Researchers have often found it useful to separate emotions into two basic processes, one that represents the valence of the state (positive or negative) and another that describes the level of physical arousal (high arousal or low arousal). In this two-dimensional model, one can have positive feelings involving high arousal. This state occurs when the arrival of some positive event (for example, a loved one or the smell of a tasty cheeseburger) triggers pleasurable feelings. Contrasting this, the arrival of a negative event (for example, bad news or the immediate threat of physical harm) can induce a feeling of dread or anxiety.
It’s important to remember that in this model, pleasurable feelings can also be elicited in the low-arousal state by the removal of a previous threat. Likewise, the removal or loss of a potentially useful event can lead to negative emotions. Psychologists like this model because it aligns well with experimental findings. For instance, the pleasure associated with the introduction of a positive stimulus is typically accompanied by relative increases in clinical indicators of arousal (for example, blood pressure and cortisol levels). Likewise, pleasure elicited by the removal of a constant threat (or negative stimulus) is usually associated with relative decreases in these same clinical indicators. In each case we have the same emotional end point, but an asymmetry in how one arrives at the destination.
Neuroscientists who study emotions from an evolutionary perspective also like this two-dimensional model since it corresponds well with the idea that emotions are important for identifying fitness indicators in one’s environment. An example of this is the high positive correlation between an individual’s facial symmetry and his or her perceived attractiveness by others (see chapter 9). Our world is full of fitness indicators that range from those that can be used to determine the ripeness of fruit to others that allow us to choose a suitable mate. This simple two-dimensional model of emotions extends naturally to the traditional view that hedonic states evolved as internal measurement devices for assessing fitness (see chapter 9). In this view, a given stimulus carries emotional value only if it can serve (indirectly or directly) as a fitness indicator.You might argue that this is a drastically oversimplified view of emotions, and I would agree. We will use it here only to introduce a perspective for understanding how the pleasure instinct relates to the initial attraction and subsequent abuse of drugs and other potentially addictive phenomena.
In this two-dimensional fitness model, pleasurable feelings occur with the presence of fitness benefits or with the absence of fitness decrements. Negative feelings occur with the presence of fitness decrements or with the absence of fitness increments.This model, although simple, is consistent with a large body of experimental findings in humans, nonhuman primates, and mammals.
We all know, however, that a fitness indicator that is useful at one point in historical time may not be useful at another time if the environment in which natural selection takes place changes dramatically. For example, in earlier chapters we learned that our intrinsic fondness for sweets in the forms of fructose and lactose serves an important function of feeding the metabolic machinery of each cell in our body. This fondness, which was forged by selection pressures in our prehistoric hunter-gatherer days, has turned into a pathological condition in modern environments with the advent of refined sugars. It now contributes to a number of modern health problems, including obesity, diabetes, and heart disease, to name just a few.
While this particular example makes sense, one might ask how this general process extends to a fondness for drugs or alcohol. Lactose and fructose were clearly available in our hunter-gatherer days, so it was at least possible that they might be used as selection factors. Those who could identify and consume these resources stood a better chance at surviving to reproductive age. But were alcohol and other psychoactive compounds available? Certainly we can’t expect the synthetic forms we have today to have existed during hunter-gatherer times, but what about their precursors? If such substances did not exist during ancestral times, they never could have been used as selection factors, and hence an evolutionary theory of addiction based on the hedonic model would not make much sense.
People often think psychoactive drugs are modern phenomena; they are not. They are a modern problem, to be sure, but their precursors have coevolved with hominoids through the millennia. Many anthropologists have pointed out that
Homo sapiens
have enjoyed a coevolutionary relationship with psychotropic plants for millions of years. In this coevolutionary arms race, mammals have evolved mechanisms to metabolize certain plant substances, and at the same time, plants have evolved toxins that mimic the chemical structure of many endogenous neurotransmitters and neuropeptides. For instance,
Areca catechu
, commonly known as betel nut, was being used at least thirteen thousand to fifteen thousand years ago in ancient Timor. You have probably never heard of betel nut, but it is currently the fourth most commonly used drug on the planet following nicotine, ethanol, and caffeine.There is also evidence that nicotine was being extracted from pituri plants by indigenous Australians in Queensland some forty thousand years ago.
An open question concerns how and when these substances were used. For many psychoactive substances, there is archaeological evidence that they were used in ceremonial contexts, but there is also evidence that they were simply everyday food sources and used for medicinal purposes. Our relationship with alcohol probably goes back even farther than the drugs just mentioned. Virtually every species that ingests fermenting fruit is subject to low levels of ethanol exposure. Indeed, the anthropoid diet has been predominantly frugivorous (fruit-eating) for some forty million years, suggesting that ethanol exposure is old and prevalent in our prehistory. Temperate-zone fruit sources have been shown to manifest ethanol concentrations ranging from 0 to 12 percent. Comparative studies have found that as most temperate fruit ripen, both their ethanol and natural sugar contents increase. Consequently, mammals that were consistently able to identify and consume fruits enjoyed the fitness benefits of fructose, but also ingested low levels of ethanol as part of their diet. Some anthropologists have suggested that ethanol plumes may have even been used by early mammals to identify fermenting fruit, making the identification of environmental ethanol a fitness indicator. Regardless of their use, hominids have clearly had a long relationship with plant-derived psychoactive compounds.
At this point we know three very important things. First, psychoactive substances were likely consumed quite commonly in ancestral environments. Second, mammals have evolved distinct mechanisms for detecting and consuming these substances. Third, these substances may have had fitness value in the form of medicines, food supplements, or a means to find either of the two. Hence our simple two-dimensional hedonic fitness model of emotions may apply to these psychoactive compounds. So how do emotions play a role in addiction? In particular, why does the pleasure instinct nudge some of us toward addiction, but not all of us?
The Many Faces of Vice
It is quite popular to experiment with potentially addictive drugs. More than 60 percent of Americans have tried an illicit substance at least once in their lifetime, and if alcohol is included, the number rises to more than 90 percent. But, of course, only a very small percentage of people who actually try a potentially addictive drug become addicted. For instance, recent studies have found that even for a highly addictive drug such as cocaine, only 15 percent of users become addicted within the first ten years of use. The addiction literature often focuses so intently on the particular psychological and biological mechanisms that might be responsible for the addictive process that we seldom ask the simple question as to why so relatively few users ever become addicted. An evolutionary perspective may prove particularly useful in addressing this question, since it assumes that we are
all
susceptible to addiction, not just some of us. Another question that can be addressed from an evolutionary view concerns why there are so many different forms of addiction. Are there psychological or biological mechanisms that are common roots for all forms of addiction, whether the compulsion is to use heroin, eat fried food, or gamble?
What are the different kinds of addiction? The answer changes depending on whom you ask. Certainly there are the classics that we all typically think of when we talk about chemical addictions such as drugs and alcohol. But what about other activities, such as food, sex, video games, surfing the Internet, thrill-seeking, shopping, and so forth, that may share common points with the more traditional forms? Let us look at the leading theories of what addiction is and how it forms.This will provide greater context for understanding how the pleasure instinct may contribute to the casual use of certain substances and how this use may transition to full-blown addiction.
There is an enormous literature in this area, but three major theories have stood the test of time. Each tries to explain the psychological variables and processes that govern the transition from casual to compulsive substance use. They are: (1) the
classic hedonic view
that drugs are taken for the pleasure they provide the user and that unpleasant withdrawal symptoms are the primary cause of addiction; (2) the
aberrant learning perspective
, which holds that addiction results from the formation of pathological stimulus-response associations; and (3) the
loss of inhibitory control theory
, which suggests that the brain systems that usually regulate impulsivity may be impaired, resulting in greater susceptibility to substances that provide immediate gratification. I will introduce and contrast these theories with a fourth, the
modified or modern hedonic view
, based on recent findings that the neural systems responsible for “wanting” a drug are different from the systems that control “liking” a drug.
The classic hedonic explanation for addiction dates to the 1940s, but it wasn’t until the work of Richard Solomon and his colleagues in the 1970s that formal theories were first developed and tested. The basic idea is that we take drugs because they bring us pleasure. Repeated exposure to the same drug, however, leads to tolerance such that ever-increasing doses are needed to get the same high. The same homeostatic neural mechanisms that lead to tolerance result in withdrawal symptoms if the drug is discontinued. Hence compulsive drug use (addiction) is maintained to avoid the unpleasant withdrawal symptoms.
The central mechanism in this theory is homeostatic in nature. There are hundreds of examples of compensatory responses that operate in living systems. All mammals live most comfortably within a specific optimal range of values for variables such as core body temperature, blood composition, blood pressure, and others. Brain cells, for example, are very temperature-sensitive. Their electrophysiological responsiveness to stimulation changes dramatically with even small deviations from a core body temperature of 37 degrees Celsius.
Cells in the hypothalamus are sensitive to temperature deviations and send feedback signals into the peripheral nervous system to make compensatory adjustments to the rest of your body that are designed to bring body temperature back into the optimal range. If you’re a member of the Polar Bear Club and just finishing a brisk winter swim in Lake Michigan, as you leave the water your hypothalamus will scream at your autonomic nervous system to make adjustments. It will send signals whose end results are to make you shiver (in an attempt to warm the muscles), develop goose bumps (to fluff your nonexistent fur), and turn your skin blue (a result of blood moving away from cold surface tissues to warm the inner sensitive core of the body).
If, on the other hand, you are involved in strenuous exercise on a very warm day, the hypothalamus activates systems to dissipate heat such as perspiration (which cools the skin by evaporation) and increasing blood flow to the skin surface, where heat can be radiated away (and make your face appear flushed). There are many other examples of homeostatic control by the hypothalamus and other brain regions, including the regulation of blood oxygen, volume, salinity, acidity, and so forth.
Ingestion of a drug that binds with brain receptors does the same thing as environmental changes do in the examples given above. It causes a shift in normal neurotransmission that will, in turn, elicit compensatory mechanisms that attempt to bring the system back to some rough homeostatic or allostatic level. But the compensatory response actually competes with the drug-induced response. This process results in users needing to increase their dosage to get the same effect.This is known as drug tolerance.When drug ingestion is stopped, the compensatory response is still active, so there is a net shift toward effects in the
opposite
direction of those induced by the drug. These effects operate at a number of levels and comprise the symptoms associated with withdrawal. Thus at the sensory level, the pleasure induced by drug ingestion is combated by unpleasant opposing processes that are left unchecked during the withdrawal state.
Although the classic hedonic model is appealing for a number of reasons, experimental and observational findings suggest that it is limited in accounting for several aspects of the addictive process. One problem with the theory is that it fails to explain why individuals addicted to drugs often relapse into use even after they are free of withdrawal symptoms.The compensatory response that underlies withdrawal decays over time, and therefore the supposed prime reason for continued use no longer exists. Another major problem for the theory is that many addictive substances are not terribly pleasant at first, yet they still drive compulsive behaviors. If there is no hedonic value from the start, why would use continue beyond the first neutral or even negative experience? A typical example of this effect is first-time cigarette use, which most people find very unpleasant.