by Gary L Wenk
Can I blame it on my parents?
The effects of a drug or your diet on your brain are greatly influenced by your genes, the nature of the drug-taking experience, and the expectations you have about the consequences of the experience. For example, if you respond strongly to one drug, you are likely to respond strongly to many drugs, and this trait is likely shared by at least one of your parents. Many biological factors such as age and weight play a crucial role in the way that food and drugs affect the brain and influence behavior. So, too, does the unique neural circuitry that you inherited from your parents and that neural circuitry sometimes influences whether a drug will be exciting or depressing to you.
This concept is known as the Law of Initial Value. According to this law, each person has an initial level of excitation that is determined by his or her genetics, physiology, sickness or health status, drug history, and environmental factors; the degree of response to a psychoactive drug depends on how all of these factors affect one’s current level of excitation. For example, patients suffering from pain, anxiety, or tension experience euphoria when they are given small doses of morphine. In contrast, a similar dose of morphine given to a happy, pain-free individual often precipitates mild anxiety and fear. If you have a fever, aspirin lowers your body temperature, but aspirin cannot cool your body on a hot day—you must first have the fever for it to work. Coffee produces elation and improves your ability to pay attention if you have been awake for a long period of time or had poor sleep the night before; in contrast, the same dose of coffee is likely to produce much less arousal, or even anxiety, if you are well rested. Catatonic patients may respond with a burst of animation and spontaneity to an intravenous injection of barbiturates, whereas most people would simply fall asleep. Sedative drugs create more anxiety in outgoing, athletic people than they do in introverted intellectual types. Obviously, it can be quite difficult to predict how some drugs or nutrients will affect your brain function. It is not safe to rely upon the experience of others; their physiology and genetic history are likely very different from yours. This principle of brain function is true even for very commonly used, apparently safe drugs, such as caffeine.
Why am I addicted to caffeine?
Studies have documented that caffeine consumption in young adults directly correlated with increased illicit drug use and generally riskier behaviors; however, these correlational studies never examined the long-term consequences of caffeine consumption. For example, does long-term coffee consumption during adolescence lead to riskier behaviors during adulthood? How might caffeine consumption produce such long-lasting changes? The answers lie in understanding the actions of caffeine in the brain. In adults, caffeine appears to enhance indirectly the activity of dopamine within the brain’s pleasure centers. Drinking coffee produces a mild euphoria due to this effect and encourages the brain to crave more coffee. Yes, coffee is addictive, but only mildly so as compared to many other drugs of abuse such as tobacco and cocaine.
The adolescent brain responds differently to caffeine as compared with the adult brain. For example, caffeine produces a more dramatic increase in motor activity in adolescents. In addition, long-term caffeine consumption produces more tolerance faster in adolescents as compared with adults. This suggests that caffeine might produce greater changes in brain chemistry in the developing adolescent brain. This speculation was strengthened by the finding that long-term caffeine consumption during adolescence leads to greater sensitivity to amphetamine-like drugs that are used to treat attention deficit hyperactivity disorders. Fortunately, there is no current evidence that caffeine consumption leads to attention deficit hyperactivity disorders in children.
A recent study determined that long-term caffeine consumption during adolescence altered the brain’s neurochemistry so that in adulthood the brain’s response to cocaine was enhanced. In contrast, consuming caffeine as an adult does not produce the same type of enhanced response to cocaine. This finding suggests that the developing adolescent brain is vulnerable to the effects of caffeine and that these changes can linger into adulthood and increase the abuse potential of euphoria-producing drugs such as cocaine. Therefore, by definition, coffee and tea are gateway drugs to cocaine. Thus, is caffeine a drug or a food? Sometimes it is very hard to tell the difference.
What should I eat to feel better?
Almost everything you consume may directly or indirectly affect brain function. In order to understand better how food and drugs affect the brain, it will be helpful to divide them into three categories. First, there are chemicals we consume that produce almost immediate effects on brain function, such as those found in coffee, heroin, alcohol, nicotine, marijuana, some spices, and a few psychoactive plants and mushrooms. Their effects depend on how much of the chemical reaches the brain. Sometimes the amount of chemical that actually enters the brain is so low that we do not notice its effects. For example, consider nutmeg: Low doses will be in pies next Thanksgiving, and most of us will not notice that it contains a chemical that our bodies convert into the popular street drug Ecstasy. Yet, if you consume the entire canister of the spice, your intestines will notice (with a terrible diarrhea), and there is a good chance, if the nutmeg is fresh, that you will hallucinate for the next 48 hours. Nutmeg abuse is often popular in prisons.
Second, there are those foods that affect our brain slowly over a period of a few days to many weeks. This is usually called “precursor-loading” and would include many different amino acids (tryptophan and lysine are good examples); carbohydrates that have a high glycemic index such as potatoes, bagels, and rice; fava beans; some minerals (iron and magnesium, in particular); lecithin-containing products such as donuts, eggs, and cakes; chocolate; and the water-soluble vitamins. The purpose of these foods is to bias the function of a specific neurotransmitter system, usually to enhance its function in the brain. For example, scientists once thought that drinking a glass of warm milk before bed or eating a large meal of protein made us drowsy because of tryptophan loading. The current evidence does not support this explanation, but the claim makes my major point: You must get enough of any particular nutrient or chemical to the right place, and at the right dose, in your brain in order for you to notice any effects. In fact, tryptophan has difficulty getting into your brain, particularly when consumed within the context of a large variety of other amino acids, as are present in meat, such as turkey, which, in fact, does not contain very high levels of tryptophan. Pumpkin seeds and egg whites contain far more tryptophan than turkey and no one has claimed that these food sources cause drowsiness. So, what is the scientific evidence for considering the cognitive effects of these foods? Mostly, it is related to what happens when we do not get enough of them. For example, studies have shown that consuming too little tryptophan makes us depressed and angry; historians now blame low-tryptophan diets for multiple wars and acts of cannibalism. Too little of water-soluble vitamins (the B’s and C) in the diet will induce changes in brain function that we will begin to notice after a few weeks of deprivation. Ordinarily, the foods in this second category require more time to affect our brains than do foods in the first category.
The third category includes the slow-acting, lifetime dosing nutrients. This category includes the antioxidant-rich foods such as colorful fruit and vegetables, fish and olive oils, fruit juices, anti-inflammatory plants and drugs such as aspirin, some steroids, cinnamon and some other spices, nicotine, caffeine and chocolate, the fat-soluble vitamins, nuts, legumes, beer, and red wine. People who eat these foods benefit from consuming them regularly over their life span.
The benefit comes from the fact that all of these foods provide our brains with some form of protection against the most deadly thing we expose ourselves to every day—namely, oxygen. Because we consume food, we must consume oxygen. Because we consume oxygen, our tissues suffer the consequences. Thus, people who live the longest tend to eat foods rich in antioxidants or simply eat much less food. Although nicotine and caffeine prevent the toxic actions
of oxygen in our brain, this should not be taken as a recommendation to smoke a cigarette with your morning coffee.
We can see here that depending upon how we frame the question about how food affects the brain we end up with a different list of foods and a different reason for consuming them. If you wish to alter your current brain function or slow your brain’s aging, you need to eat specific foods. In truth, no one ever considers these distinctions when eating—most people simply eat what tastes good, and our brains evolved to reward us for eating sugar, fat, and salt. Consequently, food, like any illicit or licit drug, has both negative and positive effects; it all depends on what drug or food you consume and how much you consume.
How do I stop eating so much food?
The real challenge for your brain is how to stop you from eating. This decision is partly determined by how fat you are. The brain learns about this through the action of two hormones—leptin and insulin—and responds by reducing food consumption. The blood levels of insulin and leptin are continuously elevated in the brains of many obese people, but their brains ignore these hormonal signals and so eating continues. The effectiveness of these hormones is influenced by fluctuating levels of estrogen; this leads to the gender dichotomy that females are more sensitive to the appetite-suppressant action of leptin (initiated by their body fat), whereas males are more sensitive to the appetite-suppressant action of insulin (induced by eating). When it comes to food, female brains do not follow the same rules as male brains.
Your brain also gets sensory feedback from your mouth and nose about the smell, taste, and feel of the food, as well as the expansion of the stomach. Unfortunately, these signals can easily be ignored by the brain—and so we keep eating. New research on how the brain gets us to stop eating has led to the development of drugs designed to reduce food intake by mimicking one or more of these feedback signals. But each time the same thing happens—caloric intake decreases for a short time and then the brain adapts to ignore the false signal; ultimately, regular caloric intake is restored. Why? Because the consequences of not ingesting a sufficient number of calories has terrible consequences for your survival. There is no evolutionary advantage to trying to lose weight by restricting eating. Four billion years of evolution have led to the following simple directive for all living things: Find and consume the energy within food, repeat often.
When an energy source is on the tongue, the brain is informed via a series of simple molecular interactions within the taste buds, which lead to the activation of reward pathways in the brain that utilize the neurotransmitters dopamine, endorphins, endocannabinoids, and orexin. Orexin was discovered only recently; it influences both our level of arousal and our craving for food. Take a moment to appreciate how orexin optimizes your daily existence and survival. Orexin-releasing neurons wake you in the morning and then make you crave food. Once food reaches your gut, it encounters still more receptors that detect sweetness, fattiness, and bitterness. It appears as though your entire gut is a continuation of the tongue with specialized taste receptors. The activation of these receptors slows the intestinal transit of the food, providing a greater opportunity for nutrient extraction within the limited length of the intestines.
Is there a good time of day to eat?
What would happen if you could only eat between the hours of 9 A.M. and 4 P.M.? Would you gain less weight and be healthier overall even if you ate a high-fat diet? The answer is yes and is based on how your body is influenced by your daily rhythms of eating and sleeping. There are always negative consequences to ignoring the role of your biorhythms. Many studies have documented that nightshift work, and the odd patterns of sleeping and waking that this lifestyle involves, has many negative health consequences, including insomnia, high blood pressure, obesity, high triglyceride levels, and diabetes—collectively known as the metabolic syndrome. In a recent study, mice were given free access to a nutritionally balanced diet or a diet that was high (61% of their daily calories!) in fat. Some mice were allowed total access to the food at all times; others were only allowed access for an eight-hour window during the early phase of their normal active period. Mice given all-day access to a high-fat diet (which the authors termed the standard American diet) developed obesity, diabetes, metabolic syndrome, and poor sleep-wake rhythms. Now for the good news! The mice that had time-restricted access to the high-fat diet were significantly healthier than the mice given all-day access to the same diet. These lucky mice lost body fat and had normal glucose tolerance, reduced serum cholesterol, improved motor function, and normal sleep cycles. Most surprising, the daily total caloric intake of all groups did not differ, regardless of their diet or feeding schedule.
Therefore, it truly does matter when you eat. The take-home message is eat early, skip dinner, and never have late-night snacks. Skipping breakfast and then overeating in the evening play a significant role in weight gain and obesity. Furthermore, people who skip breakfast report not feeling as satisfied by their food and being hungry between meals. If this sounds like you, then it’s time to change your mealtimes.
What about carbohydrates?
A carbohydrate is a molecule made of carbon, hydrogen, and oxygen. Glucose is a carbohydrate and is commonly called “sugar.” The adult brain has a very high energy demand requiring continuous delivery of glucose from the bloodstream. The brain accounts for approximately 2% of our body weight but consumes approximately 20% of glucose-derived energy, making it the main consumer of glucose. The largest proportion of energy in the brain is consumed by your neurons when they are busy processing incoming sensory information, thinking about complex problems, or contemplating your future. Your brain needs a constant supply of sugar; without it you would quickly lose the ability to think and slip into a coma. We must obtain this sugar from our diet. Somewhere in our evolutionary history, we lost the ability to convert fat into sugar; unlike a few fortunate animals, humans cannot perform this metabolic trick. So, in the morning when you wake up from a long period of fasting, your brain wants you to eat lots of sugar and other simple carbohydrate sources, such as a donut. There is a reason that donuts and sugar-laden cereals are so popular, and you can lay the blame on neurons within the feeding center of your hypothalamus. This mechanism works nicely. First thing in the morning, you eat lots of simple, easily digestible sugars and your brain rewards you with a good feeling by releasing dopamine and endogenous opiates. The amount of dopamine released into your reward center is proportional to how hungry you are; that might explain why you enjoy sugary cereals or a donut for breakfast—they simply taste much better after you have been fasting all night. Your brain needs the sugar to produce chemicals that are critical for learning and memory.
Impaired glucose regulation correlates with impaired learning in the elderly and is associated with Alzheimer’s disease. Scientists recently have discovered that the inability of specific brain regions to use glucose efficiently precedes the degeneration of those same brain region decades later. Eating more sugar is not the answer to preventing dementia. Indeed, consuming large amounts of sugar is not healthy for your pancreas or cardiovascular system. What’s good for the brain is not always good for the other organs of your body.
What about fats?
We have a fatty brain and fat plays many vital roles in brain function. In the past, very little attention was given to the influence of dietary fats on our mental state. Recent evidence indicates that it might be possible to manipulate our dietary fat intake to treat or prevent disorders of cognitive function. A recent study compared the effects of monounsaturated fats from olive and canola oils with polyunsaturated fats from meat, fish, and vegetable oils on a variety of biochemical changes and electrical properties of cells within a brain region that is critical for learning and memory. After 11 months, a diet high in monounsaturated fats, often referred to as the Mediterranean diet, altered brain chemistry in such a way that learning was enhanced, age-related cognitive decline slowed, and the risk of getting Alzheimer’s disease was reduced.
These findings support the addition of canola, olive, and fish oils to our diet and further demonstrate that sensible nutritional choices are vital for optimal brain function and good mental health.
Omega-3 fatty acids are a family of fats that are important components of the human diet. Some recent studies have concluded that being deficient in omega-3 fatty acids may affect brain physiology and increase the risk of cognitive decline. Superficially, this claim makes sense. After all, omega-3 is abundant in the brain and is involved in numerous critical functions. It also may enhance learning and memory processes in the brain. It has been argued that dietary intake of omega-3s, mainly from fish, can slow cognitive decline and the incidence of dementia. These claims may or may not be true. The problem is that the clinical trials related to these claims have either included too few patients or were conducted for quite brief periods of time. Thus, the results were highly variable and potentially misleading. Recently, a study investigating the potential benefit of omega-3s followed almost 3,000 people, aged 60 to 80 years, for 40 months. Their daily diets, medications, and health status were carefully monitored. The patients and their controls were carefully matched for education level, smoking habits, and alcohol use, among other features. The results confirmed that prolonged omega-3 intake (as fish or pill supplement) provides no significant health benefits. Cognitive decline also was unaffected. What does this mean? That a single, good dietary habit, such as high levels of specific essential nutrients, is not enough to provide protection for your aging brain.