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McLean, D. M., 1991, A climate change mammalian population collapse mechanism, in Kainlauri, E., Johansson, A., Kurki-Suonio, I., and Geshwiler, M., eds., Energy and Environment: Atlanta, Georgia, ASHRAE, p. 93-100.


Dewey M. McLean


Climatic warming and cooling beyond the optimum temperature range for conceptions, and estrual activity, can reduce mammalian fertility, leading to reduction in population numbers and, in abrupt climatic changes, collapse of mammalian populations. The greenhouse population control and extinction mechanism is triggered by environmental heat that shunts the pregnant female blood flow to peripheral tissues to dissipate heat to the environment, thus reducing blood flow to the uterus. Uterine blood flow is an embryo's source of oxygen, water, nutrients, and hormones, and also carries damaging metabolic heat away from the embryo. Modern summer heat is already killing mammalian embryos on a vast scale prior to the onset of any potential significant warming. Application of modern reproductive physiology principles to the global mammalian extinctions at the end of the last ice age, which occurred during general greenhouse conditions and climatic oscillations, accounts for the elimination of primarily large mammals, and coeval dwarfing and skeletal abnormalities.


Anthropogenic greenhouse gases are accumulating in the atmosphere, and many scientists believe that earth will experience climatic warming known as a "greenhouse" within the next century. Speculations on how a greenhouse might affect our civilization have focussed mostly on the melting of polar ices and flooding of continental margins, and effects of drought in important agricultural regions, etc. The effects of heating upon modern mammalian faunas seem to have been overlooked. In fact, reproduction among modern mammals already suffers much damage via summer heat. Environmental heat attacks the mammalian evolutionary chain via its weakest link: developing embryos. By influencing embryo survival rates, heat is a potent population control factor. Modern greenhouse warming can only expand embryo death, reduce mammalian populations and, in a major greenhouse, perhaps trigger population collapse in the more vulnerable regions.

In the 1970s, I began work on the role of CO2-induced greenhouse conditions in global extinctions, and evoked greenhouse-reproductive failure for the Cretaceous-Tertiary (K-T) dinosaurian extinctions (McLean 1978, and later). Concurrently, I was investigating the role of climatic warming in the global Pleistocene-Holocene (P-H) mammalian extinctions at the end of the last ice age about 12,000-10,000 years ago (McLean 1981, and later). I worked to isolate out a climate-bioevolution coupling that would be applicable to mammals, reptiles, and birds that would help to explain vertebrate evolution in the past, and also provide insight on how a modern climate change might affect modern mammals. I believe that I have isolated a climate-embryo coupling by which greenhouse warming has triggered global extinctions in the geological past, that will be operative in a modern greenhouse. The killing mechanism is operating all about us every summer, killing embryos on a global scale, even before the onset of any major greenhouse warming.

This paper outlines the sensitivity of mammalian reproduction systems to environmental heat, shows how heat is causing embryo failure, and explores the role of climatic warming in the global mammalian extinctions of 12,000-10,000 years ago, of which we are but the survivors. The objective will be to show us how we fit thermally into the climatology of this world so that we can best evaluate how a greenhouse might affect modern mammalian faunas. A modern greenhouse could be the most potentially dangerous phenomenon ever faced by our civilization, and one to avoid if possible.


Because mammals are homeothermic, it is widely believed that climatic warming poses little danger to them. This misconception focuses upon the effects of heat upon adult mammals, ignoring the weakest link in the mammalian evolutionary chain: heat damage of developing embryos. Embryo damage and death occur at environmental temperatures that pose little danger to adults. Embryo mortality can reach 100% in unacclimatized ewes which are not dangerously stressed (Thwaites 1985). As I will develop in the section titled "Heat Effects upon Fertility" such damage and death is commonplace every summer; environmental heat that drives up the female's core temperature kills embryos in large numbers. A modern rapid climatic warming can only increase heat damage and death among embryos. In a worst-case greenhouse, massive embryo death could produce a positive feedback between embryo and adult numbers that could trigger reduction in population numbers, and collapse in vulnerable regions.


Mammalian conception rates, as deduced from reproductive physiology studies of cows (Gwazdauskas et al. 1981), seem delicately balanced between both heat and cold. For Virginia cattle (Figure 1), the optimum environmental temperatures for conception are between 50°F (10°C) and 73°F (23°C), with maximum conceptions at about 59°F (15°C). Abrupt environmental temperature changes above or below the optimum range will reduce mammalian conception rates. The drops in fertility when the maximum temperature the day after breeding exceeds 73°F (23°C), or when a maximum daily temperature is below 50°F (10°C), will be discussed below.


A review of mammalian thermoregulation provides background on how mammals fit thermally into the modern world. In Figure 2 (after Bianca 1968) the "Zone of Survival" (D to D') denotes the range of environmental temperatures within which adult mammals can survive. The normal body temperature exists closer to the upper limits of survival than to the lower. Higher core temperature (brain, organs of the chest and the abdomen, and parts of the musculature) confers greater physiological efficiency.

Figure 2. Zone of Survival (after Bianca 1968).

Within the "Zone of Homeothermy" (C to C'), a mammal can maintain a constant, or steady state, core temperature. Within the "Zone of Thermal Comfort" (A to A'), there is little sensation of heat or cold, and a steady state core temperature can be maintained without expanding or contracting the blood vessels of the skin, evaporating excessive moisture, fluffing fur, or responding behaviorally.

With air temperature falling below the "Zone of Thermal Comfort" (A), vasoconstriction and piloerection operate to conserve body heat. At the lower critical temperature (B), heat produced by increased metabolic activity maintains homeothermy. However, at C, heat production cannot balance heat loss, the core temperature begins to fall, and the animal becomes hypothermic. With more cooling, heat production peaks, and then declines, further lowering the core temperature. At the lethal body temperature (D), an animal dies from the cold. For most species, the lower lethal temperature is 59-68°F (15-20°C), or about 36°F (20°C) below the normal core temperature.

With air temperature rising above the "Zone of Thermal Comfort" (A'), vasodilatation, and sweating and (or) panting effects heat loss. At the upper critical temperature (B'), increased sweating and (or) panting may be associated with lowered metabolic heat production. At C', further intensification of sweating and (or) panting cannot maintain homeothermy, and the animal becomes hyperthermic. The rise in core temperature increases the metabolic rate via the van't Hoff effect, triggering positive feedback, which further increases the core temperature. Thermal death of an adult occurs at D'. For mammals, the van't Hoff effect is the two-to three-fold rise in heat production caused by an 18°F (10°C) rise in tissue temperature. The temperature coefficient (Q10) of mammalian tissues is two to three. For most mammals, the upper lethal body temperature is 108-113°F (42-45°C), or about 5.4 to 10.8°F (3 to 6°C) above the normal core temperature.

As pertains to broad aspects of population dynamics, and bioevolution, however, the critical factor is not environmental heat sufficient to cause death of adult mammals via thermoregulatory breakdown. The critical factor involves environmental heat below that required to kill adults, but enough to increase embryo death rates. The cauldron of bioevolution occurs between C' and D', where pregnant adult females routinely experience mild hyperthermy during hot summers. Every summer, hyperthermy kills vast numbers of embryos on a global scale. Because it occurs out of sight within female mammals, we are generally unaware that a thermal extinction mechanism is already in operation, all about us, every summer. This coupling between air temperature and the sensitivity of embryos to excessive heat provides direct linkage between climate and bioevolution.

Humans are not immune from the effects of hyperthermy upon the fetus. For human females, a bath in water of 104°F (40°C) for 15 to 25 minutes can raise the core temperature to 101.3°F (38.5°C), sufficient to damage a fetus (Ridge and Budd 1990). At that bath temperature, 54% of the women were not uncomfortably hot, and 78% did not rate the experience as "hard." Ridge and Budd recommend that for pregnant, or potentially pregnant women, remaining immersed in water of 104°F (40°C) longer than 10 minutes may be too long.


Because females are the repository of the uterus, and the uterus is where embryos develop, females hold a special place in population dynamics and bioevolution. High environmental temperatures can reduce male fertility by damaging, or killing, sperm; however, the dominant effects of heat upon lowered fertility occur among females. By stressing the female, environmental heat triggers blood flow changes that reduce the flow of blood to the uterine tract, damaging or killing developing embryos. It is well documented that conception rates and fertility decrease in the summer in temperate zones, and in the subtropical and tropical climates (Badinga et al. 1985; Gwazdauskas et al. 1973; Gwazdauskas et al. 1975; Ingraham et al. 1974; Johnson 1985; Thatcher 1974).

The cardiovascular system exerts control upon the core temperature of an animal by influencing the flow of heat between the core and superficial tissues (Rubsamen and Hales 1985). At thermoneutrality, a balance between expansion and contraction of the peripheral blood vessels maintains thermal stability; a high temperature gradient between the skin and environment allows cooling of the animal with but small changes in surface temperature. With increasing heat load, the temperature gradient at the shell declines, and requires greater blood flow to remove heat from animal to environment. Moderate warming can elevate skin temperature by 36°F (20°C).

In protecting the adult female from high environmental temperatures, the shunting of blood to superficial tissues and respiratory muscles reduces perfusion of blood to the abdominal viscera, nonrespiratory muscles, and reproductive tract. Uterine blood flow is a developing embryo's source of oxygen, water, nutrients, and hormones, and also carries excessive, damaging, heat away from the embryo. As will be discussed below, reduced uterine blood flow (UBF) can damage, and kill, developing embryos.

Mammals: Not Exactly Homeotherms

Mammals do not have precise control over core temperature. According to Bligh (1985), temperature regulation is not the fixed property of mammals that was once supposed, and finely controlled homeothermy is not a mammalian characteristic. The rigidity (or lability) of body temperature varies among species as response of adaptation. The ability to vary core temperature is known as heterothermy.

That mammals cannot maintain a fixed body temperature with varying environmental temperatures is indicated in Figure 3 (after Yousef et al. 1968) that relates core to air temperature for lactating European-origin cattle. In rising air temperature, the core temperatures also rises. For European-type cattle such as the Holstein, Jersey, and Brown Swiss (Bos taurus), core temperatures begin to rise at 70°, 75°, and 81°F (21°, 24°, and 27°C), respectively. Core temperature of the tropical-origin Brahman cow (Bos indicus) begins to rise at 95°F (35°C). The air temperature where core temperature begins to rise in most domestic animals is from 28° to 32°C. High humidity lowers the air temperature at which core temperature begins to rise in most species.

Figure 3. Core temperature as a function of air temperature. A rise in core temperature of 1.5°C can kill most embryos (after Yousef et al. 1968).

Core temperature of the camel can vary 3.6-5.4°F (2-3°C) daily, and variations of 1.8-5.4°F (1-3°C) are common in other species. Lowest core temperatures in the early morning, and highest in the late afternoon, reflect rest during the cool night hours, and activity and feeding in the day. For cattle, absorbed solar heat may be three times greater than that produced metabolically (Bianca 1968). To avoid hyperthermia, heat gained during the day must be balanced by heat lost to the environment during the night. For cattle, night temperatures must drop below 75°F (24°C) to prevent constant hyperthermia. For ruminants, the microorganisms of the rumen produce up to 10% of an animal's basal heat production.

For other sources of heat that females must contend with, the metabolism of the fetus, and acceleration of various bodily processes of the adult, increase the total heat production. Lactation may double a cow's heat production. Because of the extra heat loads generated by pregnancy and lactation, the burden of reproduction falls more heavily upon females than males.

Environmental Heat and Conception Rates: The Mechanics

Uterine blood flow (UBF) is a developing embryo's source of oxygen, nutrients, water, and hormones (Senger et al. 1967; Bazer et al. 1969; Barron 1970), and also transports damaging heat away from the embryo (Abrams et al. 1971; Gwazdauskas et al. 1974). Reduction of UBF can damage, or kill, developing embryos. The higher the environmental temperature, the greater the reduction of UBF.

The uterus, unlike tissues that have autoregulation, cannot maintain constant blood flow as perfusion pressure decreases (Brown and Harrison 1981). Experiments by Roman-Ponce et al. (1978a, 1978b), in which cows were fitted with blood flow transducers on the mid-uterine artery, and then placed in shade and no-shade conditions, showed that animals in the hotter environment had lower UBF rates than those in the cool.

To prevent damage to developing embryos, the uterine tract must be maintained at a nearly constant and optimum temperature. A rise of uterine temperature by only 1.8-2.7°F (1.0-1.5°C) above optimum will kill an embryo. Generally, European-type lactating cattle can maintain homeothermy up to about 70-81°F (21°-27°C), above which the core temperature begins to rise. At air temperature of about 86°F (30°C), the core temperature increase significantly reduces conception rates. Figure 4, based on breeding records for over 12,000 Florida cattle (Badinga et al. 1985), shows that conception rates of lactating cows decrease sharply when the maximum air temperature on the day after insemination exceeds 86°F (30°C). With temperatures increasing from 75°F (23.9°C) to 90°F (32.2°C), conceptions dropped from 52 to 32% and stayed low during the summer months. For Virginia cattle, optimum conception temperatures are from 50°F (10°) to 73°F (23°C) (Gwazdauskas et al. 1981). Arizona and Missouri cattle conceptions range from 50% in the cool months to about 20-0% in the hot months (Johnson 1985). High humidity, reduces the animal's ability to lose heat, lowering the air temperature at which core temperatures begin to rise. Mammals that are important food sources for humanity function best in cool temperatures. According to Hahn (1976), the average daily temperatures of long-term exposure that induce nominal losses of livestock are: dairy cattle, lactating, or within two weeks of breeding, 39-75°F (4-24°C); calves, 50-79°F (10-26°C); beef cattle, 39-79°F (4-26°C); sheep, 39-75°F (4-24°C); poultry over 10 days old, 55-81°F (13-27°C); and laying hens, 45-70°F (7-21°C). For high radiant heat loads, the range should be shifted downward by 5.4°F (3°C). A major greenhouse could devastate important dairy food resources.

Figure 4. Florida cattle conceptions versus air temperature (after Badinga et al. 1985).

In addition to killing embryos, reduced UBF can produce dwarfed or stunted offspring, and skeletal abnormalities. Miniature calves are often born to unadapted European cattle following summer pregnancy in the tropics (Hafez 1968). Intrauterine growth retardation via maternal heat stress produces proportional dwarfs (Brown et al. 1977; Brown and Harrison 1981). By reducing the placental weight, heat can produce heat-stunted offspring (Thwaites 1985). High temperatures can also produce skeletal abnormalities. Hyperthermia during pregnancy can produce fetal malformations (Hafez 1968).

Mammalian embryos are most vulnerable to maternal heat stress during the first two cleavages. Ulberg and Burfening (1967) reported that slight heating of the embryo during the first few cell divisions causes delayed death. Sheep zygotes are most vulnerable during the initial stage of cleavage while yet in the oviduct (Dutt 1963), and rabbit embryos more during the first cleavage than the second (Ulberg and Sheean 1973). For cattle, Thatcher (1974) and Gwazdauskas et al. (1975) note that fertility is inversely related to the maximum air temperature the day after insemination and to uterine temperature at, and the day after, insemination. Frank Gwazdauskas (Dairy Science, VPI & SU, pers. comm.) noted that about 50% of cattle embryos die under natural conditions (10% in the first 4 days, and 40% between 6 to 15 days), implicating reduced blood supply to the oviducts as a factor. The early bovine embryo is extremely sensitive to maternal heat stress, and intermittent stress from 30 h after the onset of estrus until day seven of pregnancy increases the number of abnormal or retarded embryos; maternal heat stress between day 8 and 16 after insemination reduces conceptus weight and increases pregnancy failure (Putney et al. 1988).

Embryo failure via maternal heat stress may involve thermally-induced alterations in synthesis of conceptus proteins involved in embryonic development and maternal recognition of pregnancy (Putney et al. 1988). Alterations in the secretory activity of the uterine endometrium may affect embryo development, contributing to pregnancy failure. Because heat stress retards embryonic development, embryonic death may result from failure of embryos to produce biochemical signals at the proper time to prevent corpus luteum regression. Several authors (Northey and French 1980; Betteridge et al. 1984; Bartol et al. 1985; Knickerbocker et al. 1986a) report that the preattachment conceptus produces proteins critical to maintenance of the corpus luteum and continuation of pregnancy.

For how a greenhouse warming might affect modern mammalian populations, Figure 4 indicates that summer heat is already lowering conception rates. A greenhouse would expand the number of hot days per year, and a rapid climate change would prevent mammals from easily adapting to the new temperature regime. Increased embryo death rates would likely track the warming. Environmental heat can also reduce fertility via reducing estrual activity. Figure 6 (after Gwazdauskas et al. 1982) records a decline in estrual activity among Virginia cattle at temperatures above 86°F (30°C). Figure 5 (a causal loop diagram) shows how increased embryo death rates can generate a positive feedback collapse of mammalian populations.

Figure 5. Causal loop diagram showing how excessive environmental heat can trigger collapse of mammalian populations.


Environmental temperatures below the optimum for conception also lower mammalian fertility by reducing estrual activity. As indicated in Figure 6, estrous activity declines at temperatures below the optimum 77°F (25°C). Figure 1 indicates that conceptions decline dramatically below a maximum daily temperature of 50°F (10°C). Gwazdauskas et al. (1981) attribute this decline to effects of cold temperatures on metabolic and endocrine adjustments needed to maintain body heat, and possibly to sperm damage. Thus, environmental temperature oscillations above or below the optimum conception range can reduce mammalian fertility.


The modern climate is but a part of an ice age climate that has prevailed for the past two million years. To understand how mammals fit into the climatology of the modern world entails isolating climate-bioevolutionary couplings that have molded modern mammalian faunas. This must be done to determine how a modern greenhouse might affect mammals. Modern mammals are but the survivors of global extinctions 12,000-10,000 years ago that occurred during climatic warming that ended the last ice age, and are ice age animals trapped in a hot world. Our thermal sensitivity to this hot world is indicated in that summer heat is taking a severe toll of embryos; many species may exist near to their upper thermal limits, and may not be able to easily adapt to a climatic warming

Location of the modern climate on the cycles of coolings and warmings that have characterized the ice age climatology of the past two million years is indicated in Figure 7. We live in a relatively hot world prior to the onset of any significant greenhouse warming. For roughly 100,000 year intervals, the climate cools gradually into an ice age, and continental ice sheets expand in size. Rapid warming terminates the ice ages. The warm intervals, known as interglacials, last about 10,000 years. The modern interglacial has lasted for about 10,000 years.

Figure 7. Glacial Cycles.

The modern climate is depicted by a question mark, reflecting the uncertainty of the future climate. If humans were not present on earth, the climate would likely cool off into an ice age, as it has many times in the past. However, humans are disrupting earth's carbon cycle by burning fossil fuels, and releasing greenhouse gases into the atmosphere. By the Hansen et al. (1988) "Scenario A," the climate could warm 7.2°F (4°C) by the year 2050 should a worst-case materialize.

The cyclical ice age climatology results from variations in earth's orbit about the sun (Imbrie and Imbrie 1980), and by varying amounts of CO2 in the atmosphere (Shackleton and Pisias 1985; Lorius et al. 1988). During warming at the end of the last ice age, atmospheric CO2 rose from 190-200 parts per million by volume (ppmv) during full glacial to 270-280 ppmv during the interglacial (Delmas et al. 1980; Neftel et al. 1982). A linkage seemingly exists between climate and the carbon cycle (Lorius et al. 1988). Study of an ice core from Vostok station, Antarctica, indicates that orbital forcing, amplified by CO2 changes, plays a major role in ice age climatology. About half the 18°F (10°C) climatic warming at the end of the last ice age at Vostok can be accounted for by increased CO2. Greenhouse conditions were a factor in the climatic warming at the end of the last ice age.

The coldest conditions of the last ice age, and maximum advance of continental ice sheets in the Northern Hemisphere, occurred about 18,000-20,000 years ago. Cold conditions began to relax about 18,000 years ago (McDonald 1984). Warming from 15,000-8,000 years ago disintegrated the North American and Eurasian ice sheets (Dansgaard et al. 1989). The Glacial-Holocene transition of 15,000-8,000 years ago reflects large short-lived climatic fluctuations, the two main excursions being the Allerød warm period 12,000 to 11,000 years ago, and the Younger Dryas cold period 11,000 to 10,000 years ago (Berger et al. 1987). Major abrupt climatic changes initiated the Allerød, occurred at the boundary between Allerød and Younger Dryas, and terminated the Younger Dryas.

Figure 8 (Dansgaard and Oeschger 1989; Dansgaard et al. 1989), shows temperature oscillations about 13,000-10,000 years ago in Europe, and the North Atlantic region. Temperature records of the Dye 3 ice core of southern Greenland, and Lake Gerzensee in Switzerland, show the abrupt Bølling-Allerød (BA) warming at about 13,000 years ago, the Younger Dryas (YD) abrupt return of glacial conditions about 11,000-10,000 years ago, and subsequent warming. The Dye 3 ice core record shows the Younger Dryas ending 10,720±150 years ago by 12.6°F (7°C) warming within a 50 year period .

Radical climate changes are also indicated for central Britain. Coope's (1987) studies, based on coleoptera, indicate that 13,000 years ago the summer temperature rose 12.6°F (7°C), and the winter temperature 36°F (20°C) in about a century. Subsequent cooling in two stages at 12,000 and 11,000 years ago ushered in the Younger Dryas cold period. The Younger Dryas was terminated by climatic warming of the present interglacial which was as abrupt, and intense, as that at 13,000 years ago, with temperatures approximating modern by 9,500 years ago.

For North America, Webb and Bryson (1972) noted that the most profound climatic change in Minnesota and Wisconsin occurred within a few centuries of 11,300 years ago when the temperature rose about 5.9°F( 3.3°C) and the summer season increased by one month; the July mean temperature increase was three times the size of any change during the Holocene.

Dansgaard and Oeschger (1989) indicate that the BA-YD transition was a regional North Atlantic, rather than a global phenomenon. Peteet (1987) notes that the extent of Younger Dryas cooling outside of Europe is not well defined, and that in North America, the majority of late-glacial pollen studies do not reveal changes indicative of a climatic reversal correlative with the European sequence. Pons et al. (1987) indicate that the Younger Dryas was a back-current to the general warming that marked the end of the glacial times, and notes a rapid vanishing of its effects to the south, and a localization of its pulsations near the glaciers. However, Peteet (1987) suggests that the New England pollen record indicates cooling about 11,000-10,000 years ago. Engstrom et al. (1990) indicate that Younger Dryas climatic effects were felt well beyond the North Atlantic.

Maximum warmth of the modern interglacial was during the Altithermal about 6,000 years ago, when the temperature may have been 0.9°F (0.5°C) to 1.8°F (1.0°C) warmer than today (Broecker, in MacCracken 1980, p. 190; and Webb and Wigley 1985, respectively).

Climate Change and Mammalian Extinctions

Global mammalian extinctions of primarily large mammals, dwarfing, and skeletal abnormalities occurred during the abrupt and radical climate oscillations of the Pleistocene-Holocene transition at the end of the last ice age. Most mammals survived the extreme cold stage of the last ice age with minimal extinctions (McDonald 1984); however, the climatic warming that ended the last ice age was associated with the global Pleistocene-Holocene mammalian extinctions. Globally, mammals becoming extinct included the: mammoth, mastodon, giant bison, ground sloth, sabre-tooth cat, four-horned antelope, dire wolf, giant beaver, wooly rhinoceros, giant deer that ranged from steppe forests of Europe into Siberia and North Africa, steppe bison, cave bear, cave lion, and cave hyena.

Because the extinct mammals were so like modern mammals, physiological principles operative among modern mammals are applicable to the extinct faunas. Those extinctions, that occurred during atmospheric CO2 buildup and greenhouse conditions, provide the best analogue in earth history for determining the effects of greenhouse conditions on mammals.
For European mammals adapted to extreme ice-age cold, the abrupt and drastic Bølling climatic warming would have had devastating effects upon developing embryos. The abrupt Younger Dryas return to glacial conditions would have caught mammals attempting to adapt to warmth. Then, the abrupt and drastic warming that terminated the Younger Dryas would have caught mammals attempting to adapt to cold. Mammalian extinctions in northern Eurasia started 13,000-11,000 years ago (Martin 1967), synchronizing with the warming that ended the last ice age.

At any time, mammalian adaptation to climate involves size and S/V ratios, body shape, insulation, and metabolic rates. The climate changes cited were so abrupt that morphological/physiological adaptation protective to reproductive systems would have been nearly impossible.

Figure 1 shows declines in conception rates both above and below the optimum temperature for conception, and Figure 6 the negative effects of high and low temperatures upon estrual activity. Climate-induced decline in embryos, and reduced estrual activity, would have reduced population numbers, producing a positive feedback to further reduce, and collapse, populations (Figure 5).

For interior North American faunas, where the extreme BA-YD climatic oscillations seem not indicated, the pollen record indicates rapid climatic warming 12,000 to 10,000 years ago with the transition at any locality being abrupt, occurring just over a few hundred years. The effects of such warming on cold adapted large mammals would have created widespread maternal heat stress, and embryo death, with resultant positive feedback leading to population collapses. Mammalian extinctions, dwarfing, and skeletal abnormalities in North America occurred 12,000-10,000 years ago. North America lost 33 of its 49 genera (67%) of large mammals.

A Signature of Embryogenesis Dysfunction in Mammalian Extinctions

The mammalian extinctions at the end of the last ice age bear the "signature" of heat damage to developing embryos: extinctions of primarily large "big game" mammals, dwarfing on a global scale, and skeletal abnormalities. The latitudinal distribution of severity of the extinctions accords with greenhouse theory.

For the large size factor, Merilees (1984) noted that some process bore more heavily on large mammals than small, Martin (1984) that large size must have been a handicap as large land mammals were most affected, and McDonald (1984) that some phenomenon selected primarily against large mammals. Large mammals have relatively small surface/volume ratios, store more heat than do small mammals, and have greater difficulty getting rid of stored heat. Thus, during rapid warming, large mammals would experience greater embryogenesis dysfunction than would small ones. Elimination of large mammals is a prediction of greenhouse conditions.

Dwarfing was concurrent with the P-H extinctions, and was a global phenomenon among the mammals becoming extinct, and those that survived (Guthrie 1984). Kurten (1972) noted that dwarfing, as a prelude to extinction, occurred in many areas. In the Middle East most mammals responded to climatic warming via drastic reduction of body size (Tchernov 1984). For the Israel region, Davis (1981) reported a general size reduction 10,000-12,000 years ago. Gilbert and Martin (1984) noted that all modern large species in North America seem to have undergone size reduction during the Holocene, and general agreement that size reduction was due to climate change. Heat-induced reduction of blood flow to the uterus produces intrauterine growth retardation, or dwarfing. Heat also reduces placenta weight, producing heat-stunted offspring, and skeletal abnormalities. Dwarfing is a prediction of greenhouse conditions.

For skeletal abnormalities, Guthrie (1984) reported a size reduction of some body parts, and that nearly all mammoths associated with Clovis points in the New World are dwarfed, and had reduced tusks. High incidence of skeletal abnormalities among Bison from 11,000-9,000 years ago was reported by McDonald (1984). Hyperthermia during pregnancy can produce fetal malformations. Skeletal abnormalities are a prediction of greenhouse conditions.

The mammalian extinctions were more severe in some parts of the world than others, being maximal in the higher latitudes, and minimal in the tropical regions (Martin 1984; Guthrie 1984; Webb 1984). Climate models predict polar amplification of warming during greenhouse conditions. Of the land areas experiencing extinctions, North and South America were most severely affected, and Europe, Africa, and Asia more lightly. Variations are to be expected in that not all parts of the world heat up uniformly during a greenhouse.


If humans were not present on earth, the modern interglacial climate would likely cool directly into an ice age. However, human disruption of the carbon cycle threatens to produce a super-interglacial warming beyond the evolutionary experience of modern mammals. A Hansen et al. (1988) "Scenario A" greenhouse warming of about 7.2°F (4°C) by the year 2050, is nearly the same magnitude as the 9°F (5°C) warming that ended the last ice age (Manabe and Hahn 1977), but would hit us so rapidly that mammals would not be able to easily adapt to the abrupt and radical temperature increase. Because summer heat is already severely reducing conception rates, many species may already exist near to their upper thermal limits. Any amount of greenhouse warming can only increase maternal heat stress, and embryo damage and death, and reduce estrual activity. Mammals seem set up for maximum damage by a modern greenhouse.


In summary: (1) for the past two million years, mammals have existed mostly in cool 100,000 year glacial cycles, and but briefly in warm 10,000 year interglacials; (2) modern mammals are the survivors of global extinctions during climatic warming at the end of the last ice age; (3) we exist today in a hot interglacial world, prior to the onset of any future greenhouse warming; and (4) as indicated by widespread heat-induced embryo deaths, many mammals may already exist near to their upper thermobiological limits. (5) A major greenhouse along the lines of a Hansen et al. (1988) "Scenario A" greenhouse (7.2°F (4°C) warming by the year 2050) would create a super-interglacial hot climate beyond the evolutionary experience of modern mammals; (6) would reduce the prime cool-month breeding season; (7) reduce population numbers via embryogenesis dysfunction, with large mammals most severely affected; (8) cause dwarfing via intrauterine growth retardation due to high environmental temperatures; and (9) produce fetal malformations via hyperthermia. (10) Because of polar amplification of greenhouse warming, mammalian populations of middle and high latitudes could be vulnerable to disruption of reproductive systems.

One cannot predict with certainty that our civilization will be hit by a major greenhouse. However, examining the effects of a potential rapid climatic warming upon mammalian populations is a legitimate scientific inquiry. The sensitivity of mammalian reproductive systems to environmental heat, and the fact that greenhouse warming can only increase maternal heat stress, and its devastating effects upon embryos, suggest that mammalian faunas would not make it through a greenhouse unscathed.


I thank Dr. Joel Levine, Senior Scientist, Atmospheric Sciences Division of NASA Langley Research Center, Hampton, Virginia, whose counsel has been invaluable to me down through the years, for the invitation to participate in the 1991 International Symposium on Energy. Thanks also go to Dr. Frank Gwazdauskas, Professor of Dairy Science, Virginia Polytechnic Institute and State University, Blacksburg, Virginia, whose pioneering research on mammalian climate-reproduction coupling, and counsel, have provided valuable direction for much of my work.


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