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The Hacking of the American Mind

Page 28

by Robert H. Lustig


  Lastly, my most sincere thanks go to my family. I am indebted to my sister Carole Lustig-Berez for handling my mother’s affairs at a most difficult time, and for being our family’s primary support at a time when I couldn’t. Also thanks to my brother-in-law Mark Berez for funneling me media reports on nutrition and the business backlash. And I must reserve my most grateful appreciation to my wife, Julie, and my daughters Miriam and Meredith, whom I love more than anything. Writing this book put a strain on all of us for almost two years. Between work, travel, and book writing, I sometimes wasn’t there for family events that I should have been there for. And I heard about it. The good news is we bent but didn’t break. And now that this book is “in the can,” I can go back to being a husband and father, the two things that make me happy.

  GLOSSARY

  Addiction: a strong and harmful need to regularly have something (such as a drug) or engage in a specific behavior (such as gambling) due to an overwhelming biochemical drive, and which cannot be controlled by behavioral restraint.

  ALT: alanine aminotransferase, a blood test that tells about liver function and is very sensitive for the amount of fat in the liver.

  Amygdala: part of the stress-fear-memory pathway. This walnut-sized area of the brain generates the feelings of fear and stress, which tells the hypothalamus to tell the adrenal glands to make extra cortisol.

  Anandamide: a naturally occurring neurotransmitter that binds to the CB1 endocannabinoid receptor and that reduces levels of anxiety.

  Apoptosis: programmed cell death, in which proteins in the cell are activated to cause self-destruction.

  Autonomic nervous system: that part of the nervous system that controls unconscious functions of the body. It consists of two parts: the sympathetic system controls heart rate, blood pressure, and temperature; while the parasympathetic system (the vagus nerve) controls eating, digestion, and absorption, slows the heart rate, and lowers blood pressure. The two together control energy balance.

  Cortisol: the stress hormone released from the adrenal glands, which acutely mobilizes sugar for use but which chronically lays down visceral fat and also reduces serotonin-1a receptor number.

  Depression: a mental condition characterized by feelings of severe despondency and dejection, inadequacy, and guilt, often accompanied by lack of energy and disturbance of appetite and sleep.

  Developmental programming: alterations in brain or body functioning due to alterations in the environment that occur in the fetus prior to birth.

  Dopamine: part of the reward pathway. A neurotransmitter that, when released, can acutely cause feelings of reward but, when released, chronically reduces the number of its receptors, leading to tolerance.

  Dopamine receptor: the protein that binds dopamine to generate the reward signal and, when reduced in number, leads to tolerance.

  Endocannabinoid: a neurotransmitter, such as anandamide, that binds to brain receptors and acts like marijuana, driving reward and reducing anxiety.

  Endogenous opioid peptide (EOP): part of the reward pathway. A neurotransmitter made in the brain that binds to its receptor to signal the consummation of reward or euphoria.

  Endogenous opioid peptide (EOP) receptor: part of the reward pathway. A protein that binds either opiates (e.g., heroin) or endogenous opioid peptides (e.g., beta-endorphin) to signal the consummation of reward or euphoria.

  Epigenetics: modifications in DNA without changes in the DNA genetic sequence, usually occurring prior to birth.

  Estrogen: female sex hormone, made either in the ovary or in fat tissue.

  Excitotoxicity: the process of overstimulating a cell, leading to cell dysfunction or death.

  Fructose: half of dietary sugar or high-fructose corn syrup. The molecule that makes sugar taste sweet causes the reward system to activate, and is the addictive component.

  Glucose: half of dietary sugar or high-fructose corn syrup. Also the molecule found in starch, the molecule that every cell on the planet burns to liberate energy.

  Hippocampus: part of the stress-fear-memory pathway. The part of the brain where memories are housed and that exerts influences on the amygdala and prefrontal cortex.

  Hypothalamus: part of the stress-fear-memory pathway. The area at the base of the brain that controls various hormone systems of the body, particularly cortisol.

  Insulin resistance: the state where insulin signaling is reduced, requiring the beta-cells of the pancreas to make more insulin, which drives both obesity and chronic disease.

  Insulin secretion: the process of insulin release in response to both rising blood glucose and the firing of the vagus nerve.

  Insulin: a hormone made in the pancreas that tells fat cells to store energy and interferes with the leptin signal to increase food intake.

  Leptin resistance: the state where the leptin signal is dampened, leading to the hypothalamus interpreting starvation.

  Leptin: a hormone released from fat cells that travels in the bloodstream to the hypothalamus to report on peripheral energy stores.

  Major depressive disorder (MDD): a mental disorder characterized by at least two weeks of low mood, self-esteem, loss of interest in normally enjoyable activities, low energy, and pain without a clear cause, often needing medical treatment.

  Metabolic syndrome: a cluster of chronic metabolic diseases characterized by energy overload of cells.

  Micronutrient: vitamins or minerals found in real food, usually isolated with the fiber fraction.

  Mitochondria: subcellular organelles specialized to burn either fat or carbohydrate for energy.

  Neurotransmitter: a chemical in the brain made in one nerve cell, which, when released, causes other nerve cells to fire.

  Necrosis: cell death due to exposure to a toxin or lack of blood or oxygen.

  Nucleus accumbens (NA): the area of the brain that receives the dopamine signal and interprets the feeling as reward.

  Obesity: excess body fat deposition.

  Omega-3 fatty acids: a fatty acid found in wild fish and flax that is an important component of neuronal membranes and that reduces inflammation.

  Phenylalanine: a dietary amino acid that can be converted into dopamine.

  Prefrontal cortex (PFC): part of the stress-fear-memory pathway. The part of the brain, located in the front (above the eyes), that inhibits impulsive and socially unacceptable and potentially dangerous behaviors and actions.

  Peptide YY(3-36): a hormone made by the small intestine in response to food that signals satiety to the hypothalamus.

  Satiety: the feeling of fullness that stops further eating.

  Serotonin: part of the contentment pathway. A neurotransmitter that, when it binds to its -1a receptor on neurons, transmits feelings of contentment; and, when it binds to its -2a receptor, evokes the “mystical experience.”

  Serotonin-1a receptor: part of the contentment pathway. A protein on the surface of neurons that, when it binds serotonin, reduces neurotransmission, which leads to feelings of contentment.

  Serotonin-2a receptor: a protein on the surface of neurons that, when it binds serotonin, evokes the “mystical experience.”

  Stress: an uncomfortable state of mental or emotional strain or tension resulting from adverse or demanding circumstances. Accompanied by neural output from the amygdala, which tells the hypothalamus to signal the adrenal glands to make the hormone cortisol.

  Subcutaneous fat: the fat outside of the abdomen, which is a storehouse of extra energy but which does not signify an increased risk for metabolic syndrome.

  Sympathetic nervous system: the part of the autonomic nervous system that raises heart rate, increases blood pressure, and burns energy.

  Tetrahydrocannabinol: the active substance in marijuana that binds to the CB1 endocannabinoid receptor to reduce levels of anxiety.

  Tolerance: the state where the signal for rewar
d is dampened and can only be generated by consuming more substrate (e.g., sugar) or engaging in more behaviors (e.g., gambling).

  Transcription factor: a protein in cells that turns on genes to make the cell change its function.

  Tryptophan: a dietary amino acid that is converted into serotonin.

  Type 2 diabetes: a disease of high blood sugar due to defective insulin action on tissues.

  Tyrosine: an amino acid (which can be consumed, or derived from phenylalanine) that can be converted into dopamine.

  Vagus nerve: part of the autonomic nervous system that promotes food digestion, absorption, and energy storage, and slows heart rate.

  Ventral tegmental area (VTA): part of the reward pathway. The area of the brain that sends the dopamine signal of signifying reward to the nucleus accumbens.

  Visceral fat: the fat around the organs in the abdomen, which is a risk factor for diabetes, heart disease, and stroke, and a marker for metabolic syndrome.

  NOTES

  CHAPTER 1. THE GARDEN OF EARTHLY DELIGHTS

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  2.Oishi S et al., “Concepts of Happiness Across Time and Cultures.” Personal. and Soc. Psychol. Bull. 39, 559–77 (2013).

  3.McMahon DM, Happiness: A History. Grove, New York (2006).

  4.Helliwell J et al., World Happiness Report (2015). http://worldhappiness.report/wp-content/uploads/sites/2/2015/04/whr15.pdf

  5.Oxford Happiness Questionnaire. http://interactive.guim.co.uk/embed/labs/2014/dec/01/happiness/oxford-happiness-quiz-questionnaire/index.html

  6.Boehm JK et al. in Handbook of Positive Psychology, Lopez SJ, ed., Oxford University Press, Oxford (2015).

  7.Bartels M, “Genetics of Wellbeing and Its Components Satisfaction with Life, Happiness, and Quality of Life: A Review and Meta-Analysis of Heritability Studies.” Behav. Genetics 45, 137–56 (2015).

  8.Okbay A et al., “Genetic Variants Associated with Subjective Well-being, Depressive Symptoms, and Neuroticism Identified Through Genome-Wide Analyses.” Nat. Genet. 48, 624–33 (2016).

  9.Kharpal A, “A Scientist Has Discovered Why Happiness Might Very Well Be Genetic.” CNBC, Feb. 11, 2017. http://www.cnbc.com/2017/02/11/a-scientist-has-discovered-why-happiness-might-very-well-be-genetic.html

  10.Stanford Encyclopedia of Philosophy. http://plato.stanford.edu/entries/happiness

  11.Freudenberg N, Lethal but Legal. Oxford University Press, New York (2014).

  CHAPTER 2. LOOKING FOR LOVE IN ALL THE WRONG PLACES

  1.Freudenberg N, Lethal but Legal. Oxford University Press, New York (2014).

  2.Bradford AC et al., “Medical Marijuana Laws Reduce Prescription Medication Use in Medicare Part D.” Health Aff. 35, 1230–6 (2016).

  3.De Boer A et al., “Love Is More Than Just a Kiss: A Neurobiological Perspective on Love and Affection.” Neuroscience 201, 114–24 (2012).

  4.Coria-Avila GA et al., “Neurobiology of Social Attachments.” Neurosci. Behav. Rev. 43, 173–82 (2014).

  5.Pedersen CA et al., “Maternal Behavior Deficits in Nulliparous Oxytocin Knockout Mice.” Genes Brain Behav. 5, 274–81 (2008).

  6.Brewerton TD, “Hyperreligiosity in Psychotic Disorders.” J. Nerv. Ment. Dis. 182, 302–4 (1994).

  7.Takahashi K et al., “Imaging the Passionate Stage of Romantic Love by Dopamine Dynamics.” Front. Hum. Neurosci. 9, 191 (2015).

  8.De Boer A et al., “Love Is More Than Just a Kiss: A Neurobiological Perspective on Love and Affection.” Neuroscience 201, 114–24 (2012).

  9.Siegler IC et al., “Consistency and Timing of Marital Transitions and Survival During Midlife: The Role of Personality and Health Risk Behaviors.” Ann. Behav. Med. 45, 338–47 (2013).

  10.Palmer R, “Addicted to Love” (1985). https://www.youtube.com/watch?v=XcATvu5f9vE.

  11.Earp BD et al., “Addicted to Love: What Is Love Addiction and When Should It Be Treated?” Philos. Psychiatr. Psychol. (2015). http://www.academia.edu/3393872/addicted_to_love_what_is_love_addiction_and_when_should_it_be_treated

  12.Kelley AE et al., “The Neuroscience of Natural Rewards: Relevance to Addictive Drugs.” J. Neurosci. 22, 3306–11 (2002).

  13.Sussman S, “Love Addiction: Definition, Etiology, Treatment.” J. Treatment Prevention 17, 31–45 (2010).

  CHAPTER 3. DESIRE AND DOPAMINE, PLEASURE AND OPIOIDS

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  2.Hommel JD et al., “Leptin Receptor Signaling in Midbrain Dopamine Neurons Regulates Feeding.” Neuron 51, 801–10 (2006).

  3.Farooqi IS et al., “Leptin Regulates Striatal Regions and Human Eating Behavior.” Science 317, 1355 (2007).

  4.Jastreboff AM et al., “Leptin Is Associated with Exaggerated Brain Reward and Emotion Responses to Food Images in Adolescent Obesity.” Diab. Care 37, 3061–8 (2014).

  5.Jastreboff AM et al., “Neural Correlates of Stress- and Food Cue-Induced Food Craving in Obesity: Association with Insulin Levels.” Diab. Care 36, 394–402 (2013).

  6.Rapuano KM et al., “Genetic Risk for Obesity Predicts Nucleus Accumbens Size and Responsivity to Real-World Food Cues.” Proc. Natl. Acad. Sci. 114, 160–5 (2017).

  7.Jacobs E et al., “Estrogen Shapes Dopamine-Dependent Cognitive Processes: Implications for Women’s Health.” J. Neurosci. 31, 5286–93 (2011).

  8.Kenakin T, “The Mass Action Equation in Pharmacology.” Br. J. Clin. Pharmacol. 81, 41–51 (2015).

  9.Stice E et al., “Relation Between Obesity and Blunted Striatal Response to Food Is Moderated by Taq A1 Allele.” Science 322, 449–52 (2008).

  10.Girault EM et al., “Acute Peripheral but Not Central Administration of Olanzapine Induces Hyperglycemia Associated with Hepatic and Extra-Hepatic Insulin Resistance.” PLoS One 7, e43244 (2012).

  11.German CL et al., “Regulation of the Dopamine and Vesicular Monoamine Transporters: Pharmacological Targets and Implications for Disease.” Pharmacol. Rev. 67, 1005–24 (2015).

  12.Vaughan RA et al., “Mechanisms of Dopamine Transporter Regulation in Normal and Disease States.” Trends Pharmcol. Sci. 34, 489–96 (2013).

  13.Potenza MN, “How Central Is Dopamine to Pathological Gambling or Gambling Disorder?” Front. Behav. Neurosci. 7, 206 (2013).

  14.Yip SW et al., “Health/Functioning Characteristics, Gambling Behaviors, and Gambling-Related Motivations in Adolescents Stratified by Gambling Problem Severity: Findings from a High School Survey.” Am. J. Addict. 20, 495–508 (2011).

  15.Simmons ML et al., “Endogenous Opioid Regulation of Hippocampal Function.” Int. Rev. Neurobiol. 39, 145–96 (1996).

  16.Fournier PE et al., “Effects of a 110 Kilometers Ultra-Marathon Race on Plasma Hormone Levels.” Int. J. Sports Med. 18, 252–6 (1997).

  17.Schultz W et al., “A Neural Substrate of Prediction and Reward.” Science 275, 1593–9 (1997).

  CHAPTER 4. KILLING JIMINY: STRESS, FEAR, AND CORTISOL

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  2.Kudielka BM et al., “Human Models in Acute and Chronic Stress: Assessing Determinants of Individual Hypothalamus-Pituitary-Adrenal Axis Activity and Reactivity.” Stress 13, 1–14 (2010).

  3.Rosengren A et al., “Association of Psychosocial Risk Factors with Risk of Acute Myocardial Infarction in 11,119 Cases and 13,648 Controls from 52 Countries (The INTERHEART Study): Case-Control Study.” Lancet 364, 953–62 (2004).

  4.Crump C et al., “Stress Resilience and Subsequent Risk of Type 2 Diabetes in 1.5 Million Young Men.” Diabetologia 59, 728–33 (2016).

  5.Wilson RS et al., “Chronic Psychological Distress and Risk of A
lzheimer’s Disease in Old Age.” Neuroepidemiology 27, 143–63 (2006).

  6.Elovainio M et al., “Socioeconomic Differences in Cardiometabolic Factors: Social Causation or Health-Related Selection? Evidence from the Whitehall II Cohort Study, 1991–2004.” Am. J. Epidemiol. 174, 779–89 (2011).

  7.Williams DR, “Race, Socioeconomic Status, and Health: The Added Effects of Racism and Discrimination.” Ann. NY Acad. Sci. 696, 173–88 (1999).

  8.Mead H et al., “Racial and Ethnic Disparities in U.S. Health Care: A Chartbook” (2008). http://www.commonwealthfund.org/usr_doc/mead_racialethnicdisparities_chartbook_1111.pdf

  9.Gray JM et al., “Corticotropin-Releasing Hormone Drives Anandamide Hydrolysis in the Amygdala to Promote Anxiety.” J. Neurosci. 35, 3879–92 (2015).

 

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