Tuesday, June 14, 2016

Our Bodies Were Not Built To Last

As summer kicks in to high gear, the weather is heating up, MLB pennant races are heating up, barbecue grills are heating up, and the music is reckless and hot. Last summer witnessed the 50th anniversary of the Grateful Dead with an epic reunion and the 20th anniversary of the passing of Jerry Garcia. Yet, unbelievably, the music never stopped and the long strange trip continues. The Dead have been resurrected once again, with Dead and Company rocking a six-week US tour. With my kids finally accepting their own fate as the next generation of Deadheads, the revival of the music that makes so many of us feel alive has gotten me thinking about heritability and what information (biological or existential) is critically important to pass on to the next generation. And further, what is the meaning of life? (Full disclosure: this could simply be how I am dealing with my own process of aging, so please humor me for a moment…)
Here’s a sobering thought: the fundamental meaning of life is to get your genetic material into the next generation. There is no deeper meaning from a biological perspective than to maximize reproductive fitness. Different species take different approaches to spreading their seed, so-to-speak. On one end of the spectrum, some animals like sockeye salmon and mosquitos, which live in relatively unstable environments where the probability of survival is relatively low, focus on producing large numbers of offspring before they die, hoping that these offspring will reach sexual maturity and also reproduce. This is a good reproductive strategy in such environments because reproductive fitness is defined not by one’s ability to pass on their own genes, but by their offspring’s ability to pass on their genes.
Contrast this with the approach at the other end of the spectrum. Some animals, like orcas and primates live in much more stable environments, in population densities that are near carrying capacity for the environment (the highest density that can be supported by the resources available). These species produce many fewer offspring, but because there is a high probability of survival for offspring and parents alike, the parents invest a considerable amount of energy into raising their offspring (I know this is true because my kids exhaust me! Please help…)
In the case of primates, in particular, we know a great deal about reproduction, life history, and parental investment: primates produce few offspring, invest considerable energy into offspring care, and they generally have lengthy lives relative to other species in the same habitats. Compound this with advances in modern medicine, and human primates are enjoying lifespans that increase with successive generations. We live longer than our grandparents’ generation, and so on and so forth. And while this is fantastic news because we get to enjoy our children and grandchildren for longer than at any other time during human history, this does not come without a significant price: our skeletons break down in ways that other primates’ do not. Simply put, our bodies were not built to last.
Humans are unique among primates in that we walk around on two legs. In fact, the evolution of our bipedal locomotion predated the evolution of our large brains by several million years. And our unique mode of locomotion combined with our ever-lengthening lifespans has resulted in several musculoskeletal problems that we develop as we age. Before we get to that somber topic, it is useful to review some of the anatomical adaptations that allow us to walk around bipedally.

1. Forward position of foramen magnum. The foramen magnum – or the opening in the skull through which the brain stem/spinal cord exit – is more anterior positioned in humans compared to other primates and mammals, which places the vertebral column directly underneath the skull as opposed to behind it as in quadrupedal animals.

2. S-shaped curvature of vertebral column. By moving the vertebral column directly underneath the skull, humans require an S-shaped spinal curvature (with cervical and lumbar lordoses and a thoracic kyphosis) in order to balance the head and torso over the pelvis.

3. Broad pelvis with laterally-flared iliac blades. The iliac blades of the human bony pelvis – the parts that stick out to the side – are rotated laterally and flare outward from the midline of the body. This positions the lesser gluteal musculature (gluteus medius and gluteus minimus) lateral to the hip joint, enabling these muscles to function as abductors of the thigh at the hip joint, and prevent excessive pelvic tilt to the unsupported side during the stance phase of bipedal gait. In nonhuman great apes, this musculature is positioned posteriorly and acts synergistically with the gluteus maximus to extend the thigh, not abduct it.

4. Oversized hip and knee joints. Joint loading in response to bipedal locomotion, as well as that reflective of body mass, is borne entirely through the joint surfaces of the lower limb in humans. Therefore, we evolved expanded articular surfaces compared to our great ape relatives, which reduces shear stress in the articular cartilage. The femoral condyles and tibial condyles of the human knee are also significantly flatter in lateral profile than in nonhuman apes, which further reduces shear stress in articular cartilage. Because articular cartilage is avascular and cannot actively repair itself, reducing the shear stress borne by the cartilage also reduces the incidence of damage.

Carrying angle of the femur
5. Carrying angle of femoral shaft. The shaft of the human femur (thigh bone) is oriented obliquely relative to the femoral condyles (the part of the femur that sits on the tibia, or leg bone, to form the knee joint). This angled shaft places the knee joint directly under the center of mass. In quadrupedal animals (including our great ape relatives), the femoral shaft is more vertically oriented.

6. Adducted hallux. The human hallux – or big toe – is in line with all other digits of the foot, enabling an efficient toe off in an anterior direction in bipedal gait. In nonhuman primates, the hallux is abducted, which enables these animals to grasp with their feet in a fashion similar to manual grasping.

7. Sesamoids in tendons of flexor hallucis brevis. Sesamoid bones are bones that develop in the tendons of muscles, and the best example is the patella, or knee cap. In humans, sesamoids also develop in the tendon of flexor hallucis brevis, a muscle in the sole of the foot that flexes the big toe. These sesamoids create a tunnel through which courses the tendon of flexor hallucis longus (another big toe flexor muscle). This tunnel allows flexor hallucis longus to remain free to contract and flex big toe when all of the body weight is placed on head of the 1st metatarsal, such as when pushing off during walking.

These seven adaptations to bipedal locomotion are present in the earliest members of the fossil genus Australopithecus (and some earlier ones too), even before brains evolved to be bigger. So one can make the argument that bipedal locomotion is the hallmark of human evolution, with the evolution of big brains being a secondary adaptation that may or may not be related to the evolution of our unique locmotor mode.

Numerous hypotheses exist as to why we evolved this weird form of walking. Walking around bipedally is energetically efficient; it requires only approximately 1 calorie/min to walk. Was this the advantage it proffered over quadrupedal locomotion? Or perhaps we became bipedal in order to free our hands up to carry provisions back to our mates. Or maybe it was a way of reducing heat stress by reducing the surface area where sunrays hit directly while increasing the amount of surface area exposed to wind? Could it have evolved in order for us to see over tall grasses in the savannah? Or to increase feeding efficiency and resource exploitation? Or perhaps it was so we could posture for mates… All of these are plausible hypotheses, and there are plenty of scientific arguments in favor or one or more of these. But the fact remains, it doesn’t really matter why we evolved bipedal locomotion. Any way you slice it, we evolved it. And now we’re saddled with the baggage of our ancestors: bodies adapted to bipedal locomotion take a severe beating. Again, our bodies, especially our skeletons, were not built to last.

Vertebral compression fracture
Bone is approximately 60% mineral (calcium and phosphate) and the other 40% is collagen and other proteins. We reach our peak bone mass at about 30 years of age, which means that the most responsive time for us to build bone mass is while we are young and growing. With age, everyone loses bone mass and density; we call this osteopenia, and it is normal. But when we lose an abnormal amount of bone mass, we can this osteoporosis. Osteoporosis is common, with about 54 million Americans suffering from this disease, and often results in bone fracture. The most prevalent osteoporotic fractures are vertebral compression fractures, where the loss of bone in the vertebral column results in fracture of the body of the vertebra itself. Humans and the other great apes have an equivalent amount of bone mineral and equal bone densities, but human vertebral bodies are enlarged to absorb more compressive shock during bipedal locomotion. Therefore, they have thinner walls of the vertebral body, which are at risk of collapsing with reduced bone mass and/or density, resulting in compression fracture. These types of fractures do not occur in nonhuman apes because they have thicker walls of their vertebrae than do humans, and because their spines are parallel to the ground, not perpendicular, so there is no axial compression of the vertebral column during locomotion.

Another result of repetitive compression loading of the spine that only humans suffer is degenerative disc disease. Intervertebral discs between each of the vertebrae of the spine are comprised of two tissue types: a central, jelly-like nucleus surrounded by a strong, fibrous ring that contains the nucleus. After repeated compression, the fibrous ring of the intervertebral disc can break down, leading to a posterior bulge that impinges upon peripheral nerves that exit the spinal cord (which runs through the canal in the posterior aspect of the vertebral column). Ergo, pinched nerves. These degenerated discs do not occur with high frequency in nonhuman apes, again as a result of their quadrupedal (and less destructive) mode of locomotion.

Degenerative disc disease
One final example of how our long lifespans are not in accord with the “lifespan” of our skeleton is degenerative joint disease and osteoarthritis. The ends of bones with joint spaces are covered in a thin layer of hyaline (articular) cartilage. Hyaline cartilage is avascular, meaning that it does not have its own blood supply, and it cannot actively repair itself if damaged. In order to protect against damage, joint surfaces (of the knee at least) become flatter as body size increases during growth. This is because as body mass increases, so does the transarticular load transmitted through joint surfaces (and hyaline cartilage covering them). This has the effect of reducing shear stresses that are experienced by the cartilage and limiting the capacity to damage the cartilage by growth alone. When the hyaline cartilage breaks down, the result is damage to the bone, pain, and joint swelling – osteoarthritis. The incidence of osteoarthritis in nonhuman great apes is dramatically lower than in humans, and is attributed to a combination of shorter lifespans in the wild and the lack of a destructive, bipedal mode of locomotion.

Given all of the ways that our skeletons break down during life, it is truly quite remarkable that 60-70 year old musicians such as the surviving members of the Grateful Dead are still able to shake it, shake it in the summer of 2016. So we should embrace it while we can keep on dancing, keeping in mind that while every cloud has a silver lining; in this case, every silver lining does have a touch of grey.

Contributed by: Jason Organ, PhD

Jungers, W. (1988). Relative joint size and hominoid locomotor adaptations with implications for the evolution of hominid bipedalism Journal of Human Evolution, 17 (1-2), 247-265 DOI: 10.1016/0047-2484(88)90056-5

Jurmain R (2000). Degenerative joint disease in African great apes: an evolutionary perspective. Journal of human evolution, 39 (2), 185-203 PMID: 10968928

Latimer B (2005). The perils of being bipedal. Annals of biomedical engineering, 33 (1), 3-6 PMID: 15709701

Russo, G., & Kirk, E. (2013). Foramen magnum position in bipedal mammals Journal of Human Evolution, 65 (5), 656-670 DOI: 10.1016/j.jhevol.2013.07.007

Ward, C. (2002). Interpreting the posture and locomotion ofAustralopithecus afarensis: Where do we stand? American Journal of Physical Anthropology, 119 (S35), 185-215 DOI: 10.1002/ajpa.10185

No comments:

Post a Comment