14
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“The best doctors in the world are Doctor Diet, Doctor Quiet, and Doctor Merryman.” —Jonathan Swift |
Food for the Body, Fuel for the Brain |
As recently as World War II, scientists as well as the general public considered diet to have little or no influence on mental functioning. Research over the last 40 years, however, has revealed a close relationship between diet and the brain—so much so, in fact, that trendy brain bars are popping up that specialize in juices and foods considered to improve mentation, or mental activity. It is becoming clearer that our brain influences what and how we eat, and that what and how we eat influences our brain. This chapter identifies various specific findings in this arena of the food-brain connection.
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TOPIC 14.1 |
Two primary chemical actors head the complex cast of characters in the tense drama of appetite control: chemicals that trigger hunger and chemicals that trigger satiety. If these are in good order, much of the rest of one’s chemical makeup will have a minimal effect on appetite and weight control. Significant discoveries have come on the scene in the last five years, and huge pharmaceutical product development research efforts currently focus on finding acceptable exogenous (externally administered) ways to optimize a person’s hunger-satiety balance. Current estimates based on twin studies consider the genetic influence on weight to be extremely high—around 60–70 percent. Combined with the meager 5 percent success rate of diets, this paints a bleak picture for the role of self-control in weight management. Authorities suggest that we’d be better off changing the environment than trying to change the individual. Do we hear a movement afoot to abolish faux food? New York City Mayor Bloomberg has done his part by successfully promoting a ban on the sale of sugary drinks larger than 16 ounces in restaurants and concession stands. (Wait, this just in: a judge has blocked his honor’s ban. Watch for developments!) The environmentalists formed the Sierra Club. How about the Fiber Club for the nutritionists?
Chemicals That Signal Hunger
Sarah Leibowitz, a neurobiologist at Rockefeller University in New York City, has identified the area of the brain in which this drama plays out: the paraventricular nucleus (PVN) of the hypothalamus (see appendix A). Chemical players that trigger appetite include galanin (discovered by Leibowitz, this is a neuropeptide that craves fat), norepinephrine, neuropeptide Y, and cortisol. In addition, a research team led by Masashi Yanigasawa at the Howard Hughes Medical Institute at the University of Texas Southwestern Medical Center in Dallas reported the discovery of two hormones that send a hunger message (Cell, February 20, 1998). Yanigasawa calls these hormones orexin-A and orexin-B. The orexins have their own receptor network in the hunger section of the hypothalamus and have been found to send an extremely strong hunger signal in mice. Development is under way for use with humans as both a stimulant and a suppressant of appetite.
Another hormone related to weight is ghrelin: it makes people hungry, slows metabolism, and slows the ability to burn fat. It is highest before meals, lowest just after. Unfortunately, those who lose significant amounts of weight tend to produce more ghrelin, so it apparently serves evolutionarily as a defense against starvation. Persons injected with ghrelin report feeling hungrier and, if exposed to a buffet with a large quantity and variety of food, will eat 30 percent more than they typically would consume.
University of California, Irvine, College of Medicine researchers have identified the receptor for melanin-concentrating hormone (MCH), a key ingredient in the appetite control process. Earlier research discovered that MCH influences how often and how much rats and humans eat: the more of the hormone, the stronger the appetite. The Irvine research team, headed by pharmacology professor Olivier Civelli and senior pharmacology researchers Hans-Peter Nothacker and Yumiko Saito, located the receptors that bind with MCH in the hypothalamus, olfactory area, and the nucleus accumbens, all involved in one way or another in smell, taste, and feeding urges. Research is under way to clarify these processes and how they might be brought under control for the benefit of the masses desiring and needing to be less massive.
Sarah Leibowitz has identified the chemical sources of urges for specific food groups, as well as the time of day during which the urges are strongest (Collin, 1992, p. 74). A summary is shown in table 14.1.
At a spring 1998 meeting of the Society of Behavioral Medicine in New Orleans, Yale University researchers reported that high levels of cortisol are associated with high cravings for fatty snacks. When given a choice, high-cortisol snackers head for the nachos, low-cortisol snackers for lower-fat snacks. Cortisol levels are increased by stressful experiences.
Chemicals That Signal Satiety
Chemical players that shut down appetite include enterostatin (produced by the stomach and pancreas in response to the ingestion of fat), serotonin, dopamine, cholecystokinin (CCK), and leptin (from the Greek leptos, “thin”), a protein produced by the newly discovered “obesity gene” on chromosome 6. After you’ve eaten, cholecystokinin is released in the intestines to tell the brain you’re full. Leptin tells the body whether to burn fat you’re eating or store it as fat. GlaxoSmithKline is developing a synthetic version of cholecystokinin, with exciting early results. Regeneron is developing a synthetic version of leptin to tell the body that it has enough stored fat and it’s time to burn all calories. Houston’s M. D. Anderson Cancer Center has developed a chemical that melts fat cells in mice by attacking the proteins in blood vessels that feed their fat cells. But all is not well in leptin land. Sanofi of Paris developed rimonabant, a wonder drug that made one feel full, reduced triglycerides, increased good cholesterol, and restored sensitivity to insulin. In 2008, 56 countries were actively prescribing it when the European Medicines Agency (EMEA) declared the risks to outweigh the benefits. Sanofi suspended the drug, and the EMEA withdrew its approval of rimonabant in 2009.
Food is more than physical nourishment—it forms the basis of bonding between mother and child and, according to recent research, between friends. Eating sets off two (at least) processes: oxytocin and cholecystokinin are released to the brain. We’ve known for a while that oxytocin was released during maternal nursing (and during sexual orgasm in both sexes, and in nest building, and in uterine contraction during childbirth, and in response to massage), thus helping to cement the bond between mother and child. But we now know that nursing and eating in general not only set off oxytocin, but also cholecystokinin, the latter of which sends a message from the intestine to the brain that says, “Food has now gotten where it needed to! Thanks, system, you’re working just fine.” But Kerstin Uvnas-Moberg of Sweden’s Karolinska Institute has discovered that when oxytocin and cholecystokinin are blocked, a suckling lamb will not bond with its mother. Both messengers must be active for bonding to take place. Thus we understand why business partners, sales reps and their prospects, and friends in general like to “do lunch.” Therefrom comes bonding, and the cooperative, pleasurable mood with which it is associated. If food be the music of bonding, munch on, together. One’s associates shall be known by one’s table mates.
David York, of the Pennington Biomedical Research Center at Louisiana State University, learned that enterostatin shuts off the pleasure system of the brain (see topic 31.6), which is activated in ecstasy as a response to fat consumption. Fat loses its appeal when enterostatin levels are sufficiently high. Low galanin levels are associated with low fat intake and high galanin levels with high fat intake, unless enterostatin levels are also high, when fat intake will be limited (because fat satiety is reached quicker). If enterostatin levels are low, then fat satiety will be delayed, unless galanin is also low, when little fat will be ingested. More recently, Stephen Bloom, an endocrinologist at the Imperial College in London, announced in Nature the discovery of a suppressor similar to enterostatin named GLP-1 (glucagon-like peptide-1), whose receptors are located in the hypothalamus.
Jeffrey Friedman (The Brain in the News, April 2004, p. 5) of the Howard Hughes Medical Institute at Rockefeller University in New York discovered leptin in the 1990s. Leptin, secreted by fat cells, suppresses appetite. Leptin deficiency is associated with overeating in rats, but leptin supplements in humans have not led to the predicted appetite suppression. In a complex balance, the hypothalamus contains two opposing types of cells: NPY cells, which, when activated, stimulate appetite, and POMC cells, which suppress appetite. Both are constantly active, and the dominance of one or the other determines feeding urges. Leptin deficiency activates the NPY cells, which is why losing weight makes you hungry. This appears to be at least one aspect of the “set point” theory. The trick for researchers is to learn how to lose fat, and hence leptin, without in turn activating the NPY cells.
On another front, Merck, in partnership with Nastech Pharmaceutical Company, is in trials with a nasal spray that provides a rapid fullness message to the brain by using the natural hormone Peptide YY3-36 (PYY3-36). This hormone is made in the intestines in direct proportion to the calorie intake at mealtime. Early results indicate that use of the spray can result in a 30 percent reduction in daily calorie consumption, with an associated 50-pound annual weight loss. Long-term side effects, as well as long-term maintenance requirements, are undetermined at time of publication.
A Stab at Putting All the Appetite Chemicals Together
The spring 1997 issue of the Harvard Mahoney Neuroscience Institute Letter announced the identification of leptin receptors in the hypothalamus. Leptin is secreted by adipose tissue (fat cells) as a messenger to the hypothalamus with information about whether it wants more fat, less fat, or is just fine, thank you. Obese mice lose their excess fat when injected with leptin. Roger Unger of the University of Texas Southwestern Medical Center at Dallas reported in the Proceedings of the National Academy of Sciences that leptin is also active in burning up fat inside the adipose tissue. So leptin performs at least two functions: it metabolizes fat within fat cells, and it sends messages to the hypothalamus. Apparently, although I haven’t seen this reported, leptin is the instigator of the hypothalamic secretion of galanin. The overall process, then, is something like this: fat cells send leptin to the hypothalamus, which interprets the information and decides when to send out galanin to fish for fat, which results in the release of enterostatin when the fat hits the pancreas (figure 14.1).
Figure 14.1. How Fat Cells Work
Current Drugs for Appetite Control
Drugs now available for appetite control treat symptoms, not causes. One such symptom is the increase in dopamine and serotonin levels produced by fat consumption—a kind of reward system first discovered by Bartley Hoebel of Princeton University. The triggers and suppressants listed above relate to the causes of good and poor appetite control. Drugs like phentermine (increases dopamine), Prozac (increases serotonin), Orlistat (blocks fat absorption), fenfluramine (increases serotonin), and dexfenfluramine (a component of fenfluramine known commercially as Redux) do not address the root causes of craving and satiety, but rather provide the effect of pleasure from having eaten, thereby covering up the cravings. Recent warnings suggest that only the morbidly obese should use the powerful “Fen-phen” combination of fenfluramine and phentermine; studies show ill effects on the heart, lungs, and brain in both animals and humans. Even the drugs prescribed singly, like Redux (dexfenfluramine by itself), are overprescribed, according to Mark Molliver of Johns Hopkins University School of Medicine. Molliver was quoted in the March 17, 1997, Dallas Morning News as saying, “I’ve gotten calls from patients all over the country. They are 20 pounds overweight and were given Redux. I think it’s being used to a degree that’s completely inconsistent with medical ethics.” Part of the question has been resolved: in September 1997, the Food and Drug Administration pulled both dexfenfluramine (Redux) and fenfluramine (Pondimin, half of the Fen-phen combination) off the market because of their link to serious heart problems.
Researchers at the Eleanor Roosevelt Institute (University of Denver) have found that overweight mice lose 50 percent of their weight in two weeks when injected with melanocyte-stimulating hormone (MSH). Apparently the gene POMC controls MSH production, and mice with the POMC gene turned off fail to make enough MSH, which apparently specializes in burning fatty acids. No ill side effects accompanied the weight loss in the overweight mice. The process is just beginning (in 2004) for human research.
In a recent and related discovery, researchers at the University of California, Davis, announced in Nature Genetics the discovery of a gene that governs what one does with excess calories: whether one converts it into normal body heat or stores it as fat to “get through winter or famine.” The protein associated with this gene, UCP2, occurs at high levels in animals who do not gain weight from high-fat diets. With the discovery of this process, and of leptin receptors in particular, great strides will surely be made in carrying this new knowledge closer to a harmless drug for appetite control.
Applications
If you have a problem with being overweight, ask your doctor or pharmacist if any new drugs either limit galanin production, bind galanin receptors, or increase enterostatin or leptin levels.
If you have a problem with being underweight, have your doctor look for products that boost galanin production, stimulate galanin receptors, bind enterostatin or leptin receptors, or use some combination of these techniques.
Until better medical intervention based on recent discoveries becomes available, your best help for appetite control is to exercise regularly and to manage your environment so that fatty, sugary alternatives are not available.
Save fat consumption for evenings, when desire is strongest for most of us.
When eating an early-evening meal, minimize carbohydrate consumption and maximize protein. When eating very late, minimize protein to avoid interference with sleep.
When possible, after a stressful episode, dissipate cortisol with exercise before subjecting yourself to the temptations of fatty snacks. For example, during a break, rather than heading for the snacks, try taking a 10-minute brief walk first.
Although the research laments that diets have a high failure rate, there seems to be a common cause for such failure—the monotony, or lack of variety, in many diets. I feel that such monotony results from a failure to study the diet plan and search properly for the many ways of fulfilling the spirit of the plan. For example, the controlled carb diets report excellent initial weight loss, but participants tend to lament their boredom with eating steak and eggs every day. This is clearly an overly simplistic interpretation of the plan. The controlled carb approach allows for extensive variety.
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TOPIC 14.2 |
Paul Moe, research leader in the Energy and Protein Nutrition Laboratory of the U.S. Department of Agriculture, reports that in their human experiments in the calorimeter (a nine-by-ten-foot chamber that measures oxygen input and carbon dioxide output with 80,000 sensors to determine total energy expenditure), they found no differences in the efficiency with which different people metabolize food. Their conclusion was that differences in weight can’t be blamed on differences in metabolism; they result from excess eating or deficient exercise, or both.
William Bennett (1991) argues, however, that each body has its own “set point,” or genetically programmed level of body fat. It would be a lifelong battle to try to maintain a lower set point. For example, if a woman’s set point is 150 pounds and she decides to drop 10 pounds, her body will forever be trying to recover the lost fat. Bennett argues that to minimize fat, we should avoid the two things that tend to raise our set point: inadequate exercise and excessive consumption. He’s convinced that simple overeating in and of itself is not the culprit. In a study where subjects were overfed 900 calories a day for 14 weeks, identical twins gained weight at about the same rate; gains of 29–92 pounds were reported for unrelated people. Bennett maintains that the metabolisms of any two people at their set point would appear normal. Hence, his findings seem compatible with Moe’s.
More recently, a team of scientists from New York’s Rockefeller University determined that metabolism maintains a tenacious hold on weight. After losing 10 percent of their body weight, patients expended 15 percent less energy than expected for someone of their newly acquired reduced size. Reporting in the New England Journal of Medicine, Kassirer and Angell (1998) explained that the body resists weight change, struggling to return to its former weight. This has been explained as an evolutionary boon to more primitive peoples, subject to famine and spartan winters, but a bane to modern folk plagued with daily abundance. This regulatory system appears to keep everyone at his or her normal weight, whether slim or heavy. In a 1997 Harris poll of overweight adults who dieted, two out of three reached their target, whereas only one in nine kept the weight off (the average loss was 34 pounds, the average rebound gain 31). There is evidence that this set point can be adjusted over a substantial length of time: sustained high-fat diets can raise it and sustained exercise programs can lower it.
Recent research suggests that sleep affects metabolism. Columbia University researchers led by Steven Heymsfield (Prevention, May 2005) found from studying the sleep habits of over 18,000 subjects that, in comparison with those getting 7–9 hours of sleep each night:
• Those sleeping for less than 4 hours nightly are 73 percent more likely to be obese.
• Those sleeping around 6 hours nightly are 23 percent more likely to be obese.
• Those sleeping an average of 10 hours nightly are 11 percent less likely to be obese.
Heymsfield explains that sleep deprivation lowers leptin levels and raises ghrelin (a hormone that stimulates appetite) levels with the effect of maintaining fat storage and increasing appetite.
Applications
When there’s a choice, walk, don’t ride.
When there’s a choice, stand, don’t sit.
When there’s a choice, exercise or escape, don’t snack.
Serve smaller portions. A couple in our neighborhood maintain trim profiles without exercising, yet without giving up any favorite foods. We’ve sworn they had to have a God-given metabolism that allowed this indulgence. A while ago, we had them over for dinner. Because the serving dish was in front of the woman, she served the stew in bowls to the rest of us. To my consternation, I noticed that my portion barely covered the bottom inch of a bowl with a three-inch wall! I looked at my wife, who knowingly smiled back at me. Later that night, we agreed: it isn’t just metabolism; it’s portion size. We both grew up in homes where large portions were served. If we didn’t eat large portions and ask for seconds, our mothers took it as rejection. We have to rescript ourselves to feel all right about eating smaller portions. The task is clear—and uphill!
If you are confident that your exercise and diet levels are appropriate for you, learn to accept your set point and not feel guilty.
Get a good night’s sleep.
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TOPIC 14.3 |
Statistics on eating disorders are difficult to assess, with some estimating that upward of one-third of all people in the U.S. suffer from one of the eating disorders to some degree. Anorexia nervosa (starving oneself), bulimia nervosa (dieting, binging, and purging), binge eating disorder (compulsive eating), anorexia athletica (compulsive exercising), night-eating syndrome (consuming over one-half of one’s daily food after 7:00 P.M.), and nocturnal sleep-related eating disorder each have a complex set of causes, including biological, social, family, and psychological sources. Although anorexia and bulimia primarily afflict females between 10 and 35 years old (somewhere between 5 and 10 percent of anorexia and bulimia patients are males), cases have been reported from as young as 6 years of age to as old as 76. The lower incidence among males is attributed to societal approval of the strong, muscular, more bulky image for males. In fact, many believe that the primary cause of eating disorders is the ideal image that daily forces itself upon readers, listeners, and viewers of the popular media. In South Korea, as recently as the 1970s, the ideal image for a female was full-figured. These women were thought to be more sexy, more beautiful, and more able to bear healthy children. But decontrol of broadcasting has unleashed a flood of Western body image material throughout the culture, so that today the diet industry in Korea is flourishing, with entrepreneurs hawking everything from diet pills to liposuction. The statistics for South Korea now roughly parallel those of the United States (Los Angeles Times article, October 26, 1997).
Symptoms for each of the disorders are complex and are best not summarized. They include such diverse behaviors as skipping meals, experiencing relationship problems, and talking excessively about food. Excellent profiles of the symptoms for each disorder are available at the website for Anorexia Nervosa and Related Eating Disorders Inc.: www.anred.com.
Treatments
Without treatment, one out of five people with eating disorders will die prematurely. Treatment reduces that rate to one out of 30 to 50. About 60 percent of those who are treated recover, but not all make a full recovery. Current treatment could include one or more of the following: hospitalization, medication, dental work, individual counseling, group counseling, family counseling, nutritional counseling, and support groups. Consult a physician or mental health professional for specific recommendations.
In earlier editions of this book, I recommended the Montreux Counseling Center in Victoria, British Columbia, in spite of inadequate research in its support. In light of British Columbia authorities’ revocation of MCC’s license and having directed it to cease operations, I no longer recommend it.
Stanford University’s James Lock proposes a new treatment for anorexia nervosa developed by British therapists Christopher Dare and Ivan Eisler of Maudsley Hospital, London. The treatment sees family not as cause, but rather as ally, in getting the patient to eat more, return to a more normal weight, and establish control of her eating patterns. The treatment proceeds by observing family interactions and coming up with ways for the parents to help the child eat more. In essence, the therapists train the parents to become nurses for their child. Daniel LeGrange, director of the Eating Disorders Program at the University of Chicago, also is using and studying the treatment.
For the current status of any clinical trial mentioned in this book, check this website: www.clinicaltrials.gov.
Expect major discoveries in the next 10 years in this new field. Follow new developments with these websites: www.eating-disorder.com and www.anred.com.
Watch specifically for research on the enzyme cholecystokinin, which is lower in bulimic patients. The level of this enzyme typically increases when eating, with the result of stimulating the production of digestive enzymes that send us the message that we’re no longer hungry. Apparently bulimics fail to get this chemical message, and keep on eating.
Miscellaneous Topics, in Alphabetical Order
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TOPIC 14.4 |
Ben Feingold of the Feingold Association has found that people, especially children, react to food additives that interact with the natural salicylates in good food (A. Winter and R. Winter, 1988). Food additives include artificial sweeteners such as aspartame, artificial colors, artificial flavors, flavor enhancers such as monosodium glutamate, and preservatives such as nitrites. Aluminum-based additives (found in antacids and double-acting baking powder) appear to have especially adverse effects on the nervous system. Reactions include poor concentration, short attention span, fidgeting, aggressiveness, excitability, impulsivity, a low frustration threshold, clumsiness, and insomnia.
High-fructose corn syrup (HFCS) and common table sugar are chemically similar. Both are common additives. Both in excess will make you fat. HFCS is a liquid that food manufacturers slip into everything from baby food to bread for enhancing flavor. For some reason, HFCS not only can make you fat—it can also affect your brain function. Researchers are unsure why. Mercury has been found in some samples of HFCS. Experiments indicate decreased learning ability and decreased retention when individuals have diets high in HFCS, especially if they do not consume substantial levels of omega-3 fatty acids. Because HFCS is in so many manufactured foods, and because it is so tedious to read the small print on labels, the only sure way to avoid it is to obtain only foods with the organic seal. Note: Fructose that occurs naturally in fruits is okay. Here we are referring to the industrial strength additive.
Applications
Avoid foods with additives for yourself, your loved ones, friends, and co-workers. Just don’t make them available. While this subject is still being hotly debated, it would seem wise to minimize or eliminate additives in the diet, especially for expectant mothers and children exhibiting the symptoms described above.
Read food labels to check for additives, especially aluminum.
Candace Pert (1997) cautions us not to eat any food that is not 4,000 years old! In other words, let the test of time guide food selection.
Prefer the organic label at the grocer’s. Then rest assured you’re not getting HFCS added to your products. Request that your grocer clearly label products that contain HFCS.
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TOPIC 14.5 |
Ernesto Pollitt of the University of Texas Health Science Center at Houston (now at the University of California, Davis) compared the school performance of children who skipped breakfast to the performance of those who ate a good breakfast (Pollitt, Leibel, and Greenfield, 1981). Those who ate breakfast made measurably fewer errors as the morning wore on. Other studies of both children and adults have confirmed this finding.
Application
Don’t skip breakfast. If you must eat on the fly, grab a banana, a glass of milk, or at least a piece of bread that’s not dredged in fat and sugar.
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TOPIC 14.6 |
Much to the delight of the world’s chocolate lovers, research (see Science News, March 18, 2000) has found that chocolate consumption is healthy. The cocoa bean contains flavonoids, a natural antioxidant. One 40-gram serving (about the size of one typical chocolate candy bar) of pure milk chocolate contains about 400 mg of antioxidants, the rough equivalent of that contained in a glass of red wine. One serving of dark chocolate contains more than double the quantity of antioxidants found in one cup of black tea. Furthermore, when matching chocolate molecule for molecule with ascorbic acid (vitamin C), chocolate’s flavonoids are more powerful at limiting plaque development by preventing the oxidation of cholesterol. Also, chocolate’s power pack increases levels of nitric oxide, which work to relax the inner wall of blood vessels, thereby improving circulation and reducing risk of both stroke and heart disease. In fact, say researchers, chocolate’s flavonoids appear to have the same anticoagulant effect as that of a mild aspirin. So, as long as we can minimize the butter fats and sugars associated with chocolate, we shouldn’t feel guilty about consuming, on average, 12 pounds of chocolate per year in the U.S.!
Application
Prefer dark chocolates with minimal sugar and fat added. For example, try 100 percent cocoa powder with fat-free milk for a cold or hot treat.
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TOPIC 14.7 |
Fats, or more properly, fatty acids, are chains of carbon. Some, having a complete set of hydrogen atoms, are said to be “saturated” with hydrogen; hence, they are known as saturated fatty acids. Saturated fats are solid under normal conditions; unsaturated fats, which lack one or more hydrogen atoms, are liquids. Those missing only one hydrogen are called monounsaturated; those missing more than one, polyunsaturated. Saturated fats include animal fat, such as the solid fat surrounding a beef steak. Unsaturated fats include vegetable oils such as olive oil. For the convenience of modern homemakers, a process was invented in the U.S. in 1910 that turned liquid vegetable oils into solids. This process, called hydrogenation, had the effect of “saturating” vegetable oils with hydrogen atoms and turning liquids into solids. The resulting product is called a transformed, or “trans,” fat. Crisco and margarine are prime examples.
Stay away from trans fats—don’t put them in your body. Though trans fats are not harmful in small amounts—e.g., the occasional cookie—a steady diet of them has been associated with heart disease, diabetes, cancer, low birth weight, obesity, and immune disfunction. Trans fats also interfere with the proper conversion of the essential fatty acids omega-3 and omega-6 (see topic 14.9), leading to a deficiency of these vital nutrients. The problem is that trans fats are everywhere: baked goods (doughnuts, cookies, pastry), deep-fried foods, imitation cheeses, chips, crackers, and so forth. The word to the wise: consume vegetable oils in their natural, liquid form. Say no to hydrogenated, even so-called “partially” hydrogenated oils. Among the natural fats, prefer unsaturated ones to saturated ones.
Fat is the dietary source of acetylcholine, a neurotransmitter that is crucial to maintaining the condition of neural cell membranes. Too much fat is unhealthy, but too little fat is also unhealthy: with too little acetylcholine, the neural cell membranes will become brittle and deteriorate over time. The result of this deterioration is memory loss and a general decrease in brain function. Dietary fat metabolizes into lecithin, which further metabolizes into choline, which then, with the help of the catalyst cholinacetyltransferase, metabolizes into acetylcholine. Some research indicates that doses of choline can improve the problem of severe memory loss.
A series of meta-analyses (DeAngelis, 1992) suggests that low-fat diets, though improving death rates from heart disease, increase death rates that result from suicides, homicides, and accidents. This apparent relationship between low-fat diets and negative affect adds emphasis to the potential dangers to the human system of too little fat.
Dr. Michael Zemel of the University of Tennessee’s Nutrition Institute published a study in Journal of Obesity Research (April 2004) that found diets with three daily servings of dairy (serving = one cup of milk or yogurt, or 1½ ounces of cheese) resulted in more weight loss than diets either with low dairy or with calcium supplements. Apparently there is a hormone in dairy products that influences the size and quantity of fat cells, resulting in more and larger fat cells in its absence.
Applications
Do not eliminate fat from your diet!
Prefer unsaturated fats, especially olive oil and canola oil.
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TOPIC 14.8 |
The four food groups act on mood and the brain in the following ways:
Protein (in flesh, legumes, tofu): Contains an abundance of the amino acid L-tyrosine, which produces norepinephrine and dopamine (leading to elevated alertness and stable memory).
Complex carbohydrates (in vegetables, grains, fruits): Contain an abundance of the amino acid L-tryptophan, which is necessary to produce serotonin (leading to a sense of satiety and relaxation).
Fats (in dairy, meat, oils): Important for the production of acetylcholine, which is crucial for memory formation and general neural integrity (an absence of acetylcholine leads to the breakdown of neural membranes and advanced aging).
Simple carbohydrates (sugars): A quick energy booster, but without the “time-release” quality of complex carbohydrates, which provide glucose for longer periods (sugars alone lead to sluggishness).
Complex carbohydrates—those with a low glycemic index (grains, seeds, beans, fruits, and vegetables)—metabolize more gradually and provide a steadier release of glucose for use by the body. Simple carbohydrates such as sugar, on the other hand, provide a quick rise in blood sugar followed by a letdown.
Haas (1994) points out that the sequencing of proteins and carbohydrates is important. If you’re having a “California-style” salad for lunch and want to be alert after lunch, eat the chicken (protein) first, so that the L-tyrosine gets to your brain first. Then eat the rest of the salad, with L-tryptophan lagging. This ensures that you get the energy from the carbohydrates without the sleepiness. If you eat the carbohydrates first or simultaneously with the protein, the tryptophan will dominate and reach the brain first, thus establishing lower arousal and higher relaxation.
A Hebrew University research team led by Nachum Vaisman learned that children 11–13 years old showed improved performance on cognitive tests when they consumed milk and cereal within 30 minutes of the test. Children who had eaten breakfast at home two hours before the test showed no improvement in cognitive performance over children who hadn’t eaten breakfast at all. Apparently the boost in brain sugar levels just preceding the test also boosted performance.
Applications
Serve primarily carbohydrates and fats before events for which you want people relaxed and easy to please, such as a sales presentation.
Serve primarily proteins before events for which you want people alert and analytical, such as a staff meeting. Or put protein out first, carbohydrates later.
Save fats for the evening, when you crave them most and when you have the least need for alertness.
Time snacks to just precede a time of day when you need a boost in mental performance (a test, a presentation, a meeting, a new learning challenge, an important new sales call).
Follow this recommended daily meal and snack content:
Breakfast: complex carbohydrates + protein (skim milk + cereal)
Mid- to late-morning snack: complex carbohydrates (fruits or grains)
Lunch: protein first (chicken or shrimp cocktail), then complex carbohydrates
Afternoon snack: complex carbohydrates (fruits, vegetable juice, or grains)
Dinner: complex carbohydrates, fats, minimal protein
Bedtime snack: complex carbohydrates, sugar, fats (at last, banana ice cream!)
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TOPIC 14.9 |
Omega-3 fatty acids have a well-earned reputation for benefits to the circulatory system and the joints (helps with arthritis), and for treating diabetes, but only recently have they acquired a reputation for addressing issues of the nervous system. Found naturally in fish, flaxseed, canola oil, nuts, and avocados, these essential fatty acids (fats the body can’t make, but which are required for optimum health) have shown promise in the prevention and treatment of many nervous system disorders, including depression, bipolar disorder, ADHD, alcoholism, Alzheimer’s disease, and postpartum depression. Although the trials are incomplete, the consumption of the foods containing omega-3s is certainly benign, so let’s review how they work in the spirit of knowing why we might increase consumption of omega-3-containing foods as a kind of self-treatment.
Omega-3s must stay in balance with omega-6 fatty acids. Omega-3s come in fish, canola oil, and flaxseed. Omega-6s come in oils from soybean, safflower, and corn, as well as meat, poultry, and fish. Over the last 100 years, Americans have undergone a thousandfold increase in the amount of soybean in their diet, with an accompanying overbalance favoring omega-6 that results in higher incidences of depression and heart disease. The solution is to bring omega-3 back into balance by including more omega-3-containing foods in the diet. In support of this notion, countries with the highest fish consumption also have the lowest rates of depression and suicide: Korea, Taiwan, Norway, Portugal, Hong Kong, and Japan; countries with the lowest fish consumption have the highest rates of depression and suicide: the United States, France, West Germany, Canada, New Zealand, Hungary, Bulgaria, and Austria.
Pregnancy entails a double whammy: the embryo’s mother is the only source of a particular omega-3 fatty acid, and the child drains the mother of her normal supplies. Postpartum depression can be the result; in countries with lowest fish consumption, postpartum depression is 50 times higher than in countries with higher fish consumption.
Alcoholism depletes supplies of omega-3s, but research to date has not established whether increasing consumption of omega-3 foods can prevent or offset the physical effects of alcoholic excesses.
(Source: Sally Squires, “The Omega Principle,” Washington Post, August 18, 2003. Available online at www.washingtonpost.com/wp-dyn/articles/A11623-2003Aug18.html)
Application
Set a goal of averaging one serving of fish daily. Go for variety: canned salmon spreads, canned clam spreads, smoked fish, scrambled with eggs, in tomato sauces, and so forth.
Mix 1 tsp of flax seeds with your breakfast, wrap, sandwich, soup, and so forth.
Prefer unsalted nuts for snacks and meals.
Although olive oil should be your number one source of fat, canola should be number two.
At least once a week, slice an avocado onto your salad, sandwich, wrap, as a side, or into your favorite guacamole recipe.
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TOPIC 14.10 |
At the request of the U.S. Army Research Laboratory’s Military Nutrition Division, the National Academy of Sciences’ Committee on Military Nutrition Research looked at the contribution of six food groups to various aspects of military performance. The goal: to improve soldiers’ physical and mental performance through nutrition by 10–15 percent by fiscal 1998. Their recommendations are listed here as applications.
Applications
Use carbohydrates (found in cereals, grains, vegetables, and fruits) to increase your capacity for physical work and reduce anxiety. A special Kool-Aid type of brew boosted with powdered carbohydrates has been found to enhance performance.
Use caffeine to increase mental alertness and physical endurance. (For proper dosage, see topic 12.3.)
Use tyrosine (this amino acid is found in proteins, especially nuts, and is particularly high in cashews and sesame seeds) to better withstand extreme cold and to better adjust to high altitudes. The Army uses a powdered supplement in a food such as applesauce.
Use choline (found in egg yolks, liver, and soybeans) to increase mental clarity. Choline also has been shown to take five minutes off a marathoner’s time.
Use carnitine (found in red meat, liver, and heart) to increase physical performance over a long period.
Use structured lipids (a manufactured product used in hospitals to boost the caloric intake of some patients) to strengthen immune responses and to decrease susceptibility to disease and infection.
For more detailed information, as well as a listing of reports published by the NAS committee, visit www.iom.edu/CMS/3788/4615.aspx.
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TOPIC 14.11 |
Sodium is not just bad for hypertension and the heart—overconsuming sodium can also lead to electrolyte imbalances and accompanying mental dysfunction. The typical body requires about 1,000 mg of sodium daily and about five times that much potassium. (The balance between sodium and potassium is important for effective neural transmission.) To give you a rough idea of how easy it is to overconsume sodium, one tablespoon of soy sauce contains about 1,000 mg, the recommended daily allowance.
Applications
Don’t salt your food, or at least limit yourself to one shake or pinch.
Use a variety of spices and peppers to compensate tastewise for lessened salt intake.
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TOPIC 14.12 |
The tongue recognizes different tastes differently. Sweet is identified on the tip of the tongue, sour on the sides, bitter on the back of the tongue (hence the gagging that often accompanies bitter tastes), and salt all over, but especially in the front (Ackerman, 1990).
Applications
If you are tasting an unpleasantly sour substance, try to avoid having the substance touch the sides of your tongue.
If you are tasting something to determine if it is bitter, understand that you are not getting an accurate reading until the substance hits the back of your tongue. It is then natural to gag it up and out, as that is the only way to bypass the back of your tongue if you don’t want further experience with the substance.
If you are eating something too sweet or salty and you must continue, avoid placing the substance on the front of your tongue.
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TOPIC 14.13 |
Researchers have identified three levels of taste bud chemistry: nontasters, tasters, and supertasters. One’s level is determined by two genes: the gene for tasting PROP (6-n-propylthiouracil) and the gene for determining the density, or number per unit area, of fungiform papillae on the tongue (the housings for taste buds). Nontasters cannot taste PROP (it tastes just like water or paper) and have fewer papillae. Tasters can taste PROP; it tastes bitter to them. Supertasters have denser concentrations of papillae, and PROP tastes extremely bitter to them. Not only does the intensity of taste increase as the number of papillae rises, the number of pain receptors also increases. Roughly 25 percent of people in the United States are nontasters and 25 percent are supertasters, with tasters holding the middle at 50 percent of the population.
Nontasters eat a wider variety of foods than the other two groups. A higher proportion of females, Asians, and blacks are supertasters. Supertasters tend to have lower cholesterol and to be less obese. To the supertaster, bitter tastes more bitter, sweet tastes more sweet, fat tastes more creamy, and salty tastes more salty. Ginger, alcohol, carbonated beverages, and the capsaicin in chili peppers all create a greater sensation of burning on the supertaster’s tongue. Supertasters are more likely to reject bitter foods such as green tea, soy products, grapefruit, coffee, cabbage, broccoli, mustard greens, saccharine, brussels sprouts, and spinach. The University of Washington at Seattle’s Adam Drewnowski, a professor of environmental and industrial health, is using a National Cancer Institute grant to determine if such taste preferences are causing women with breast cancer to reject foods high in antioxidants. Supertasters appear to experience an advantage in the battle of the bulge. Some research suggests that they find fatty and sugary foods too intense and avoid them (reported in the APA Monitor, January 1998, p. 13). Because the aversion to bitter foods in supertasting women increases significantly during the first trimester of pregnancy (when toxins can do the most damage to a fetus), researchers suspect that the supertaster status prevalent among women is an evolutionary advantage.
Understand that preferences and aversions in regard to certain foods are not imaginary; they are genetic. To find out how you stack up, do two things. First, get some phenylthiocarbamide (PTC) paper from your local chemical supply store. Tasting these paper strips will let you know if you can taste PROP. If they just taste like paper, you are 50 percent on your way to being a nontaster. Second, swab your tongue with some blue food coloring. Then find one of the small, circular, lifesaver-like stickers used for reinforcing the holes in notebook paper. Place it in the center of your tongue, toward the tip. Near a mirror, shine a flashlight on the circumscribed area and count the number of papillary bumps (the blue sticks to everything but the bumps). The more bumps, the more of a taster you are. Nontasters tend to have around five bumps, while supertasters can have thirty or more.
Applications
If you’re a nontaster, you have a natural tendency to shovel it in, hoping that by assaulting your tongue with quantity you will experience pleasant tastes. However, quantity doesn’t lead to quality here. Alter your eating habits by highly seasoning your food—if you assault your tongue with spices and peppers and other assorted strong flavors, you are more likely to resist the push for quantity.
If you’re a supertaster, then you are less likely to have a tendency to shovel it in, because your taste buds are more sensitive, easier to please. However, should you have a problem with overeating, you might try seasoning your foods stronger than your comfort level as a way of toning down your cravings.
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TOPIC 14.14 |
In the February 1996 issue of Scientific American, Larry Brown, of the Tufts University Center on Hunger, Poverty and Nutrition Policy, and Ernesto Pollitt, of the University of California, Davis, School of Medicine, reported on a major study involving over 2,000 children in Central America. After providing calories, protein, vitamins, and minerals, researchers observed reverses in poor academic performance that had been attributed to poverty. Other research has demonstrated that a major effect of undernourishment is significantly lessened social interaction, adding lack of exposure to lack of mental energy.
Application
For children in poverty, academic intervention alone is not enough to improve performance. They need protein and calories as well as instruction and caring. Support programs in your region and elsewhere that provide nutritional supplements for children in poverty.
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TOPIC 14.15 |
Many studies report drops in violent acts when, for example, residents of detention centers are fed low- or no-sugar diets. Stephen Schoenthaler (1983), of the Social Justice Program at California State College, Stanislaus, reports from a 1980 study at the Tidewater Detention Center in Chesapeake, Virginia, that high-sugar diets promote violence in this way: Whenever the limbic system and the cerebral cortex have to vie for scant supplies of glucose, the limbic system always wins. With a high-sugar diet, the body is left depleted of blood sugar when a hit of dietary sugar wears off, because insulin is released to shut down the body’s production of glucose; the limbic part of the brain then gobbles up the available glucose, starving the cerebral cortex and thereby making emotional behavior dominant (the limbic system is in control) and pushing rational behavior into the background.
When I taught high school, I once had a violent student in my 11th-grade homeroom. I called his parents in for a conference. The mother (the father was on the road) described a typical day. I noticed that the boy was rising at 5:30 A.M. in order to catch a 6:15 A.M. bus to school. Meanwhile, the mother stayed in bed. The son left the house without human contact or food intake, stopped by a convenience store on the way to the bus stop, grabbed a grape soda and a pack of doughnuts or cookies, and caught the bus. When he arrived at school, therefore, he was on a sugar high and was affable and demonstrative for about one hour; then, after the sugar wore off, he started hitting people. Why didn’t his mother fix breakfast? Because he didn’t like her breakfasts. I asked what he’d eat if she fixed it. We agreed on a hamburger and a glass of milk, of all things. Within two weeks, his pattern had changed, reverting to that of a reasonably likable 17-year-old. I’m sure that he benefited not only from the substantial breakfast, but from having some contact with his mother before leaving home.
Applications
Ensure that sugary foods do not replace healthy foods; at most they should only supplement them.
Look for other causes of behavioral problems than sugar and sweeteners.
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TOPIC 14.16 |
Vitamin and mineral deficiencies result from either insufficient intake or inadequate absorption. The first can be fixed by a varied and balanced diet composed primarily of fresh or frozen foods. The second can be fixed by appropriate injections administered by a physician. The consequences of a sustained deficiency are fatigue, loss of appetite, poor concentration, failing memory, depression, and insomnia. You can confirm and specify a suspected deficiency through a blood test at a laboratory qualified to test for vitamin and mineral content.
Now that I have said that, consider what Jane E. Brody describes as “Vitamania” (New York Times, October 26, 1997). From 1990 to 1997, spending on vitamin and mineral products more than doubled, from roughly $3 billion to $6.5 billion, according to the Council for Responsible Nutrition in Washington, D.C. Yet this buying pattern is not based on any clear results. The notion that vitamin and mineral supplements benefit healthy people who consume a balanced diet is supported by meager evidence. And even for those who need more vitamins and minerals—the elderly, smokers, the undernourished, the sick, pregnant women—the research findings are uncertain. Interestingly, most of the consumers of supplements are active nonsmokers who avoid heavy alcohol consumption, eat more fruits and vegetables, are better educated than the norm, and have comfortable incomes. One thing is clear: vitamin takers do not live longer or die less frequently from cancer, based on a 13-year study of over 10,000 Americans by Atlanta’s Centers for Disease Control and Prevention, and this 1993 report (available from their website at www.cdc.gov) also found no support for the notion that vitamin and mineral supplements can compensate for slack eating habits.
Brody concludes that consumers are, in essence, voluntary subjects in a national marketing-driven experiment. Enough good, long-term studies on the effects of vitamin and mineral supplements are simply not available, and the jury is still out on their relative helpfulness and harmfulness. A few bits of good news are available: supplements can remedy the deficiencies that cause such diseases as scurvy and rickets. But nothing conclusive is available for cancer, heart disease, osteoporosis, longevity, and overall well-being. In a 20-year study (The Lancet, October 2, 2004) of some 170,000 persons at risk for developing gastrointestinal cancers, antioxidant pills (for vitamins A, C, and E) were found to have no effect in reducing cancer risk, further supporting the notion that antioxidants should be taken through normal diet that includes fruits and vegetables. In addition, a considerable list of dangers is emerging, including the following:
• Vitamin E megadoses (a relative term, but suggesting more than the RDA) can interfere with vitamin K (which affects blood clotting).
• Calcium megadoses limit the absorption of iron and perhaps that of other trace elements.
• Although taking 500 mg of vitamin C daily does have an antioxidant effect, British doctors at the University of Leicester reported in Nature (April 1998) that it also has a pro-oxidant effect, attacking DNA. They join Victor Herbert of Mount Sinai School of Medicine in New York, who has been arguing for decades that extra vitamin C promotes free radicals (unlike the vitamin C in orange juice, which is an antioxidant).
• Zinc megadoses can reduce the body’s copper levels, interfere with immune responses, and decrease levels of high-density lipoproteins (the “good” cholesterol).
• Folic acid megadoses can mask vitamin B-12 deficiency and adversely affect anticonvulsant medications.
The one certainty that emerges is the benefit of eating a variety of foods, minimizing fat, and maximizing fruits, vegetables, and complex carbohydrates. And to hedge your bets, take a daily multivitamin. In fact, on April 7, 1998, reversing a trend of discouraging vitamin supplements, the National Academy of Sciences recommended for the first time that the following two groups take specific supplements:
1. Women of childbearing age need 400 micrograms of folic acid daily. That amount is guaranteed in most multivitamins and is difficult to get through a normal diet. Insufficient folic acid in these women increases the chance of birth defects in their offspring.
2. Adults over age 50 need 2.4 micrograms of vitamin B-12 daily in order to minimize the chance of developing anemia. Between 10 and 30 percent of people over the age of 50 lose the ability to absorb B-12 from food.
Applications
Vitamin supplements are best absorbed when taken with other foods. Caffeine, however, obstructs absorption, so take your multivitamins with a meal that does not include coffee, tea, or caffeinated sodas.
Mineral supplements are best absorbed between meals.
If you think that you have some of the symptoms of a deficiency, take a blood test to determine your vitamin and mineral content.
To get the most nutrition from your foods:
• Replace canned food with fresh or frozen food.
• If you use canned food, retain and use the juices in other dishes, unless you detest high sodium.
• Keep milk and bread in opaque containers.
• Don’t leave food in the freezer too long.
• Use fresh juice immediately, preferably the same day it is squeezed.
• Avoid soaking vegetables.
• Choose pressure cooking, steaming, or boiling to cook vegetables, using minimum water, leaving skins on, and cooking the vegetables the shortest amount of time possible.
Factors that obstruct absorption, destroy nutrients, or both include the following:
• Excessively low calorie count
• Alcohol
• Nicotine
• Tannin
• High fiber in the diet
• Aspirin
• Medications
• Overcooking
Hedge your bets and take a multivitamin! I do.
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Claude-Pierre, P. (1999). The Secret Language of Eating Disorders: The Revolutionary New Approach to Understanding and Curing Anorexia and Bulimia. New York: Vintage.
Gibbs, W. W. (1996, August). “Gaining on Fat.” Scientific American, 88–94.
Haas, R. (1994). Eat Smart, Think Smart. New York: HarperCollins.
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Thomas, P. R. (Ed.). (1995). Weighing the Options: Criteria for Evaluating Weight-Management Programs. Washington, D.C.: National Academy of Sciences Press.
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