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9.5: Bone Classification - Biology


Learning Objectives

  • Classify bones according to their shapes
  • Describe the function of each category of bones

The 206 bones that compose the adult skeleton are divided into five categories based on their shapes (Figure 1). Their shapes and their functions are related such that each categorical shape of bone has a distinct function.

Long Bones

A long bone is one that is cylindrical in shape, being longer than it is wide. Keep in mind, however, that the term describes the shape of a bone, not its size. Long bones are found in the arms (humerus, ulna, radius) and legs (femur, tibia, fibula), as well as in the fingers (metacarpals, phalanges) and toes (metatarsals, phalanges). Long bones function as levers; they move when muscles contract.

Short Bones

A short bone is one that is cube-like in shape, being approximately equal in length, width, and thickness. The only short bones in the human skeleton are in the carpals of the wrists and the tarsals of the ankles. Short bones provide stability and support as well as some limited motion.

Flat Bones

The term flat bone is somewhat of a misnomer because, although a flat bone is typically thin, it is also often curved. Examples include the cranial (skull) bones, the scapulae (shoulder blades), the sternum (breastbone), and the ribs. Flat bones serve as points of attachment for muscles and often protect internal organs.

Irregular Bones

An irregular bone is one that does not have any easily characterized shape and therefore does not fit any other classification. These bones tend to have more complex shapes, like the vertebrae that support the spinal cord and protect it from compressive forces. Many facial bones, particularly the ones containing sinuses, are classified as irregular bones.

Sesamoid Bones

A sesamoid bone is a small, round bone that, as the name suggests, is shaped like a sesame seed. These bones form in tendons (the sheaths of tissue that connect bones to muscles) where a great deal of pressure is generated in a joint. The sesamoid bones protect tendons by helping them overcome compressive forces. Sesamoid bones vary in number and placement from person to person but are typically found in tendons associated with the feet, hands, and knees. The patellae (singular = patella) are the only sesamoid bones found in common with every person. Table 1 reviews bone classifications with their associated features, functions, and examples.

Table 1. Bone Classifications
Bone classificationFeaturesFunction(s)Examples
LongCylinder-like shape, longer than it is wideLeverageFemur, tibia, fibula, metatarsals, humerus, ulna, radius, metacarpals, phalanges
ShortCube-like shape, approximately equal in length, width, and thicknessProvide stability, support, while allowing for some motionCarpals, tarsals
FlatThin and curvedPoints of attachment for muscles; protectors of internal organsSternum, ribs, scapulae, cranial bones
IrregularComplex shapeProtect internal organsVertebrae, facial bones
SesamoidSmall and round; embedded in tendonsProtect tendons from compressive forcesPatellae

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NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Gilbert SF. Developmental Biology. 6th edition. Sunderland (MA): Sinauer Associates 2000.

  • By agreement with the publisher, this book is accessible by the search feature, but cannot be browsed.


The Skeleton

The adult human skeleton has a total of 213 bones, excluding the sesamoid bones (1). The appendicular skeleton has 126 bones, axial skeleton 74 bones, and auditory ossicles six bones. Each bone constantly undergoes modeling during life to help it adapt to changing biomechanical forces, as well as remodeling to remove old, microdamaged bone and replace it with new, mechanically stronger bone to help preserve bone strength.

The four general categories of bones are long bones, short bones, flat bones, and irregular bones. Long bones include the clavicles, humeri, radii, ulnae, metacarpals, femurs, tibiae, fibulae, metatarsals, and phalanges. Short bones include the carpal and tarsal bones, patellae, and sesamoid bones. Flat bones include the skull, mandible, scapulae, sternum, and ribs. Irregular bones include the vertebrae, sacrum, coccyx, and hyoid bone. Flat bones form by membranous bone formation, whereas long bones are formed by a combination of endochondral and membranous bone formation.

The skeleton serves a variety of functions. The bones of the skeleton provide structural support for the rest of the body, permit movement and locomotion by providing levers for the muscles, protect vital internal organs and structures, provide maintenance of mineral homeostasis and acid-base balance, serve as a reservoir of growth factors and cytokines, and provide the environment for hematopoiesis within the marrow spaces (2).

The long bones are composed of a hollow shaft, or diaphysis flared, cone-shaped metaphyses below the growth plates and rounded epiphyses above the growth plates. The diaphysis is composed primarily of dense cortical bone, whereas the metaphysis and epiphysis are composed of trabecular meshwork bone surrounded by a relatively thin shell of dense cortical bone.

The adult human skeleton is composed of 80% cortical bone and 20% trabecular bone overall (3). Different bones and skeletal sites within bones have different ratios of cortical to trabecular bone. The vertebra is composed of cortical to trabecular bone in a ratio of 25:75. This ratio is 50:50 in the femoral head and 95:5 in the radial diaphysis.

Cortical bone is dense and solid and surrounds the marrow space, whereas trabecular bone is composed of a honeycomb-like network of trabecular plates and rods interspersed in the bone marrow compartment. Both cortical and trabecular bone are composed of osteons.

Cortical osteons are called Haversian systems. Haversian systems are cylindrical in shape, are approximately 400 mm long and 200 mm wide at their base, and form a branching network within the cortical bone (3). The walls of Haversian systems are formed of concentric lamellae. Cortical bone is typically less metabolically active than trabecular bone, but this depends on the species. There are an estimated 21 × 10 6 cortical osteons in healthy human adults, with a total Haversian remodeling area of approximately 3.5 m 2 . Cortical bone porosity is usually υ%, but this depends on the proportion of actively remodeling Haversian systems to inactive cortical osteons. Increased cortical remodeling causes an increase in cortical porosity and decrease in cortical bone mass. Healthy aging adults normally experience thinning of the cortex and increased cortical porosity.

Cortical bone has an outer periosteal surface and inner endosteal surface. Periosteal surface activity is important for appositional growth and fracture repair. Bone formation typically exceeds bone resorption on the periosteal surface, so bones normally increase in diameter with aging. The endosteal surface has a total area of approximately 0.5 m 2 , with higher remodeling activity than the periosteal surface, likely as a result of greater biomechanical strain or greater cytokine exposure from the adjacent bone marrow compartment. Bone resorption typically exceeds bone formation on the endosteal surface, so the marrow space normally expands with aging.

Trabecular osteons are called packets. Trabecular bone is composed of plates and rods averaging 50 to 400 mm in thickness (3). Trabecular osteons are semilunar in shape, normally approximately 35 mm thick, and composed of concentric lamellae. It is estimated that there are 14 × 10 6 trabecular osteons in healthy human adults, with a total trabecular area of approximately 7 m 2 .

Cortical bone and trabecular bone are normally formed in a lamellar pattern, in which collagen fibrils are laid down in alternating orientations (3). Lamellar bone is best seen during microscopic examination with polarized light, during which the lamellar pattern is evident as a result of birefringence. The mechanism by which osteoblasts lay down collagen fibrils in a lamellar pattern is not known, but lamellar bone has significant strength as a result of the alternating orientations of collagen fibrils, similar to plywood. The normal lamellar pattern is absent in woven bone, in which the collagen fibrils are laid down in a disorganized manner. Woven bone is weaker than lamellar bone. Woven bone is normally produced during formation of primary bone and may also be seen in high bone turnover states such as osteitis fibrosa cystica, as a result of hyperparathyroidism, and Paget's disease or during high bone formation during early treatment with fluoride.

The periosteum is a fibrous connective tissue sheath that surrounds the outer cortical surface of bone, except at joints where bone is lined by articular cartilage, which contains blood vessels, nerve fibers, and osteoblasts and osteoclasts. The periosteum is tightly attached to the outer cortical surface of bone by thick collagenous fibers, called Sharpeys’ fibers, which extend into underlying bone tissue. The endosteum is a membranous structure covering the inner surface of cortical bone, trabecular bone, and the blood vessel canals (Volkman's canals) present in bone. The endosteum is in contact with the bone marrow space, trabecular bone, and blood vessel canals and contains blood vessels, osteoblasts, and osteoclasts.


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Flat Bones

Flat bones are the armor of the body. Flat bones provide structure, such as the shape of the head and torso, and the foundation of the shoulder and hip. Flat bones can also provide protection of soft tissues underneath. Like short bones, flat bones have walls that are made of compact bone and a center of spongy bone that forms something like a sandwich.

The cranial bones, scapula (shoulder blade), sternum (breast bone), ribs, and iliac bone (hip) are all flat bones. Of these, the scapula, sternum, ribs, and iliac bone all provide strong insertion points for tendons and muscles.

Skull

The bones of the cranium are the part of the skull that encapsulates the brain. The bones of the cranium are connected together through joints called sutures, which look like they are stitched. Sometimes, additional small bones can develop between sutured bones of the cranium along the suture lines. These small bones are called sutural bones. They develop randomly and are not named bones.


Bones: All you need to know

Bones are more than just the scaffolding that holds the body together. Bones come in all shapes and sizes and have many roles. In this article, we explain their function, what they are made of, and the types of cells involved.

Despite first impressions, bones are living, active tissues that are constantly being remodeled.

Bones have many functions. They support the body structurally, protect our vital organs, and allow us to move. Also, they provide an environment for bone marrow, where the blood cells are created, and they act as a storage area for minerals, particularly calcium.

At birth, we have around 270 soft bones. As we grow, some of these fuse. Once we reach adulthood, we have 206 bones.

The largest bone in the human body is the thighbone or femur, and the smallest is the stapes in the middle ear, which are just 3 millimeters (mm) long.

Bones are mostly made of the protein collagen, which forms a soft framework. The mineral calcium phosphate hardens this framework, giving it strength. More than 99 percent of our body’s calcium is held in our bones and teeth.

Bones have an internal structure similar to a honeycomb, which makes them rigid yet relatively light.

Bones are composed of two types of tissue:

1. Compact (cortical) bone: A hard outer layer that is dense, strong, and durable. It makes up around 80 percent of adult bone mass.

2. Cancellous (trabecular or spongy) bone: This consists of a network of trabeculae or rod-like structures. It is lighter, less dense, and more flexible than compact bone.

  • osteoblasts and osteocytes, responsible for creating bone
  • osteoclasts or bone resorbing cells
  • osteoid, a mix of collagen and other proteins
  • inorganic mineral salts within the matrix
  • nerves and blood vessels
  • bone marrow
  • cartilage
  • membranes, including the endosteum and periosteum

Below is a 3D map of the skeletal system. Click to explore.

Bones are not a static tissue but need to be constantly maintained and remodeled. There are three main cell types involved in this process.

Osteoblasts: These are responsible for making new bone and repairing older bone. Osteoblasts produce a protein mixture called osteoid, which is mineralized and becomes bone. They also manufacture hormones, including prostaglandins.

Osteocytes: These are inactive osteoblasts that have become trapped in the bone that they have created. They maintain connections to other osteocytes and osteoblasts. They are important for communication within bone tissue.

Osteoclasts: These are large cells with more than one nucleus. Their job is to break down bone. They release enzymes and acids to dissolve minerals in bone and digest them. This process is called resorption. Osteoclasts help remodel injured bones and create pathways for nerves and blood vessels to travel through.

Bone marrow

Bone marrow is found in almost all bones where cancellous bone is present.

The marrow is responsible for making around 2 million red blood cells every second. It also produces lymphocytes or the white blood cells involved in the immune response.

Extracellular matrix

Bones are essentially living cells embedded in a mineral-based organic matrix. This extracellular matrix is made of:

Organic components, being mostly type 1 collagen.

Inorganic components, including hydroxyapatite and other salts, such as calcium and phosphate.

Collagen gives bone its tensile strength, namely the resistance to being pulled apart. Hydroxyapatite gives the bones compressive strength or resistance to being compressed.

Bones serve several vital functions:

Bones serve several vital functions:

Mechanical

Bones provide a frame to support the body. Muscles, tendons, and ligaments attach to bones. Without anchoring to bones, muscles could not move the body.

Some bones protect the body’s internal organs. For instance, the skull protects the brain, and the ribs protect the heart and lungs.

Synthesizing

Cancellous bone produces red blood cells, platelets, and white blood cells. Also, defective and old red blood cells are destroyed in bone marrow.

Metabolic

Storing minerals: Bones act as a reserve for minerals, particularly calcium and phosphorous.

They also store some growth factors, such as insulin-like growth factor.

Fat storage: Fatty acids can be stored in the bone marrow adipose tissue.

pH balance: Bones can release or absorb alkaline salts, helping blood to stay at the right pH level.

Detoxification: Bones can absorb heavy metals and other toxic elements from the blood.

Endocrine function: Bones release hormones that act on the kidneys and influence blood sugar regulation and fat deposition.

Calcium balance: Bones can raise or reduce calcium in the blood by forming bone, or breaking it down in a process called resorption.


Blood and Nerve Supply

The spongy bone and medullary cavity receive nourishment from arteries that pass through the compact bone. The arteries enter through the nutrient foramen (plural = foramina), small openings in the diaphysis (Figure 6.3.10). The osteocytes in spongy bone are nourished by blood vessels of the periosteum that penetrate spongy bone and blood that circulates in the marrow cavities. As the blood passes through the marrow cavities, it is collected by veins, which then pass out of the bone through the foramina.

In addition to the blood vessels, nerves follow the same paths into the bone where they tend to concentrate in the more metabolically active regions of the bone. The nerves sense pain, and it appears the nerves also play roles in regulating blood supplies and in bone growth, hence their concentrations in metabolically active sites of the bone.

Figure 6.3.10 – Diagram of Blood and Nerve Supply to Bone: Blood vessels and nerves enter the bone through the nutrient foramen.

External Website

Watch this video to see the microscopic features of a bone.

Chapter Review

A hollow medullary cavity filled with yellow marrow runs the length of the diaphysis of a long bone. The walls of the diaphysis are compact bone. The epiphyses, which are wider sections at each end of a long bone, are filled with spongy bone and red marrow. The epiphyseal plate, a layer of hyaline cartilage, is replaced by osseous tissue as the organ grows in length. The medullary cavity has a delicate membranous lining called the endosteum. The outer surface of bone, except in regions covered with articular cartilage, is covered with a fibrous membrane called the periosteum. Flat bones consist of two layers of compact bone surrounding a layer of spongy bone. Bone markings depend on the function and location of bones. Articulations are places where two bones meet. Projections stick out from the surface of the bone and provide attachment points for tendons and ligaments. Holes are openings or depressions in the bones.

Bone matrix consists of collagen fibers and organic ground substance, primarily hydroxyapatite formed from calcium salts. Osteogenic cells develop into osteoblasts. Osteoblasts are cells that make new bone. They become osteocytes, the cells of mature bone, when they get trapped in the matrix. Osteoclasts engage in bone resorption. Compact bone is dense and composed of osteons, while spongy bone is less dense and made up of trabeculae. Blood vessels and nerves enter the bone through the nutrient foramina to nourish and innervate bones.


Bones

Bones from the skeleton of the body. There are more than 200 separate bones forming the skeleton. The study of bone is called “Osteology”. many blood cells — red blood cells, white blood cells, and platelets — are formed within your bones, This process is called hematopoiesis, and it occurs in the red marrow.

The skeleton

  1. Axial skeleton: Skull, Vertebra, Sternum, and Ribs.
  2. Appendicular skeleton: Bones of Upper limb: ( pectoral girdle, Bone of arm, Bones of the forearm, Bones of hand), Bones of the lower limb: ( Pelvic girdle, bone of the thigh, Bones of the leg, and bones of the foot).

Bones are divided according to their shape into:

  1. Long bones such as humerus, femur, and radius.
  2. Short bones such as metacarpal bones.
  3. Flat bones such as scapula or ilium.
  4. Irregular bones such as vertebrae.
  5. Pneumatic bones such as the skull.
  6. Sesamoid bones such as patella.

The humerus is the bone of the arm. It is one of the long bones. Each long bone has an upper end, shaft, and lower end. The metacarpal bones form the skeleton of the palm of the hand. They are examples of short bones as they have the same parts as the long bone but they are small in size. The patella in front of the knee joint is an example of the sesamoid bone.

Each long bone has a growing end (that ossifies later) and a non-growing end. The growing end of the humerus is the upper end. The growing ends of the radius and ulna are the lower ends. As for the bones of the lower limb is the opposite. This means that the growing end of the femur is the lower end whereas the growing ends of the tibia and the fibula are the upper ends.

Nutrient Artery

Each bone is capable of growth and repair. Thus, each bone receives its nutrient artery. It enters the bone at a certain place and in a certain direction. The nutrient artery in the long bones is directed towards the non-growing end. Thus in the humerus, it runs towards the lower end of the bone or the elbow.

Parts of a Growing Long Bone:

  • A long bone consists of two ends and a shaft.
  • Each end is called an epiphysis.
  • The shaft is called the diaphysis.
  • In a growing bone, the epiphysis is separated from the diaphysis by a plate of cartilage, an epiphyseal plate. This epiphyseal plate is the site of an increase in the length of the bone. The region of the shaft close to the epiphyseal plate is called metaphysis. At a certain age, when growth is completed, these plates ossify.
  • The shaft of a long bone is formed of compact bone enclosing a cavity which is filled with bone marrow. This cavity is called: a medullary cavity or a bone marrow cavity.
  • The epiphysis is formed of spongy, cancellous bone.
  • The shaft is covered by a fibrous membrane: the periosteum.
  • The parts of the bone that articulate are covered with hyaline articular cartilage.

Functions of Bones

  1. Bones form the supporting frame-work of the body.
  2. Bones protect the underlying structures, e.g. the skull protects the brain.
  3. Bones give attachments to the muscles and also act as levers for movement.
  4. Bones store calcium and phosphorus.
  5. The bone marrow acts as a factory for the formation of blood cells.

There are sex differences between male and female bones. Usually, the male bones are loner, heavier thicker, stronger, and possess prominent impressions for muscular attachments.

Applied Anatomy

Osteoporosis: It is the most common bone disease. It affects more the elderly white woman. The bones lose their mass and become brittle and subject to fracture. Milk and other calcium sources and moderate exercise can slow the progress of osteoporosis.

Bone fractures: Bone is a living tissue. When it is fractured it heals by callus formation. Fractures result from accidents. Patients with osteoporosis are more liable to fractures. The most common fracture in elderly is the fracture neck femur.

The vertebral column

The vertebral column (backbone or spine) is a midline column formed of 33 Vertebrae separated by intervertebral cartilaginous discs. It houses and protects the spinal cord in its spinal canal. In the side view, the vertebral column presents several curves, which correspond to the different regions of the column.

Curvature of the Spine in Adults

The shape of a normal adult human spine has 4 curves:

  1. Cervical curve: formed by 7 cervical vertebrae.
  2. Thoracic curve: formed by 12 thoracic vertebrae.
  3. Lumbar curve: formed by 5 lumbar vertebrae.
  4. Sacral curve: formed by 5 sacral vertebrae.

All vertebrae share a basic common structure. Each consists of a vertebral body, situated anteriorly, and a posterior vertebral arch.

Vertebral body

The vertebral body is the anterior part of the vertebrae. It is the weight-bearing component and its size increases as the vertebral column descends (having to support increasing amounts of weight.

Vertebral Arch

The vertebral arch refers to the lateral and posterior parts of the vertebrae. With the vertebral body, the vertebral arch forms an enclosed hole, called a vertebral foramen. The foramina of all vertebrae line up form the vertebral canal, which encloses the spinal cord. The vertebral arches have a number of bony prominences, which act as attachment sites for muscles and ligaments:

  • Pedicles: There are two of these, one left and one right. They point posteriorly, meeting the laminae.
  • Lamina: The bone between the transverse and spinous processes.
  • Transverse processes: These extend laterally and posteriorly away from the pedicles. In the thoracic vertebrae, the transverse processes articulate with the ribs.
  • Articular processes: At the junction of the lamina and the pedicles, superior and inferior processes arise. These articulate with the articular processes of the vertebrae above and below.
  • Spinous processes: Posterior and inferior projection of bone, a site of attachment for muscles and ligaments.

Thoracic Vertebrae

Sacrum and Coccyx

The sacrum is a collection of five fused vertebrae. It is described as an inverted triangle, with the apex pointing inferiorly. On the lateral walls of the sacrum are facets, for articulation with the pelvis at the sacroiliac joints.

The coccyx is a small bone, which articulates with the apex of the sacrum. It is recognized by its lack of vertebral arches. Due to the lack of vertebral arches, there is no vertebral canal, and so the coccyx does not transmit the spinal cord.


Compact Bone Structure

The basic units of compact bone are called osteons or Haversian systems. These are cylinder-shaped structures that have a mineral matrix and are home to osteocytes (mature bone cells) that are trapped in the matrix. Lamellae are formed by osteons that align themselves in a parallel orientation to form layers along the long axis of the bone. The small open spaces created in the lamellae by the osteocytes are called lacunae. Canaliculi are small channels that create a network between the lacunae to aid in the diffusion of material between the bone cells. The lamellae create circular canals called Haversian canals that contain nerves and blood vessels


Race Is Real, But It’s Not Genetic

A friend of mine with Central American, Southern European and West African ancestry is lactose intolerant . Drinking milk products upsets her stomach, and so she avoids them. About a decade ago, because of her low dairy intake, she feared that she might not be getting enough calcium, so she asked her doctor for a bone density test . He responded that she didn’t need one because “blacks do not get osteoporosis.”

My friend is not alone. The view that black people don’t need a bone density test is a longstanding and common myth. A 2006 study in North Carolina found that out of 531 African American and Euro-American women screened for bone mineral density, only 15 percent were African American women — despite the fact that African American women made up almost half of that clinical population. A health fair in Albany, New York, in 2000, turned into a ruckus when black women were refused free osteoporosis screening. The situation hasn’t changed much in more recent years.

Meanwhile, FRAX, a widely used calculator that estimates one’s risk of osteoporotic fractures, is based on bone density combined with age, sex and, yes, “race.” Race, even though it is never defined or demarcated, is baked into the fracture risk algorithms.

Let’s break down the problem.

First, presumably based on appearances, doctors placed my friend and others into a socially defined race box called “black,” which is a tenuous way to classify anyone.

Race is a highly flexible way in which societies lump people into groups based on appearance that is assumed to be indicative of deeper biological or cultural connections. As a cultural category, the definitions and descriptions of races vary. “Color” lines based on skin tone can shift, which makes sense, but the categories are problematic for making any sort of scientific pronouncements.

Second, these medical professionals assumed that there was a firm genetic basis behind this racial classification, which there isn’t.

Third, they assumed that this purported racially defined genetic difference would protect these women from osteoporosis and fractures.

Some studies suggest that African American women — meaning women whose ancestry ties back to Africa — may indeed reach greater bone density than other women, which could be protective against osteoporosis. But that does not mean “being black” — that is, possessing an outward appearance that is socially defined as “black” — prevents someone from getting osteoporosis or bone fractures. Indeed, this same research also reports that African American women are more likely to die after a hip fracture. The link between osteoporosis risk and certain racial populations may be due to lived differences such as nutrition and activity levels , both of which affect bone density.

But more important: Geographic ancestry is not the same thing as race . African ancestry, for instance, does not tidily map onto being “black” (or vice versa). In fact, a 2016 study found wide variation in osteoporosis risk among women living in different regions within Africa. Their genetic risks have nothing to do with their socially defined race.

When medical professionals or researchers look for a genetic correlate to “race,” they are falling into a trap: They assume that geographic ancestry, which does indeed matter to genetics, can be conflated with race, which does not. Sure, different human populations living in distinct places may statistically have different genetic traits — such as sickle cell trait (discussed below) — but such variation is about local populations (people in a specific region), not race.

Like a fish in water, we’ve all been engulfed by “ the smog ” of thinking that “race” is biologically real. Thus, it is easy to incorrectly conclude that “racial” differences in health, wealth and all manner of other outcomes are the inescapable result of genetic differences.

The reality is that socially defined racial groups in the U.S. and most everywhere else do differ in outcomes. But that’s not due to genes. Rather, it is due to systemic differences in lived experience and institutional racism.

Communities of color in the United States, for example, often have reduced access to medical care, well-balanced diets and healthy environments . They are often treated more harshly in their interactions with law enforcement and the legal system . Studies show that they experience greater social stress, including endemic racism , that adversely affects all aspects of health. For example, babies born to African American women are more than twice as likely to die in their first year than babies born to non-Hispanic Euro-American women.

As a professor of biological anthropology, I teach and advise college undergraduates. While my students are aware of inequalities in the life experiences of different socially delineated racial groups, most of them also think that biological “races” are real things. Indeed, more than half of Americans still believe that their racial identity is “determined by information contained in their DNA .”

For the longest time, Europeans thought that the sun revolved around the Earth. Their culturally attuned eyes saw this as obvious and unquestionably true. Just as astronomers now know that’s not true, nearly all population geneticists know that dividing people into races neither explains nor describes human genetic variation.

Yet this idea of race-as-genetics will not die. For decades, it has been exposed to the sunlight of facts, but, like a vampire, it continues to suck blood — not only surviving but causing harm in how it can twist science to support racist ideologies. With apologies for the grisly metaphor, it is time to put a wooden stake through the heart of race-as-genetics. Doing so will make for better science and a fairer society.

In 1619, the first people from Africa arrived in Virginia and became integrated into society. Only after African and European bond laborers unified in various rebellions did colony leaders recognize the “need” to separate laborers. “Race” divided indentured Irish and other Europeans from enslaved Africans, and reduced opposition by those of European descent to the intolerable conditions of enslavement. What made race different from other prejudices, including ethnocentrism (the idea that a given culture is superior), is that it claimed that differences were natural, unchanging and God-given. Eventually, race also received the stamp of science.

Over the next decades, Euro-American natural scientists debated the details of race, asking questions such as how often the races were created (once, as stated in the Bible, or many separate times), the number of races and their defining, essential characteristics. But they did not question whether races were natural things. They reified race, making the idea of race real by unquestioning, constant use.

In the 1700s, Carl Linnaeus, the father of modern taxonomy and someone not without ego, liked to imagine himself as organizing what God created . Linnaeus famously classified our own species into races based on reports from explorers and conquerors.

The race categories he created included Americanus , Africanus , and even Monstrosus (for wild and feral individuals and those with birth defects), and their essential defining traits included a biocultural mélange of color, personality and modes of governance. Linnaeus described Europeaus as white, sanguine and governed by law, and Asiaticus as yellow, melancholic and ruled by opinion. These descriptions highlight just how much ideas of race are formulated by social ideas of the time.

In line with early Christian notions, these “racial types” were arranged in a hierarchy: a great chain of being , from lower forms to higher forms that are closer to God. Europeans occupied the highest rungs, and other races were below, just above apes and monkeys.

So, the first big problems with the idea of race are that members of a racial group do not share “essences,” Linnaeus’ idea of some underlying spirit that unified groups, nor are races hierarchically arranged. A related fundamental flaw is that races were seen to be static and unchanging. There is no allowance for a process of change or what we now call evolution.

There have been lots of efforts since Charles Darwin’s time to fashion the typological and static concept of race into an evolutionary concept. For example, Carleton Coon, a former president of the American Association of Physical Anthropologists, argued in The Origin of Races (1962) that five races evolved separately and became modern humans at different times.

One nontrivial problem with Coon’s theory, and all attempts to make race into an evolutionary unit, is that there is no evidence. Rather, all the archaeological and genetic data point to abundant flows of individuals, ideas and genes across continents, with modern humans evolving at the same time, together.

A few pundits such as Charles Murray of the American Enterprise Institute and science writers such as Nicholas Wade , formerly of The New York Times , still argue that even though humans don’t come in fixed, color-coded races, dividing us into races still does a decent job of describing human genetic variation. Their position is shockingly wrong. We’ve known for almost 50 years that race does not describe human genetic variation.

In 1972, Harvard evolutionary biologist Richard Lewontin had the idea to test how much human genetic variation could be attributed to “racial” groupings. He famously assembled genetic data from around the globe and calculated how much variation was statistically apportioned within versus among races. Lewontin found that only about 6 percent of genetic variation in humans could be statistically attributed to race categorizations. Lewontin showed that the social category of race explains very little of the genetic diversity among us.

Furthermore, recent studies reveal that the variation between any two individuals is very small, on the order of one single nucleotide polymorphism (SNP), or single letter change in our DNA, per 1,000. That means that racial categorization could, at most, relate to 6 percent of the variation found in 1 in 1,000 SNPs. Put simply, race fails to explain much.

In addition, genetic variation can be greater within groups that societies lump together as one “race” than it is between “races.” To understand how that can be true, first imagine six individuals: two each from the continents of Africa, Asia and Europe. Again, all of these individuals will be remarkably the same: On average, only about 1 out of 1,000 of their DNA letters will be different. A study by Ning Yu and colleagues places the overall difference more precisely at 0.88 per 1,000.

The researchers further found that people in Africa had less in common with one another than they did with people in Asia or Europe. Let’s repeat that: On average, two individuals in Africa are more genetically dissimilar from each other than either one of them is from an individual in Europe or Asia.

Homo sapiens evolved in Africa the groups that migrated out likely did not include all of the genetic variation that built up in Africa. That’s an example of what evolutionary biologists call the founder effect , where migrant populations who settle in a new region have less variation than the population where they came from.

Genetic variation across Europe and Asia, and the Americas and Australia, is essentially a subset of the genetic variation in Africa. If genetic variation were a set of Russian nesting dolls, all of the other continental dolls pretty much fit into the African doll.

What all these data show is that the variation that scientists — from Linnaeus to Coon to the contemporary osteoporosis researcher — think is “race” is actually much better explained by a population’s location . Genetic variation is highly correlated to geographic distance . Ultimately, the farther apart groups of people are from one another geographically, and, secondly, the longer they have been apart, can together explain groups’ genetic distinctions from one another. Compared to “race,” those factors not only better describe human variation, they invoke evolutionary processes to explain variation.

Those osteoporosis doctors might argue that even though socially defined race poorly describes human variation, it still could be a useful classification tool in medicine and other endeavors. When the rubber of actual practice hits the road, is race a useful way to make approximations about human variation?

When I’ve lectured at medical schools, my most commonly asked question concerns sickle cell trait. Writer Sherman Alexie, a member of the Spokane-Coeur d’Alene tribes, put the question this way in a 1998 interview : “If race is not real, explain sickle cell anemia to me.”

OK! Sickle cell is a genetic trait: It is the result of an SNP that changes the amino acid sequence of hemoglobin, the protein that carries oxygen in red blood cells. When someone carries two copies of the sickle cell variant, they will have the disease. In the U.S., sickle cell disease is most prevalent in people who identify as African American, creating the impression that it is a “black” disease.

Yet scientists have known about the much more complex geographic distribution of sickle cell mutation since the 1950s. It is almost nonexistent in the Americas, most parts of Europe and Asia — and also in large swaths of Northern and Southern Africa. On the other hand, it is common in West-Central Africa and also parts of the Mediterranean, Arabian Peninsula, and India. Globally, it does not correlate with continents or socially defined races.

In one of the most widely cited papers in anthropology, American biological anthropologist Frank Livingstone helped to explain the evolution of sickle cell. He showed that places with a long history of agriculture and endemic malaria have a high prevalence of sickle cell trait (a single copy of the allele). He put this information together with experimental and clinical studies that showed how sickle cell trait helped people resist malaria, and made a compelling case for sickle cell trait being selected for in those areas. Evolution and geography , not race, explain sickle cell anemia.

What about forensic scientists: Are they good at identifying race? In the U.S., forensic anthropologists are typically employed by law enforcement agencies to help identify skeletons, including inferences about sex, age, height and “race.” The methodological gold standards for estimating race are algorithms based on a series of skull measurements, such as widest breadth and facial height. Forensic anthropologists assume these algorithms work .

The origin of the claim that forensic scientists are good at ascertaining race comes from a 1962 study of “black,” “white” and “Native American” skulls, which claimed an 80–90 percent success rate. That forensic scientists are good at telling “race” from a skull is a standard trope of both the scientific literature and popular portrayals . But my analysis of four later tests showed that the correct classification of Native American skulls from other contexts and locations averaged about two incorrect for every correct identification. The results are no better than a random assignment of race.

That’s because humans are not divisible into biological races. On top of that, human variation does not stand still. “Race groups” are impossible to define in any stable or universal way. It cannot be done based on biology — not by skin color, bone measurements or genetics. It cannot be done culturally: Race groupings have changed over time and place throughout history.

Science 101: If you cannot define groups consistently, then you cannot make scientific generalizations about them.

Wherever one looks, race-as-genetics is bad science. Moreover, when society continues to chase genetic explanations, it misses the larger societal causes underlying “racial” inequalities in health, wealth and opportunity.

To be clear, what I am saying is that human biogenetic variation is real. Let’s just continue to study human genetic variation free of the utterly constraining idea of race. When researchers want to discuss genetic ancestry or biological risks experienced by people in certain locations, they can do so without conflating these human groupings with racial categories . Let’s be clear that genetic variation is an amazingly complex result of evolution and mustn’t ever be reduced to race.

Similarly, race is real, it just isn’t genetic. It’s a culturally created phenomenon. We ought to know much more about the process of assigning individuals to a race group, including the category “white.” And we especially need to know more about the effects of living in a racialized world: for example, how a society’s categories and prejudices lead to health inequalities . Let’s be clear that race is a purely sociopolitical construction with powerful consequences.

It is hard to convince people of the dangers of thinking race is based on genetic differences. Like climate change, the structure of human genetic variation isn’t something we can see and touch, so it is hard to comprehend. And our culturally trained eyes play a trick on us by seeming to see race as obviously real. Race-as-genetics is even more deeply ideologically embedded than humanity’s reliance on fossil fuels and consumerism. For these reasons, racial ideas will prove hard to shift, but it is possible.

Over 13,000 scientists have come together to form — and publicize — a consensus statement about the climate crisis, and that has surely moved public opinion to align with science. Geneticists and anthropologists need to do the same for race-as-genetics. The recent American Association of Physical Anthropologists’ Statement on Race & Racism is a fantastic start.

In the U.S., slavery ended over 150 years ago and the Civil Rights Law of 1964 passed half a century ago, but the ideology of race-as-genetics remains. It is time to throw race-as-genetics on the scrapheap of ideas that are no longer useful.

We can start by getting my friend — and anyone else who has been denied — that long-overdue bone density test.

Alan Goodman is a professor of biological anthropology at Hampshire College in Massachusetts. This story was originally posted on SAPIENS . Read the original article here.


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