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29
E. Dirinck et al., “Obesity and Persistent Organic Pollutants: Possible Obesogenic Effect of Organochlorine Pesticides and Polychlorinated Biphenyls,”
Obesity
19, no. 4 (2011): 709–14.

30
D. Mullerova et al., “Negative Association between Plasma Levels of Adiponectin and Polychlorinated Biphenyl 153 in Obese Women under Non-Energy-Restrictive Regime,”
International Journal of Obesity
32, no. 12 (2008):1875–78.

31
E. R. Hugo et al., “Bisphenol A at Environmentally Relevant Doses Inhibits Adiponectin Release from Human Adipose Tissue Explants and Adipocytes,”
Environmental Health Perspectives
116, no. 12 (December 2008): 1642–47.

32
F. Grün and B. Blumberg, “Environmental Obesogens: Organotins and Endocrine Disruption via Nuclear Receptor Signaling,”
Endocrinology
147, 6 Suppl. (2006): S50–55.

33
A. Santacruz et al., “Gut Microbiota Composition Is Associated with Body Weight, Weight Gain, and Biochemical Parameters in Pregnant Women,”
British Journal of Nutrition
104, no. 1 (2010): 83–92.

34
K. Stanhope, “Adverse Metabolic Effects of Dietary Fructose: Results from the Recent Epidemiological, Clinical, and Mechanistic Studies,”
Current Opinion in Lipidology
24, no. 3 (2013): 198–206.

35
———, “Consuming Fructose-Sweetened, not Glucose-Sweetened, Beverages Increases Visceral Adiposity and Lipids and Decreases Insulin Sensitivity in Overweight/Obese Humans,”
Journal of Clinical Investigation
119, no. 5 (2009): 1322–34.

36
G. Bray, “Consumption of High-Fructose Corn Syrup in Beverages May Play a Role in the Epidemic of Obesity,”
American Journal of Clinical Nutrition
79, no. 4 (2004): 537–43.

37
Stanhope, “Consuming Fructose-Sweetened, not Glucose-Sweetened, Beverages,” 1322–34.

38
T. Nakagawa, “A Causal Role for Uric Acid in Fructose-Induced Metabolic Syndrome,”
American Journal of Physiology—Renal Physiology
290, no. 3 (2006): F625–31.

39
X. Ouyang, “Fructose Consumption as a Risk Factor for Non-Alcoholic Fatty Liver Disease,”
Journal of Hepatology
48, no. 6 (2008): 993–99.

40
H. Basciano et al., “Fructose, Insulin Resistance, and Metabolic Dyslipidemia,”
Nutrition and Metabolism
2 (February 2005): 5.

41
K. Page et al., “Effects of Fructose vs. Glucose on Regional Cerebral Blood Flow in Brain Regions Involved with Appetite and Reward Pathways,”
Journal of the American Medical Association
309, no. 1 (2013): 63–70.

42
A. Shapiro, “Fructose-Induced Leptin Resistance Exacerbates Weight Gain in Response to Subsequent High-Fat Feeding,”
American Journal of Physiology—Regulatory, Integrative, and Comparative Physiology
295, no. 5 (2008): R1370–75.

43
http://www.odwalla.com/products/smoothies/original-superfood

44
Centers for Disease Control and Prevention (CDC), “Trends in Intake of Energy and Macronutrients—United States, 1971–2000,”
Morbidity and Mortality Weekly Report
53, no. 4 (2004): 80.

45
E. Ford and W. Dietz, “Trends in Energy Intake among Adults in the United States: Findings from NHANES,”
American Journal of Clinical Nutrition
97, no. 4 (April 2013): 848–53.

46
Q. Zhou et al., “Dopamine-Deficient Mice Are Severely Hypoactive, Adipsic, and Aphagic,”
Cell
83 (1995): 1197–1209.

47
M. Yeomnans et al., “Palatability: Response to Nutritional Need or Need-Free Stimulation of Appetite?”
British Journal of Nutrition
92, Suppl. S1 (2004): S3–14.

48
R. J. Johnson et al., “Potential Role of Sugar (Fructose) in the Epidemic of Hypertension, Obesity and the Metabolic Syndrome, Diabetes, Kidney Disease, and Cardiovascular Disease,”
American Journal of Clinical Nutrition
86, no. 4 (October 2007): 899–906.

49
ers.usda.gov/data-products/food-expenditures.aspx

50
fmi.org/research-resources

51
K. Chen, “Induction of Leptin Resistance through Direct Interaction of C-Reactive Protein with Leptin,”
Nature Medicine
12 (2006): 425–32.

52
A. Shapiro, “Fructose-Induced Leptin Resistance Exacerbates Weight Gain in Response to Subsequent High-Fat Feeding,”
Integrative and Comparative Physiology
295, no. 5 (November 1, 2008): R1370–75.

53
J. M. de Castro and E. M. Brewer, “The Amount Eaten in Meals by Humans Is a Power Function of the Number of People Present,”
Physiology and Behavior
51, no. 1 (1992): 121.

54
J. Danguir and S. Nicolaidis, “Dependence of Sleep on Nutrients’ Availability,”
Physiology and Behavior
22, no. 4 (1979): 735–40.

55
C. A. Everson, B. M. Bergmann, and A. Rechtschaffen, “Sleep Deprivation in the Rat: III. Total Sleep Deprivation,”
Sleep
12, no. 1 (1989): 13–21.

56
D. Kripke, R. Simons, L. Garfinkel et al., “Short and Long Sleep and Sleeping Pills. Is Increased Mortality Associated?”
Archives of General Psychiatry
36, no. 1 (1979): 103–16.

57
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Chapter 2

1
A. Barletta, G. et al.,
Journal of Endocrinological Investigation
3 (1980): 293–96.
2
F. Goglia, G. Liverini, T. De Leo, and A. Barletta, “Thyroid State and Mitochondrial Population during Cold Exposure,”
Pflügers Archiv-European Journal of Physiology
396, no. 1 (1983): 49–53.

3
H. Sul and D. Wang, “Nutritional and Hormonal Regulation of Enzymes in Fat Synthesis: Studies of Fatty Acid Synthase and Mitochondrial Glycerol-3-Phosphate Acultransferase Gene Transcription,”
Annual Review of Nutrition
18 (1998): 331–51.

4
G. J. Canaris, N. R. Manowitz, G. Mayor, and E. C. Ridgway, “The Colorado Thyroid Disease Prevalence Study,”
Archives of Internal Medicine
160 (2000): 526–34.

5
T. Teixeira, “Potential Mechanisms for the Emerging Link between Obesity and Increased Intestinal Permeability,”
Nutrition Research
32, no. 9 (September 2012): 637–47.

6
F. Grün and B. Blumberg, “Environmental Obesogens: Organotins and Endocrine Disruption via Nuclear Receptor Signaling,”
Endocrinology
147, no. 6 Suppl. (2006): S50–55.

7
A. Shapiro, W. Mu, C. Roncal, K. Y. Cheng, R. J. Johnson, and P. J. Scarpace, “Fructose-Induced Leptin Resistance Exacerbates Weight Gain in Response to Subsequent High-Fat Feeding,”
Amercian Journal of Physiology—Regulatory, Integrative, and Comparative Physiology
295, no. 5 (2008): R1370–75.

Chapter 3

1
R. R. Wing and R. W. Jeffery, “Benefits of Recruiting Participants with Friends and Increasing Social Support for Weight Loss and Maintenance,”
Journal of Consulting and Clinical Psychology
7, no. 1 (1999): 132–38.

2
K. Hwang et al., “Social Support in an Internet Weight Loss Community,”
International Journal of Medical Informatics
79, no. 1 (2010): 5–13.

3
M. Gailliot et al., “Self-Control Relies on Glucose as a Limited Energy Source: Willpower Is More Than a Metaphor,”
Journal of Personality and Social Psychology
92, no. 2 (2007): 325–36.

Chapter 4

1
Ancel Keys,
Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease
(Cambridge, MA: Harvard University Press, 1980).

2
R. Chowdhury et al., “Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-Analysis,”
Annals of Internal Medicine
160, no. 6 (2014): 398–406.

3
J. F. Mauger et al., “Effect of Different Forms of Dietary Hydrogenated Fats on LDL Particle Size,”
American Journal of Clinical Nutrition
78, no. 3 (2003): 370–75.

4
R. Khanal, “Potential Health Benefits of Conjugated Linoleic Acid (CLA): A Review,”
Asian-Australasian Journal of Animal Sciences
17, no. 9 (2004): 1315–28.

5
Z. Gao et al., “Butyrate Improves Insulin Sensitivity and Increases Energy Expenditure in Mice,”
Diabetes
58, no. 7 (2009): 1509–17.

6
A. Christianson,
The Adrenal Reset Diet
(New York: Harmony Books, 2014).

7
S. W. Souci, E. Fachmann, and H. Kraut,
Food Composition and Nutrition Tables
(Stuttgart, Germany: Medpharm Scientific Publishers, 2008).

8
A. Afshin, “Consumption of Nuts and Legumes and Risk of Incident Ischemic Heart Disease, Stroke, and Diabetes: A Systematic Review and Meta-Analysis,”
American Journal of Clinical Nutrition
100, no. 1 (July 1, 2014): 278–88.

9
A. Salehi-Abargouei et al., “Effects of Non-Soy Legume Consumption on C-Reactive Protein: A Systematic Review and Meta-Analysis,”
Nutrition
31, no. 5 (2015): 631–39.

10
H. Hermsdorff, “A Legume-Based Hypocaloric Diet Reduces Proinflammatory Status and Improves Metabolic Features in Overweight/Obese Subjects,”
European Journal of Nutrition
50, no. 1 (2011): 61–69.

11
D. Birt et al., “Resistant Starch: Promise for Improving Human Health,”
Advances in Nutrition
4, no. 6 (2013): 587–601.

12
M. Säemann et al., “Anti-Inflammatory Effects of Sodium Butyrate on Human Monocytes: Potent Inhibition of IL-12 and Up-Regulation of IL-10 Production,”
FASEB Journal
14, no. 15 (December 2000): 2380–82.

13
O. Kanauchi et al., “Butyrate from Bacterial Fermentation of Germinated Barley Foodstuff Preserves Intestinal Barrier Function in Experimental Colitis in the Rat Model,”
Journal of Gastroenterology and Hepatology
14, no. 9 (1999): 880–88.

14
D. Robertson et al., “Insulin-Sensitizing Effects of Dietary Resistant Starch and Effects on Skeletal Muscle and Adipose Tissue Metabolism,”
American Journal of Clinical Nutrition
82, no. 3 (2005): 559–67.

Chapter 5

1
C. S. Johnston et al., “Ketogenic Low-Carbohydrate Diets Have No Metabolic Advantage over Nonketogenic Low-Carbohydrate Diets,”
American Journl of Clinical Nutrition
83, no. 5 (May 2006): 1055–61.

2
S. Soenen et al., “Relatively High-Protein or ‘Low-Carb’ Energy-Restricted Diets for Body Weight Loss and Body Weight Maintenance?”
Physiology & Behavior
107, no. 3 (October 10, 2012): 374–80.

3
A. Raben, I. Macdonald, and A. Astrup, “Replacement of Dietary Fat by Sucrose or Starch: Effects on 14 d ad libitum Energy Intake, Energy Expenditure and Body Weight in Formerly Obese and Never-Obese Subjects,”
International Journal of Obesity and Related Metabolic Disorders
21, no. 10 (1997): 846–59.

4
M. Mattson and R. Wan, “Beneficial Effects of Intermittent Fasting and Caloric Restriction on the Cardiovascular and Cerebrovascular Systems,”
Journal of Nutritional Biochemistry
16, no. 3 (2005): 129–37.

5
A. Muller et al., “Ghrelin Drives GH Secretion during Fasting in Man,”
European Journal of Endocrinology
146, no. 2 (2002): 203–7.

Chapter 6

1
S. Haskins, “4 Reasons Why Diets Don’t Work,” retrieved from
health.usnews.com/health-news/blogs/eat-run/2015/01/21/4-reasons-why-diets-dont-work
(Jan. 21, 2015).

2
Boston Medical Center, “Nutrition and Weight Management,” retrieved from
bmc.org/nutritionweight/services/weightmanagement.htm
(2014).

3
P. Schnohr, J. H. O’Keefe, J. L. Marott, P. Lange, and G. B. Jensen, “Dose of Jogging and Long-Term Mortality: The Copenhagen City Heart Study,”
Journal of the American College of Cardiology
65, no. 5 (2015): 411–19.

4
J. Talanian et al., “Two Weeks of High-Intensity Aerobic Interval Training Increases the Capacity for Fat Oxidation during Exercise in Women,”
Journal of Applied Physiology
102, no. 4 (April 2007): 1439–47.

5
M. Gibala and S. McGee, “Metabolic Adaptations to Short-Term High-Intensity Interval Training: A Little Pain for a Lot of Gain?”
Exercise and Sport Sciences Reviews
36, no. 2 (2008): 58–63.

6
D. Malatesta et al., “Effect of High-Intensity Interval Exercise on Lipid Oxidation during Postexercise Recovery,”
Medicine and Science in Sports and Exercise (Journal Impact Factor: 4.48)
41, no. 2 (February 2009): 364–74.

7
L. Deldicque, K. De Bock, M. Maris et al., “Increased p70s6k Phosphorylation during Intake of a Protein-Carbohydrate Drink Following Resistance Exercise in the Fasted State,”
European Journal of Applied Physiology
108, no. 4 (2009): 791–800.

8
L. Baylor and A. Hackney, “Resting Thyroid and Leptin Hormone Changes in Women Following Intense, Prolonged Exercise Training,”
European Journal of Applied Physiology
88, no. 4–5 (2003): 480–84. Epub 2002 Nov 22.