Bibliography: Foods That Lie

For the sake of keeping the print edition of Foods That Lie affordable and accessible, a comprehensive bibliography with live links to referenced sources is available below. I am deeply grateful to all of those whose work is referenced within.

Please note that the content of third-party websites may change over time, and any alterations or inaccuracies that may occur on these sites after the publication of this book is not the responsibility of the author.

Furthermore, as the ideas expressed within this book have been gathered over the course of two decades, it is possible that I have inadvertently misattributed an idea or failed to give credit where it is due. If you believe this to be the case, please get in touch with me, and I will rectify the error as soon as possible.

Please note this document isn’t quite finished – and is currently in draft form.

1.1 Who am I?

[1] Calories Needed Each Day, National Institutes of Health

2.0 Behavior

[2] “…it is largely an organism’s behavior that determines whether it will survive, that is, live long enough to pass on its genes.” – W. David Pierce and Carl D. Cheney, Behavior Analysis and Learning: A Biobehavioral Approach, Sixth Edition (2017)

[3] “Single-celled organisms, such as Escherichia coli, developed multiple chemical receptors critical for such survival. The rotatory direction of their flagellae – whip-like appendages used to propel them through their environment – is altered by the type of chemical encountered. Thus, chemicals important for sustenance induce a counterclockwise rotation of the flagella, facilitating a smooth and somewhat linear swimming path, whereas toxic chemicals provoke a clockwise flagellar rotation, resulting in tumbling and turning away from the offending stimulus (Larsen et al., 1974).” – Christopher H Hawkes, Smell and Taste Disorders (2018)

2.1 Emotions

[4] “Happiness is the result of making progress and of goal-attainment at any of the diverse aspects of life that are inherently important: romance, friendships, health, material comfort, security, family, and social regard. These are inherently important because each has been intimately related to successful DNA reproduction throughout the history of our species.” – Douglas J. Lisle and Alan Goldhamer, The Pleasure Trap (2003)

2.2 Pattern and Prediction

[5] “Medieval water torture exploited the punishing effects of forcing a person to drink water beyond capacity. These tendencies for reinforcers to wax and wane and even turn to punishers evolved because individuals that possessed them survived and reproduced better than those that lacked them.” – William M. Baum, Understanding Behaviorism: Behavior, Culture, and Evolution, Third Edition (2017)

[6] “Toxicologists view all chemicals as potentially poisonous—the key issue is determining the relationship between dosage and lethality.” – Danielle Renee Reed, and Antti Knaapila, Genetics of Taste and Smell: Poisons and Pleasures (2012)

[7] “Since information is costly, rational decision makers can be expected to look for ways to reduce the average costs of attention, computation, calculation, and search.” – James G. March, A Primer on Decision Making: How Decisions Happen (2009)

[8] “For instance, animals that startle and run in response to a sudden noise may escape a predator, hence the startle reflex may have provided an adaptive advantage over organisms that did not run, or that ran less quickly in response to the noise. Thus, reflexes are selected across the history of the species.” – W. David Pierce and Carl D. Cheney, Behavior Analysis and Learning: A Biobehavioral Approach, Sixth Edition (2017)

2.3 Recalibration of the Rules (Learning)

[9] “Model parameters are continually updated until prediction error is minimised, up to expected levels of noise. This is learning (Friston 2003; Friston and Stephan 2007).” – Jacob Hohwy, The hypothesis testing brain: Some philosophical applications (2010)

[10] “All species that have been tested, including humans, show this kind of conditioning.” – W. David Pierce and Carl D. Cheney, Behavior Analysis and Learning: A Biobehavioral Approach, Sixth Edition (2017)

[11] “The sequences animals learn in some serial pattern experiments seem to extend well beyond the limits of working memory. They would thus appear to require an ability to compare what is going on now with what has gone on in the past.” – Claude G. Cech, Chapter 6: Resistance to Extinction (1999)

[12] “…present behavior depends not only on present events, but on many past events. These past events affect behavior as an aggregate, not as momentary happenings.” – William M. Baum, Understanding Behaviorism: Behavior, Culture, and Evolution, Third Edition (2017)

[13] “Many scientists now believe that the brain is basically a Bayesian hypothesis tester. One of its primary activities is making predictions about what input it expects to receive and then updating these predictions in the light of the actual input. – Neil Levy, Addiction as a disorder of belief (2014)

[14] “…the goal of the brain is to explore the world and register the consequences of successful exploratory actions to improve the efficacy of future actions.” – György Buzsáki, The Brain from Inside Out (2019)

[15] “…[the brain] computes a weighted running average of all rewards received previously in the presence of the stimulus, with the most recent reward weighted most heavily and the weight for prior rewards declining exponentially in their lag.” – Nathaniel D. Daw and Philippe N. Tobler, Neuroeconomics: Chapter 15. Value Learning through Reinforcement: The Basics of Dopamine and Reinforcement Learning (2014)

2.4 Deception

[16] Deirdre Barrett, Supernormal Stimuli (2010)

[17] Kathleen McAuliffe, This is Your Brain on Parasites: How Tiny Creatures Manipulate Our Behavior and Shape Society (2017)

Robert Trivers, The Folly of Fools: The Logic of Deceit and Self-Deception in Human Life (2014)

3.0 Eating Behavior

[18] N.A.A Rahman, A Fazilah, and M.E Effarizah, Toxicity of Nutmeg (Myristicin): A Review (2015)

[19] Olumayokun A. Olajide, Franklin F. Ajayi, Ambrose I. Ekhelar, S. Olubusayo Awe, J. Modupe Makinde, A. R. Akinola Alada, Biological effects of Myristica fragrans (nutmeg) extract (1999)

[20] Jessica Elizabeth De La Torre Torres, Fatma Gassara, Anne Patricia Kouassi, Satinder Kaur Brar & Khaled Belkacemi, Spice Use in Food: Properties and Benefits, Critical Reviews in Food Science and Nutrition (2015)

[21] S.H. Nasr, Y. Kashtanova, V. Levchuk, G.S. Markowitz, Secondary oxalosis due to excess vitamin C intake (2006)

[22] Vasu Sunkara , Timothy D. Pelkowski, Darren Dreyfus, Anjali Satoskar, Acute Kidney Disease Due to Excessive Vitamin C Ingestion and Remote Roux-en-Y Gastric Bypass Surgery Superimposed on CKD (2015)

[23] R. Weindruch, R. Walford, D. Guthrie, The retardation of aging in mice by dietary restriction: longevity, cancer, immunity and lifetime energy intake (1986)

[24] Stephen Strauss, Clara M. Davis and the wisdom of letting children choose their own diets (2006)

[25] Fred Provenza, Nourishment: What Animals Can Teach Us about Rediscovering Our Nutritional Wisdom (2018)

[26] Mark Schatzker, The Dorito Effect: The Surprising New Truth About Food and Flavor (2016)

[27]

[28] “Nutrition is such a new science that we’ve barely touched the surface as to the power it has over our health and well-being. As scientific studies reveal more, we realize that we have mislabeled good things as bad and bad things as good.” – Kate Deering, How to Heal Your Metabolism (2015)

[29] Louis Rosenfeld, Vitamine – Vitamin. The early years of discovery (1997)

3.1 The Role of Flavor

[30] James Kennedy, Ingredients of an All-Natural Banana (2013)

[31] Paul A. S. Breslin, Alan C. Spector, Mammalian taste perception (2008)

[32] Paul A. S. Breslin, An Evolutionary Perspective on Food and Human Taste (2013)

[33] Scott Herness, Fang-li Zhao, The neuropeptides CCK and NPY and the changing view of cell-to-cell communication in the taste bud (2009)

[34] Linda A. Barlow, Ophir D. Klein, Developing and regenerating a sense of taste (2016)

[35] Mirre Viskaal van Dongen, Marjolijn C van den Berg, Nicole Vink, Frans J Kok, Cees de Graaf, Taste-nutrient relationships in commonly consumed foods (2011)

[36] Paul A. S. Breslin, An Evolutionary Perspective on Food and Human Taste (2013)

[37] Institute for Quality and Efficiency in Health Care, How does our sense of taste work? (Updated 2016)

[38] “In addition to the five canonical taste qualities, there is growing evidence that many vertebrates and invertebrates use their gustatory systems to detect the presence of other compounds, that may include Ca2+, CO2, water and fats…” – Emily R. Liman, Yali V. Zhang, and Craig Montell, Peripheral coding of taste (2014)

[39] Paul A. S. Breslin, An Evolutionary Perspective on Food and Human Taste (2013)

[40] “Whereas humans are able to distinguish between only five or six primary taste qualities, people are able to differentiate more than a trillion odors…” – Cees de Graaf and Sanne Boesveldt, Flavor, Satiety and Food Intake (2017)

[41] Stephen A. Goff, Harry J. Klee, Plant Volatile Compounds: Sensory Cues for Health and Nutritional Value? (2006)

[42] Gordon Shepherd, Neurogastronomy: How the Brain Creates Flavor and Why It Matters (2013)

[43] Institute for Quality and Efficiency in Health Care, How does our sense of taste work? (Updated 2016)

[44] “It is now estimated that there are between 500-1000 odorant receptor genes in both humans and mice. This number of genes, specific to the olfactory system, comprises 1-2% of the 50,000 to 100,000 genes thought to make up the human genome. This number is second only to the receptors of the immune system.” – John C. Leffingwell, Olfaction (2001)

[45] “Nonhuman species provide evidence that the sense of taste has been shaped by evolution; for instance, cats and some other carnivorous species, in addition to chickens, have lost the function of their sweet receptor—they no longer need to taste “sweet” because the foods they eat, the flesh of other animals or starchy grains, contain little sugar.” – Danielle Renee Reed and Antti Knaapila, Genetics of Taste and Smell: Poisons and Pleasures (2012)

[46] “Compared to mammals, chickens have fewer genes for taste receptors, e.g., lacking the taste receptor T1R2 for sweet…” – Hong-Xiang Liu, Prasangi Rajapaksha, Zhonghou Wang, Naomi E Kramer, and Brett J Marshall, An Update on the Sense of Taste in Chickens: A Better Developed System than Previously Appreciated (2018)

[47] “Aquatic carnivorous mammals, such as sea lions […] appear to have lost a large number of taste receptors, perhaps because most of their prey are swallowed whole and would not be tasted. In this case, the identification of swimming fish via visual recognition and the body and kinetic senses of pursuing prey may have replaced taste.” – Paul A. S. Breslin, An Evolutionary Perspective on Food and Human Taste (2013)

[48] Danielle Renee Reed and Antti Knaapila, Genetics of Taste and Smell: Poisons and Pleasures (2012)

[49] Richard D. Mattes, Orosensory Considerations (2012)

3.2 Flavor-Nutrition Relationships

[50]

[51] “Flavor is information. Compounds like phosphorus and vitamin C are stable. They don’t waft off food. So the body senses what it can—those unstable floaty aromas—and associates them with the post-ingestive effects on our bodies.” – Mark Schatzker, The Dorito Effect: The Surprising New Truth About Food and Flavor (2016)

[52] “Flavor evaluation is influenced by learning from experience with foods. One main influence is flavor-nutrient learning (FNL), a Pavlovian process whereby a flavor acts as a conditioned stimulus (CS) that becomes associated with the postingestive effects of ingested nutrients (the US).” – Kevin P. Myers, The convergence of psychology and neurobiology in flavor-nutrient learning (2018) (PDF available here)

[53] “Sheep can make multiple flavor-feedback associations with minerals. We designed a study in which we made lambs deficient in one of three minerals – phosphorus, calcium or sodium – and gave them a choice of the three differently flavored foods. The lambs had previously ingested these flavored foods with one of the three minerals. Lambs preferred the flavor previously paired with repletion of the mineral – phosphorus, calcium, or sodium – they were lacking.” – Fred Provenza, Nourishment: What Animals Can Teach Us about Rediscovering Our Nutritional Wisdom (2018)

[54] “He wanted to set up an “association” between the flavor of maple and the nutritional payload of phosphorus. A few days later, when these same phosphorus-deficient sheep were offered maple-flavored feed, they gobbled it up, even though there wasn’t so much as a speck of phosphorus in it. To their bodies, maple flavor meant one thing: phosphorus.” – Mark Schatzker, The Dorito Effect: The Surprising New Truth About Food and Flavor (2016)

[55] “When sheep eat a meal of four familiar foods (alfalfa, barley, oats, and corn) and one novel food (rye), and then get an orally administered nauseating capsule of lithium chloride, they subsequently ignore the novel food, but not the familiar foods.” – Fred Provenza, Nourishment: What Animals Can Teach Us about Rediscovering Our Nutritional Wisdom (2018)

[56] Emily R. Liman, Yali V. Zhang, and Craig Montell, Peripheral coding of taste (2015)

[57] “You can get along with other people only if you can accurately gauge whether their intentions are benign or dangerous. Even a slight misreading can lead to painful misunderstandings in relationships at home and at work.” – Bessel van der Kolk, The Body Keeps the Score (2015)

[58] “Our own studies have shown that sniffing in a smell gives rise to a spatial pattern of activity in the brain. These patterns function as images of smell, with different images for different smells, much as different faces form different images in our visual system. Human brains are very good at recognizing faces, which can be thought of as a highly developed form of pattern recognition. From our studies we think that the same ability occurs with the patterns laid down by smells—that is, the ability to recognize many different patterns representing as many different smells.” – Gordon Shepherd, Neurogastronomy: How the Brain Creates Flavor and Why It Matters (2013)

[59] “Importantly, flavor evaluation is neither innate nor fixed.” – Kevin P. Myers, The convergence of psychology and neurobiology in flavor-nutrient learning (2018) (PDF available here)

[60] “Our likes and wants are subjective properties we assign to food based on our past experiences, and our current state of satiation and satiety.” – J. Stanton, What Is Hunger, and Why Are We Hungry? (2012)

3.3 Hunger and Satiety

[61] Zata Vickers, Flavor, Satiety and Food Intake (2017)

[62] Cees de Graaf and Sanne Boesveldt, Flavor, Satiety and Food Intake (2017)

[63] “In the orbitofrontal cortex, feeding to satiety with one food decreases the responses of these neurons to that food, but not to other foods, showing that sensory-specific satiety is computed in the primate (including human) orbitofrontal cortex.” – Edmund Rolls, Brain mechanisms underlying flavour and appetite (2006)

[64] “…dopamine neurons come to respond with bursts to stimuli that immediately precede and reliably predict the reward…” –  Roy A. Wise, and Mykel A. Robble, Dopamine and Addiction (2020)

[65] Richard D. Mattes, Orosensory Considerations (2012)

[66] Keri McCrickerd, Flavor, Satiety and Food Intake (2017)

[67] Paul A. S. Breslin, An Evolutionary Perspective on Food and Human Taste (2013)

[68] Christopher H Hawkes, Smell and Taste Disorders (2018)

[69] “Eating two oranges [for breakfast] made participants feel physically full, but they were still mentally hungry – looking for or wanting something else to eat.” – Zata Vickers, Flavor, Satiety and Food Intake (2017)

3.4 Sham Eating

[70] “The behavioural sequence of satiety occurred after the first sham-fed meal, but meal size doubled and the intermeal interval was about 50% shorter than was observed in the preceding real feeding test.” – Gerard P. Smith, Satiation: From Gut to Brain (1998)

[71] “…after 17 hours of food deprivation, sham feeding continued for 7.5 hours in rats without the occurrence of the behavioural sequence of satiety (Young et al.,). Continuous sham feeding has also been observed in rhesus monkeys after overnight food deprivation.” – Gerard P. Smith, Satiation: From Gut to Brain (1998)

[72] “The observation of absence of satiety when food drained out of the upper small intestine has been confirmed in monkeys…” – Danielle Greenberg, Satiation: From Gut to Brain (1998)

[73] “The observation of absence of satiety when food drained out of the upper small intestine has been confirmed in monkeys…” – Danielle Greenberg, Satiation: From Gut to Brain (1998)

[74] “The infusions elicited the complete behavioral sequence for satiety, and the reductions in sham feeding were related to the chemical concentration of the nutrient infusions.” – Danielle Greenberg, Satiation: From Gut to Brain (1998)

[75] “The duodenal infusion had been shown to stop sham feeding and elicit the behavioural sequence of satiety after 17 hours of food deprivation (Liebling et al., 1975).” – Gerard P. Smith, Satiation: From Gut to Brain (1998)

[76] “The satiating effect of intestinal nutrient infusions in the sham-feeding preparation indicates, however, that gastric distention is not necessary for the inhibition of meal size.” – Danielle Greenberg, Satiation: From Gut to Brain (1998)

[77] “The satiating effect of intestinal nutrient infusions in the sham-feeding preparation indicates, however, that gastric distention is not necessary for the inhibition of meal size.” – Danielle Greenberg, Satiation: From Gut to Brain (1998)

[78] “If intestinal infusions were given 6-12 minutes before sham feeding was initiated, no suppression of intake was observed. Maximal suppression of sham feeding was obtained when the [nutrient] infusion began 12 minutes after the onset of sham feeding.” – Danielle Greenberg, Satiation: From Gut to Brain (1998)

[79] “…a synergistic interaction between post-pyloric and gastric stimuli in the control of compensatory intake…”  – Gerard P. Smith, Satiation: From Gut to Brain (1998)

[80] “Roux-en-Y gastric bypass surgery (RYGB) and other bariatric procedures alter gastrointestinal processing of food in a number of ways. Thus, it is plausible that these procedures alter post-oral unconditioned stimuli that support flavor-consequence learning, leading to altered food selection, amount eaten, and affect. Surprisingly, however, there is almost no research on the role of flavor-consequence learning in the effects of bariatric surgery on appetite. This issue urgently warrants investigation.” –  Lori Asarian, Nori Geary, RYGB and flavor-consequence learning (2020)

[81] “…total subdiaphragmatic vagotomy abolished the suppression of sham feeding elicited by intestinal infusion of sodium oleate.”  – Danielle Greenberg, Satiation: From Gut to Brain (1998)

[82] “When the caloric density of their food was cut in half, after a few days rats doubled the volume of food that they ate. Other labs found similar results.” – Seth Roberts, What makes food fattening (2005)

[83] “However, studies in which food has been calorically diluted (i.e., by the addition of nonnutritive bulk so that more volume must be eaten to achieve the same caloric load) have shown that animals easily adapt to this manipulation by increasing their meal size (Adolph, 1947; Janowitz & Grossman, 1949). They readily consume a larger volume to get their calories, which suggests that gastric capacity is rarely a factor in normal consumption.” – The Eating Paradox: How We Tolerate Food (1991)

4.0 Deceptive Flavor

[84] “A soft drink with low natural juice content may require a clouding agent to boost the turbidity [haziness] in order for it to resemble the cloudy natural juice of the fruit it is named after.” – Joanna Blythman, Swallow This: Serving Up the Food Industry’s Darkest Secrets (2015)

[85] Avery Gilbert, What the Nose Knows (2015)

[86] “When they see something they like, they extract its flavor molecules from the fruit on the tree. Then, back in the lab, they mimic mother nature’s molecules with chemicals.” – Morley Safer, Tweaking tastes and creating cravings, CBS News (2011) 2:30

4.1 Concealing Flavor

[87] Glanbia Nutritionals, Flavor Masking Challenges and How to Solve Them

[88] Jeff Gelski, Eliminating the pea flavor in pea protein, (2018)

[89] “Sweetness is used to mask not only bitter but also acidic tastes. This is important in wines or fruit juices, especially citrus juices that can contain strong-flavored volatile oils from pith, seeds, and peels that are the result of large-scale juice operations.” – Florentine Hilty-Vancura, New Strategies For Masking And Modifying Flavor (2017)

[90] Innova Flavors, Understanding Flavor Masking Agents: 5 Things You Need to Know (2021)

[91] “Trying to block bitter flavours is far more practical than, say, trying to remove any of the vast range of compounds that can make food taste unpleasant. And only tiny amounts of bitter blockers are required to stop the bitter signal reaching the brain.” – Celeste Biever, Bitter pills banished by taste-blocking compounds (2003)

[92] Danielle Andrews, Smita Salunke, Anne Cram, Joanne Bennett, Robert S. Ives, Abdul W. Basit, Catherine Tuleu, Bitter-blockers as a taste masking strategy: A systematic review towards their utility in pharmaceuticals (2021)

[93] Celeste Biever, Bitter pills banished by taste-blocking compounds (2003)

[94] Florentine Hilty-Vancura, New Strategies For Masking And Modifying Flavor (2017)

4.2 Transporting Flavor

[95] Mark Schatzker, The Dorito Effect: The Surprising New Truth About Food and Flavor (2016)

4.3 Strengthening Flavor

[96] “Dutch chemists soon discovered that the compound diacetyl, produced either synthetically or by microorganisms, could add a “buttery” flavor to foods. Creameries then started adding a chemical that doesn’t naturally occur in butter to actual butter in order to make it taste more like…butter.” – Alison Herman, The Absurd History of Artificial Flavors (2015)

[97] “Enhanced or value-added meat and poultry products are raw products that contain flavor solutions added through marinating, needle injecting, soaking, etc. The presence and amount of the solution will be featured as part of the product name, for example, “Chicken Thighs Flavored with up to 10% of a Solution” or “Beef Steak Marinated with 6% of a Flavor Solution.”” – United States Department of Agriculture, Water in Meat and Poultry (2013)

[98] “Monosodium glutamate (MSG) is perhaps the most common of the glutamates added to foods. Many consumers, however, have been avoiding MSG when it appears on a label. But extracts and concentrations of tomatoes and mushrooms, rich in natural glutamic acid compounds, are stepping up to take MSG’s place.” – Florentine Hilty-Vancura, New Strategies For Masking And Modifying Flavor (2017)

[98] “MSG enhancement of flavour appears to require some existing umami-like element to be present: thus when MSG is added to boiled rice alone, it elicits either neutral or negative palatability ratings, but when added to fried rice, palatability ratings increase.” – Martin R Yeomans, Flavor, Satiety and Food Intake (2017)

[99] “The perfect illusion is one that does not depart too much from reality, but has a touch of the unreal to it, like a waking dream. Lead the seduced to a point of confusion in which they can no longer tell the difference between illusion and reality.” – Robert Greene, The Art of Seduction (2003)

[100] “…the most often selected foods were chocolate (selected by 54 % of participants), candy (46 %), cookies (25 %), chips (25 %), pastries (21 %), cake (21 %), pasta (18 %), pizza (18 %), ice cream (16 %), and French fries (14 %). These foods correspond to the most often craved foods identified in previous studies on food craving.” – Adrian Meule and Ashley N. Gearhardt, Five years of the Yale Food Addiction Scale: Taking stock and moving forward (2014)

[101] Pizza Hut Ingredient Listing (2014)

4.4 Supplements and Fortification

[102] Tod Cooperman, Which supplements should be taken with food? (2021)

[103] Ranjani R. Starr, Too Little, Too Late: Ineffective Regulation of Dietary Supplements in the United States (2015)

4.5 Flavor: The Most Important Stimulus

[104]

[105] “When questioned about cravings, sensory properties are the attributes most commonly reported.” –Richard D. Mattes, Orosensory Considerations (2012)

4.6 Masters of Deception

[106] “More intelligent individuals, who were better at spotting contradictions, would have been at an evolutionary advantage as they would be less readily duped. The better they were at detecting lies, the better they would have also been at preventing any of their own lies from being spotted and thus at manipulating others. The standards of lying and storytelling would then increase, driving the need to be even more intelligent and linguistically able to stay ahead.” – Enrico Coen, The storytelling arms race: origin of human intelligence and the scientific mind (2019)

[107] “Once one agent learns how to become more competitive by sacrificing a common value, all its competitors must also sacrifice that value or be outcompeted and replaced by the less scrupulous.” – Scott Alexander, Meditations on Moloch (2014)

[108] “The smallest package, the machine-made cigarette, blended shredded tobacco, flavoring agents, and humectants to create a product that was cheap, addictive, and universal, cutting across class and occupational lines.” – David T. Courtwright, The Age of Addiction (2019)

[109] “In 1910 German health officials complained that certain shopkeepers were selling morphine-laced candies, along with discount morphine injections for “delicate nerves.”” – David T. Courtwright, The Age of Addiction (2019)

[110] Jonathan Rees, Food Adulteration and Food Fraud (2020)

[111] William Krohn, Graded Lessons in Physiology and Hygiene (1906)

[112] Jonathan Rees, Food Adulteration and Food Fraud (2020)

[113] Larry Olmsted, Real Food/Fake Food: Why You Don’t Know What You’re Eating and What You Can Do About It (2017)

5.1 Increased Engagement

[114] B.F. Skinner, Science and Human Behavior (1965)

5.3 Obsession

[115] Robert Sapolsky, excerpt from Stanford University lecture on Human Sexual Behavior

[116] “In PG, accumbens DA is maximal during a gambling task when the probability of winning and losing money is identical—a 50% chance for a two-outcome event representing maximal uncertainty (Linnet et al., 2012).” – Patrick Anselme, Mike J. F. Robinson, What motivates gambling behavior? Insight into dopamine’s role (2013)

[117] “…only in the presence of uncertainty is it anticipated that there will be information available in the outcome. If reward (P = 1) or no reward (P = 0) occurs exactly as predicted, that event contains no information beyond that already given by the conditioned stimulus; that is, it is redundant. However, when the prediction of reward is uncertain, the outcome (reward or no reward) always contains information. The outcome at P = 0.5 contains, on average, the maximal amount of information (one bit) of any probability.” – Christopher D. Fiorillo, Philippe N. Tobler, and Wolfram Schultz, Discrete Coding of Reward Probability and Uncertainty by Dopamine Neurons (2003)

[118] “…Martha Weiss and her students let these butterflies loose on a field of yellow and magenta flowers. Sometimes only the yellow flowers had nectar, sometimes only the magenta ones (Weiss and company had fun arranging this). The butterflies quickly learned which color signaled the consequence they wanted.” – Susan Schneider, The Science of Consequences: How They Affect Genes, Change the Brain, and Impact Our World (2012)

[119] “At the start of training, before the animal has learned to discriminate among stimuli, it ought to treat all stimuli along the relevant dimension as equivalent. So, rather than exhibit a tent-shaped gradient, animals at this point ought to have a flat-line gradient in which the same proportion of responses is given to all similar stimuli.” – Claude G. Čech, Chapter 7: Attention & Categorization (1998)

[120] “By reinforcing responses to a circular red spot while extinguishing responses to circular spots of all other colors, we may give the red spot exclusive control over the behavior. This is discrimination.” – B.F. Skinner, Science and Human Behavior (1965)

[121] “Each time the system is recalculated, the posterior becomes the prior of the new iteration. It was an evolving system, which each new bit of information pushed closer and closer to certitude.” – Sharon Bertsch McGrayne, The Theory That Would Not Die: How Bayes’ Rule Cracked the Enigma Code, Hunted Down Russian Submarines, and Emerged Triumphant from Two Centuries of Controversy (2012)

[122] “Some birds plagued by the cuckoo do eventually evolve a detector and begin to reject the intruder’s egg after centuries of victimization.” – Deirdre Barrett, Supernormal Stimuli: How Primal Urges Overran Their Evolutionary Purpose (2010)

5.4 The Normal Response

[123] “…many behavioral experiments have shown that contingencies of reinforcement generalize across species, type of reinforcement, diverse settings, and different operants.” – W. David Pierce and Carl D. Cheney, Behavior Analysis and Learning: A Biobehavioral Approach, Sixth Edition (2017)

[124] “This general result has been obtained with goldfish (Igaki & Sakagami, 2004), rats (e.g., Blackman, 1968; Shahan & Burke, 2004), pigeons (e.g., Nevin, 1974; Nevin, Tota, Torquato, & Shull, 1990), normal children (Tota-Faucette, 1991), children with developmental disabilities (Ahearn et al., 2003; Mace et al., 2010), college students (Cohen, 1996), and adults with mental retardation (Mace et al., 1990). These studies have employed different sorts of responses and reinforcers, and have evaluated resistance to change by presenting various disruptors including response-independent reinforcers between schedule components, pre-session feeding to devalue reinforcers, response-contingent punishment, conditioned suppression, concurrent distraction, and extinction – i.e., withholding all reinforcers…” – John A. Nevin, Resistance to extinction and behavioral momentum (2012)

6.0 A New Understanding of Addiction

[125] “Fentanyl selectively binds to the mu-receptor in the central nervous system (CNS) thereby mimicking the effects of endogenous opiates.” – Fentanyl, Compound Summary, US National Library of Medicine

[126] Caffeine, Compound Summary, US National Library of Medicine

[127]

[128] J P Boulenger, J Patel, R M Post, A M Parma, P J Marangos, Chronic caffeine consumption increases the number of brain adenosine receptors (1983)

[129] Paul J. Marangos, Jean-Philippe Boulenger, Jitendra Patel, Effects of chronic caffeine on brain adenosine receptors: Regional and ontogenetic studies (1984)

[130] “Individuals who regularly consume caffeine have increased the number of adenosine receptors in their central nervous system (CNS) and become more sensitive to normal physiologic effects of adenosine.” – Karima R. Sajadi-Ernazarova, Jackie Anderson, Aayush Dhakal, Richard J. Hamilton, Caffeine Withdrawal (2023)

[131] Britannica, acetylcholine, chemical compound (2024)

[132] Marina R. Picciotto, Michael J. Higley, and Yann S. Mineur, Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior (2012)

6.1 Tolerance and Escalation

[133] “…compatible with the idea that the brain transforms all rewards onto a single scale of value that facilitates decision making when different actions may procure different types of rewards…” – Kelly Diederen and Paul Fletcher, Dopamine, Prediction Error and Beyond (2020)

[134] Armin Lak, William R. Stauffer, and Wolfram Schultz, Dopamine prediction error responses integrate subjective value from different reward dimensions (2014)

[135] “According to the now canonical theory, reward predictions are represented as a single scalar quantity, which supports learning about the expectation, or mean, of stochastic outcomes.” – Will Dabney, Zeb Kurth-Nelson, Naoshige Uchida, Clara Kwon Starkweather, Demis Hassabis, Rémi Munos, Matthew Botvinick, A distributional code for value in dopamine-based reinforcement learning (2020)

[136] Paul W. Glimcher, Understanding dopamine and reinforcement learning: The dopamine reward prediction error hypothesis (2011)

6.2 The Downfall

[137] Abraham H. Maslow, A Theory of Human Motivation (1943)

[138] “Negative prospection and even depression itself is not inherently dysfunctional, maladaptive, or problematic; indeed, both could be essential for adaptive functioning, because incessant optimism would have serious costs (Nesse, 2004; Norem & Chang, 2002).” – Martin Seligman, Peter Railton, Roy Baumeister, Chandra Sripada, Homo Prospectus (2016)

6.3 1.1 Hypothesis Testing

[139] Matt Ridley, The Red Queen (2003)

6.4 Vulnerability

[140] Rajita Sinha, Chronic Stress, Drug Use, and Vulnerability to Addiction (2008)

[141] George F. Koob, A Role for Brain Stress Systems in Addiction (2008)

[142] Jean Lud Cadet, Epigenetics of Stress, Addiction, and Resilience: Therapeutic Implications (2014)

[143] Nick E. Goeders, The impact of stress on addiction (2003)

[144] Rajita Sinha, Ania M. Jastreboff, Stress as a Common Risk Factor for Obesity and Addiction (2013)

[145] “Cortisol levels rise during any kind of exercise. If the exercise is moderate and enjoyable, cortisol drops below its normal level soon after we stop exercising. If the exercise is extreme or unpleasant, cortisol levels stay high for a long time.” – Russell Farris and Per Marin, The Potbelly Syndrome: How Common Germs Cause Obesity, Diabetes, and Heart Disease (2005)

[146] Kevin Laland, Darwin’s Unfinished Symphony: How Culture Made the Human Mind (2017)

[147] “The first individuals to solve the mazes are those driven to find novel foraging solutions by hunger, or by the metabolic costs of growth, or pregnancy. […] Motivation, rather than cleverness or ability, is what explains patterns of innovation here. Fishes are typically reluctant to swim into dark holes and through dark compartments, since predators might be lurking behind them. The hungrier an individual, the more likely it will be to take risks and try out new solutions to find food.” – Kevin Laland, Darwin’s Unfinished Symphony: How Culture Made the Human Mind (2017)

6.5 Recognition

[148] “As David Sloan Wilson discovered, a group usually solves problems better than the individuals within it. Pit one socially networked problem-solving web against another—a constant occurrence in nature—and the one which most successfully takes advantage of complex adaptive system rules, that which is the most powerful cooperative learning contraption, will almost always win.” – Howard Bloom, Global Brain: The Evolution of Mass Mind from the Big Bang to the 21st Century (2001)

[149] “The striking technologies that characterize our species, from the kayaks and compound bows used by hunter-gatherers to the antibiotics and airplanes of the modern world, emerge not from singular geniuses but from the flow and recombination of ideas, practices, lucky errors, and chance insights among interconnected minds and across generations.” – Joseph Henrich, The Secret of Our Success: How Culture Is Driving Human Evolution, Domesticating Our Species, and Making Us Smarter (2015)

[150] “[Heyes, Jaldow, and Dawson] did an experiment on observational learning in which one group of rats saw another go through extinction (i.e., our group saw the others perform a response they had also learned, but they also saw that the response [no] longer resulted in reinforcement). As you might expect […] the observational group exhibited faster extinction.” – Claude G. Čech, Chapter 6: Resistance to Extinction (1999)

[151] “…consistent with observational learning and perceptual learning, animals that observe other animals making a discrimination will learn that discrimination more rapidly (the Kohn and Dennis study mentioned in Chapter 5). Also, stimulus differentiation will speed up discrimination learning, as we saw in the Gibson, Walk, and Tighe study.” – Claude G. Čech, Chapter 7: Attention & Categorization (1998)

[152] Paul Schmid-Hempel, Immune defence, parasite evasion strategies and their relevance for ‘macroscopic phenomena’ such as virulence (2009)

[153] “…one of the most exciting insights of recent years is the gathering evidence for the generality and multitude of mechanisms by which parasites evade the host’s immune responses, gain entrance to tissues or by which they manipulate the signalling network of the immune system. Indeed, the mechanisms of immune evasion are mind-boggling in their subtlety and diversity, and have been described for all major parasite groups…” – Paul Schmid-Hempel, Immune defence, parasite evasion strategies and their relevance for ‘macroscopic phenomena’ such as virulence (2009)

7.1 Downregulation of Taste and Smell

[154] Harvard Health Publishing, Potassium lowers blood pressure (2017)

[155] “Bodies counter nutrient deficits or excesses. To maintain homeostasis, cells can increase (up-regulate) or decrease (down-regulate) the number of receptors on the membrane, thus altering sensitivity to a compound.” – Fred Provenza, Nourishment: What Animals Can Teach Us about Rediscovering Our Nutritional Wisdom (2018)

[156] “Conditioning (also referred to as learning) is a change in behavior due to experience (exposure to stimuli that cause small-scale physical changes to the body that behaves), and a stimulus is anything that can potentially control behavior (Chance, 2009; Fraley, 2008, p. 64).” – James O’Heare, Changing Problem Behavior (2010)

Conditioning creates changes to the structure of the body of the learner via stimulation from the environment, which change the evocative capacity of the SD on subsequent presentations. – James O’Heare, Changing Problem Behavior (2010)

[157]

[158] “A decrease in olfactory sensitivity can be seen as part of the food intake control mechanism, where appetite regulation hormones may be able to shift olfactory sensitivity to achieve nutritional homeostasis.” – Cees de Graaf and Sanne Boesveldt, Flavor, Satiety and Food Intake (2017)

[159] “The group with higher taste bud densities gave significantly higher average intensity ratings for sucrose (196%), NaCl (135%) and PROP (142%), but not for citric acid (118%) and quinine HCl (110%) than the lower density group. Thus, the subjects with higher fungifrom taste bud densities also reported some tastes as more intense than subjects with fewer fungiform taste buds.” – J. Miller, Frank E. Reedy, Variations in human taste bud density and taste intensity perception (1990)
https://www.sciencedirect.com/science/article/abs/pii/003193849090374D

[160] Pu Feng, Liquan Huang, and Hong Wang, Taste Bud Homeostasis in Health, Disease, and Aging (2014)

[161] “So critical are taste sensations to the recognition and enjoyment of foods, and the appropriate digestion and utilization of nutrients, that humans who acutely lose their sense of taste, such as following radiotherapy, for example, often will not eat.” – Paul A. S. Breslin, Alan C. Spector, Mammalian taste perception (2008)

[162] Pu Feng, Liquan Huang, and Hong Wang, Taste Bud Homeostasis in Health, Disease, and Aging (2014) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3864165/

[163] “Many people with anosmia are known to skip meals because the appeal for food is not there. Nothing seems to taste good anymore and the flavor is gone. Another reason appetite is affected, is that the aroma of foods does not cause a desire for food because the person cannot detect the luring odors from the food. Not eating results in malnutrition and involuntary weight loss. This can also lead to illness because the proper foods are not being eaten to keep a person healthy.” – Lora Muxworthy, The Dangers and Safety Precautions Related to the Olfactory Dysfunction Anosmia (1999)

[164] Annette Heist, With No Sense Of Smell, The World Can Be A Grayer, Scarier Place (2016)

[165] “Obese individuals have been reported to display a weakened sense of taste and thus may be driven to consume more calories to attain such reward.” – Andrew Kaufman, Ezen Choo, Anna Koh, and Robin Dando, Inflammation arising from obesity reduces taste bud abundance and inhibits renewal (2018)

[166] Z. M. Patel, J. M. DelGaudio, and S. K. Wise,  Higher Body Mass Index Is Associated with Subjective Olfactory Dysfunction (2015)

[167] “Obese women required higher MSG concentrations to detect a taste and preferred significantly higher MSG concentrations in a soup‐like vehicle.” – M. Yanina Pepino, Susana Finkbeiner, Gary K. Beauchamp, Julie A. Mennella, Obese Women Have Lower Monosodium Glutamate Taste Sensitivity and Prefer Higher Concentrations Than Do Normal-weight Women (2012)

[168] Johanna Overberg, Thomas Hummel, Heiko Krude, Susanna Wiegand, Differences in taste sensitivity between obese and non-obese children and adolescents (2012)

[169] “However, certain eating behaviors may be altered in some cases of chemosensory dysfunction, such as increased seasoning and sugar use in anosmic individuals. Changes in related culinary practices, such increased salt, sugar, and fat use, could complicate issues with hypertension, diabetes and cardiovascular disease, respectively.” – Jonathan C. Kershaw, Richard D. Mattes, Nutrition and taste and smell dysfunction (2018)

[170] “…it is well known that diabetes and obesity affect taste preferences in adults. For example, in diabetic patients, taste responses, especially to sweet, are blunted (Wasalathanthri et al., 2014), and obese individuals also have decreased taste sensitivity (Stewart et al., 2010; Stewart et al., 2011).” – Linda A. Barlow, and Ophir D. Klein, Developing and regenerating a sense of taste (2015)

[171] “Type 2 diabetic patients had a blunted taste response for sweet followed by sour and salt tastes. This taste abnormality may influence the choice of nutrients, with a preference for sweet-tasting foods, thereby exacerbating hyperglycemia.” – S.M. Gondivkar, A. Indurkar, S. Degwekar, R. Bhowate, Evaluation of gustatory function in patients with diabetes mellitus type 2 (2009)

[172] M. Balslev Jørgensen, Nils H. Buch, Studies on the Sense of Smell and Taste in Diabetics (1960)

[173] Brynn E Richardson, Eric A Vander Woude, Ranjan Sudan, Jon S Thompson, Donald A Leopold, Altered Olfactory Acuity in the Morbidly Obese (2004)

[174] “Smell dysfunction is associated with age and degenerative complications of diabetes, suggesting a degenerative mechanism related to diabetes.” – J.P. Le Floch, G. Le Lièvre, M. Labroue, M. Paul, R. Peynegre, and L. Perlemuter, Smell dysfunction and related factors in diabetic patients (1993)

[175] “Mortality for anosmic older adults was four times that of normosmic individuals while hyposmic individuals had intermediate mortality (p<0.001), a “dose-dependent” effect present across the age range.” – Jayant M Pinto, Kristen E Wroblewski, David W Kern, L Philip Schumm, Martha K McClintock, Olfactory dysfunction predicts 5-year mortality in older adults (2014)

[176] “Kaufman has found that heavier mice have fewer taste buds present in their tongues. In addition, he has observed slower taste bud cell regeneration in these heavier mice, which may be a reason for why they have fewer cells. […] Promisingly, if the heavier mice are switched back to a lean diet, there appears to be a reversal of this effect.” – Ava Fan, Obesity, Could it be Taste Buds? (2016)

[177] L. Graham, G. Murty, D. J. Bowrey, Taste, Smell and Appetite Change After Roux-en-Y Gastric Bypass Surgery (2014)

[178] National Institutes of Health, Overweight & Obesity Statistics (2021)

7.2 Insulin Resistance: A Lifesaving Response

[177] Maja Divjak, Insulin Receptor and Type 2 Diabetes, Part 2 (2015)

[178] “Upon binding to its receptor, insulin triggers a chain of molecular interactions inside the cell. The signal propagates through the cytoplasm and eventually renders glucose uptake (the response).” –  Guanyu Wang, Raison d’être of insulin resistance: the adjustable threshold hypothesis (2014)

[179] “The predominate pathologies of hyperinsulinemia, type 2 diabetes are athero-arteriosclerosis, cardiovascular disease, cerebral vascular disease, hypertension, nephropathy, retinopathy, peripheral and central neuropathy, and penile erectile dysfunction.” – Joseph R. Kraft, Diabetes Epidemic & You (2008)

[180] “During pregnancy, for example, the thresholds increase consistently to strengthen the mother’s insulin resistance to meet the increasing glucose demand of the expanding fetal brain.” – Guanyu Wang, Raison d’être of insulin resistance: the adjustable threshold hypothesis (2014)

[181] “Contrary to the common belief that insulin promotes glucose disposal, the results imply that insulin is the body’s ‘ration stamp’ to restricting glucose utilization by peripheral tissues and that insulin resistance is primarily a well-evolved mechanism.” – Guanyu Wang, Raison d’être of insulin resistance: the adjustable threshold hypothesis (2014)

[182] “According to the hypothesis, a typical cell exhibits an all-or-none response to insulin (figure 2b). The switching between all and none occurs at two threshold insulin concentrations I_on and I_off, which render hysteresis: the delayed switch-on to spare glucose for the brain and the delayed switch-off to avoid hyperglycaemia.” – Guanyu Wang, Raison d’être of insulin resistance: the adjustable threshold hypothesis (2014)

[183] “By varying the levels of insulin and the degree of insulin sensitivity of tissues the energy budget allocation to different organs can be finely manipulated.” – Milind Watve and Chittaranjan Yajnik, Evolutionary origins of insulin resistance: a behavioral switch hypothesis (2007)

[184] “Longer-term studies of the Atkins diet failed to confirm the much hoped-for benefits. Dr. Gary Foster from Temple University published two-year results showing that both the low-fat and the Atkins groups had lost but then regained weight at virtually the same rate.” – Jason Fung, The Obesity Code (2016)

[185] Stephan Guyenet, Interview with Chris Voigt of 20 Potatoes a Day (2010)

[186] “This was (for me) the instant cure to a life-long battle with binge eating disorder. […] I was eating to “satisfied” and finding satisfied well before “painfully gorged” which was something I had never experienced in my life. A switch had been flipped.

That scoreboard is getting recalibrated!” – M. Stone, Amazon Review of The Potato Hack by Tim Steel (2016)

[187] “In comparison with sucrose alone, ingestion of sucrose with whole berries resulted in reduced glucose and insulin concentrations during the first 30 min and a slower decline during the second hour and a significantly improved glycemic profile. Berries prevented the sucrose-induced late postprandial hypoglycemic response and the compensatory free fatty acid rebound. Nearly similar effects were observed when sucrose was consumed with berry nectars. The improved responses were evident despite the higher content of available carbohydrate in the berry and nectar meals, because of the natural sugars present in berries.” – Riitta Törrönen, Marjukka Kolehmainen, Essi Sarkkinen, Hannu Mykkänen, Leo Niskanen, Postprandial glucose, insulin, and free fatty acid responses to sucrose consumed with blackcurrants and lingonberries in healthy women (2012)

[188] “Weight loss was higher in the moderate natural fructose group (4.19 ± 0.30 kg) than the low-fructose group (2.83 ± 0.29 kg) (P = .0016).” – Magdalena Madero, Julio C Arriaga, Diana Jalal, Christopher Rivard, Kim McFann, Oscar Pérez-Méndez, Armando Vázquez, Arturo Ruiz, Miguel A Lanaspa, Carlos Roncal Jimenez, Richard J Johnson, Laura-Gabriela Sánchez Lozada, The effect of two energy-restricted diets, a low-fructose diet versus a moderate natural fructose diet, on weight loss and metabolic syndrome parameters: a randomized controlled trial (2011)

[189] Michael A Nauck, Juris J Meier, The incretin effect in healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions (2016)

[190] “Although a PIR [pre-absorptive insulin release] comprises a tiny portion of the overall insulin secreted, it is responsible for decreasing blood sugar during a meal by 50%. When the PIR is experimentally blocked in humans during feeding, dysregulation of blood sugar (dysglycemia) ensues and high levels of plasma insulin are attained. A blunted PIR is associated with obesity, exacerbating if not causing metabolic problems.” – Paul A. S. Breslin, An Evolutionary Perspective on Food and Human Taste (2013)

[191] “The proof of this is easily demonstrable. When an animal is prevented from secreting insulin cephalically (typically accomplished by the cutting of the neural link between the brain and the pancreas, the vagus nerve) and then the animal is given the same caloric load as that given to a control animal, the animal is glucose intolerant (Berthoud, Bereiter, Trimble, Siegel, & Jeanrenaud, 1981; Louis-Sylvestre, 1978b). This means that the
amount of glucose detectable in the blood after a test meal attains significantly higher levels when there is no cephalic insulin. Another way of saying this is that without cephalic insulin, animals secrete insufficient insulin during a meal to eliminate the ingested glucose from the blood in the normal time, and they therefore appear diabetic after meals (see Berthoud et al., 1981; Nicolaidis, 1977).” – Stephen C. Woods, The Eating Paradox: How We Tolerate Food (1991)

[192] “Comparable results in terms of abnormally elevated blood glucose levels occur if food is simply put into the stomach so that the mouth-to-brain-to-pancreas reflex is circumvented (Proietto, Rohner-Jeanrenaud, Ionescu, & Jeanrenaud, 1987; Steffens, 1976).” – Stephen C. Woods, The Eating Paradox: How We Tolerate Food (1991)

[193] “A key factor in anticipating incoming nutrients, particularly sugars, is the taste receptor responses. It is well established that humans show a PIR [pre-absorptive insulin release] to oral glucose, activated presumably via a carbohydrate taste receptor, such as T1R2/T1R3 25, 54, 55.” – Paul A. S. Breslin, An Evolutionary Perspective on Food and Human Taste (2013)

“The taste buds also serve as endocrine organs and secrete regulatory hormones in response to nutrient stimulation, including glucagon like peptide-1 (GLP-1) and glucagon, among other endocrine peptides [52]. The secretory responses of digestive hormones by peripheral tissues would signal to digestive organs, such as the pancreas, that nutrients are being ingested and prepare metabolic systems to respond, such as insulin secretion to control elevated blood glucose. These anticipatory processes are essential to optimal metabolism during and after feeding.” – Paul A. S. Breslin, An Evolutionary Perspective on Food and Human Taste (2013)

[194] Tino Just, Hans Wilhelm Pau, Ulrike Engel, Thomas Hummel, Cephalic phase insulin release in healthy humans after taste stimulation? (2008)

[195] “It is well established that animals, including people, begin secreting insulin as soon as they start eating, before any increase of ingested fuels into the blood. Such insulin is called cephalic insulin because its secretion is triggered more by food-related stimuli such as tastes or smells…” – Stephen C. Woods, The Eating Paradox: How We Tolerate Food (1991)

“After first demonstrating that animals can
be trained to secrete insulin (Woods, Alexander, & Porte, 1972; Woods, Hutton, & Makous, 1970), my colleagues and I found that arbitrary stimuli associated with food presentation can develop the ability to elicit insulin secretion (Woods, 1976; Woods et al., 1977). These stimuli included specific sounds, odors, and even the time of day (Woods et al., 1977). Anything that informed the animals that food was imminent seemed capable of acquiring this ability. – Stephen C. Woods, The Eating Paradox: How We Tolerate Food (1991)

[196] “…a two‐ to three‐fold higher insulin secretory response to oral as compared to intravenous glucose administration. In subjects with type 2 diabetes, this incretin effect is diminished or no longer present.” –  Michael A. Nauck, Juris J. Meier, Incretin hormones: Their role in health and disease (2018)

[197] “…the ones who used AS had a higher insulin resistance. The study also showed that the duration of use of artificial sweeteners had a direct impact on insulin resistance.” – Kushagra Mathur, Rajat Kumar Agrawal, Shailesh Nagpure, and Deepali Deshpande, Effect of artificial sweeteners on insulin resistance among type-2 diabetes mellitus patients (2020)

[198] “Recent results from both human epidemiological and experimental studies with animals suggest that intake of noncaloric sweeteners may promote, rather than protect against, weight gain and other disturbances of energy regulation. […] Using a rat model, the present research showed that intake of noncaloric sweeteners reduces the effectiveness of learned associations between sweet tastes and postingestive caloric outcomes…” – Terry L. Davidson, Ashley A. Martin, Kiely Clark, and Susan E. Swithers, Intake of high-intensity sweeteners alters the ability of sweet taste to signal caloric consequences (2010)

7.3 Disruption of Circadian Rhythm

[199] “When we reviewed eating patterns from the myCircadianClock app, we found that the traditional breakfast-lunch-dinner pattern is no longer observed, even among healthy non–shift-working adults. In fact, the number of eating occasions ranged from 4.2 times a day to 10.5 times a day.” – Satchin Panda, The Circadian Code (2018)

[200] Shubhroz Gill and Satchidananda Panda, A smartphone app reveals erratic diurnal eating patterns in humans that can be modulated for health benefits (2016)

[201] Roberto Salgado-Delgado, Manuel Angeles-Castellanos, Nadia Saderi, Ruud M. Buijs, Carolina Escobar, Food Intake during the Normal Activity Phase Prevents Obesity and Circadian Desynchrony in a Rat Model of Night Work (2010)

[202] Carlos López-Otín, Lorenzo Galluzzi, José M.P. Freije, Frank Madeo, Guido Kroemer, Metabolic Control of Longevity (2016)  

[203] Shubhroz Gill and Satchidananda Panda, A smartphone app reveals erratic diurnal eating patterns in humans that can be modulated for health benefits (2016)

[204] Satchin Panda, The Circadian Code (2018)

[205] “If the mice ate a healthy diet within 8 to 10 hours, they gradually increased their muscle mass, and after 36 weeks, they had 10 to 15 percent more muscle mass than mice that ate whenever they wanted.” – Satchin Panda, The Circadian Code (2018)

[206] “We also learned from this experiment that a daily eating– fasting cycle drives almost every rhythm in the liver. Instead of thinking that all timing information comes from the outside world through the eye’s blue light sensor, we learned that just like the first light of the morning resets our brain clock, the first bite of the morning resets all other organ clocks.” – Satchin Panda, The Circadian Code (2018)

[207] “The absorption of glucose, amino acids, and fat is strongly circadian. Nutrient absorption requires a lot of energy, which is why it can’t happen all the time. Gut cells that absorb these nutrients and other chemicals in food have different channels or doors that allow only certain types of molecules to go through, and the opening and closing of these doors is circadian.” – Satchin Panda, The Circadian Code (2018)

[208] Satchin Panda, The Circadian Code (2018)

[209] “Just like our plumbing gets weaker and leaks after a while, we have hundreds of miles of blood vessels that need to be checked for leakage and repaired. Similarly, our gut lining and skin needs daily repair to keep bacteria, chemicals, and toxins from entering our body. Inside every organ, many cells die and need to be replaced. Our blood cells also need replacement. This repair, through the production of new replacement cells, does not happen randomly; rather it occurs at a specific time of the day: at night, when we’re asleep.” – Satchin Panda, The Circadian Code (2018)

[210] John Nash Ott, The Effects of Natural and Artificial Light on Living Organisms ( 1975)

[211] Kylie A. Robert, John A. Lesku, Jesko Partecke, and Brian Chambers, Artificial light at night desynchronizes strictly seasonal reproduction in a wild mammal (2015)

[212] “[Yvonne] Foss believes that vitamin D is the cause of common obesity through a survival strategy developed by the organism during the evolutionary pathway to protect the organism from a cold climate. She theorises that vitamin D originated as a photoreceptor system in primitive organisms, which were responsible to inform and defend the body against lower climates. The body would respond to lower UV radiation with reduced skin production of vitamin D that would signal the increase of fat tissue accumulation, enhancing organism protection from the cold weather by reducing heat conduction and increasing its thermogenic capacity. A higher production of vitamin D3 by the skin, induced by increased presence of sunlight in summer, would inhibit this response and promote a reduction in fat deposits.” – Fernanda Reis de Azevedo and Bruno Caramelli, Hypovitaminosis D and Obesity – Coincidence or Consequence? (2013)

[213] Rosa M Ortega, Aránzazu Aparicio, Elena Rodríguez-Rodríguez, Laura M Bermejo, José M Perea, Ana M López-Sobaler, Baltasar Ruiz-Roso, Pedro Andrés, Preliminary data about the influence of vitamin D status on the loss of body fat in young overweight/obese women following two types of hypocaloric diet (2008)

[214] “Compared to reading a printed book, reading on an iPad suppressed melatonin release by over 50 percent at night. Indeed, iPad reading delayed the rise of melatonin by up to three hours, relative to the natural rise in these same individuals when reading a printed book.” – Matthew Walker, Why We Sleep (2017)

[215] “When it comes to information processing, think of the wake state principally as reception (experiencing and constantly learning the world around you), NREM sleep as reflection (storing and strengthening those raw ingredients of new facts and skills), and REM sleep as integration (interconnecting these raw ingredients with each other, with all past experiences, and, in doing so, building an ever more accurate model of how the world works, including innovative insights and problem-solving abilities).” – Matthew Walker, Why We Sleep (2017)

[216] “Worse, should you attempt to diet but don’t get enough sleep while doing so, it is futile, since most of the weight you lose will come from lean body mass, not fat.” – Matthew Walker, Why We Sleep (2017)

[217] “…short sleep was associated with lower fat loss during caloric restriction in overweight subjects.” – Omar Mesarwi, Jan Polak, Jonathan Jun, and Vsevolod Y. Polotsky, Sleep disorders and the development of insulin resistance and obesity (2014)

7.4 Disruption of the Microbiome

[218] “From the output, computers calculated the size of the microbiota community—the sum total of viruses, bacteria, fungi, protozoa, and other organisms that dwell within each of us. The final tally came to more than one hundred trillion organisms, dwarfing the population of human cells by a factor of 10. The amount of genetic material of microbial origin surpassed our own by 150 times.” – Kathleen McAuliffe, This is Your Brain on Parasites: How Tiny Creatures Manipulate Our Behavior and Shape Society (2017)

[219] “In the gut, resident microbes take a share of every meal you eat, but in return they aid in digestion, synthesizing vitamins and disarming dangerous bacteria that you ingest. They also churn out virtually every major neurotransmitter that tunes our emotions—notably, GABA, dopamine, serotonin, acetylcholine, and noradrenaline—as well as hormones with psychoactive properties.” – Kathleen McAuliffe, This is Your Brain on Parasites: How Tiny Creatures Manipulate Our Behavior and Shape Society (2017)

[220] “Regress evolutionary time still further and we have discovered that the very simplest forms of unicellular organisms that survive for periods exceeding twenty-four hours, such as bacteria, have active and passive phases that correspond to the light-dark cycle of our planet. It is a pattern that we now believe to be the precursor of our own circadian rhythm, and with it, wake and sleep.” – Matthew Walker, Why We Sleep (2017)

[221] “Plentiful sleep maintains a flourishing microbiome within your gut from which we know so much of our nutritional health begins.” – Matthew Walker, Why We Sleep (2017)

[222] Mahesh S. Desai, Anna M. Seekatz, Nicole M. Koropatkin, Thaddeus S. Stappenbeck, Gabriel Núñez, Eric C. Martens, A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility (2016)

[223] “The same species of bacteria may be a helper (a symbiont), a harmless freeloader (a commensal), or a hurter (a parasite), depending on circumstances that are constantly in flux.” – Kathleen McAuliffe, This is Your Brain on Parasites: How Tiny Creatures Manipulate Our Behavior and Shape Society (2017)

[224] “Additives found in many health foods have also been implicated in killing beneficial gut microbes and they can irritate and damage the intestinal wall directly.” – John Douillard, Eat Wheat: A Scientific and Clinically-Proven Approach to Safely Bringing Wheat and Dairy Back Into Your Diet (2017)

[225] Satchin Panda, The Circadian Code (2018)

[226] “Emulsifiers are used to improve a food’s texture and to prevent mixtures from separating, particularly in ice cream. Last year, Benoit Chassaing of Georgia State University showed that mice that drank water containing one of two emulsifiers underwent changes in gut bacteria and inflammation of the gut – changes that led to obesity and diabetes in these animals.” – Michael Le Page, Surge in obesity and diabetes could be linked to food additives (2016)

[227] Fred Provenza, Nourishment: What Animals Can Teach Us about Rediscovering Our Nutritional Wisdom (2018)

[228] “Intestinal bacteria regulate hormones your own body makes to stoke or suppress your appetite—for example, ghrelin, the molecule that goads you to get a second serving at the buffet, and leptin, which tells you to push your plate away. It’s also s In ecology, biome refers to the sets of plants and animals in a community such as a jungle, forest, or coral reef. An enormous diversity of species, large and small, interact to form complex webs of mutual support. When a keystone species (think wolves in Scotland) disappears or goes extinct the ecology suffers. It can even collapse.” – Martin J. Blaser, Missing Microbes: How the Overuse of Antibiotics Is Fueling Our Modern Plagues (2014)

[229] “Diet strongly affects human health, partly by modulating gut microbiome composition. We used diet inventories and 16S rDNA sequencing to characterize fecal samples from 98 individuals. Fecal communities clustered into enterotypes distinguished primarily by levels of Bacteroides and Prevotella. Enterotypes were strongly associated with long-term diets, particularly protein and animal fat (Bacteroides) versus carbohydrates (Prevotella). A controlled-feeding study of 10 subjects showed that microbiome composition changed detectably within 24 hours of initiating a high-fat/low-fiber or low-fat/high-fiber diet, but that enterotype identity remained stable during the 10-day study. Thus, alternative enterotype states are associated with long-term diet.” – Gary D Wu, Jun Chen, Christian Hoffmann, Kyle Bittinger, Ying-Yu Chen, Sue A Keilbaugh, Meenakshi Bewtra, Dan Knights, William A Walters, Rob Knight, Rohini Sinha, Erin Gilroy, Kernika Gupta, Robert Baldassano, Lisa Nessel, Hongzhe Li, Frederic D Bushman, James D Lewis, Linking long-term dietary patterns with gut microbial enterotypes (2011)

[230] “When the ill mice stopped consuming emulsifiers, their gut bacteria gradually returned to normal.” – Michael Le Page, Surge in obesity and diabetes could be linked to food additives (2016)

[231] “Gary Wu, a professor of gastroenterology at the University of Pennsylvania, has shown that diet over the long term—a year or more—correlated very strongly with the overall microbiome.” – Rob Knight and Brendan Buhler, Follow Your Gut (2015)

7.5 Degradation, Sickness, and Death

[232] Diabetes Research Institute Foundation, Diabetes Statistics (2022)

[233] Centers for Disease Control and Prevention, National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States (2023)

[234] Centers for Disease Control and Prevention, Leading Causes of Death, US (2024)

[235] Timothy A Welborn, Satvinder S Dhaliwal, Stanley A Bennett, Waist–hip ratio is the dominant risk factor predicting cardiovascular death in Australia (2003)

[236] Centers for Disease Control and Prevention, National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States (2020)

[237] National Institute of Diabetes and Digestive and Kidney Diseases, Overweight & Obesity Statistics, UK (2021)

8.1 Traditional Processing

[238]

Food Processing Externalizes Digestion Compared to other primates, humans have an unusual digestive system. Starting at the top, our mouths, gapes, lips, and teeth are oddly small, and our lip muscles are weak. Our mouths are the size of a squirrel monkey’s, a species that weighs less than three pounds.” – Joseph Henrich, The Secret of Our Success (2015)

“We also have puny jaw muscles that reach up only to just below our ears. Other primates’ jaw muscles stretch to the tops of their heads, where they sometimes even latch onto a bony central ridge. Our stomachs are small, having only a third of the surface area that we’d expect for a primate of our size, and our colons are too short, being only 60% of their expected mass. Our bodies are also poor at detoxifying wild foods. Overall, our guts—stomachs, small intestines, and colons—are much smaller than they ought to be for our overall body size.” – Joseph Henrich, The Secret of Our Success (2015)

8.2 Sugar, Honey, and Fruit

[239] U.S. Environmental Protection Agency, Sugarcane Processing

[240] Robert Lustig, Sugar: The Bitter Truth (2009)

[241] Thomas Jensen, Manal F. Abdelmalek, Shelby Sullivan, Kristen J. Nadeau, Melanie Green, Carlos Roncal, Takahiko Nakagawa, Masanari Kuwabara, Yuka Sato, Duk-Hee Kang, Dean R. Tolan, Laura G Sanchez-Lozada, Hugo R. Rosen, Miguel A. Lanaspa, Anna Mae Diehl, and Richard J Johnson, Fructose and Sugar: A Major Mediator of Nonalcoholic Fatty Liver Disease (2018)

[242] “Flavors and phytochemicals decline after harvest, more rapidly in some fruits and vegetables than others. For example, by the time broccoli is purchased at the store, typically ten days to two weeks since harvest, it loses more than 75 to 80 percent of health-promoting phytochemicals, 50 percent of its vitamin C, and most of its sugars and antioxidants. Loss of sugars, due to respiration after picking, reduces palatability.” – Fred Provenza, Nourishment: What Animals Can Teach Us about Rediscovering Our Nutritional Wisdom (2018)

[243] Julia Phillips, Why Fruit Has a Fake Wax Coating (2017)

[244] “It is a common practice to color the skins of oranges in certain orange growing areas of the country because of climatic or cultural conditions which cause the oranges to mature while still green in color.” –  US FDA, Compliance Policy Guide, Sec 550.625 Oranges – Artificial Coloring (1980)

[245] J. Johnson, F.M. Clydesdale, Perceived Sweetness and Redness in Colored Sucrose Solutions (1982)

[246] “Citrus juices are excellent sources of vitamin C and contribute other key nutrients such as potassium, folate, magnesium, and vitamin A. OJ [orange juice] intake has been associated with better diet quality in children and adults. OJ intake has not been associated with adverse effects on weight or other body measures in observational studies in children and adults.” – Gail C. Rampersaud, M. Filomena Valim, 100% citrus juice: Nutritional contribution, dietary benefits, and association with anthropometric measures (2016)

[247] Ahmad Adnan, Muhammad Mushtaq, Tanveer ul Islam, Fruit Juices: Extraction, Composition, Quality and Analysis, Chapter 12 – Fruit Juice Concentrates (2018)

[248] “Do you remember what canned orange juice tasted like? It was sweet and it had a pleasant acidity, and the color was about right, but it wasn’t “orangey”.” – Society of Flavor Chemists Inc. and the Chemical Sources Association Inc., A Short History of the Flavor Industry (2020)    

[249] “Daily consumption of dried fruits is recommended in order to gain full benefit of essential nutrients, health-promoting phytochemicals, and antioxidants that they contain, together with their desirable taste and aroma.” – Sui Kiat Chang, Cesarettin Alasalvar, and Fereidoon Shahidi, Review of dried fruits: Phytochemicals, antioxidant efficacies, and health benefits (2016)

[250] Gary Williamson and Arianna Carughi, Polyphenol content and health benefits of raisins (2010)

[252] Lara Pizzorno, Nothing Boring About Boron (2015)  

[252] “The Mbuti pygmies of the Congo obtain as much as 80 YO of their dietary energy from honey during the honey season (Crane, 1983), but this lasts for only 2 months of the year (Turnbull, 1963).” – K A Allsop, J B Miller, Honey revisited: a reappraisal of honey in pre-industrial diets (1996)

[253] “…every drop of honey is packed with up to two hundred beneficial bionutrients such as vitamins, minerals, amino acids, bioflavonoid (plant molecules that are anti-diabetic), disease-fighting antioxidants, organic acids, monosaccharides and obligosaccharides (sugars) and numerous enzymes.” – Mike McInnes, The Honey Diet (2014)

[254] “In North America, maple sap, which is boiled down to syrup, has long been enjoyed as a spring tonic, believed to increase health and vitality.” – Joey Lott, In Defense of Sugar: The Sweet Truth about the Diet Industry’s Latest Evil (2015)

[255] “…a number of studies performed by a University of Rhode Island team have shown that maple syrup contains many novel compounds that are antibacterial and that help to modulate the immune system.” – Joey Lott, In Defense of Sugar: The Sweet Truth about the Diet Industry’s Latest Evil (2015)

[256] “In addition, total phenol content and phenolic acid composition were also determined. Results indicated a total phenolic content of 26.5, 31.5, 372 and 3837 μg GAE/g for refined, white, brown and jaggery, respectively. The HPLC analysis revealed the presence of different phenolic acids in brown sugar and jaggery.” –  M.A. Harish Nayaka, U.V. Sathisha, M.P. Manohar, K.B. Chandrashekar, Shylaja M. Dharmesh, Cytoprotective and antioxidant activity studies of jaggery sugar (2009)

[257] “Ancient medical scriptures, Sushruta Sanhita (Chapter 45, sloka 146), dating back to 2500 years states how Jaggery is useful in purification of blood, prevents rheumatic afflictions and disorders of bile and possess nutritive properties of high order. It supplements the requirement of iron and calcium in women and children, prevents anemia and increases vitality in men and help in digestion. Magnesium in jaggery strengthens the nervous system and potassium conserve the acid balance in the cells and combats acids and acetones. The preventive action of jaggery on smoke-induced lung lesions (Sahu and Saxena 1994) and the presence of micronutrients in jaggery have antitoxic and an anticarcinogenic property suggests the potential of jaggery as protective agent for workers in industry in smoky environments (Nrashant Singh et al., 2008). In addition, it has potential antioxidant activity owing to the presence of polyphenolic compounds in cane juice (Harish et al., 2009).” – M. Esther Magdalene Sharon, Cv Kavitha Abirami, K Alagusundaram, Energy Losses in Traditional Jaggery Processing (2013)

[258] Lucía Seguí, Laura Calabuig‐Jiménez, Noelia Betoret, and Pedro Fito, Physicochemical and antioxidant properties of non‐refined sugarcane alternatives to white sugar (2015)

[259] “Several recent meta-analyses have attempted to put human fructose-alone experimentation into a dose-dependent perspective. In a series of papers from the research group of Sievenpiper and Jenkins, isocaloric comparisons of fructose with other carbohydrates (sucrose, HFCS, lactose, starch) were found not to affect weight gain (33) or blood pressure (38), did not increase uric acid in nondiabetic and diabetic subjects (39), and improved glycemic control (40). Some differences were observed with hypercaloric feeding trials, but that was likely due to confounding from extra calories rather than fructose.” – John S. White, Challenging the Fructose Hypothesis: New Perspectives on Fructose Consumption and Metabolism (2013)

8.3 Grains, Nuts, Seeds, and Legumes

[261] “…it appears that people who lived in what is now Mozambique may have eaten a diet based on sorghum as far back as 105,000 years ago, Neanderthals apparently consumed grains 44,000 years ago, and there is evidence to suggest that grains were consumed in Europe over 30,000 years ago.” – Rosane Oliveira, Busting the (Whole) Grain Myth (2016)

[262] “Arguments that the currently consumed wheat has been genetically modified resulting in adverse effects on body weight and illnesses cannot be substantiated. In particular, populations in some countries have obtained the major part of their daily energy intake from wheat-based foods for many years, such as Turkey, without reporting any detrimental effects on body weight or chronic disease. In line with this is the evidence that grains and grasses have already been consumed and processed throughout Europe during the Mid-Upper Palaeolithic era.” – Fred Brouns, Vincent van Buul, and Peter Shewry, Does wheat make us fat and sick? (2013)

[263] Francisco Bernardino Castillo Rodriguez, Gerardo Alberto Sanchez Olivares, GRUPO ALTEX SA de CV patent, Process for the production of refined whole wheat flour with low coloration (2014)

[264] Francisco Bernardino Castillo Rodriguez, Gerardo Alberto Sanchez Olivares, GRUPO ALTEX SA de CV patent, Process for the production of refined whole wheat flour with low coloration (2014)

[265] Fred Brouns, Vincent van Buul, and Peter Shewry, Does wheat make us fat and sick? (2013)

[266] – Find reference

[267] “The flour diets were compared to a control purified diet. Four groups of 10 male Wistar rats each were fed one of the experimental diets for 6 wk and mineral status and tissue retention as well as bone characteristics were determined. As expected, mineral intake, except for calcium, was significantly lesser in rats fed the white flour diet than in the other groups. The rats fed the white flour diet had the lowest food intake, weight gain, fecal excretion and intestinal fermentation. The most important result was that Mg and Fe status were drastically lower in rats fed the white flour diet than in those fed whole flour or control diets.” – Charles Coudray, Marie A. Levrat-Verny, Jean C. Tressol, Christine Feillet-Coudray, Noëlle M. Horcajada-Molteni, Christian Demigné, Yves Rayssiguier, Christian Rémésy, Mineral supplementation of white wheat flour is necessary to maintain adequate mineral status and bone characteristics in rats (2001)

[268] “With three thousand inmates in the institution the annual death-rate from beriberi prior to the use of unpolished rice was 201 per 1,000; this fell to nil in 21 months when unpolished rice was used, and when polished rice was resumed it again rose to 157 per 1, 000, to disappear a second time when the unpolished rice was supplied.” – [access restricted since this quote was first sourced, so unable to identify authors or full title], Beriberi. An Additional Experience at… (1915)

[269]

“The quarantine officer estimates that in 1922 about one-fifth of the men developed the disease. The diet consisted essentially of, white flour, polished rice, and tinned foods. The officer at Port Darwin reported only six severe cases in sixteen months, all Europeans from the interior who had been living exclusively on white flour and corned beef; about six months of this diet is sufficient to produce beriberi.” – [access restricted since this quote was first sourced, so unable to identify authors or full title], Advantages of Nation-Wide and International… (1925) (Potential source here)

[271]

“For centuries, dark bread was considered a sign of poverty, food only for the peasantry; in oriental countries, unpolished rice is consumed only by the poorest of the natives; whole grain cereals, containing the entire kernel including the seed germ, have been considered food fit only for animals, not for civilized man. Yet the peasants maintain a degree of health unknown to their wealthier lords living upon refined foods; the poor oriental, who must of necessity mill his rice by hand, never suffers from beri-beri, an affliction of those who live upon the polished rice from commercial mills; and the animal fed a whole grain ration attains a rapid growth and healthy vigor unexperienced by others fed a more artificial diet.” – C. Ulysses Moore and Jessie Laird Brodie, The Comparative Nutritional Value of White and Whole Wheat Flour (1925)

[272] Mary Spencer, The behaviour of rats and mice feeding on whole grains (1953)

[273] “While there are numerous studies labelling WGA and other lectins as toxic, inflammatory, neurotoxins, cancer-causing and a reason to avoid all grains, some studies are beginning to change our understanding. For example, one study demonstrated that the WGA has beneficial effects on the gastrointestinal tract and have anti-tumor properties.” – John Douillard, Eat Wheat: A Scientific and Clinically-Proven Approach to Safely Bringing Wheat and Dairy Back Into Your Diet (2017)

[274] Ibrahim Abdulwaliyu, Shefiat Olayemi Arekemase, Judy Atabat Adudu, Musa Latayo Batari, Mercy Nwakamaswor Egbule, Stanley Irobekhian Reuben Okoduwa, Investigation of the medicinal significance of phytic acid as an indispensable anti-nutrient in diseases (2019)

[275] “The chief foods of the Tarahumara are corn and beans, other vegetables and fruits, and small quantities of game, fish, and eggs. If sufficient calories are provided, their diet, which has been the traditional fare of Mesoamerica for several thousand years, is nutritionally adequate.” – Martha P. McMurry, Maria Teresa Cerqueira, Sonja L. Connor, and William E. Connor, Changes in Lipid and Lipoprotein Levels and Body Weight in Tarahumara Indians after Consumption of an Affluent Diet (1991)

[276] “Phytates are considered an anti-nutrient because they bind to minerals (e.g. zinc, calcium, and magnesium) and prevent their absorption. However, when analyzed carefully, the ‘anti-nutrient’ effect of phytates seems only to appear when a large quantity of phytates are consumed in conjunction with a nutrient-poor diet.  Also, cooking, boiling, fermenting, soaking or germinating whole grains will inactivate phytic acid and free minerals up for absorption by the body.” – Rosane Oliveira, Busting the (Whole) Grain Myth (2016)

[277] “Eating organic, slow fermented sourdough bread with no preservatives or oils is a great option over other breads. The fermented culture of lactic acid and probiotic strains used to make sourdough actually help to break down gluten and, according to some studies, even render the bread gluten-free.” – John Douillard, Eat Wheat: A Scientific and Clinically-Proven Approach to Safely Bringing Wheat and Dairy Back Into Your Diet (2017)

[278] “It should be noted that typical white flour is usually “treated” using a combination of chlorine, benzoyl peroxide and/or azodicarbonamide. These oxidants exert their action by oxidizing the carotenoid pigments that give the yellow color to flour.” – Adelmo Monsalve-Gonzalez, Aruna Prakash, General Mills Inc patent, Bran and bran containing products of improved flavor and methods of preparation (2001)

[279] Francisco Bernardino Castillo Rodriguez, Gerardo Alberto Sanchez Olivares, GRUPO ALTEX SA de CV patent, Process for the production of refined whole wheat flour with low coloration (2014)

[280] “Through a particular treatment process, the present invention is able to lighten the darker color of whole wheat flour, and all but eliminate the bitter flavors. As a result, the present invention provides whole wheat flours that can be used to provide finished whole wheat products that look and taste as good as those made with regular white flour.” – Lloyd E. Metzger, General Mills Inc patent,  Method of bleaching cereal grains (2002)  

[281] Adelmo Monsalve-Gonzalez, Aruna Prakash, General Mills Inc patent, Bran and bran containing products of improved flavor and methods of preparation (2001)

[282] US Department of Agriculture, Wheat flour, white, all-purpose, enriched, bleached (2018)

[283] “To compensate for the loss of nutrients, government regulations dictate the addition of vitamins and minerals into these flours and label the modified flour as refined flour. These additives are primarily niacin, reduced iron, thiamine mononitrate, riboflavin and folic acids. As practiced with whole wheat flour, ascorbic acid, amylase and azodicarbonamide are also added.” – Lilei Yu, Anne-Laure Nanguet, and Trust Beta, Comparison of Antioxidant Properties of Refined and Whole Wheat Flour and Bread (2013)

[284] Lisa Petrison, A Foodie’s Guide to Avoiding Glyphosate (And Other Bad Stuff) – Grain Overview (2020)

[285] NZ Ministries for Primary Industries, The 2015/2016 Report on Pesticides in Fresh and Frozen Produce (2017)

[286] Consumer NZ, How did a banned herbicide end up in organic grain? (2019)

[287] Surabhi Awasthi, Reshu Chauhan, Sudhakar Srivastava, Rudra D. Tripathi, The Journey of Arsenic from Soil to Grain in Rice (2017)

8.4 Vegetables and Tubers

[288] Fred Provenza, Nourishment: What Animals Can Teach Us about Rediscovering Our Nutritional Wisdom (2018)

[289] D.E. Yen, The Adaptation of Kumara by the New Zealand Maori (1961)  

[290] “The potato became the major contributor to the European population explosion of 1750–1850 which in turn resulted in increased urbanization and contributed to the underpinning of the Industrial Revolution in England in the nineteenth century. By feeding rapidly growing populations the potato permitted a small number of nations in northern Europe to assert dominion over much of the world between 1750 and 1950. The failure of the potato crop in Ireland in the 1840s led Britain to repeal the protectionist Corn Laws and set the country on a path of free trade.” –  H. De Jong, Impact of the Potato on Society (2016)

[291] Stanisław Kazimierz Kon and Aniela Klein, The value of whole potato in human nutrition (1928)

[292] “Populations who have long been dependent on eating high-starch diets have between 6.5 and 7 copies, on average. The Hadza, African hunter-gatherers who live in savannah woodlands and rely on starchy roots and tubers, have the most, at almost 7 copies, on average, and some Hadza have as many as 15 copies. European-Americans and Japanese are not far behind, at 6.8 and 6.6 copies. By contrast, populations long dependent on low-starch diets have copy counts around 5.5.” – Joseph Henrich, The Secret of Our Success (2015)

[293] Mnason Tweheyo, Kåre A. Lye, Robert B. Weladji, Chimpanzee diet and habitat selection in the Budongo Forest Reserve, Uganda (2004)

[294] “Potato protein content is fairly low but has an excellent biological value of 90–100. Potatoes are particularly high in vitamin C and are a good source of several B vitamins and potassium. The skins provide substantial dietary fiber. Many compounds in potatoes contribute to antioxidant activity and interest in cultivars with pigmented flesh is growing.” – Mary Ellen Camire, Stan Kubow, Danielle J. Donnelly, Potatoes and Human Health (2009)

[295] “Prior efforts to increase the crispiness of snack food products made from dehydrated potato products have included the addition of fibrous cellulosic material to the snack food dough, as described in U.S. Patent No. 4,876,102 issued October 24, 1989 to Feeney et al. U.S. Patent No. 4,219,575, issued August 26, 1980 to Saunders et al, teaches the addition of modified food starch to potato-based dough in order to increase the crispiness of French fries made therefrom.” – Maria Dolores Martinez-Serna Villagran, Jianjun Li, David K. Yang, Joel F. Evans, David S. Chang, Procter and Gamble Co patent, Potato chips based on potato flakes (2001)

[296] “These snack products are largely characterized by a bland potato flavor profile and possibly off-flavors because of the large extent of processing to which the potato material is subjected. For the most part, these snack products are made from dehydrated potatoes which have already been subjected to losses of flavor attributable to leaching, plus changes in flavor due to intensive mixing and dehydration; and they are often subjected further to intensive moist heat treatment and, in most cases, to exposure to a second heat treatment by frying or high temperature extrusion.” – Miles Willard, Patent, Potato flavor enhancing composition and method of use (1987)

[297] “The formed products have less fried potato flavor because the fried outside areas have had much of the soluble flavor precursors extracted, and the internal portions comprise only the relatively flavorless particles that are bound together in a watery mass.” – Miles Willard, Patent, Potato flavor enhancing composition and method of use (1987)

[298] “A process for producing a potato-chip flavor concentrate which comprises the steps of heating a potato material until a browned product is formed; extracting the browned potato material with a solvent; contacting the extract with a cation-exchange resin, thereby to adsorb flavoring compounds onto the resin; and eluting the adsorbed flavoring compounds from the resin by means of a suitable solvent. Preferred process conditions involve heating comminuted potato material, slurrying the browned potato material in a water-and-alcohol extraction solvent, contacting the resulting extract with a cation-exchange resin and eluting the adsorbed flavoring material by addition of a strong base or acid.” – M Sevenants, Procter and Gamble Co patent, Processing for producing potato chip flavor concentrate (1974)

9.2 The First Diet

[400] “If a Stone Age girl wasn’t the prettiest in her small tribe, the difference wasn’t likely to be dramatic. Everyone had opportunities to see others looking their worst—tired, bedraggled, sick—as well as on their best days. Now society culls from millions of young women to select the best faces and bodies, and then perfects these with Adobe Photoshop. The difference between the resulting magazine cover and our average modern girl is staggering.” – Deirdre Barrett, Supernormal Stimuli: How Primal Urges Overran Their Evolutionary Purpose (2010)

[401] Radoslav Detchev, Actors Give Advice on Diet & Exercise (2017)

[402] “In normal living there is an ebb and flow among drives and impulses, first one dominating, then another. In starvation this pleasant balancing process is upset, and the hunger drive gradually dominates more and more of the person’s activities and thoughts.” – Ancel Keys, Men and Hunger (1946)

[403] “Over eons, the organisms left standing are those with exquisitely tuned strategies for acquiring and spending their calories.” – Herman Pontzer, Burn: The Misunderstood Science of Metabolism (2021)

9.3 Extreme Hunger and Anorexia

[404] Leah M. Kalm, Richard D. Semba, They Starved So That Others Be Better Fed: Remembering Ancel Keys and the Minnesota Experiment (2005)

[405] Vicente Javier Clemente-Suárez, Maria Isabel Ramírez-Goerke, Laura Redondo-Flórez, Ana Isabel Beltrán-Velasco, Alexandra Martín-Rodríguez, Domingo Jesús Ramos-Campo, Eduardo Navarro-Jiménez, Rodrigo Yáñez-Sepúlveda, José Francisco Tornero-Aguilera, The Impact of Anorexia Nervosa and the Basis for Non-Pharmacological Interventions (2023)

[406] Carolina Lopez, Daniel Stahl, Kate Tchanturia, Estimated intelligence quotient in anorexia nervosa: a systematic review and meta-analysis of the literature (2010)

[407] Simona Giordano, Anorexia Nervosa: A Case for Exceptionalism in Ethical Decision Making (2019)

[408] Simona Giordano, Secret Hunger: The Case of Anorexia Nervosa (2020)

[409] Simona Giordano, Secret Hunger: The Case of Anorexia Nervosa (2020)

[410] Helene Tran, Pierre Poinsot, Sebastien Guillaume, Dominique Delaunay, Marion Bernetiere, Catherine Bégin, Pierre Fourneret, Noel Peretti, Sylvain Iceta, Food Addiction as a Proxy for Anorexia Nervosa Severity: New Data Based on the Yale Food Addiction Scale 2.0 (2020)

[411] “Although it appears that anorectics do not experience hunger because they eat so little, most do get hungry and at times their hunger is so extreme that it frightens them.” – Jean Antonello, Breaking Out of Food Jail (1996)

[412] Lea Muldtofte, The Grace of my Perfect Skeleton: an Autoethnographic Analysis of the Anorexic Body (2018)

[413] Vicente Javier Clemente-Suárez, Maria Isabel Ramírez-Goerke, Laura Redondo-Flórez, Ana Isabel Beltrán-Velasco, Alexandra Martín-Rodríguez, Domingo Jesús Ramos-Campo, Eduardo Navarro-Jiménez, Rodrigo Yáñez-Sepúlveda, José Francisco Tornero-Aguilera, The Impact of Anorexia Nervosa and the Basis for Non-Pharmacological Interventions (2023)

9.4 Binge Eating, Bulimia, and Yo-yo Dieting

[414] Darcy K Groesbeck, Renee M Bluml, Eric H Kossoff, Long-term use of the ketogenic diet in the treatment of epilepsy (2006)

[415] “A 15-month longitudinal prospective study used dual energy X-ray absorptiometry (DEXA) every 3 months to measure bone mineral content (BMC) in children on the KD [ketogenic diet]. Whole body and spine BMC for-age and height declined…” – A.G. Christina Bergqvist, Long-term monitoring of the ketogenic diet: Do’s and Don’ts (2012)

[416] “As in humans, animals are assumed to have a limited capacity for noticing or attending things in their environments (indeed, presumably a smaller capacity than we do). Thus, only what the animal pays attention to may be coded as a hypothesis. As a simplifying assumption, most theorists start with a model in which animals attend only a single dimension or feature.” – Claude G. Čech, Chapter 7: Attention & Categorization (1998)

[417] “Complications such as heart arrhythmias, cardiac contractile function impairment, sudden death, osteoporosis, kidney damage, increased cancer risk, impairment of physical activity and lipid abnormalities can all be linked to long-term restriction of carbohydrates in the diet.” – Shane A. Bilsborough and Timothy C Crowe, Low Carbohydrate Diets: what are the potential short- and long-term health implications? (2003)

[418] Thomas DeLauer, 5 Things Paul Saladino Changed His Mind on After Quitting Carnivore (2023)

[419] Claude G. Čech, Chapter 7: Attention & Categorization (1998)

9.6 Compulsive’ Eating / Obesity

[420] “…binge eating does occur in children, particularly among those who are overweight. In one sample of 112 overweight children, over 5% met the criteria for binge eating disorder.” – Christopher Fairburn, Overcoming Binge Eating, Second Edition (2013)

9.7 The Dark Before the Dawn

[420b] William Miller and Janet C’de Baca, Quantum Change: When Epiphanies and Sudden Insights Transform Ordinary Lives (2001)

10.0 Errors of Perception

[421] “These beliefs always look very convincing: they have to be in order to fool you. You would not think, for example, that smoking enables you to leap tall buildings in a single bound. That’s too absurd.” – Gillian Riley, How to Stop Smoking and Stay Stopped For Good (2007)

[422] “Averaging across several studies, there seems to be no net advantage to having privileged information about ourselves: the amount of accuracy obtained by people about the causes of their responses is nearly identical with the amount of accuracy obtained by strangers.” – Timothy D. Wilson, Strangers to Ourselves: Discovering the Adaptive Unconscious (2004)

[433] Kevin Simler and Robin Hanson(describing studies on split brain patients by Roger Sperry and Michael Gazzaniga), The Elephant in the Brain: Hidden Motives in Everyday Life (2020)

10.1 Fat Genes

[434] “The results of a large-scale adoption study in Denmark and of twin studies in the United States and Sweden are noteworthy in this regard (Stunkard 1991). The former study found a high correlation between the body weight of adoptees and those of their biological parents, coupled with little or no correlation between the weights of adoptees and those of their adoptive parents. The twin studies revealed quite high indices of heritability (0.75–0.80) for obesity in monozygotic pairs, even when the twins were raised apart under disparate conditions.” – Richard E. Keesey, Matt D. Hirvonen, Body Weight Set-Points: Determination and Adjustment (1997)

[435] “A gene for growth during pregnancy – once for making insulin-like growth factor 2 or IGF2 – was more active (less methylated) in people conceived during the worst days of starvation. The children and grandchildren were also more susceptible to obesity, diabetes, cardiovascular disease, microalbuminuria (increase in urine alcumin), and other health problems.” – Fred Provenza, Nourishment: What Animals Can Teach Us about Rediscovering Our Nutritional Wisdom (2018)

[436] “Dr. David Ludwig recently examined the relationship between the weights of 513,501 women and their 1,164,750 offspring. Increased maternal weight gain is strongly associated with increased neonatal weight gain. Because both the mother and the fetus share the same blood supply, any hormonal imbalances, such as high insulin levels, are automatically and directly transmitted through the placenta from the mother to the growing fetus. – Jason Fung, The Obesity Code (2016)

[437] Fred Provenza, Nourishment: What Animals Can Teach Us about Rediscovering Our Nutritional Wisdom (2018)

[438] “The thrifty-gene hypothesis assumes chronic food shortages prevented obesity. However, many traditional societies had plentiful food year round. For example, the Tokelau, a remote tribe in the South Pacific, lived on coconut, breadfruit and fish, which were available year round. Regardless, obesity was unknown among them until the onset of industrialization and the Westernization of their traditional diet.” – Jason Fung, The Obesity Code (2016)

[439] Richard E. Keesey, Matt D. Hirvonen, Body Weight Set-Points: Determination and Adjustment (1997)

[440] Ruth B. S. Harris, Role of set-point theory in regulation of body weight (1990)

[441] “Leptin is known to play a key role in appetite and thus weight regulation, and may be important in regulating the set point and regulating body weight towards the set point.” – Ruth B. S. Harris, Role of set-point theory in regulation of body weight (1990)

[442] “While set point theory has been supported in animals and humans, it may not apply to humans eating a western diet, which may be obesogenic to an extent that it overcomes the homeostatic process set forth in set point theory.” – Ruth Harris, Role of set-point theory in regulation of body weight (1990)   

[443] “By being the most efficient forager it can be, it effectively minimizes the time that it spends in the prey cycle, leaving it free for other activities.” – Paul Glimcher, Decisions, Uncertainty, and the Brain: The Science of Neuroeconomics (2004)

[444] “Since 2005, the genome-wide association study (GWAS) has made it possible to identify 119 independent loci associated with BMI and common obesity status in large populations.” – Hélène Huvenne, Béatrice Dubern, Karine Clément, Christine Poitou, Rare Genetic Forms of Obesity: Clinical Approach and Current Treatments in 2016 (2016)

[445] John R. Speakman, David A. Levitsky, David B. Allison, Molly S. Bray, John M. de Castro, Deborah J. Clegg, John C. Clapham, Abdul G. Dulloo, Laurence Gruer, Sally Haw, Johannes Hebebrand, Marion M. Hetherington, Susanne Higgs, Susan A. Jebb, Ruth J. F. Loos, Simon Luckman, Amy Luke, Vidya Mohammed-Ali, Stephen O’Rahilly, Mark Pereira, Louis Perusse, Tom N. Robinson, Barbara Rolls, Michael E. Symonds, and Margriet S. Westerterp-Plantenga, Set points, settling points and some alternative models: theoretical options to understand how genes and environments combine to regulate body adiposity (2011)

[446] “The identified variants mostly have small to very small effect sizes; only 1-2% of the BMI variance is explained. Currently, a consensus explanation for this ‘missing heritability’ in complex diseases has not yet emerged.” – Johannes Hebebrand, Anna-Lena Volckmar, Nadja Knoll, Anke Hinney, Chipping Away the ‘Missing Heritability’: GIANT Steps Forward in the Molecular Elucidation of Obesity – but Still Lots to Go (2010)

[447] Hélène Huvenne, Béatrice Dubern, Karine Clément, Christine Poitou, Rare Genetic Forms of Obesity: Clinical Approach and Current Treatments in 2016 (2016)

[448] “Despite the tremendous increase in our knowledge of the many genetic variants that differentiate the obese from the non-obese, we still do not understand how these genotypes translate into phenotypes in terms of eating behaviour or energy expenditure.” – John R. Speakman, David A. Levitsky, David B. Allison, Molly S. Bray, John M. de Castro, Deborah J. Clegg, John C. Clapham, Abdul G. Dulloo, Laurence Gruer, Sally Haw, Johannes Hebebrand, Marion M. Hetherington, Susanne Higgs, Susan A. Jebb, Ruth J. F. Loos, Simon Luckman, Amy Luke, Vidya Mohammed-Ali, Stephen O’Rahilly, Mark Pereira, Louis Perusse, Tom N. Robinson, Barbara Rolls, Michael E. Symonds, and Margriet S. Westerterp-Plantenga, Set points, settling points and some alternative models: theoretical options to understand how genes and environments combine to regulate body adiposity (2011) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3209643/

[449] Veronique Beauloye, Gwenaelle Diene, Renske Kuppens, Francis Zech, Coralie Winandy, Catherine Molinas, Sandy Faye, Isabelle Kieffer, Dominique Beckers, Ricard Nergårdh, Berthold Hauffa, Christine Derycke, Patrick Delhanty, Anita Hokken-Koelega & Maithé Tauber, High unacylated ghrelin levels support the concept of anorexia in infants with prader-willi syndrome (2016)

[450] Johannes Hebebrand, Anna-Lena Volckmar, Nadja Knoll, Anke Hinney, Chipping Away the ‘Missing Heritability’: GIANT Steps Forward in the Molecular Elucidation of Obesity – but Still Lots to Go (2010)

[451] Johannes Hebebrand, Anna-Lena Volckmar, Nadja Knoll, Anke Hinney, Chipping Away the ‘Missing Heritability’: GIANT Steps Forward in the Molecular Elucidation of Obesity – but Still Lots to Go (2010)

[452] Johannes Hebebrand, Anna-Lena Volckmar, Nadja Knoll, Anke Hinney, Chipping Away the ‘Missing Heritability’: GIANT Steps Forward in the Molecular Elucidation of Obesity – but Still Lots to Go (2010)

[453] D. Haslam, Weight management in obesity – past and present (2016) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4832440/[453]

[454] Martin Wainwright, Bones reveal chubby monks aplenty (2004)

[455] Martin Davies, The role of GABAA receptors in mediating the effects of alcohol in the central nervous system (2003)

[456] “The results of a large-scale adoption study in Denmark and of twin studies in the United States and Sweden are noteworthy in this regard (Stunkard 1991). The former study found a high correlation between the body weight of adoptees and those of their biological parents, coupled with little or no correlation between the weights of adoptees and those of their adoptive parents. The twin studies revealed quite high indices of heritability (0.75–0.80) for obesity in monozygotic pairs, even when the twins were raised apart under disparate conditions.” – Richard E. Keesey, Matt D. Hirvonen, Body Weight Set-Points: Determination and Adjustment (1997)

10.2 Slim Junk Food Eaters

[457] “The category of teenagers who play computer games four times a week or more (25.3% of the sample) is at increased risk of meal skipping; those who play more than four times a week are 10 times more likely weekly to skip a meal.” – J. Van den Bulck, S. Eggermont, Media use as a reason for meal skipping and fast eating in secondary school children (2006)

[458] Harvard Health Publishing, Howard E. LeWine, Taking aim at belly fat (2024)

[459] Michael Orthofer, Armand Valsesia, Reedik Mägi, Qiao-Ping Wang, Joanna Kaczanowska, Ivona Kozieradzki, Alexandra Leopoldi, Domagoj Cikes, Lydia M. Zopf, Evgenii O. Tretiakov, Egon Demetz, Richard Hilbe, Anna Boehm, Melita Ticevic, Margit Nõukas, Alexander Jais, Katrin Spirk, Teleri Clark, Sabine Amann, Maarja Lepamets, Christoph Neumayr, Cosmas Arnold, Zhengchao Dou, Volker Kuhn, Maria Novatchkova, Shane J.F. Cronin, Uwe J.F. Tietge, Simone Müller, J. Andrew Pospisilik, Vanja Nagy, Chi-Chung Hui, Jelena Lazovic, Harald Esterbauer, Astrid Hagelkruys, Ivan Tancevski, Florian W. Kiefer, Tibor Harkany, Wulf Haubensak, G. Gregory Neely, Andres Metspalu, Jorg Hager, Nele Gheldof, Josef M. Penninger, Identification of ALK in Thinness (2020)

[460] NIH National Library of Medicine, Congenital generalized lipodystrophy

[461] All3Media, Raising Kids on Junk Food, Fast Food Baby (2020)

[462] “Far from being an insurmountable obstacle to the analysis of an organic system, a pathological disorder is often key to understanding it. We know of many cases in the history of physiology where a scientist became aware of an important organic system only after a pathological disturbance had caused it’s disease.” – Konrad Lorenz, Civilized Man’s Eight Deadly Sins (1974)

10.3 Sluggish Metabolism

[463] J.L Hornick, C Van Eenaeme, O Gérard, I Dufrasne, L Istasse, Mechanisms of reduced and compensatory growth (2000)

[464] “Catch-up growth has been observed for many years (Reed 1921) in plants, in-vertebrates, and vertebrates, both in the laboratory and in the wild (Albon et al. 1987) and both in juveniles and in adults.” – Marc Mangel, Stephan Munch, A Life‐History Perspective on Short‐ and Long‐Term Consequences of Compensatory Growth (2006)

[465] “Despite a significant amount of weight regain 6 years later, the mean RMR was 1,903 ± 466 kcal/day, which was not significantly different from the end of the competition…” – Erin Fothergill, Juen Guo, Lilian Howard, Jennifer C. Kerns, Nicolas D. Knuth, Robert Brychta, Kong Y. Chen, Monica C. Skarulis, Mary Walter, Peter J. Walter, Kevin D. Hall, Persistent metabolic adaptation 6 years after “The Biggest Loser” competition (2016)

[466] R L Weinsier 1, T R Nagy, G R Hunter, B E Darnell, D D Hensrud, H L Weiss, Do adaptive changes in metabolic rate favor weight regain in weight-reduced individuals? An examination of the set-point theory (2000)

[467] “Frequent dieters (yo-yo) and women without a dietary history (non-yo-yo) were matched into the following groups: diet-exercise yo-yo (DE-Y), diet-exercise non-yo-yo (DE-NY), and diet-non-yo-yo group (D-NY). After 14 wk significant differences in weight loss and fat loss were revealed between D and DE groups but not between yo-yo and non-yo-yo dieters.” – D van Dale, W H Saris, Repetitive weight loss and weight regain: effects on weight reduction, resting metabolic rate, and lipolytic activity before and after exercise and/or diet treatment (1989)

[468] A Bosy-Westphal, B Schautz, M Lagerpusch, M Pourhassan, W Braun, K Goele, M Heller, C-C Glüer, M J Müller, Effect of weight loss and regain on adipose tissue distribution, composition of lean mass and resting energy expenditure in young overweight and obese adults (2013)

10.4 Large Serving Sizes

[469] “Portion sizes began to grow in the 1970s, rose sharply in the 1980s, and have continued in parallel with increasing body weights.” – Lisa R. Young, Marion Nestle, The Contribution of Expanding Portion Sizes to the US Obesity Epidemic (2002)

[470] “Restaurants are using larger dinner plates, bakers are selling larger muffin tins, pizzerias are using larger pans, and fast-food companies are using larger drink and french fry containers.” – Lisa R. Young, Marion Nestle, The Contribution of Expanding Portion Sizes to the US Obesity Epidemic (2002)

[471] Buzzfeed Multiplayer, McDonald’s: 1955 Vs. Now (2015)

[472] Brian Wansink, James E Painter, Jill North, Bottomless bowls: why visual cues of portion size may influence intake (2005)

[473] Stephanie M. Lee, Here’s How Cornell Scientist Brian Wansink Turned Shoddy Data Into Viral Studies About How We Eat (2018)

[474] Ellie Kincaid, Cornell food marketing researcher who retired after misconduct finding is publishing again (2022)

[475] C. Peter Herman, Janet Polivy, Lenny R. Vartanian, and Patricia Pliner, Are large portions responsible for the obesity epidemic? (2016)

[476] Eleni Mantzari, Gareth J Hollands, Rachel Pechey, Susan Jebb, Theresa M Marteau, Perceived impact of smaller compared with larger-sized bottles of sugar-sweetened beverages on consumption: A qualitative analysis (2018)

[477] M. M. Hetherington, P. Blundell‐Birtill, The portion size effect and overconsumption – towards downsizing solutions for children and adolescents (2018)

10.6 The Cost of Genuine Food

[478] Hollie A. Raynor, Colleen K. Kilanowski, Irina Esterlis, Leonard H. Epstein, A cost-analysis of adopting a healthful diet in a family-based obesity treatment program (2002)

[479] “Dogs fed on demineralized food died in twenty-six to thirty days; whereas dogs completely deprived of all food lived for forty to sixty days.” – Herbert M. Shelton, The Science and Fine Art of Fasting (1934) 

[480] “…rats deprived of all food and given a sweet saccharine solution to consume died significantly sooner than rats similarly deprived and given unflavored water to drink.” – Stephen Woods, The Eating Paradox: How We Tolerate Food (1991) 

10.7 Bariatric Surgery

[481] Emily Tate Sullivan, Some doctors slam anti-obesity device as ‘medically sanctioned bulimia’ (2016)  

[482] John E Pandolfino, Brintha Krishnamoorthy, Thomas J Lee, Gastrointestinal Complications of Obesity Surgery (2004)

[483] Anita Berg, Untold stories of living with a bariatric body: long-term experiences of weight-loss surgery (2019)  

[484] Anita Berg, Untold stories of living with a bariatric body: long-term experiences of weight-loss surgery (2019)

[485] John E Pandolfino, Brintha Krishnamoorthy, Thomas J Lee, Gastrointestinal Complications of Obesity Surgery (2004)

[486] Anita Berg, Untold stories of living with a bariatric body: long-term experiences of weight-loss surgery (2019)

[487] John E Pandolfino, Brintha Krishnamoorthy, Thomas J Lee, Gastrointestinal Complications of Obesity Surgery (2004)

[488] “Metabolic bone disease is a well-documented long-term complication of obesity surgery. It is often undiagnosed, or misdiagnosed, because of lack of physician and patient awareness. Abnormalities in calcium and vitamin D metabolism begin shortly after gastrointestinal bypass operations; however, clinical and biochemical evidence of metabolic bone disease may not be detected until many years later.” – Whitney S Goldner, Thomas M O’Dorisio, Joseph S Dillon, Edward E Mason, Severe Metabolic Bone Disease as a Long-Term Complication of Obesity Surgery (2002)

[489] Reddit thread, Wife wants gastric sleeve and I don’t support it. Help me change my mind (2023)

[490] “Weight regain is unfortunately a common phenomenon associated with all weight loss modalities including bariatric surgery.” – Saketh R. Velapati, Meera Shah, Aravind R. Kuchkuntla, Barham Abu-dayyeh, Karen Grothe, Ryan T. Hurt, Manpreet S. Mundi, Weight Regain After Bariatric Surgery: Prevalence, Etiology, and Treatment (2018)

[491] Pinterest-mom, reddit thread, Just canceled my weight loss surgery 3 days before it was scheduled. I’m going to do this myself. Am I nuts?? (2020)

[492] Jacqueline Odom, Kerstyn C. Zalesin, Tamika L. Washington, Wendy W. Miller, Basil Hakmeh, Danielle L. Zaremba, Mohamed Altattan, Mamtha Balasubramaniam, Deborah S. Gibbs, Kevin R. Krause, David L. Chengelis, Barry A. Franklin, Peter A. McCullough, Behavioral Predictors of Weight Regain after Bariatric Surgery (2009)

[493] John E Pandolfino, Brintha Krishnamoorthy, Thomas J Lee, Gastrointestinal Complications of Obesity Surgery (2004)

[494] Anita Berg, Untold stories of living with a bariatric body: long-term experiences of weight-loss surgery (2019)

10.8 Weight Loss Drugs

[495] R. John Rodgers, Matthias H. Tschöp, John P. H. Wilding, Anti-obesity drugs: past, present and future (2012)

[496] Timo D. Müller, Matthias Blüher, Matthias H. Tschöp, Richard D. DiMarchi, Anti-obesity drug discovery: advances and challenges (2021) h

[497] Chang Beom Lee, Weight Loss Drugs Recently Approved by the FDA (2013)

[498] Joram D. Mul,Denovan P. Begg, Jason G. Barrera, Bailing Li, Emily K. Matter, David A. D’Alessio, Stephen C. Woods, Randy J. Seeley, Darleen A. Sandoval, High-fat diet changes the temporal profile of GLP-1 receptor-mediated hypophagia in rats (2013)

[499] Kristin C. C. Petri, Steen H. Ingwersen, Anne Flint, Jeppe Zacho, Rune V. Overgaard, Exposure-response analysis for evaluation of semaglutide dose levels in type 2 diabetes (2018)

[500] Chuanfeng Liu, Yuzhao Liu, Yu Xin, Yangang Wang, Circadian secretion rhythm of GLP-1 and its influencing factors (2022)

[501] L R Ranganath, J M Beety, L M Morgan, J W Wright, R Howland, V Marks, Attenuated GLP-1 secretion in obesity: cause or consequence? (1996)

[502] Joaquín Santiago Galindo Muñoz, Diana Jiménez Rodríguez, Juan José Hernández Morante, Diurnal rhythms of plasma GLP-1 levels in normal and overweight/obese subjects: lack of effect of weight loss (2014)

[503] OkDocument8476, Reddit thread, I can eat whatever I want (2023)

[504] “…my stomach for really the first time in my life felt full. Not the type of full that I feel sick if I eat anymore, just content and full. On the way home I almost broke down in tears thinking to myself “is this how normal people feel?”” – Nova-star561519, Reddit thread, I almost broke down in tears after going out to eat with my fiancé (2023)

[505] “It is suggested that up to 75% of secreted GLP-1 is degraded within the gut, with an additional 50% then degraded in the liver, before even entering the general circulation (Deacon et al., 1996). Within the circulation, GLP-1 binds and activates the GLP-1R expressed on various sites throughout the body.” – Neil Tanday, Peter R. Flatt, Nigel Irwin, Metabolic responses and benefits of glucagon-like peptide-1 (GLP-1) receptor ligands (2021)

[506] “With 94% amino acid sequence homology to native GLP-1,4 semaglutide has three structural modifications that prolong its half-life to ~1 week, making it appropriate for once-weekly administration.” – Kristin C. C. Petri, Steen H. Ingwersen, Anne Flint, Jeppe Zacho, Rune V. Overgaard, Exposure-response analysis for evaluation of semaglutide dose levels in type 2 diabetes (2018)

[507] “Nausea occurred in 17.0%, diarrhea in 12.2% and vomiting in 6.4% of patients treated with semaglutide 0.5 mg. As for patients treated with semaglutide 1.0 mg, nausea occurred in 19.9%, diarrhea in 13.3% and vomiting in 8.4% of cases.” – Kristin C. C. Petri, Steen H. Ingwersen, Anne Flint, Jeppe Zacho, Rune V. Overgaard, Exposure-response analysis for evaluation of semaglutide dose levels in type 2 diabetes (2018)

[507] “Compared with placebo, liraglutide delayed gastric emptying of solids at 5 weeks (median 70 min [IQR 32 to 151] vs 4 min [-21 to 18]; p<0·0001) and 16 weeks (30·5 min [-11 to 54] vs -1 min [-19 to 7]; p=0·025).” – Houssam Halawi, Disha Khemani, Deborah Eckert, Jessica O’Neill, Hoda Kadouh, Karen Grothe, Matthew M Clark, Duane D Burton, Adrian Vella, Andres Acosta, Alan R Zinsmeister, Michael Camilleri, Effects of liraglutide on weight, satiation, and gastric functions in obesity: a randomised, placebo-controlled pilot trial (2017)

[509] Girish P Joshi, Anesthetic Considerations in Adult Patients on Glucagon-Like Peptide-1 Receptor Agonists: Gastrointestinal Focus (2024)

[510] Emily Cooke, Can Ozempic and Wegovy cause ‘stomach paralysis’ and ‘cyclic vomiting’? (2023)

[511] Brenda Goodman, They took blockbuster drugs for weight loss and diabetes. Now their stomachs are paralyzed (2023)

[512] Michael A. Nauck, Guido Kemmeries, Jens J. Holst, Juris J. Meier, Rapid Tachyphylaxis of the Glucagon-Like Peptide 1–Induced Deceleration of Gastric Emptying in Humans (2011)

[513] Tuuli Sedman, Maarja Krass, Kertu Rünkorg, Eero Vasar, Vallo Volke, Tolerance develops toward GLP-1 receptor agonists’ glucose-lowering effect in mice (2020)

[514] N.M. Kushnarova, O.V. Zinych, V.V. Korpavchev, A.V. Kovalchuk, O.V. Prybyla, K.O. Shyshkan-Shishova, Decrease in the efficacy of glucagon-like peptide-1 receptor agonists: what is the reason? (2021)

[515] Shu Meguro, Toshihide Kawai, Tomohiro Matsuhashi, Motoaki Sano, Keiichi Fukuda, Hiroshi Itoh, Yoshihiko Suzuki, Basal-Supported Oral Therapy with Sitagliptin Counteracts Rebound Hyperglycemia Caused by GLP-1 Tachyphylaxis (2014)

[516] Shu Meguro, Toshihide Kawai, Tomohiro Matsuhashi, Motoaki Sano, Keiichi Fukuda, Hiroshi Itoh, Yoshihiko Suzuki, Basal-Supported Oral Therapy with Sitagliptin Counteracts Rebound Hyperglycemia Caused by GLP-1 Tachyphylaxis (2014)

[517] “The increased pulse rate from baseline to end-of-trial compared with placebo has been seen previously with semaglutide8-11, 15, 16 and other GLP-1RAs,25 although there is no evidence of an increased cardiovascular risk.” – Kristin C. C. Petri, Steen H. Ingwersen, Anne Flint, Jeppe Zacho, Rune V. Overgaard, Exposure-response analysis for evaluation of semaglutide dose levels in type 2 diabetes (2018)

[518] “Rodent studies have indicated an increased risk of developing medullary thyroid carcinoma following treatment with GLP-1 RAs, but without existing confirmation of these results in humans (72,73).” – Kristin C. C. Petri, Steen H. Ingwersen, Anne Flint, Jeppe Zacho, Rune V. Overgaard, Exposure-response analysis for evaluation of semaglutide dose levels in type 2 diabetes (2018)

[519] Anita Kabahizi, Briana Wallace, Linh Lieu, Dominic Chau, Yanbin Dong, Eun-Sang Hwang, Kevin W. Williams, Glucagon-like peptide-1 (GLP-1) signalling in the brain: From neural circuits and metabolism to therapeutics (2021)

[520] “The GLP-1 receptor is expressed throughout many regions of the brain including the brainstem, cerebellum, cerebral cortex, hippocampus, hypothalamus, substantia nigra and thalamus (Cork et al., 2015). As a result, GLP-1 receptors have important and potential pharmacologically exploitable effects within the CNS.” – Neil Tanday, Peter R. Flatt, Nigel Irwin, Metabolic responses and benefits of glucagon-like peptide-1 (GLP-1) receptor ligands (2021)

[521] “Besides its appetite suppressing effect, GLP-1 acts on areas of the brain involved in stress response and emotion regulation. However, the role of GLP-1 in emotion and stress regulation, and whether it is a viable treatment for stress-induced compulsive overeating, has yet to be established.” – Eva Guerrero-Hreins, Anthony P. Goldstone, Robyn M. Brown, Priya Sumithran, The therapeutic potential of GLP-1 analogues for stress-related eating and role of GLP-1 in stress, emotion and mood: a review (2021)

[522] Katdicko, Reddit thread, One year on and the colour is gone from life (2023)

[523] Clubmasterc, Reddit thread, Why I Quit Ozempic (and don’t regret it) (2023)

[524] Jens Juul Holst, quoted by Matt Reynolds, What the Scientists Who Pioneered Weight-Loss Drugs Want You to Know (2023)

[525] Joram D. Mul,Denovan P. Begg, Jason G. Barrera, Bailing Li, Emily K. Matter, David A. D’Alessio, Stephen C. Woods, Randy J. Seeley, Darleen A. Sandoval, High-fat diet changes the temporal profile of GLP-1 receptor-mediated hypophagia in rats (2013)

[526] “I’ve seen some people say their cravings come back after the year mark.🤷🏻‍♀️ I haven’t really had a lot of appetite suppression but I have a lot of friends who have lost tons of weight that started taking ozempic in October of 2022. Many of them are starting to have increased hunger.” – International-Unit85 commenting on Reddit thread by ClinTrial-Throwaway, People on Drugs Like Ozempic Say Their ‘Food Noise’ Has Disappeared (2023)

[527] Sinker12344, Reddit thread, Ozempic tolerance (2023)

[528] KayCJones, Reddit thread, Has anyone experienced tolerance? (2022)

[529] John P. H. Wilding, Rachel L. Batterham, Melanie Davies, Luc F. Van Gaal, Kristian Kandler, Katerina Konakli, Ildiko Lingvay, Barbara M. McGowan, Tugce Kalayci Oral, Julio Rosenstock, Thomas A. Wadden, Sean Wharton, Koutaro Yokote, Robert F. Kushner, Weight regain and cardiometabolic effects after withdrawal of semaglutide: The STEP 1 trial extension (2022)

[530] GreenFlatworm9675, I now understand why people gain the weight back (2023)

[531] R. John Rodgers, Matthias H. Tschöp, John P. H. Wilding, Anti-obesity drugs: past, present and future (2012)

[532] Timo D. Müller, Matthias Blüher, Matthias H. Tschöp, Richard D. DiMarchi, Anti-obesity drug discovery: advances and challenges (2021)

[533] Calley Means, X status (2024)

[534] Anita Kabahizi, Briana Wallace, Linh Lieu, Dominic Chau, Yanbin Dong, Eun-Sang Hwang, Kevin W. Williams, Glucagon-like peptide-1 (GLP-1) signalling in the brain: From neural circuits and metabolism to therapeutics (2021)

[535] “…individuals with obesity who consumed higher levels of dietary added sugar had the lowest postprandial GLP-1 response.” – Sabrina Jones, Shan Luo, Hilary M. Dorton, Alexandra G. Yunker, Brendan Angelo, Alexis Defendis, John R. Monterosso, Kathleen A. Page,  Obesity and Dietary Added Sugar Interact to Affect Postprandial GLP-1 and Its Relationship to Striatal Responses to Food Cues and Feeding Behavior (2021)

[536] “…a disruption of diurnal GLP-1 levels in overweight/obese subjects, which worsen as body fat progresses.” – Joaquín Santiago Galindo Muñoz, Diana Jiménez Rodríguez, Juan José Hernández Morante, Diurnal rhythms of plasma GLP-1 levels in normal and overweight/obese subjects: lack of effect of weight loss (2014)

[537] “We found that the gut hormone GLP-1 and its receptor are present in taste buds and that GLP-1 signaling plays an important role in the modulation of sweet and umami taste.” – Bronwen Martin, Cedrick D. Dotson, Yu-Kyong Shin, Sunggoan Ji, Daniel J. Drucker, Stuart Maudsley, and Steven D. Munger, Modulation of taste sensitivity by GLP-1 signaling in taste buds (2013)

[538] Yu-Kyong Shin, Bronwen Martin, Erin Golden, Cedrick D. Dotson, Stuart Maudsley, Wook Kim, Hyeung-Jin Jang, Mark P. Mattson, Daniel J. Drucker, Josephine M. Egan, Steven D. Munger, Modulation of taste sensitivity by GLP-1 signaling (2008)

10.11 Boredom Eating

[539] A.M. Koball, M.R. Meers, A. Storfer-Isser, S.E. Domoff, D.R. Musher-Eizenman, Eating when bored: Revision of the Emotional Eating Scale with a focus on boredom (2012)

[540] Edward E. Abramson, Shawn G. Stinson, Boredom and eating in obese and non-obese individuals (1977)

10.12 Stress and Emotional Eating

[541] Bruce K. Alexander, Addiction: The View from Rat Park (2010)

[542] “Stress is the nonspecific response of the body to any demand.” – Hans Selye, Stress in Health and Disease (1976)

[543] “It is difficult to see at first how such essentially different things as cold, heat, drugs, hormones, sorrow and joy could provoke an identical biological reaction. Nevertheless this is the case; it can now be demonstrated by highly objective, quantitative biochemical and morphologic parameters that certain reactions are totally nonspecific and common to all types of agents, whatever their superimposed effects may be.” – Hans Selye, Stress in Health and Disease (1976)

10.13 Self-sabotage

[544] Justin Faden, Douglas Leonard, John O’Reardon, Robin Hanson, Obesity as a defense mechanism (2013)

[545] “Others willfully put on weight to desexualize, in the hope that what happened to them as children will never happen again.” – Olga Khazan, The Second Assault (2015)

[546] “Perceived burdensomeness significantly correlated with completer status and with more lethal means of suicide, even controlling for other relevant dimensions.” – Thomas E. Joiner, Jeremy W. Pettit, Rheeda L. Walker, Zachary R. Voelz, Jacqueline Cruz, M. David Rudd, David Lester, Perceived Burdensomeness And Suicidality: Two Studies On The Suicide Notes Of Those Attempting And Those Completing Suicide (2005)

[547] Amanda J. Edmondson, Cathy A. Brennan, Allan O. House, Non-suicidal reasons for self-harm: A systematic review of self-reported accounts (2015)

[548] “Generally, Premack’s analysis indicates that, like reinforcement, punishment is relative, not absolute. Even electric shock, which is usually viewed as an aversive stimulus or punisher, can function as reinforcement under appropriate conditions—as when a FI schedule of shock is superimposed on a schedule of food reinforcement for lever pressing or on a schedule of brain stimulation reinforcement in humans and other animals (Heath, 1963; Sidman, Brady, Boren, Conrad, & Schulman, 1955).” – W. David Pierce and Carl D. Cheney, Behavior Analysis and Learning: A Biobehavioral Approach, Sixth Edition (2017)

[549] Amanda J. Edmondson, Cathy A. Brennan, Allan O. House, Non-suicidal reasons for self-harm: A systematic review of self-reported accounts (2015)

10.14 Entrenched Habits

[550] Donald Hebb, The Organization of Behavior: A Neuropsychological Theory (1949)

10.15 Delicious Taste

[551] Steven Slate, Do Alcoholics Lose Control? The Results of Priming Dose Experiments Say NO (2013)

[552] Karen Dion, My Sinclair Method Experience | Daily Drinker to Sobriety | Some Reflections (2019)

[553]

10.16 A Mild Problem

[554] “Recent work on food use disorders has demonstrated that the same neurobiological pathways that are implicated in drug abuse also modulate food consumption. […] Work presented in this review strongly supports the notion that food addiction is a real phenomenon.” – Mark S. Gold, Damian M. Blumenthal, Neurobiology of food addiction (2010)

[555] “Cigarettes cause about one death per million smoked with a latency of about 25 years…” – Robert N Proctor, The shameful past: The history of the discovery of the cigarette–lung cancer link: evidentiary traditions, corporate denial, global toll (2012)

[556] W. David Pierce and Carl D. Cheney, Behavior Analysis and Learning: A Biobehavioral Approach, Sixth Edition (2017)

[557] GBD 2017 Diet Collaborators, Health effects of dietary risks in 195 countries, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017 (2019)

10.17 Powerlessness

[558] Fulton Timm Crews, Charlotte Ann Boettiger, Impulsivity, frontal lobes and risk for addiction (2009)

[559] “Both obese rats and chronic drug users have low basal dopamine levels (Hamdi, Porter, & Prasad, 1992), experience periodic exaggerated dopamine release associated with either food (Fetissov et al., 2002) or drug intake (Worsley et al., 2000), and have reduced dopamine D2 receptor and increased D1 receptor expression (Fetissov et al., 2002). A number of addictive behaviors (alcoholism; cocaine, heroin, marijuana, and nicotine use; and glucose bingeing) have been associated with low expression or dysfunction of D2 receptors (Comings & Blum, 2000).” – Leonard H. Epstein, John J. Leddy, Jennifer L. Temple, Myles S. Faith, Food Reinforcement and Eating: A Multilevel Analysis (2007)

[560] Kenneth Blum, Thomas McLaughlin, Abdalla Bowirrat, Edward J. Modestino, David Baron, Luis Llanos Gomez, Mauro Ceccanti, Eric R. Braverman, Panayotis K. Thanos, Jean Lud Cadet, Igor Elman, Rajendra D. Badgaiyan, Rehan Jalali, Richard Green, Thomas A. Simpatico, Ashim Gupta, Mark S. Gold, Reward Deficiency Syndrome (RDS) Surprisingly Is Evolutionary and Found Everywhere: Is It “Blowin’ in the Wind”? (2022)

[561] Leonard H. Epstein, John J. Leddy, Jennifer L. Temple, Myles S. Faith, Food Reinforcement and Eating: A Multilevel Analysis (2007)

[562] Jakob Hohwy, The hypothesis testing brain: Some philosophical applications (2010)

[563] “The idea is that the patient knows she had the intention to move, that she acted on the intention, probably she also knows that no-one physically pushed her around, and she knows how her body actually moved. The best explanation of the unusual experience, under these circumstances, is that some supernatural force, like a demon, initiated the movement. And this is then adopted as belief.” – Jakob Hohwy, The hypothesis testing brain: Some philosophical applications (2010)

[564] “…deeper studies of the logistic map and related maps have resulted in an equally surprising and profound positive result—the discovery of universal characteristics of chaotic systems.” – Melanie Mitchell, Complexity: A Guided Tour (2011)

[565] Melanie Mitchell, Complexity: A Guided Tour (2011)

[566] “For many substance users, their substance use escalates after they go to treatment. Additionally, their binge usage becomes more frequent and their behavior in other areas may become more erratic.” – Michelle L Dunbar, Steven Slate, and Mark W Scheeren, The Freedom Model for the Family (2018) 

[567] “The relevant research shows most of those who meet the American Psychiatric Association’s criteria for addiction quit using illegal drugs by about age 30, that they usually quit without professional help, and that the correlates of quitting include legal concerns, economic pressures, and the desire for respect, particularly from family members.” – Gene M. Hayman, Addiction and choice: theory and new data (2013)

[568] Steven Slate, Over 90% of addicts will recover even though less than 25% will get treatment (2019)

[569] “Analyses were done for the sub-sample of individuals with lifetime history of abuse or dependence on sedatives (n = 402), tranquilizers (n = 372), opioids (n = 521), and stimulants (n = 765) at Wave 1 of the National Epidemiological Survey on Alcohol and Related Conditions (NESARC). Cumulative probability estimates and hazard ratios for remission from PDUD were obtained for the general population. Lifetime cumulative probability estimates of remission were above 96% for all substances assessed.” – Carlos Blanco, Roberto Secades-Villa, Olaya García-Rodríguez, Marta Labrador-Mendez, Shuai Wang, Robert P. Schwartz, Probability and predictors of remission from life-time prescription drug use disorders: Results from the National Epidemiologic Survey on Alcohol and Related Conditions (2013)

[570] Gene M. Heyman, Verna Mims, Chapter 21, What addicts can teach us about addiction: A natural history approach from Addiction and Choice: Rethinking the relationship (2016)  

[571] Gene M. Heyman, Verna Mims, Chapter 21, What addicts can teach us about addiction: A natural history approach from Addiction and Choice: Rethinking the relationship (2016)  

11.2 Never

[572] National Institute on Alcohol Abuse and Alcoholism, US NIH, Alcohol Facts and Statistics (2023)

[573] Bridget F. Grant, S. Patricia Chou, Tulshi D. Saha, Prevalence of 12-Month Alcohol Use, High-Risk Drinking, and DSM-IV Alcohol Use Disorder in the United States, 2001-2002 to 2012-2013: Results From the National Epidemiologic Survey on Alcohol and Related Conditions (2017)

[574] Substance Abuse and Mental Health Services Administration, U.S. Department of Health & Human Services, National Survey on Drug Use and Health (2018)

[575] National Library of Medicine, US NIH, National Academy of Sciences, Food Additives, Contaminants, Carcinogens, and Mutagens (1983)

11.3 Avoidance

[576] M J Jarvis, M A Russell, C Feyerabend, Absorption of nicotine and carbon monoxide from passive smoking under natural conditions of exposure (1983)

11.4 The Recalibration Process

[577] Lotfi B. Merabet, Roy Hamilton, Gottfried Schlaug, Jascha D. Swisher, Elaine T. Kiriakopoulos, Naomi B. Pitskel, Thomas Kauffman, Alvaro Pascual-Leone, Rapid and Reversible Recruitment of Early Visual Cortex for Touch (2008)

[578] Matthew Walker, Why We Sleep (2017)

[579] Robert T. Mallet, Johannes Burtscher, Vincent Pialoux, Qadar Pasha, Yasmin Ahmad, Grégoire P. Millet, Martin Burtscher, Molecular Mechanisms of High-Altitude Acclimatization (2023)  

[580] “One interesting property about taste bud cells is that they are constantly undergoing apoptosis and regeneration. The average lifespan of a taste bud cell has been estimated to be about 10 days.” – Paul A. S. Breslin, Alan C. Spector, Mammalian taste perception (2008)

[581] Gordon Shepherd, Neurogastronomy: How the Brain Creates Flavor and Why It Matters (2013)

[582] Linda A. Barlow, and Ophir D. Klein, Developing and regenerating a sense of taste (2015)

11.5 Dissolving Cravings

[583] “Birds were exposed to the schedule of reinforcement plus punishment at several levels of food deprivation. Recall that food deprivation is an establishing operation that should increase pecking of the key for food (and increase the reinforcement effectiveness of food). The animals were punished for responding at 60, 65, 70, 75, and 85% of free-feeding body weight. At 85% weight, punishment virtually stopped the birds’ responding. However, at 60% weight the pigeons maintained a high, stable rate of response. […] …rate of response was ordered by level of deprivation—the less the deprivation for food (satiation), the more effective was punishment.” – W. David Pierce and Carl D. Cheney, Behavior Analysis and Learning: A Biobehavioral Approach, Sixth Edition (2017)

[584] Karl Schlechta, A Reliability Theory of Truth (2017)

[585] Platistocrates, Reddit thread, Truth & reliability: an etymology (2024)

11.7 The Capacity for Instant Change

[586] Michael Chaiton, Lori Diemert, Joanna E Cohen, Susan J Bondy, Peter Selby, Anne Philipneri, Robert Schwartz, Estimating the number of quit attempts it takes to quit smoking successfully in a longitudinal cohort of smokers (2016)

[587] “The closest I can come to describing it is with metaphor, such as a switch being flipped, or a pivot point being reached.” – Marc Lewis, quoted by Walter Armstrong, Interview With an Addicted Brain (2012)

[588] “Of particular interest are abrupt dynamic events that cause networks to irreversibly fail. However, in many real-world phenomena, such as brain seizures in neuroscience or sudden market crashes in finance, after an inactive period of time a significant part of the damaged network is capable of spontaneously becoming active again. The process often occurs  repeatedly.” – Antonio Majdandzic, Boris Podobnik, Sergey V. Buldyrev, Dror Y. Kenett, Shlomo Havlin, H. Eugene Stanley, Spontaneous recovery in dynamical networks (2013)

12.0 The Escape Method

[589] M.A. Di Muro, C.E. La Rocca, H.E. Stanley, S. Havlin, L.A. Braunstein, Recovery of Interdependent Networks (2016)

12.2 Prioritize Nourishment

[590] “One of the most common ways to change behavior–environment relationships is to have the person (or other organism) experience a period of deprivation or satiation. For example, a pigeon will peck a key for food only if it is deprived of food for some period of time. More specifically, the peck-for-food contingency depends on level of food deprivation. – W. David Pierce and Carl D. Cheney, Behavior Analysis and Learning: A Biobehavioral Approach, Sixth Edition (2017)

[591] “If we reinforce a response in a group of organisms at the same level of deprivation and extinguish it in subgroups at different levels, we find that the number of responses in the extinction curve is a function of deprivation. The hungrier the organism, the more responses it will emit during extinction. If, on the other hand, we condition at different levels of deprivation and extinguish at the same level, we find, surprisingly enough, that the two extinction curves contain approximately the same number of responses. The effect of deprivation is felt during extinction, not during conditioning.” – B.F. Skinner, Science and Human Behaviour (1965)

[592] Paul Jaminet, Hunter-Gatherer Macronutrient Ratios: More Data (2011)

12.3 Eat Until Completely Full

[593] Leah M. Kalm, Richard D. Semba, They Starved So That Others Be Better Fed: Remembering Ancel Keys and the Minnesota Experiment (2005)

12.4 Eat at Regular Mealtimes

[594] “The change does not happen instantly, however (Collier, 1982, 1989), and I suspect that the animal, as it adapts to consuming larger and larger meals, also learns to anticipate such meals by secreting more and more cephalic insulin and developing other adaptive responses. As long as the environment is perfectly predictable, large meals can be consumed and well tolerated. Cephalic insulin and other processes enable such consumption.” – Stephen C. Woods, The Eating Paradox (1991) 

[595] Neil E. Rowland, Order and disorder: Temporal organization of eating (2012)

[596] Christopher Fairburn, Overcoming Binge Eating, Second Edition (2013)

12.5 Fast between meals (unless ravenous)

[597] C Lee, V D Longo, Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients (2011)

[598] Elizabeth F. Sutton, Robbie Beyl, Kate S. Early, William T. Cefalu, Eric Ravussin, Courtney M. Peterson, Early Time-Restricted Feeding Improves Insulin Sensitivity, Blood Pressure, and Oxidative Stress Even without Weight Loss in Men with Prediabetes (2018)

[599] Ameneh Madjd, Moira A Taylor, Alireza Delavari, Reza Malekzadeh, Ian A Macdonald, Hamid R Farshchi, Beneficial effect of high energy intake at lunch rather than dinner on weight loss in healthy obese women in a weight-loss program: a randomized clinical trial (2016)

[560] M. Garaulet, P. Gómez-Abellán, J.J. Alburquerque-Béjar, Y-C. Lee, J.M. Ordovás, F.A.J.L. Scheer, Timing of food intake predicts weight loss effectiveness (2013)

[561] Improvement Gnome, Kidney Failure After 20 Day Water Fast (2018)

[562] Herbert M. Shelton, The Science and Fine Art of Fasting (1934)

12.8 Weight Loss and Healing

[563] “The gut resets itself so that it produces digestive juice just before the food appears, and the liver clock resets to process nutrients that are absorbed in the gut.” – Satchin Panda, The Circadian Code (2018)