Iconoclast: A Neuroscientist Reveals How to Think Differently (31 page)

Cortisol also has direct effects on the brain. Synthetic versions of steroids, such as prednisone, are an order of magnitude more potent than cortisol and sometimes result in bizarre changes in mood and thought. For many years, both synthetic and natural steroids were thought to alter moods in a negative way, but in the 1990s two different classes of steroid receptor were discovered in the brain, each with a different effect on mood. The mineralocorticoid receptor (MR) is a steroid receptor concentrated in the hippocampus, while the glucocorticoid receptor (GR) is found throughout the brain but especially in the striatum. The overall effect of steroids on mood appears linked to the ratio of activated MRs and GRs.
²⁴
Under the right conditions, cortisol increases arousal, concentration, and mood.
²⁵
Cortisol also acts synergistically with dopamine. As a result, many of cortisol’s acute effects resemble amphetamine’s. At high doses, however, steroids hit the receptors in the hippocampus and interfere with memory. Because of cortisol’s wide-ranging effects on the body, chronic use of cortisol, or any steroid, will cause detrimental effects to many organ systems. Side effects of regular steroid use include hypertension, GI bleeding, diabetes, obesity, osteoporosis, and because of the redistribution of fat, “moon face” and “buffalo hump.”

Another type of steroid hormone that has received a great deal of recent attention as a potential cognitive enhancer is testosterone. Like cortisol, testosterone is derived from cholesterol. In men, it is synthesized primarily in the testes, but women have testosterone too, made in
the adrenal glands. Interestingly, the effect of testosterone depends on the age of the person. During puberty, testosterone causes the development of the external genitalia, grows body hair, and increases muscle mass. After about age twenty-five, however, testosterone levels decline steadily, so that it is cut in half by age eighty. As a consequence, the geriatric literature is burgeoning with anecdotal reports that testosterone, taken in late life, is some sort of fountain of youth, restoring failing memory and even staving off Alzheimer’s disease. A chemical precursor to testosterone, DHEA, has received a lot of hype. DHEA was easily available over the Internet or through health stores. The FDA wants to regulate it. But in a two-year double-blind, placebo-controlled study of DHEA and testosterone in elderly men and women, no significant effects were found on either physical or mental function.
²⁶
There weren’t even any improvements in quality of life. Although neither testosterone nor DHEA has been conclusively shown to aid memory, testosterone does affect the emotional system of the brain. Neuroscientists in the Netherlands have found that giving a single, sublingual dose of testosterone to healthy women did two things. First, when the women viewed movies of actors making facial expressions of different emotions, the women didn’t subconsiously mimic the actors’ expressions. Normally, when people view these movies, they subconsciously mimic the expressions, implying that testosterone somehow decreased normal empathic responses. Second, testosterone decreased their startle responses by about 20 percent.
²⁷
So, although testosterone might make you braver, or at least less prone to being startled, it might also make you a jerk. Plus, if you’re a woman, you’ll start growing chest hair.

Conclusion: testosterone and maybe DHEA do have effects on social and emotional processing (not necessarily in a good way), but their effects on memory are more hype than reality. These hormones don’t appear to have good potential for iconoclasm, and may raise the risk of prostate cancer.

One hormone that might actually live up to the hype is oxytocin. Also secreted by the pituitary gland, oxytocin is released in massive amounts during labor. In women, it strengthens uterine contractions. In animals, oxytocin acts in the amygdala to reduce fear and aggressive behavior. Mice that have been genetically engineered to lack oxytocin show a profound deficit in social recognition behaviors for other mice. In some animals, oxytocin promotes monogamous pair-bonding. In humans, oxytocin can be injected, as when it is used to induce labor, or it can be absorbed intranasally through a small puffer device (Syntocinon).

A handful of recent experiments have unequivocally demonstrated that intranasal oxytocin enhances several aspects of social function in humans. A test called the “Reading the Mind in the Eyes Test” asks the subject to infer a mental state from a picture of someone’s eyes. Most people do pretty well on this, although some pictures are a bit tricky. Interestingly, in a placebo-controlled study, healthy volunteers who received intranasal oxytocin did better on the difficult pictures.
²⁸
Another study used an experimental economic procedure called the “trust game.” In this game, two people take turns sending money back and forth. At each turn, the individual has the choice of keeping some money or returning some to the other player. The amount returned triples in value. Thus, there is a financial incentive to return all the money because it will triple, but each player must trust that the other person will do the same. Amazingly, oxytocin increased participants’ willingness to trust other each other.
²⁹
Much of this effect seems to be mediated by the amygdala. An fMRI study found that the amygdala activation in response to fear-inducing pictures was decreased by oxytocin.
³⁰

Summary: of all the hormones studied, oxytocin appears to have real potential for decreasing fear, especially in social situations. It may augment an individual’s ability to read another person’s intentions,
increase empathy, and promote trusting behavior. The side effects appear to be minimal. Because of its labor-inducing properties,
oxytocin should definitely not be used by pregnant women
.

Summary

So there you have it. The quick road to iconoclasm (well, not really).

Some of the drugs described here may have a limited role in augmenting certain iconoclastic brain functions while diminishing other mental processes that seem to get in the way. The SSRIs and beta-blockers have real potential to decrease performance-related anxiety and social phobia. They are also fairly safe to use and carry only mild side effects. Benzodiazepines may do the same, but you can get addicted to them. Stay away from the stimulants—too much addiction potential, and they just make you impatient and impulsive. The hallucinogens might have potential for creating new insights and perceptions, but they are, of course, illegal. And finally, the hormone oxytocin seems to function broadly to promote social bonding, which may be a boon for social intelligence.

Introduction: Doing What Can’t Be Done

1.
Details surrounding Armstrong’s life and death are from Thomas Lewis,
Empire of the Air: The Men Who Made Radio
(New York: HarperCollins, 1991).

2.
Ibid., 254.

One: Through the Eye of An Iconoclast

1.
Dale Chihuly, interview with author, Seattle, WA, November 15, 2006.

2.
See Sammy Davis Jr., Jane Boyar, and Burt Boyar,
Yes I Can: The Story of Sammy Davis, Jr
. (New York: Farrar, Straus and Giroux, 1965).

3.
See Nancy Etcoff,
Survival of the Prettiest: The Science of Beauty
(New York: Anchor Books, 1999).

4.
See Brian A. Wandell,
Foundations of Vision
(Sunderland, MA: Sinauer Associates, 1995).

5.
See Kristin Koch et al., “How Much the Eye Tells the Brain,”
Current Biology
16 (2006): 1428–1434.

6.
See G. Kanizsa, “Margini quasi-percettivi in campi con stimolazione omogenea,”
Rivista di Psicologia
49, no. 1 (1955): 7–30.

7.
See Cindy Gill, “Magnetic Personality,”
Pitt Magazine
, Fall 2004.

8.
See Leila Reddy and Nancy Kanwisher, “Coding of Visual Objects in the Ventral Stream,”
Current Opinion in Neurobiology
16 (2006): 408–414.

Two: From Perception to Imagination

1.
See Gerald L. Edelman,
Neural Darwinism: The Theory of Neuronal Group Selection
(New York: Basic Books, 1987).

2.
See Neal Gabler,
Walt Disney: The Triumph of the American Imagination
(New York: Alfred A. Knopf, 2006).

3.
For an excellent discussion of the evolutionary theory of perception, as well as many beautiful illustrations of optical illusions, see Dale Purves and R. Beau Lotto,
Why We See What We Do: An Empirical Theory of Vision
(Sunderland, MA: Sinauer Associates, 2003).

4.
See Xiong Jiang et al., “Categorization Training Results in Shape- and Category-Selective Human Neural Plasticity,”
Neuron
53 (2007): 891–903.

5.
See W. Schultz et al., “Neuronal Activity in Monkey Ventral Striatum Related to the Expectation of Reward,”
Journal of Neuroscience
12 (1992): 4595–4610.

6.
See Kalanit Grill-Spector, Richard Henson, and Alex Martin, “Repetition and the Brain: Neural Models of Stimulus-Specific Effects,”
Trends in Cognitive Sciences
10 (2006): 14–23.

7.
See Martha Farah,
The Cognitive Neuroscience of Vision
(Malden, MA: Blackwell Publishing, 2000).

8.
See S. M. Kosslyn et al., “Topographical Representations of Mental Images in Primary Visual Cortex,”
Nature
6556 (1995): 496–498; and Xu Cui et al., “Vividness of Mental Imagery: Individual Variability Can Be Measured Objectively,”
Vision Research
47 (2007): 474–478.

9.
See William James,
The Principles of Psychology
, vol. 1 (New York: Dover Publications, 1950).

10.
See A. C. Nobre et al., “Functional Localization of the System for Visuospatial Attention Using Positron Emission Tomography,”
Brain
120 (1997): 515–533.

11.
See Farah,
The Cognitive Neuroscience of Vision
.

12.
Sporting News
, March 3, 1948, in Jules Tygiel,
Baseball’s Great Experiment: Jackie Robinson and His Legacy
(New York: Oxford University Press, 1983).

13.
Look
, March 19, 1946, cited in Tygiel,
Baseball’s Great Experiment
.

14.
Tygiel,
Baseball’s Great Experiment
, 52.

15.
See David J. Walsh, transcript of interview with Branch Rickey, 1955, ed. Manuscript Division and Branch Rickey Papers, Library of Congress.

16.
See Kary B. Mullis, “The Polymerase Chain Reaction,” Nobel Lecture, 1993.

Three: Fear—The Inhibitor of Action

1.
See Jackie Robinson and Alfred Duckett,
I Never Had It Made
(New York: G. P. Putnam’s Sons, 1972).

2.
Ibid.

3.
Ibid.

4.
Ibid.

5.
For an excellent explanation of the human stress system, see Robert M. Sapol-sky,
Why Zebras Don’t Get Ulcers
, 3rd ed. (New York: Owl Books, 2004).

6.
Emily Robison, interview on
60 Minutes
, May 14, 2006.

7.
See Adam Sweeting, “How the Chicks Survived Their Scrap with Bush,”
Telegraph
, June 15, 2006; and Christoph Dallach and Matthias Matussek, “Let Them Hate Us,”
Spiegel Online
, July 11, 2006.

8.
Natalie Maines, interview on
60 Minutes
, May 14, 2006.

9.
See Whitney Pastorek, “Heart of Dixie,”
EW.com
, January 2006.

10.
For an excellent review of the amygdala, see Elizabeth A. Phelps and Joseph E. LeDoux, “Contributions of the Amygdala to Emotion Processing: From Animal Models to Human Behavior,”
Neuron
48 (2005): 175–187.

11.
See Alex Berenson, “A Software Company Runs Out of Tricks; The Past May Haunt Computer Associates,”
New York Times
, April, 29, 2001; and William M. Bulkeley and Charles Forelle, “Directors’ Probe Ties CA Founder to Massive Fraud; Report Suggests Suing Wang for $500 Million; Evidence of Backdating,”
Wall Street Journal
, April 14, 2007.

12.
See William McCracken and Renato Zambonini,
CA, Inc. Special Litigation Committee Report
, Chancery Court, Delaware, 2007, 5.

13.
Quotes in this section from Jim Lavoie and Joe Marino, interview with author, Newport, RI, June 7, 2007.

14.
See Daniel Ellsberg, “Risk, Ambiguity, and the Savage Axioms,”
Quarterly Journal of Economics
75 (1961): 643–669.

15.
See Ronald C. Kessler, Murray B. Stein, and Patricia Berglund, “Social Phobia Subtypes in the National Comorbidity Study”
American Journal of Psychiatry
155, no. 5 (1998): 613–619.

16.
See K. N. Ochsner et al., “Rethinking Feelings: An fMRI Study of the Cognitive Regulation of Emotion,”
Journal of Cognitive Neuroscience
14 (2002): 1215–1229.

17.
See Phelps and LeDoux, “Contributions of the Amygdala,” 175–187.