Why We Eat (Too Much)

by Andrew Jenkinson

  3 R. H. Lustig et al. (2003). Suppression of insulin secretion is associated with weight loss and altered macronutrient intake and preference in a subset of obese adults. Int J Obes Relat Metab Disord, 27(2), February, 219–26.

  4 C. S. Lieber et al. (1991). Perspectives: do alcohol calories count? Am J Clin Nutr, 54(6), 976–82.

  5 P. Suter (2005). Is alcohol consumption a risk factor for weight gain and obesity? Crit Rev Clin Lab Sci, 42(3), 197–227.

  6 L. Cordain et al. (1997). Influence of moderate daily wine consumption on body weight regulation and metabolism in healthy free-living males. J Am Coll Nutr, 16(2), April, 134–9.

  7 A. Arif and J. Rohrer (2005). Patterns of alcohol drinking and its association with obesity: data from the Third National Health and Nutrition Survey 1988–1994. BMC Public Health, 5, December, 126.

  8 T. Stalder et al. (2010). Use of hair cortisol analysis to detect hypercortisolism during active drinking phase in alcohol-dependent individuals. Biol Psychol, 85(3), December, 357–60.

  11 The French Paradox

  1 P. MacLean and R. Batterham et al. (2017). Biological control of appetite: a daunting complexity. Obesity (Silver Spring), 25(1), March, S8–S16.

  2 D. Treit and M. L. Spetch (1986). Caloric regulation in the rat: control by two factors. Physiology & Behavior, 36(2), 311–17.

  13 The Fat of the Land

  1 M. Sladek et al. (2016). Perceived stress, coping, and cortisol reactivity in daily life: a study of adolescents during the first year of college. Biol Psychol, 117, May, 8–15; A. Bhende et al. (2010). Evaluation of physiological stress in college students during examination. Biosc Biotech Res Comm, 3(2), December, 213–16.

  2 S. Gropper et al. (2012). Changes in body weight, composition, and shape: a 4-year study of college students. Appl Physiol Nutr Metab, 37(6), 1118–23.

  3 L. Dinour et al. (2012). The association between marital transitions, body mass index, and weight: a review of the literature. J Obes, 2012(294974), May.

  4 T. Robles and J. Kiecolt-Glaser (2003). The physiology of marriage: pathways to health. Physiol Behav, 79(3), August, 409–16.

  5 P. B. Gray et al (2004). Social variables predict between-subject but not day-to-day variation in the testosterone of US men. Psychoneuroendocrinology, 29(9), October, 1153–62; E. Barrett et al. (2015). Women who are married or living as married have higher salivary estradiol and progesterone than unmarried women. Am J Hum Biol, 27(4), July–August, 501–7.

  6 B. Leeners et al. (2017). Ovarian hormones and obesity. Hum Reprod Update, 23(3), May, 300–321.

  7 J. Cipolla-Neto et al. (2014). Melatonin, energy metabolism, and obesity: a review. J Pineal Res, 56(4), May, 371–81.

  8 Cipolla-Neto et al. Melatonin, energy metabolism, and obesity.

  9 M. Mankowska et al. (2017). Confirmation that a deletion in the POMC gene is associated with body weight of Labrador Retriever dogs. Res Vet Sci, 112, June, 116–18.

  10 H. Eicher-Miller et al. (2012). Contributions of processed foods to dietary intake in the US from 2003–2008: a report of the Food and Nutrition Science Solutions Joint Task Force of the Academy of Nutrition and Dietetics, American Society for Nutrition, Institute of Food Technologists, and International Food Information Council. J Nutr, 142(11), November, 2065S–2072S.

  11 C. Monteiro et al. (2018). Household availability of ultra-processed foods and obesity in nineteen European countries. Public Health Nutr, 21(1), January, 18–26.

  14 Prepare to Do It Yourself

  1 Z. T. Segal et al. (2012). Mindfulness-Based Cognitive Therapy for Depression, 2nd edn. New York: The Guilford Press.

  15 Eat More, Rest More

  1 M. Walker (2017). Why We Sleep: Unlocking the power of sleep and dreams. London: Penguin Books.

  16 Your Personal Blue Zone

  1 R. De Souza et al. (2015). Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ, 351, August, h3978.

  2 H. Pontzer et al. (2012). Hunter-gatherer energetics and human obesity. PLoS One, 7(7), July, e40503.

  Appendix 1: The Cholesterol Debate

  1 M. Gladwell (2000). The Tipping Point: How little things can make a big difference. London: Little, Brown.

  2 A. Keys (1980). Seven Countries: A multivariate analysis of death and coronary heart disease. Cambridge, MA: Harvard University Press.

  3 C. Kearns et al. (2016). Sugar industry and coronary heart disease research: a historical analysis of internal industry documents. JAMA Intern Med, 176(11), November, 1680–85.

  4 S. Hamley (2017). The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials. Nutr J, 16(1), May, article no. 30; S. Berger et al. (2015). Dietary cholesterol and cardiovascular disease: a systematic review and meta-analysis. Am J Clin Nutr, 102(2), August, 276–94.

  5 R. De Souza et al. (2015). Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ, 351, August, h3978.

  6 P. Siri and R. Krauss (2005). Influence of dietary carbohydrate and fat on LDL and HDL particle distributions. Curr Atheroscler Rep, 7(6), November, 455–9; P. Siri-Tarino et al. (2010). Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr, 91(3), March, 502–9.

  7 J. Durstine et al. (2002). Lipids, lipoproteins, and exercise. J Cardiopulm Rehabil, 22(6), November–December, 385–98.

  8 F. Sacks et al. (2017). Dietary fats and cardiovascular disease: a presidential advisory from the American Heart Association. Circulation, 136(3), July, e1–e23.

  9 R. Krauss (1995). Dense low density lipoproteins and coronary artery disease. Am J Cardiol, 75(6), February, 53B–57B.

  10 World Health Organization (2003). Diet, Nutrition and the Prevention of Chronic Diseases. WHO Technical Report Series, 916, 10, 88.

  11 De Souza et al. (2015). Intake of saturated and trans unsaturated fatty acids.

  Appendix 2: Glycaemic Load and Omega-3 to Omega-6 Ratio of Common Foods

  1 S. A. Khan (2017). Comparative study of fatty-acid composition of table eggs from Jeddah food market and effect of value addition in omega-3 bio-fortified eggs. Saudi J Biol Sci, 24(2), 929–35.

  2 Khan (2017). Comparative study of fatty-acid composition of table eggs.

  Glossary

  adenosine triphosphate (ATP) – ATP is the chemical found within the cells of all living organisms on Earth. It acts as an energy currency that cells can understand and use. ATP stores the energy that is released when food is broken down and transports it to the area of the cell requiring energy for building and repair.

  ATP batteries – ATP molecules act like mini cellular batteries, charging up (on food) and discharging their energy in other parts of the cell.

  autonomic nervous system (ANS) – The autonomic nervous system describes a part of our nervous system that is not under our conscious control (it is automatic). It is split into two parts: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS). These two systems work either to optimize physical activity (in times of danger) or to preserve energy.

  basal metabolic rate (BMR) – BMR describes the amount of energy that the body uses when at rest, including the energy required for cellular chemical reactions (building and repair), temperature control, breathing and heart rate.

  dinitrophenol (DNP) – A chemical substance that causes the release of the energy stored in ATP to thermal (heat) rather than to chemical energy.

  epigenetics – The study of the way inherited traits from DNA can be altered during pregnancy and early childhood in response to the environment.

  ghrelin – A hormone produced by the stomach (and upper GI tract) that acts (via the hypothalamus) to produce a voracious appetite and food-seeking behaviour. Ghrelin increases
in response to starvation (and dieting) and decreases after eating.

  GLP-1 – Glucagon-like peptide-1 is a hormone released by the small bowel when food is being digested. It acts (via the hypothalamus) to increase satiety and is part of the signal to stop eating. It also acts to improve the efficiency of insulin.

  hypothalamus – The pea-sized gland within the brain that is responsible for processing incoming sensory information such as the state of hydration and nutrition. In response to incoming signals it determines thirst, hunger and metabolic rate.

  insulin – A hormone produced by the pancreas in response to food, particularly carbohydrates. It works to clear excess glucose (sugar) from the blood by opening the channels in the cells that suck in glucose.

  leptin – A hormone produced by fat cells. Leptin acts as the ‘master regulator’ of body weight. When fat accumulates, leptin levels rise. This signals to the hypothalamus that enough energy is stored, resulting in an increase in metabolism and decreased appetite. When there is less fat, leptin levels fall, resulting in the hypothalamus increasing appetite and decreasing metabolism.

  leptin resistance – The presence of very high levels of leptin that are not sensed by the hypothalamus. The leptin signal is blocked by insulin and TNF-alpha (inflammation). Despite there being a high level of fat in the body, the hypothalamus does not sense this and therefore does not correct it.

  metabolic adaptation – Alterations in the amount of energy expended in response to the amount of energy consumed in order to defend a weight set-point and stop extreme weight fluctuations. The metabolic rate shifts downwards in response to calorie restriction (opposing extreme weight loss), and upwards in response to excess calories (opposing extreme weight gain).

  metabolic rate – In this book metabolic rate refers to resting metabolic rate, i.e. the amount of energy required by the body to function while at rest.

  micro-batteries – In this book the term micro-batteries is used to describe the function of ATP, small cellular chemicals that constantly charge and then discharge their energy, acting like mobile chargers.

  negative feedback system – A system that is designed to maintain order by automatically correcting changes away from the pre-set desired equilibrium.

  obesogenic – Something that promotes obesity.

  omega fatty acids – The term refers to the two polyunsaturated fatty acids omega-3 and omega-6. Omega fatty acids are essential for cellular health. Humans are unable to make them and therefore foods that contain them should be part of a healthy diet.

  parasympathetic nervous system (PNS) – Part of the autonomic nervous system. The PNS promotes energy conservation by decreasing pulse and blood pressure.

  peptide-YY (PYY) – A hormone originating in the small intestine that is released after food is sensed within the bowel. It acts on the hypothalamus to promote feelings of satiety, or fullness, and forms part of the signal to stop eating.

  sympathetic nervous system (SNS) – Part of the autonomic nervous system. The SNS triggers the fight or flight response to danger, enhancing strength, speed, and clarity of thought by increasing blood (and oxygen) flow to the muscles and brain.

  thermogenesis – The process by which cellular energy, in the form of ATP, is converted to thermal energy (heat) rather than to chemical or mechanical energy.

  TNF-alpha – Tumour necrosis factor-alpha is a protein that is released by inflammatory cells in response to the threat of attack (real or perceived). It helps to stimulate the inflammatory response seen in both infection and in autoimmune disease.

  weight-control centre – A term used in this book to describe the hypothalamus.

  weight set-point – The term refers to the weight that the body senses is safest for its survival and reproduction. The weight set-point is determined by genetic, epigenetic and environmental factors.

  Bibliography

  Allport, Susan, The Queen of Fats (Berkeley, CA: University of California Press, 2006)

  Briffa, John, Escape the Diet Trap (London: Fourth Estate, 2012)

  Buettner, Dan, The Blue Zones (Washington DC: National Geographic, 2008)

  Davis, William, Wheat Belly (London: HarperThorsons, 2014)

  Guyenet, Stephan, The Hungry Brain (London: Vermilion, 2017)

  Hoffmann, Peter, Life’s Ratchet (New York: Basic Books, 2012)

  Lewis, David, and Margaret Leitch, Fat Planet (London: Random House Books, 2015)

  Lustig, Robert, Fat Chance (London: Fourth Estate, 2014)

  Moalem, Sharon, Survival of the Sickest (London: HarperCollins, 2008)

  Nesse, Randolph, and George Williams, Why We Get Sick (New York: Vintage Books, 1996)

  Pollan, Michael, In Defence of Food (London: Allen Lane, 2008)

  Sisson, Mark, The Primal Blueprint (London: Ebury Press, 2012)

  Taubes, Gary, The Case against Sugar (London: Portobello Books, 2017)

  Teicholz, Nina, The Big Fat Surprise (London: Scribe, 2014)

  Wrangham, Richard, Catching Fire (London: Profile Books, 2009)

  Acknowledgements

  As I stated at the start of this book, the inspiration for writing it came from the many patients that I listened to and befriended in my clinics. They are the reason I wrote this book and it is to them that I am truly thankful for their early encouragement. I hope this book will repay the faith they have in me. A special mention should go to Jak, the first patient that I operated on, and in particular to his mother Dina, and to her family and community, for their support. Panny, Jerry, Satish, Alicia, Elisa, Yenti, Norma and all of you, thanks for your support.

  Obviously, a book takes time to write and preparation to write it. Thanks to my wonderful loving girls at home, Rina, Jessica and Hannah, for your support and constant good humour. Thanks to Mum, who read the first draft and, unsurprisingly, loved it; Dad, who did the DIY in the study (at the age of eighty); and Richard and Sarah (and their families) for their support.

  The book would not have been possible without my eighteen-month sabbatical from NHS duties, so I am indebted to Richard Cohen and Sarah Shaw at UCLH for facilitating this – I hope I have repaid that trust with this book.

  I am also indebted to the surgeons that inspired and trained me, particularly David McLean, Don Menzies, Abrie Botha and Kesava Mannur. My research thesis would not have been possible without the intervention of Professor Norman Williams – thank you. Appreciation to my friends in the lab: Sri, Etsuro, Scotty, David Evans and, obviously, Charlie Knowles (now Professor).

  Thanks to the support of the bariatric team, past and present, at UCLH, particularly my friends Marco Adamo, Rachel Batterham, Mo, Majid, Naim, Andrei, Andrea Pucci, Himender Makker, Muntzer Mughal, Billy White, James Holding, Jackie Doyle, Kate Waller, Lise, Alison and Dr Maan Hasan, the safest and most interesting anaesthetist in London. Not to forget the admin team, past and present, at UCH: Jason Willis, Andreas Mann, Jade O’Connell, Maleika Pitterson … all of you – thanks.

  Thanks to the research team I am currently working with at UCLH to investigate the effect of dieting on resting metabolic rate: Belinda Dury, Jessica Mok, Rob Stephens and Rachel Batterham (again).

  A special mention should go to Natalie Cole – the highly efficient manager of my private practice in Harley Street … keep those twenty to thirty emails a day coming; I need the reminders!

  I am grateful for my friends and colleagues in the United Arab Emirates for their unwavering support and their enthusiasm for this book: Rola Ghali, Mike Stroud, Alaa, Dr Bilal, Samer, Medhat, Fahmeeda, and Chandni Sharma.

  Appreciation to Dr John Briffa, author and GP, for his advice to ‘write like you talk’ – thanks, John. And to Kevin Harvey for reading an early manuscript and giving me invaluable advice.

  I am truly grateful to Elizabeth Sheinkman, my literary agent, for her fantastic enthusiasm for the book, and for recommending (from many offers) Penguin Life as publishers. At Penguin, I am indebted to Venetia Butterfield and Marianne Tatepo for moulding the book into th
e finished product it now is, and finally to Jane Robertson, my copy-editor, for adding clarity and focus to my writing.

  Index

  The page references in this index correspond to the print edition from which this ebook was created, and clicking on them will take you to the the location in the ebook where the equivalent print page would begin. To find a specific word or phrase from the index, please use the search feature of your ebook reader.

  Page references in italic indicate Figures.

  5:2 diet 221

  16/8 diet 221

  Abu Dhabi 54

  acetaldehyde 205

  adenosine triphosphate (ATP) 75

  ATP batteries 112, 114, 135, 205–6

  adipocytes 5

  adrenaline 72

  African slaves

  and Caribbean sugar trade 131

  migration to America 48–9

  agricultural age 128–9, 130–31

  Aiello, L. C.: ‘The Expensive Tissue Hypothesis’ (with P. Wheeler) 115–16

  alcohol

  and appetite 207

  beer 133, 204

  and beer belly 206–7

  and blood sugar 207

  and cortisol 206–7, 208

  and insulin 207

  and the liver 204, 205–6

  and Victorian diet 133

  and weight set-point theory 204–8

  almonds 261, 291

  Alzheimer’s disease 189

  American Heart Association 282, 283

  anaemia 40

  anxiety mood disorders 189

  appetite

  after bariatric surgery 79–80

  and alcohol 207

  and animals in approach to winter 28, 191–2

  of baby of a starving mother 52