aquaporin] works, what was required to invent it in the first place?” 

Solving the Next Hard Problem of Life

Life is a series of millions of hard problems that must be solved all the time, or else. My last article looked at how the embryo has the foresight to solve one of its first hard problems, getting an adequate supply of oxygen and nutrients throughout gestation, by helping to form the placenta. But for the embryo there are still lots of hard problems ahead. In our book Your Designed Body, this is how we explained the embryo’s next major causal hurdle.

The placenta is just the first step in the continuous and increasing supply of essential building blocks the developing child needs. After conception the number of cells in the embryo begins to multiply and, before long, to differentiate into the hundreds of different cell types the body will need. For this differentiation process to work, order and timing are everything. Much of what the baby will need at birth will take the full nine months of the gestation process. Some body systems can wait till near the end of the gestation process; others must arrive much sooner. Since oxygen and nutrients must be distributed to every cell in this little body, which organ system would you guess needs to develop first if the embryo is to survive?

Think about the answer to this question for a few seconds, then read how we started to answer it in our book. 

The cells of the endoderm will form the lungs and the digestive system. But those aren’t needed right away, since the mother has the duties of the lungs and digestive system covered via the placenta. The cells of the ectoderm differentiate to form the skin and nervous system. Once outside the womb, they will allow this new human life to interact with and be protected from her surroundings. But for now, she’s safe in her mother’s womb, so she can do without this as well for now. Some of the mesoderm will differentiate to form the musculoskeletal system. Once outside the womb, this system will allow this new person to move around and handle things. But for now, where does she need to go and what does she need to do? Her job is just to sit tight and let her mother provide her with what she needs to grow and develop. Other cells in the mesoderm will differentiate to form the kidneys. Once outside the womb, they’ll allow the baby to control her salt and water content. But for now, her mother, through the placenta, has that covered too. So, what’s left?

Here’s how we explained the embryo’s solution to its distribution problem.

For this the embryo needs a cardiovascular system — a heart, blood vessels, and blood — and these also come from the mesoderm. At about three weeks, the new heart begins pumping blood through its developing circulatory system. Over the next several weeks and months, as the embryo becomes a fetus and grows and develops, the heart provides the driving force for life. The cardiovascular system begins its life-critical role even as it’s still developing. If it couldn’t manage this extraordinary feat, the unborn baby would not survive.

But when she learns how to crawl, walk, jump, and run, what will it take for her body to be able to do these things? Take a moment to think about the laws of motion and the forces of nature which her heart will have to overcome! Here’s how we explained it in our book:

Just as it takes energy to roll a ball up a hill (against gravity) or push a chair across the floor (against friction) or accelerate a car (against inertia), the heart pumps blood throughout your body by way of about 60,000 miles of pipe called blood vessels. The cardiovascular system is a closed system composed of two circular pathways, or circuits. As the blood transits a complete route, it’s pumped twice by the heart, once to drive to the lungs to pick up oxygen, and a second time to drive the oxygenated blood throughout the body. Because the blood flows continuously around this closed system, O₂ delivery to the body can be adjusted simply by varying the rate the blood is pumped. That’s why your heart beats harder and faster when you get more active.

Adequate cardiac function is important for survival. At complete rest, for your organs and tissues to work properly, your heart must pump out about five liters of blood per minute. But when it comes to maximal activity, what would have meant “eating or being eaten” to our ancient ancestors, your heart must pump out about 25 liters per minute. It’s just like with your car. When you want to speed up, or go up a hill, you have to press the accelerator down to give the engine more gas so it has the requisite energy. The engine also has to big enough to do the job. A lawnmower engine just won’t do!   

This shows you that real numbers have objective consequences for life and death. All physicians and engineers know that no amount of imaginary thinking would have allowed for human survival without the heart being able to have the right specifications to do what it needs to do at exactly the right times.  

But how did the human heart get to be that way? Here’s one neo-Darwinian explanation. 

Selective Pressure to the Rescue

A recent article at Science Daily claims, “Study on architecture of heart offers new understanding of human evolution.” It promotes a new study, published in the journal Communications Biology, “Left ventricular trabeculation in Hominidae: divergence of the human cardiac phenotype.” The study, they say, “has uncovered a new insight into human evolution by comparing humans’ hearts with those of other great apes”

The Science Daily article states that 

despite humans and non-human great apes having a common ancestor, the former has evolved larger brains and the ability to walk or run upright on two feet to travel long distances, likely to hunt. A human’s larger brain and greater physical activity compared to other great apes can also be linked to higher metabolic demand, which requires a heart that can pump a greater volume of blood to the body. Similarly, higher blood flow contributes to humans’ ability to cool down, as blood vessels close to the skin dilate — observed as flushing of the skin — and lose heat to the air.

The article goes on to say, 

Now, through a new comparative study of the form and function of the heart, researchers believe they have discovered another piece of the evolutionary puzzle. The team used echocardiography — a cardiac ultrasound — to produce images of the left ventricle, the chamber of the heart that pumps blood around the body. Within the non-human great ape’s left ventricle, bundles of muscle extend into the chamber, called trabeculations.

Ventricular trabeculations are finger-like projections of muscle that protrude into the ventricular cavity. Says co-author Bryony Curry, 

the left ventricle of a healthy human is relatively smooth, with predominately compact muscle compared to the more trabeculated, mesh-like network in the non-human great apes. In humans, who have the least trabeculation, we observed comparatively greater cardiac function. This finding supports our hypothesis that the human heart may have evolved away from the structure of other non-human great apes to meet the higher demands of humans’ unique ecological niche.

The Science Daily article ends by quoting co-author Dr. Aimee Drane, “In evolutionary terms, our findings may suggest selective pressure was placed on the human heart to adapt to meet the demands of walking upright and managing thermal stress.”  

It’s important to point out that one footnoted source from the Communications Biology article states that in humans, 

Excessive trabeculation is frequently observed by imaging studies in healthy individuals, as well as in association with pregnancy, athletic activity, and with cardiac diseases of inherited, acquired developmental or congenital origins.

Petersen, S.E. et al. Excessive Trabeculation of the Left Ventricle. JACC Cardiovasc. Imaging 16, 408-425 (2023)

Regarding possible causation, it states that “reversible excessive trabeculation is known to develop secondarily to increased preload in a sizeable proportion of individuals who are pregnant with otherwise normal hearts” and “a reversible phenotype of excessive trabeculation has been reported in athletes related to high cardiac preload demand associated with intensive physical exercise.” Finally, research has shown that there seem to be forty or more “gene loci associated with trabecular development.”

What do these statements mean in practical terms? Preload is the amount the heart muscle stretches after the ventricle fills with blood during the relaxation phase (diastole). The more blood there is in the left ventricle at the end of diastole, the more pressure the blood applies against the left ventricular wall. This is called the left ventricular end-diastolic pressure (LVEDP). LVEDP is a marker for the preload and is measurable on echocardiography. 

More LVEDP causes the heart muscle to stretch more, which makes it reflexively contract more to pump out more blood per contraction (stroke volume). Since the amount the heart pumps out per minute (cardiac output) is directly related to the stroke volume, this means that an increase in preload generally causes an increase in cardiac output.

Due to their unique physiological situations, pregnant women and athletes have more preload. This increase in LVEDP is thought to explain why the hearts of some pregnant women and athletes develop excessive trabeculations, similar to the hearts of non-human great apes. Moreover, this is reversible, meaning that sometime after pregnancy and high-level athletic activity ceases, the excessive trabeculations disappear and the left ventricle goes back to being smooth.     

In other words, the adaptive response of the human heart to the increase in preload during pregnancy and high-level athletics results for some people in the reversible development of the phenotype (excessive trabeculations) that predominates in non-human great apes. Research seems to indicate that there are forty or more gene loci that may be involved in the phenomenon of left ventricular trabeculation.  

Points to Ponder

Evolution involves two steps. The first is the generation of a new variation by mutation, and the second determines which randomly generated variant(s) will persist into the next generation. Selective pressure is the concept that internal and external factors can reduce or increase reproductive success in a portion of a population, thereby driving natural selection. In other words, natural selection and selective pressure generate absolutely nothing. All they do is preserve a given variation based on the effects of certain internal and external factors on the ability to survive, flourish, and reproduce.  

In this case, the assumption is that as our ancient ancestors acquired a higher metabolic rate to allow for upright bipedal mobility, larger brains, and more complicated temperature control, they would have at the same time acquired better heart function, manifesting as higher rates of blood flow. This study seems to show that the trabeculated left ventricle of the non-human great apes does not function as well as the smooth left ventricle of humans. Since, as the theory goes, humans and non-human great apes evolved from a common ancestor, this means, as the co-authors state, “selective pressure was placed on the human heart to adapt to meet the demands of walking upright and managing thermal stress” and “the human heart may have evolved away from the structure of other non-human great apes to meet the higher demands of humans’ unique ecological niche.” 

The scientists here are just stating the obvious. Their investigation shows that the human heart has a smoother left ventricle than the trabeculated one of the non-human great apes. For now, we’ll accept the conclusion that this difference affords humans better heart function — although the fact that many high-level athletes have reversible excessive trabeculations makes this highly suspect. At the same time, humans have evolved larger brains and the ability to walk or run upright on two feet to travel long distances compared to other great apes, linked to higher metabolic demand, which requires a heart that can pump a greater volume of blood to the body. Once again, we’ll accept this conclusion — although exercise physiology involves factors beyond cardiac function, such as respiration, oxygen uptake, the oxygen-carrying capacity of the blood, and neuromuscular function, to name but a few. 

Remember, natural selection and selective pressure don’t generate anything. So, one must ask the obvious question: From what specific mutations involving which specific genes and their specific regulation, and in what specific order, did this “evolution” of the smooth left ventricle develop? Remember, studies have shown that forty or more different genes are associated with this trabeculation phenomenon, but nobody knows exactly how they work. 

None of this is even mentioned as something that would be necessary to verify causation. Selective pressure seems to be a magical force by which Nature is given agency by neo-Darwinists so that it could give humanity what is needed to survive within its “unique ecological niche.” No wonder, as Shedinger relates, that several critics found the Origin of the Species “laughable” especially “the reference to Darwin’s argument that when species engage in behaviors not normal to their kind, these new habits may in time lead to large-scale evolutionary change.” 

This leads to another glaring lacuna. There is no detailed explanation of all the specific genetic and regulatory changes that would have needed to take place for a non-human great ape to evolve into a human with upright bipedal mobility, a larger brain, higher metabolic rate, and more complex thermoregulation — while at the same time the heart was adapting to allow for this increase in functional ability at each step along the way. As Shedinger notes, “Asa Gray, Professor of Botany at Harvard University, though a supporter, told Darwin ‘Well, what seems to be the weakest point in the book is the attempt to account for the formation of organs by natural selection. Some of this reads quite Lamarckian.’” 

In his book The Design and Origin of Man, Stuart Burgess details several unique features along with unique abilities present in bipedal humans compared to our nearest relative, the quadrupedal ape. He notes that “according to evolution, humans have gradually evolved an upright stature over millions of years [but] to stand upright, humans need many design features not present in quadrupeds and these must all be in place simultaneously.” 

In contrast to the neo-Darwinian narrative, which totally ignores the required anatomical and physiological features, Burgess applies his extensive award-winning mechanical engineering experience to explain this, literally from the ground up. Our upright bipedalism and the unique mobility and functional capabilities it affords us starts with having the right types of feet and ends with having the right type of brain to maintain control — and includes the right types of knees, hips, spine, and spinal cord connection to the brain through the bottom of the skull (not the back of it like in quadrupeds). In addition, as alluded to by Asa Gray’s critique, besides cardiac function, one has to also take into account a whole host of other physical, metabolic, respiratory, endocrine, and hematological differences. None of these are alluded to by these scientists. But now you know because you read it here — so don’t be misled.  

Finally, it’s interesting to note that the Science Daily article makes no mention of the fact that humans can have excessive trabeculation in their left ventricle. And the Communications Biology paper only mentions it in passing with respect to an ongoing debate within human cardiology. What are we to make of this revelation that even though “selective pressure was placed on the human heart to adapt to meet the demands of walking upright and managing thermal stress,” it appears that in certain circumstances (such as increased preload in pregnancy and high-level athletics) the smooth compact phenotype can revert to the trabeculated mesh-like network phenotype, apparently without affecting survival? Does this mean that in these cases we’re seeing “devolution before our eyes”? And since this is reversible after pregnancy and when high-level athletics cease, does this mean that we’re also seeing “repeated evolution before our eyes?” 

Does This Even Make Sense? 

What seems to stand out here is that the basis for a trabeculated left ventricle is still present within the human genome and its regulatory mechanisms. Given the right circumstances, reversible left ventricular trabeculations can develop. One might ask, What is it about human existence that is so different from that of the non-human great apes? One obvious answer is that we have upright bipedal mobility. This capacity naturally causes gravity to reduce the return of blood from the lower half of the body to the heart, thereby possibly reducing the relative preload of the human heart, compared to that of the non-human ape. 

A different theory to consider is that, given our upright posture and gravity-related reduced venous return to the heart from the lower half of the body, humans may, in general, have a lower preload than non-human great apes. This is because non-human great apes, being quadrupeds, spend more time in the horizontal position, which would preclude this gravity-related reduced venous return to the heart from the lower half of the body and so, in general, may result in a higher preload (LVEDP).  But we know that one factor that results in excessive trabeculations in humans is a high preload. So, it is plausible that a lower preload may prevent the left ventricle from forming excessive trabeculations. This could be accomplished by a control mechanism that senses the LVEDP (there are many pressure sensors in the atria and ventricles) and, depending on the level, turns on or off certain genes to cause the smooth compact phenotype seen in humans. 

This would mean that the underlying genetic and regulatory information needed to make the human left ventricle become smooth and compact may even still be present within the genome of the non-human great apes. But because their preload remains relatively higher than for humans, their left ventricles stay trabeculated. It would also mean that it would have been this innate engineered genome that allowed the human heart to adapt to meet the demands of walking upright and managing thermal stress, instead of the vacuous and magical “selective pressure” espoused by neo-Darwinists.