The Pleasure Instinct: Why We Crave Adventure, Chocolate, Pheromones, and Music (13 page)

 

 

By the beginning of the second trimester of pregnancy—just about the time when Melissa was regaining her desire to eat and morning sickness was making a thankful exit—Kai’s taste buds were beginning to mature. It is probably no coincidence that his first real sucking and swallowing behaviors also started at about this time, since the continued development of his taste buds, and most importantly their anatomical connection into functional taste circuitry in the brain-stem, depend on stimulation. The brain-stem sites mature very early as well and will provide Kai with a complete set of reflexive movement patterns for getting the nutrition he needs—everything from sucking and swallowing behavior to changes in facial expression in response to sweet versus bitter tastes. But it is unlikely that fetuses can consciously perceive tastes at this point in their development, since cortical taste sites are not yet mature. Anencephalic newborns lack most of their cerebral cortex, yet they are capable of the same behaviors. These include tongue protrusions to reject bitter-tasting liquids, and salivation in response to sweets, even though detailed investigations show that these infants have no genuine awareness of such tastes.

Comparisons across a wide range of mammalian species has shown that the taste circuitry that projects from the epithelial cells to brainstem sites is highly conserved across very different animals, and hence is likely to have evolved rather early in the evolutionary lineage of hominids. Just as the conscious perception of taste and its integration with brain systems that regulate pleasure are likely to be relatively newer adaptations built on existing brain-stem circuitry, so it is for the developing fetus, who fails to show signs of real taste preferences until about the third trimester, when brain-stem connections to cortical and limbic regions are complete.

At this point in his development, Kai is experiencing all sorts of tastes—sweets, sours, bitters, you name it—all of which are incorporated into the amniotic fluid through Mom’s diet. Even before my son is born, he has a sweet tooth.Although he tends to move most in the late evening hours, his fetal gymnastics can be brought on at any time of the day if his mother indulges in a bowl of Häagen-Dazs’s Dulce de Leche. And this is not unusual. Before the days of ultrasound, X-ray contrasts were commonly used to assess fetus health in the final trimester. Studies performed during this time show that fetuses increase their swallowing behavior and movements if a sweet solution such as saccharine is injected into the amniotic fluid, while they decrease their swallowing if a bitter or noxious-tasting substance is injected. These results are consistent with the idea that taste perception and preferences emerge during this developmental period.

Well before Kai has any exposure to the outside world, he is already establishing taste preferences that will form a lifetime of eating habits. Evidence from both animal and human research indicates that taste variety is remarkably important during this stage of development. For instance, rats born to mothers who have had their salt intake curtailed during the final stages of gestation lack the ability to perceive the substance after birth. Likewise, rats born to mothers who consume diets rich in particular tastes such as apple juice or alcohol show an enhanced preference for the taste after birth when compared to rats born from mothers with a normal diet. Both of these forms of experience-expectant learning also occur in humans. Finally, it is important to note that a very general relationship appears to exist between the experience of taste variety in the womb and acceptance of novel foods after birth. Newborn rats and humans exposed to an increased variety of tastes in utero typically show less fear of novel foods when compared to newborns from mothers who had a more restricted diet.

Much like we saw with smell, although newborns have an innate preference for specific tastes such as sweets and certain fats, they also exhibit an impressive potential for developing novel taste preferences based on what was experienced in the womb. Moreover, these experiments demonstrate that the development of normal taste perception depends critically on experiencing a wide variety of tastes while in the womb, since limited exposure to a taste class (for example, salts) can result in a reduced ability to detect and perceive these tastes after birth.

So far we’ve seen that humans find the consumption of sweets innately pleasurable, and that the evolution of this tendency can be traced to the evolutionary pressure to identify and
desire
high-energy foods (such as fruits and mother’s milk) that are rich in natural sugars and relatively plentiful and safe to consume. But what about fats? Why do humans have such an insatiable appetite for fatty foods?

Although many of the ancient Greeks, including Aristotle, considered fat a basic taste class, it has only been in the past few years that food scientists and psychologists are willing to accept the idea that fat has a specific taste. Previously, most scientists believed that fat only acted as a food texture or flavor carrier. But this has changed with the discovery that simply putting a fatty food such as cream cheese into your mouth raises blood serum levels of triacylglycerol (TAG), an indicator of blood fat loading, even if the food is never swallowed. Richard Mattes, a food scientist at Purdue University, and his students followed up on this original study by showing that blocking the subjects’ ability to smell the cream cheese has no effect on the outcome, suggesting that it is the taste component of a fat that produces this change in blood TAG levels.

These findings are probably no surprise to researchers such as physiologist Adam Drewnowski, who in the early 1980s showed that subjects’ rating of the pleasantness of a food is directly related to the relative proportions of sucrose and fat in the samples tested. We all love foods that are laden with sugar, but there is a limit beyond which we find a food to be too sweet. Hedonic preference ratings first rise and then typically decline with increasing sucrose concentration in these experimental studies. This is not, however, what happens with fatty foods. Surprisingly, hedonic preference ratings typically continue to rise with increases in dietary fat content. It is possible, then, that our innate fondness for fats is even more intense than for sweets. And this makes perfect sense from both evolutionary and developmental perspectives.

Let’s start with evolution. In the past 2.5 million years, the hominid lineage leading to humans has evolved significantly larger brains relative to body size when compared to other primates. Understanding the reason for this dramatic expansion has been a long-standing question for those concerned with human evolution. Many theories argue that brain expansion followed the development of some key cognitive or behavioral milestone such as the emergence of bipedalism or language or social group formation or toolmaking, and so on. The list is long and varied, but the question remains: Did these new functional capacities result from or cause the dramatic increase in hominid brain size?

Michael Crawford of the Institute for Brain Chemistry and Human Nutrition in London has argued that hominid brain expansion is the direct result of dietary shifts that accompanied the migration of
Homo sapiens
from the open savannas to freshwater and saltwater shoreline regions, predominantly in the East African Rift Valley some 250,000 years ago. Human babies have combined brain and body fat that accounts for a whopping 22 to 28 percent of their total body weight, a finding that is not seen in any other terrestrial animals. Fats are an indispensable component for building brains.The very foundation of life—the cell membrane—is made from a double layer of lipids that protects and shields the internal organs of the cell while at the same time permitting the perfect amount of elasticity so the cell can respond to physical changes in the extracellular environment. In human babies, a high level of dietary fat is critical for normal brain development because it provides energy for growth in the form of fatty acids found in triglycerides; contains important chemical precursors to ketone bodies that regulate brain lipid synthesis; and provides a store of long-chain polyunsaturated fatty acids, most notably docosahexaenoic acid (DHA) and arachidonic acid (AA), which are essential for the formation of retinas and synaptic junctions where brain cells communicate.

Both DHA and AA are present in abundance in human milk but noticeably absent in cow’s milk. Recognizing the importance of these fatty acids for human brain growth and development, many formula manufacturers have begun supplementing their existing recipes with DHA and AA. Human body fat contains more DHA and AA at birth than at any other time during life, and in the newborn approximately 75 percent of its total energy expenditure goes to brain growth. Hence the fatty acids DHA and AA are important for brain development because they serve as an energy supply to fuel cell growth and proliferation, and because they have a molecular structure that is a unique component for building synapses.

Michael Crawford and his colleagues have suggested that since the natural supply of DHA and AA in human newborns is only enough to last the first three months of life or so, the continued supply of these fatty acids must occur through the child’s diet. This means that the availability of foods that are natural sources of DHA and AA is a rate-limiting factor on human brain development and would naturally restrict the expansion of hominid brain size throughout evolutionary history. So where do you find rich veins of DHA and AA? Both are part of the larger omega family of fats whose synthesis requires the presence of two essential fatty acids that are not manufactured by the body, and consequently must be obtained through the diet. Alpha-linolenic acid (ALA) is the foundation of the omega-3 family of fatty acids that your body uses to make DHA, and linoleic acid (LA) is the foundation of the omega-6 family that is used to make AA. Both substances emerged in response to evolutionary pressures in plants to efficiently store and access energy reserves. Photoplankton, algae, and green leaves synthesize ALA in their chloroplasts, while flowering, seed-bearing plants store lipids in the form of seed oils loaded with LA.

Crawford’s group has argued that the evolution of the hominid brain to the human form we know today would have been impossible unless early
Homo sapiens
incorporated large amounts of both ALA and LA into their daily diet. They suggest that the most dramatic increase in hominid brain expansion co-occurred with the migration of
Homo sapiens
to shoreline environments and lacustrine estuaries, where dietary ALA and LA were plentiful.

Whether or not Crawford’s hypothesis is correct, two things are absolutely clear: growing brains require significant amounts of both ALA and LA, and these critical ingredients must be obtained through diet. ALA and LA deficiency in animals and humans results in altered structure and function of brain cell membranes and can lead to severe cerebral abnormalities. These anatomical changes have been linked to a number of disorders. For instance, both ALA and LA are involved in the prevention of some aspects of cardiovascular disease (including cerebral vascularization), and reduced levels of the fatty acids have recently been attributed as a cause of stroke, visual deficits, and several neuropsychiatric disorders, including depression, presenile dementia, and most notably Alzheimer’s disease. Another study showed that ALA deficiency decreases the perception of pleasure by directly altering the efficacy of sensory organs and by creating abnormal changes in frontal cortex anatomy.

Taken together, these findings provide compelling evidence that many selection factors were operating to ensure that early
Homo sapiens
with a taste for foods containing ALA or LA would have a survival advantage over their peers who lacked this preference. Nature has solved this problem by giving us not just a “sweet tooth,” but also an appetite for fats. Given these findings and the results of Drewnowski’s experiments in the early 1980s, it is possible that we may find eating fats even more pleasurable than sweets.

It is known that humans and other animals can discriminate among different dietary fats and have a preference for corn oil, which can be used as a positive reinforcer in conditioning experiments. Corn oil has three major fatty acid components: linoleic acid (52%), oleic acid (31%), and palmitic acid (13%). Recent experiments in rats have shown that LA has an important effect on the physiological responses of the epithelial taste cells that make up taste buds. It appears that when LA binds to these cells, it increases the strength of the electrical signal that they normally send to the brain-stem in response to a food source. For instance, if LA and sucrose are consumed together, the combined signal sent from the taste bud that announces the arrival of food is stronger than would be the case with sucrose alone. This physiological response has a marked impact on food intake regulation. In a series of behavioral experiments, psychologist David Pittman and his students at Wofford College found that in rats, LA acts to increase the intensity of sweet, salty, and sour tastes such that the natural preference or avoidance of each is enhanced.As predicted from the physiological findings, animals preferred the taste of a solution containing LA and sucrose together more so than a solution with sucrose alone. Likewise, when Pittman’s rats were given a mixture of LA with salt or citric acid, they consumed less than when the salt or citric acid solution was offered alone.

Linoleic acid is present in a variety of natural vegetable oils, and since it has a direct effect on the physiological responsiveness of epithelial cells, it is likely to be one of several compounds that give fats their pleasurable taste. The fact that LA can be used as a positive reinforcing stimulus in conditioning tasks tells us that humans and animals are motivated to consume foods that contain the substance. Hence, the pleasure we find in eating fats may serve to ensure that enough essential fatty acids are included in our typical diet to promote and maintain normal brain growth and development. At the same time, this pleasure-mediated mechanism provides yet another example of how modern food manufacturing technology, in proliferating the availability of refined sugars and fats, has essentially removed the selection factors that originally led to these important adaptations. In doing so, we are a society vulnerable to a number of disorders, such as obesity and diabetes, that emerge when the pleasure we receive from eating certain foods is filled well beyond the natural limits imposed by the environmental circumstances of younger hominids.