Modern evidence has defined dinosaur mysteries.(Bakker 2001) Dinosaurs dominated vertebrate life on land for 160 million years. They did not thrive in water. They evolved from reptiles, but the biggest dinosaurs were larger than any terrestrial reptile or mammal. Dinosaurs experienced a series of partial extinctions, followed by resurgences of new and different species before they disappeared altogether. Like mammals, dinosaurs had enhanced exercise tolerance and could chase their prey, whereas reptiles have limited exercise tolerance that usually necessitates a “lie in wait” predation strategy. Like warm-blooded birds and mammals, dinosaurs grew and matured quickly and exhibited rapid evolutionary adaptation. In contrast, cold-blooded reptiles seldom produce new species, and they grow and mature slowly unless they are maintained with abundant food and warm temperatures. Some dinosaurs were bipedal (they walked on two legs), whereas reptiles are exclusively quadrupeds. Pterosaurs were dinosaurs that flew in the manner of mammalian bats (neither had feathers) but reptiles have never achieved flight. These dinosaur mysteries have inspired speculation about mass homeothermy (body heat retention due to large size), giant meteors colliding with the earth, “death stars” at million-year intervals, catastrophic volcanic activity, reduced earth gravity, and whether dinosaurs were warm-blooded, but none of these explanations are convincing.
Mammals and reptiles differ from each other almost as much as both differ from dinosaurs, and yet all three are closely related vertebrate cousins. Euthermic (warm-blooded) mammals maintain their body temperature around 100 degrees Fahrenheit regardless of environmental temperatures. This entails increased food requirements, but it somehow confers superior exercise tolerance that enhances their ability to obtain food and thrive in cold climates where reptiles cannot survive. Reptiles are poikilothermic (“cold-blooded”) animals whose bodies assume the temperature of the environment. Because they do not waste food energy maintaining their body temperature, they can survive for extended periods of time with far less food than mammals. They function best at mammalian body temperatures, but their exercise tolerance is inferior to mammals even when they are warm. They become extremely sluggish when cold. The author once witnessed this dramatic cold sensitivity on a raft trip in the Grand Canyon when guides employed cold river water to immobilize a rattlesnake that lurked near the latrine. The snake could then be safely picked up and flung into the bushes.
I hypothesize that the differences between reptiles, mammals and dinosaurs are caused by their adaptations to different climates. The focus of these adaptations is temperature-dependent lipoprotein solidification that affects blood turbulence. The pivotal role of blood turbulence in vertebrate hemodynamic physiology remains largely unappreciated. Blood turbulence inhibits atherosclerosis, increases blood flow resistance, and generates lateral forces that account for the palpable pulse and blood pressure measurement. At cool temperatures, lipoproteins exist as solid particles that exaggerate turbulence, accelerate atherosclerosis, and increase blood flow resistance, but at or above mammalian body temperatures (around 100 degrees Fahrenheit) they liquefy and these effects are neutralized.(Dintenfass 1965) Reptilian red blood cells exaggerate blood turbulence to inhibit atherosclerosis caused by solidified lipoproteins at low temperatures. Mammalian red blood cells inhibit blood turbulence to reduce flow resistance, and thereby optimize cardiac efficiency and exercise tolerance. Vertebrate adaptations to climate thus involve alterations in both body metabolism and red cell morphology. The adaptations involve “trade-offs” between exercise tolerance, food requirements, and cold sensitivity.
Temperature-dependent lipoprotein solidification can be observed in venous blood drawn from humans after a meal. As the blood samples cool, lipoproteins solidify and float to the top of the test tube, where they form a white layer. The author has observed that portal veins turn pearly white due to lipoprotein solidification when exposed intestines are cooled during surgery, but systemic vessels remain unaffected. The portal veins conduct blood from the intestines to the liver, so that blood flowing from the intestines must pass through the liver before entering the systemic circulation. This prevents harmful solidified lipoproteins as well as toxins from entering systemic circulation.
Hemodynamic Physiology and Blood Turbulence
Hemodynamic physiology in vertebrates remains stubbornly mysterious. For example, water is incompressible, so that the palpable arterial pulse should appear simultaneously and with equal force throughout the arterial tree with each heartbeat. Instead, the pulse inexplicably appears as a wave that travels proximal to distal, and its speed increases as arterial diameter decreases. Blood pressure and flow are classically attributed to variations of cardiac contractility and arteriolar vasoconstriction. However, vascular smooth muscle contraction is energy-intensive, short-lived, and followed by obligatory relaxation, so that it cannot explain prolonged elevations of blood pressure such as occur in essential hypertension. Meanwhile, the heart muscle generates a consistent force with each contraction. Its ability to increase this force is limited, and it cannot endure prolonged increases in vascular resistance and workload, which cause congestive heart failure. This consistency of cardiac contraction is reflected by the striking similarity of blood pressure measurements among most mammalian species (with exceptions such as the giraffe) regardless of temperature and activity. In contrast, reptilian blood pressure varies substantially among species and is affected by both temperature and activity. Vasoconstriction and cardiac contractility thus provide a tenuous explanation of organ regulation, essential hypertension, blood pressure, and blood flow regulation. Also, there is no satisfactory explanation of bruits and Korotkoff sounds. These and other puzzling observations are readily explained by blood turbulence.
Water, oil, and most other fluids are called “Newtonian” because they exhibit exponential increases in turbulence when they are accelerated in pipes. The turbulence causes exponential increases in flow resistance and generates lateral forces that press on the inner walls of the pipe. Belgian mechanical engineers recently photographed Newtonian pipe flow turbulence and showed that it consists of small “jet streams” that flow forward along the inner walls of the pipe and force slower-moving fluid elements to the center of the pipe, where they flow backward. This explains how turbulence inhibits forward flow in pipes, and also how it mobilizes particulates that would otherwise deposit on the walls of the pipe.(Chris Woodyard 2006; Hof et al. 2004) In contrast, mammalian blood is “non-Newtonian” because it exhibits exponential declines in turbulence and flow resistance when it is accelerated in arteries.
Vertebrate pulsatile arterial blood flow accelerates forward during systole, when the heart contracts. During diastole, when the heart relaxes, arterial flow decelerates and briefly halts. Pulsatile flow thus induces periodic bursts of arterial turbulence. Vertebrate arterial turbulence is similar to water pipe turbulence, except that blood contains red blood cells that alter turbulence in accord with their shape and size. Rotund, nucleated reptilian red cells exaggerate systolic blood turbulence to inhibit atherosclerosis. Biconcave, enucleated mammalian red cells inhibit systolic blood turbulence to enhance cardiac efficiency and exercise tolerance. This explains the presence of red blood cells in vertebrates, because hemoglobin encapsulation does not enhance oxygen delivery, and red cell mass is far greater than necessary to oxygenate tissues.
Blood turbulence inhibits atherosclerosis. Blood contains numerous particulates in addition to lipoproteins and red cells. Like sludge formation in oil pipes, blood particulates form deposits on the inner walls of arteries if blood turbulence is inadequate.(Chris Woodyard 2006) Such deposits induce an inflammatory reaction that results in the formation of atherosclerotic plaque. Athletic activity exaggerates blood turbulence that inhibits and can even reverse atherosclerosis. Anemia likewise increases blood turbulence and inhibits atherosclerosis. Polycythemia and sedentary life style reduce blood turbulence and accelerate atherosclerosis. Atherosclerosis is a natural consequence of aging and inactivity, as cardiac vigor and blood turbulence decline. Insoluble Fibrin is generated in flowing blood by the SRM in accord with stressful forces and stressful stimuli that affect autonomic balance, and this reduces turbulent mixing in blood and thereby accelerates atherosclerosis. This explains why atherosclerosis is accelerated by disease, surgery, and emotional stress. (Coleman 2006; Coleman 2010)
Pulsatile arterial turbulence also inhibits coagulation, which explains why clot formation is rare in uninjured arteries, while thrombophlebitis is common in veins, where flow is sluggish and turbulence is minimal. Insoluble fibrin generated by the Stress Repair Mechanism (SRM) induces clot formation by reducing blood turbulence below a threshold, and then binding red blood cells into a viscoelastic clot.(Coleman 2005; Coleman 2010)
Mammals are “Euthermic” (warm-blooded). They have adapted to cold climates by adjusting their metabolism to maintain their body temperature continuously above the threshold of lipoprotein liquefaction, and by ejecting the nucleus of their red blood cells to create biconcave red cells that enhance cardiac efficiency and exercise tolerance. Maintaining elevated body temperatures substantially increases food requirements, but it prevents lipoprotein solidification and enables mammals to remain active at cold temperatures, and the enhanced exercise capacity enables them to satisfy their increased food requirements. Superior mammalian intelligence further enhances their ability to obtain food. Humans are born with immature “fetal” red blood cells that are spherical and nucleated. These are gradually replaced by mature biconcave, enucleated red blood cells during the first year of life. The fetal red cells exaggerate systolic blood turbulence to inhibit atherosclerosis during embryological development, when blood turbulence is otherwise inadequate in the quiescent developing fetus. The increased turbulent flow resistance caused by fetal red blood cells explains the limited exercise tolerance and increased risk of general anesthesia during the first year of human life.
“Newtonian” fluids such as water and oil produce exponential increases in viscosity (flow resistance) as they are accelerated in pipes. In contrast, mammalian blood is a “non-Newtonian” fluid that exhibits exponential declines in viscosity when it is accelerated in arteries. The nucleus of maturing mammal red blood cells is ejected and engulfed by immune cells, causing the rotund cell to partially collapse to create its distinctive biconcave shape. During systole, when the heart contracts and ejects blood, these biconcave red cells spontaneously form “aggregate patterns” that inhibit blood turbulence and flow resistance so that the mammalian heart expels its contents much more efficiently. The mammalian heart is thus able to accelerate arterial blood flow from 0 to 125 cm/sec in a tenth of a second with minimal effort. This enhanced cardiac efficiency confers a substantial increase in exercise capacity.
During diastole, when the mammalian heart has emptied its contents and blood flow decelerates, the aggregate formations disintegrate, causing the kinetic energy of moving blood to convert to a burst of turbulence. This manifests as a traveling pulse wave that propagates throughout the arterial tree with each cardiac cycle, halting blood flow as it travels. The turbulence generates lateral forces that press on the inner walls of arteries. These lateral forces make the pulse wave palpable and blood pressure measureable. Arterial strictures and blood pressure cuff inflation accelerate blood flow and elevate turbulent frequencies to audible levels, which explains bruits and blood pressure measurement.
Blood turbulence clarifies mammalian hemodynamic physiology. Red blood cells are nearly identical among mammalian species because their size and shape minimizes turbulence and flow resistance. Mammalian blood pressure varies little between individuals and among species because cardiac power, force and work vary little from beat to beat, and because mammalian physiology controls temperature within a narrow range, so that turbulent forces remain consistent with each heartbeat and similar among species. This produces the misleading impression that blood pressure, cardiac contractility and tissue perfusion are directly related. However, turbulent relationships are exponential in nature, and blood pressure is not linearly related to cardiac output or tissue perfusion as often presumed. For example, cardiac output remains intact in resting trained athletes. This is because aerobic conditioning stimulates capillary formation in muscles affected by exercise, and this reduces flow resistance, which increases stroke volume, so that heart rate and blood pressure are reduced at rest. This reflects enhanced cardiac efficiency in the athlete. The heart itself is little affected by exercise, and does not become “stronger” or larger. The weak cardiac force that propels blood cannot readily perfuse distant or elevated tissues, which explain why the head is usually located close to the heart. Exceptions such as the giraffe require exaggerated heart mass. In contrast to mammals, reptilian blood turbulence, and therefore blood pressure, is affected by temperature, activity and other factors, so that it varies substantially in individuals as well as among species.
Reptiles are “cold-blooded” (poikilothermic). They are adapted to warm climates. They do not waste food energy to maintain their body temperature above the level of lipoprotein liquefaction. Their food requirements are therefore modest compared to mammals. Their body temperature fluctuates in accord with environmental temperatures, so that lipoproteins in their blood solidify at cool temperatures. Lipoprotein solidification inhibits blood flow and accelerates atherosclerosis. However, unlike mammalian red blood cells, reptilian red blood cells retain their nucleus, which causes their shape to remain rotund. This rotund shape exaggerates systolic blood turbulence, which offsets the acceleration of atherosclerosis caused by lipoprotein solidification. The exaggerated systolic blood turbulence simultaneously inhibits cardiac function by increasing flow resistance. The combined effect of rotund red cells and solidified lipoproteins severely reduces cardiac efficiency and exercise tolerance at cool temperatures. This explains why reptiles become extremely sluggish at low temperatures. Reptiles typically bask in the morning sun to raise their body temperatures to mammalian levels, which is where they function best. However, even when their blood temperature is elevated above the level of lipoprotein liquefaction, their exercise tolerance remains inferior to that of mammals on account of the exaggerated turbulent systolic flow resistance caused by their rotund, nucleated red cells. Because of this, most reptiles employ a “lie in wait” style of predation that requires minimal exercise capacity. Vegetarian reptiles are rare, presumably because their limited exercise tolerance restricts their ability to obtain adequate quantities of low-energy plant food sources.
Dinosaurs were adapted to continuously hot temperatures. They thrived during the unique era when all the continents of the earth were fused together into a single land mass called “Pangaea”. This caused interior land temperatures to become continuously elevated above the level of lipoprotein liquefaction. I hypothesize that under these conditions, certain reptile species transmogrified into dinosaurs by ejecting the nucleus of their reptilian red blood cells to create biconcave red blood cells similar to those of mammals. In the presence of continuously hot temperatures, this single change in red cell structure would explain how dinosaurs added the superior hemodynamic efficiency (exercise tolerance) of mammals to the superior metabolic efficiency (modest food requirements) of reptiles to enable them to become energetic monsters that dominated terrestrial life for millions of years. The combination of metabolic and hemodynamic efficiency explains how plant-eating dinosaurs attained gigantic size despite small heads that limited their food intake. Their enhanced exercise tolerance facilitated their ability to obtain fresh plant food sources, but their additional food energy was not wasted to maintain body temperature, so that their conserved caloric intake exaggerated body size. Enhanced dinosaur exercise capacity enabled dinosaur predators to run on two legs to chase after their prey and increase their caloric intake, while their metabolic efficiency exaggerated their size and strength, so that they become the most formidable predators ever known. The enhanced exercise capacity likewise enabled Pterosaurs to fly in the manner of mammalian bats (both lacked feathers). The combination of hemodynamic and metabolic efficiency also enabled rapid growth, maturation and evolutionary diversification similar to warm-blooded mammals and birds.
Dinosaurs were not mammals, because they lacked the ability to maintain their body temperature above the level of lipoprotein liquefaction. Their adaptation to sustained high temperatures rendered them exquisitely vulnerable to cool temperatures. Because of this, they did not thrive in water, where temperatures are usually below the threshold of lipoprotein liquefaction. The fossil record reflects a series of catastrophic dinosaur extinctions followed by resurgences in which new and different dinosaur species appeared, and this is best explained by temporary declines in ambient land temperature below the level of fat liquefaction. When Pangaea disintegrated into separate continents, causing land temperatures to permanently fall below the threshold of lipoprotein liquefaction, the dinosaur life form became extinct. The final chapter in the dinosaur saga likely resembled Armageddon, as doomed dinosaurs clustered together in a desperate search for warmth. The contorted postures of their fossilized bodies may reflect their final agony as lipoprotein solidification disrupted their hemodynamic function.
This hypothesis is limited to reptiles, mammals and dinosaurs. It cannot explain the hemodynamic efficiency of birds, because the distinctive oval red blood cells of birds are nucleated. However, birds are euthermic, which suggests that lipoprotein liquefaction plays an important role in their physiology. Perhaps the distinctive oval shape of bird red cells confers the ability to control blood turbulence and enhance hemodynamic efficiency in a manner different from that of mammalian red cells.
The evolution of dinosaurs is often associated with cosmic climatic cataclysms, but the evidence suggests that the earth’s climate is remarkably temperate. It never becomes so extreme as to render either reptiles or mammals extinct. Instead, mild cyclical temperature fluctuations temporarily favor one versus the other. Dinosaurs represent a vertebrate adaptation to a period of unusually elevated land temperatures. The dinosaur evidence provides insights to vertebrate physiology, embryology and evolution. The ability to eject the nucleus of red blood cells may be retained by reptiles as well as mammals, and it may represent one of many potential adaptations hidden in the vertebrate genome. It illustrates how simple physiological adaptations to moderate environmental changes can produce diverse new life forms that disappear as suddenly as they appeared. (Kirschner and Gerhart 2005)
This hypothesis of dinosaur origin and physiology resulted from the extensive review of published medical research literature that identified the “Stress Repair Mechanism” (SRM) that maintains and repairs the vertebrate body and governs hemodynamic physiology.(Coleman 2010) Confirmation of the dinosaur hypothesis initially appeared impossible, because the shape of dinosaur red blood cells was unknown. However, Dr. Mary Schweitzer recently discovered intact dinosaur bone marrow tissue,(Fields 2006; Schweitzer et al. 2005; Schweitzer et al. 1997). Electron microscopy studies have subsequently produced evidence that dinosaurs had biconcave red blood cells.(Liangtai 2009) This evidence remains controversial. However, the ability of reptiles to transmogrify into dinosaurs could be tested by maintaining a selected group of reptiles with temperatures continuously above the threshold of lipoprotein liquefaction and abundant food. Under these conditions, dinosaurs might eventually appear spontaneously.
The secret of vertebrate hemodynamic physiology is efficiency rather than power and work. The modest force generated by cardiac muscle is consistent within a narrow range, and flow resistance readily inhibits the ability of the heart to expel its contents. Both turbulent flow resistance and capillary flow resistance are simultaneously regulated in accord with autonomic balance by the capillary gate component of the Stress Repair Mechanism (SRM).(Coleman 2010) The combined effects of turbulent flow resistance and capillary gate closure reduces cardiac output, cardiac efficiency, and exercise tolerance.(Ades et al. 1996) Capillary gate component regulation provides an improved explanation of the regulation of blood flow and organ function, because capillary blood flows, pressures and turbulence are minimal, and the combined surface area of capillaries is vastly greater than that of larger vessel, so that flow regulation by fibrinogenesis and fibrinolysis in capillaries is more efficient and effective than vasoconstriction of arterioles. Capillary gate operation also explains numerous experimental observations, such as the increase in fibrin split products after treatment with “vasoactive” pharmaceuticals.(Holemans 1965)