Genetic change in a population is not the only way to survive stress. The ability to make quick physiological adjustments is also an adaptation and does not require genetic change in the population every time a stress occurs. If one is able to adjust quickly to changes in the environment, then the need for rapid genetic change is not as great.
For example, humans who move to high altitude locations will quickly experience increased red blood cell density in their blood. It does not take years or generations. This is a physiological response to living in low oxygen environments and is one of the great many physiological adjustments humans can make to maintain our internal homeostasis. As “warm-blooded” creatures, we must maintain a relatively constant internal environment no matter what the external environment may be and our physiological flexibility is absolutely key to that.
Our ability to make these changes is genetic trait for rapid physiological adjustment; there is no need for our circulatory system to genetically adapt to life in the mountains. Humans are very flexible in this way and we are able to live in and adjust to a wide variety of environments. This flexibility is common to all species (especially plants) and we refer to the trait as phenotypic plasticity. It is the ability to change one’s physiological and sometimes physical status, whether internal or external, in response to the conditions one experiences.
A well-known plant example of phenotypic plasticity is seen in the common ornamental Hydrangea bush. When growing in acidic soil (low pH), the flowers are blue, but when in neutral to basic soil (high pH), the flowers are pink. The feedback from the external conditions changes the internal conditions and this is reflected in the appearance of the flowers.
There might be no genetic difference between a pink bush and a blue bush, just a difference in the quality of the soil where the two plants are growing. And if a plant with blue flowers in low pH soil is transplanted to a higher pH soil, it will begin to produce pink flowers. (This, of course, is a source of frustration to gardeners who intentionally buy blue Hydrangeas, but begin to get pink flowers after the plants have been in the new garden soil for a while.)
This plasticity allows organisms to adjust quickly to changing conditions. By adjusting to better tolerate the conditions, plasticity can help an organism buy the time necessary for adapting to stress. If a biochemical adjustment reduces the effects of a stress long enough for the individual to reproduce, then the alleles for making that adjustment will be passed on to the next generation and individuals with those alleles will increase in number.
If the stress is present over a long period of time, those individuals able to make such adjustments will come to dominate the population, better versions of the tolerance alleles (or combinations of them) will be favored, and the negative effect of the stress will be lower with succeeding generations. The population will have changed genetically, and therefore it adapted, but the adaptation is for the ability to alleviate the stress by making quick physiological adjustments.
Plasticity is an efficient mechanism for responding to changes in the environment. It’s genetically based, but relies on environmental cues to trigger the appropriate response and these cues might be changes in temperature, day length, humidity, food quality, or even soil pH. In fact, all organisms depend on environmental cues for a tremendous variety of growth, reproductive, and behavioral processes.
For example, zookeepers that tend flocks of flamingoes know that little if any mating and egg-laying will take place unless there is a threshold number of birds. That is, flamingoes rely on visual cues related to group size to stimulate the behaviors that lead to successful mating. Once the females are surrounded by a sufficient number of neighbors, the females are stimulated to begin the mating and nest-building processes. The minimum number of birds ranges from 14 to about 40, depending on the flamingo species. By synchronizing the mating and egg-laying among all females, the chicks are born simultaneously. Theoretically, the larger numbers of chicks reduce predation risk for each individual because the probability of being killed by a predator goes down when there is a larger number of chicks for the predator to choose from.
In plants, flowering is often tied to the length of the periods of light and dark, that is, the length of the day and night. Some plants flower as the nights get shorter (and the days longer), some flower as the nights get longer (and the days shorter). In our gardens, these plants flower very predictably at the same time each year. So how is it that we can go to the market or florist and buy flowers out of season?
The horticultural world manipulates the flowering in the plants by using greenhouses to change the length of the night period. Summer flowering plants will flower in the spring if the lights in the greenhouse are kept on for longer periods of time; spring flowers can be produced in the fall by turning on the lights at night to make the nighttime seem shorter. The plants respond to the light and dark periods and not to the time of year. These are genetically fixed responses to light and dark, but plants also demonstrate a wide variety of plastic responses to other environmental cues. A very obvious flowering response is to temperature. Unseasonably warm early spring weather will result in early flowering in fruit trees.
Some plastic responses become stronger over time as sequential triggers cause the physiological response to become stronger with each episode. One obvious example in humans is the release of histamines triggered by pollen and the subsequent allergic reaction. Many allergy sufferers know that the response can become more and more emphatic with continued exposure to the environmental trigger. These responses are essentially defensive as the body is reacting to foreign proteins and it attempts to eliminate or neutralize those proteins once they have entered our bodies. Many serious allergies are an ever-increasing over-reaction to the foreign molecules and this is brought on by repetitive triggers from the environment. However, allergic responses may be useful for defending the body from invasion by foreign proteins and microbes.
Genetically-based defenses require a trigger, a response, and deployment of the response to affected areas. However, acquiring new defenses (new adaptations) is still dependent on generation time and is not realistic for dealing with novel challenges from the environment. As BIGS, we are certainly capable of handling environmental stresses from our evolutionary past, but how do we acquire new capacity to respond to new stresses and how do we do that in a reasonably short amount of time?
I suggest that human evolutionary history has favored a strategy for survival that is related to the food we eat. As Michael Pollan elegantly explained in The Omnivore's Dilemma (2006, Penguin Press), humans are faced with interesting problems by being omnivores. Carnivores and herbivores do not share our problems because they eat one kind of food: mostly proteins or mostly plant materials, and the herbivores are often very specific in their preferences. The digestive systems are less complex, chemically speaking.
In contrast, an omnivore’s digestive system must be very flexible and able to tolerate and manage a wide variety of food types. That plasticity does not come easily because the ability to digest is a biochemical ability; an omnivore’s digestive system must be able to produce a range of digestive enzymes and manage a wide range of food quality. And the range of food quantity and quality may change daily, monthly, and seasonally. For example, a traditional human diet may follow a sequence where winter greens are replaced by spring root vegetables followed by summer fruits and grains. These are very different types of foods with very different digestive requirements. How did BIGS like us adapt to be able to eat such a variety of foods? Perhaps, we didn’t have to.
BUGS adapt in very short amounts of time. Bacteria, in particular, are the most adept at shifting rapidly to accommodate change (as we noted earlier) and every human maintains trillions of these little fast responders. With a microbiome numbering in the tens of trillions with hundreds to thousands of species, perhaps humans and other BIGS have a stimulus-reaction system already in place. If our microbiota can respond to the food we eat within a few hours, the microbiome could be acting as the rapid-response system we need.
We already know that BUGS can evolve faster than BIGS. Modifying the genetic architecture of a BIG takes many generations measured in years, but changes in food quality happen over months and weeks and even days. Unless we possess a very large number of genes for producing a wide array of enzymes for digesting food of unpredictable quality (we don’t) and those genes can be turned on and off easily (probably not), it is possible that that the possession of a diverse microbiome reduces and even eliminates that need.
And as previously discussed, genetic responses to changes in the environment are hampered by the requirement of having appropriate mutations already present in the population, but such mutations are random. Random and chance processes in small populations (which is typical of humans throughout history) are inefficient for developing rapid and directed responses to stress. Forming symbiotic associations with BUGS may have become an evolutionary answer for all BIGS to the problem of rapid response to environmental change or of long-term response to environmental stresses for which there are no available mutations.
The diversity of the digestive microbiome in an omnivore and its ability to further diversify quickly represents an ideal mechanism for living in unpredictable, variable, diverse, and hazardous environments. Survival depends on adjusting and adapting to stress relatively quickly.
While BUGS are small and vulnerable to physical threats, they can manage the evolutionary process faster and more efficiently than BIGS who are at a distinct disadvantage in that regard. We should not be surprised that symbiotic relationships between small and large organisms are common and very likely even a requirement for survival as a BIG. The rapid evolutionary response of the BUGS and the physical hardiness of the BIGS is an ecological combination that provides an ideal arrangement for meeting the challenges of a shifting and unpredictable environment.
We don’t need no stinkin’ adaptations!
The original question of whether we humans are adapting to our world should probably be answered with, “No, but we might not need to.” We have BUGS on our side. Without a doubt, our systems do need to respond to environmental triggers that indicate stress, but our first response system in some, maybe many, cases is being managed by symbiotic microbes that can handle chores that are outside of our genetic capacity.
One estimate of the genetic diversity of the digestive microbiome is five million genes (and that may be on the low side). That is, our microbiome has 5,000,000 genes representing an incredible diversity of biochemical processes. In comparison, the Human Genome Project identified a paltry 20,000 genes in humans. In other words, we have a very small base from which to draw when it comes to potentially useful mutations and it takes us years, nay decades, to produce more of them.
Again, this is not to say we don’t have a long history of adapting to the environment, but that history is fraught with examples of how uncertain the process of adaptation can be. The period of 1347-1351 in Europe and the Mediterranean Basin is perhaps the most famous historical example of the human race being faced with an environmental challenge. Over the course of five years, the Bubonic Plague took an estimated 25-50 million lives representing about 40-60% of the regional population.[i] While it’s hard to know the exact numbers, the consequences of losing nearly half the total population probably had a significant effect on the genetic make-up of the region.
Did the human population adapt? No, not overall, because 40% mortality is not strong enough to cause a rapid adaptive shift in the population. However, in some areas, entire villages were lost and, in those areas, the effects of the plague might be noticeable. The Plague returned many times over the subsequent 150 years, but if the necessary evolutionary requirement of genetic variation is not met (that is, there are no mutations for genetic resistance), then there is no possibility of the survivors of the plague being anything other than lucky or hardy.
However, in Scandinavian countries, it appears there was a mutated gene (CCR5-D32) that conferred a resistance to infection and that mutation remains very common in some areas to this day.[ii] It is very likely the carriers of the gene survived the onslaught of the plague and produced the majority of the offspring for several generations. The result is a regional population that is more resistant to plague than other areas of Europe despite the fact that all of Europe and the Mediterranean felt the ravages of the disease.[iii]
The necessity of high mortality for genetic adaptation is unavoidable, but absolute numbers are not the same as relative numbers. The Spanish Flu pandemic of 1918 killed at least 50 million and perhaps as many as 100 million people worldwide making it the worst epidemic in history in terms of the number of people killed. However, with a world population of about 1.9 billion, mortality was about 2.5-5.0% compared to the 40% mortality of the Bubonic Plague in Europe (and many other epidemics in that region). Consequently, the effects of what appears to be a devastating stress are not imprinted in some populations, but not in the genetic architecture of our species as a whole.
Technology to the rescue?
With the rise of public vaccinations as a common medical procedure, starting about 1900, first for diphtheria and then for many others in rapid succession, the era of modern medicine began. At this point, the human species was able to protect itself from the many dangerous pathogens in our environment that had regularly taken a toll, especially on children. Prior to 1900, about 25% of children died before the age of two and another 25% died during the toddler to teenage years.
Because of high child mortality, life expectancy was 40-50 years in 1900 (often much lower is less developed countries) and had been for a very long time. If there had been a steady pressure on humans to adapt to these diseases, that pressure was eliminated by vaccines and later antibiotics. Very quickly, the western world made the transition from being a world of infectious diseases to one dominated by age-related diseases (notably, cardiovascular diseases and cancers). This was a transition from death before reproduction to death after reproduction and this meant the era of potentially adapting to our environment was probably over.
[i] Estimates range as high as 200 million, but 28-50 million is more likely. McNeill, William H. (1976). Plagues and Peoples. Anchor/Doubleday. Sephanie Haensch et al. 2010. Distinct clones of Yersinia pestis caused the black death. PLoS pathogens, 6(10), p.e1001134. [ii] Duncan, S.R., Scott, S. and Duncan, C.J. 2005. Reappraisal of the historical selective pressures for the CCR5-Δ32 mutation. Journal of Medical Genetics, 42(3), pp.205-208. [iii] This is the same mutation that confers resistance to HIV infection noted earlier. This is linked to the fact that both Plague and HIV attack the immune system through the T-helper cells. The similarities are remarkable, however, because Plague is caused a bacterium and HIV is a virus.