Dysphoria & Obesity
Cortisol stimulates our appetites, and it makes fat stick to our bellies. It also makes us obese by raising our glucose and insulin levels, as shown below.
 
 
Insulin resistance. It has been known for more than 60 years that infections cause insulin resistance and hyperglycemia. Insulin resistance makes more glucose (blood sugar) available to our brains, but it deprives liver and muscle cells of glucose they need to function and repair themselves.
         Fat cells do not become insulin resistant; when insulin and glucose are high, fat cells will happily convert the extra glucose to fat, even if our liver and muscle cells are starving. (Note to people with atrial fibrillations or congestive heart failure: Your heart is a muscle, and it can be starving even though you are eating enough to make you gain weight.)
 
Dysphoria. Insulin resistance makes us feel tired and restless. We don't feel terrible, but we don't feel good--we feel dysphoric. Dysphoric people don't feel like getting up to change TV channels, much less to go jogging around the park. Dysphoria is relieved temporarily by eating carbohydrates. When we are insulin resistant, the urge to eat carbohydrates can be overwhelming.
         What happens if you don't eat the extra carbohydrates? You feel rotten. If you eat enough carbohydrates to feel OK, to drive to work, and to function reasonably well, you are probably eating too many carbohydrates to lose weight. This is explained in more detail on page 86 of The Potbelly Syndrome.
 
Obesity. Eating lots of carbohydrates forces glucose into our muscle cells and relieves our dysphoria. Unfortunately, this makes us gain weight and it contributes to the development of metabolic syndrome. That, of course, makes our insulin resistance and dysphoria worse in the long run. Then we will need to eat still more carbohydrates to fight the increased feelings of dysphoria. Our weight goes up and down, but mostly up. If we lose a few pounds, they always come back, and they always bring a few friends with them.
 
Health spas. Insulin resistance and dysphoria explain how "health" spas help us loose weight. At a spa, we are coddled or bullied into doing a little exercise. Then we are coaxed or coerced into eating reasonable meals. The dysphoria would be intolerable if we were at work, or at home picking up after the kids. At a spa the dysphoria is ameliorated by massages, mud baths, hot tubs, reading, naps, and the company of fellow sufferers. Spas work as long as you are in them, and for a little while after you leave. I suspect that the television show The Biggest Loser works the same way.
         I'm having a little trouble imagining my giant HMO paying for me to spend a few weeks at Two Bunch Palms. On the other hand, it might save them money in the long run.
 
A good question. A good question at this point might be: "If all adults are infected with germs that raise their cortisol levels and make them insulin resistant, why aren't they all fat?"
         This question stumped me until I read a book called Fight Fat After Forty by Pamela Peeke, M.D. She explains that cortisol is produced by a group of organs called the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis produces other hormones besides cortisol, and one of them is corticotropin-releasing hormone (CRH). Dr. Peeke calls CRH the "alarm hormone." She wrote: "The Alarm Hormone is one of the most potent appetite suppressants we know of" (page 47).
         The interaction of CRH and cortisol makes some people slender and other people fat. That's not the only reason why some people stay slim, but it's an important reason.
 
More information on infections and obesity
The adaptations that lead from infections to obesity are described in more detail in the middle chapters of The Potbelly Syndrome. You can find still more details in the papers listed below.
 
Pasarica M, Dhurandhar NV. Infectobesity: obesity of infectious origin. Adv Food Nutr Res. 2007;52:61-102. Review.
 
Roberge C, Carpentier AC, Langlois MF, Baillargeon JP, Ardilouze JL, Maheux P, Gallo-Payet N. Adrenocortical dysregulation as a major player in insulin resistance and onset of obesity. Am J Physiol Endocrinol Metab. 2007 Oct 2
 
Godoy-Matos AF, Vieira AR, Moreira RO, Coutinho WF, Carraro LM, Moreira DM, Pasquali R, Meirelles RM. The potential role of increased adrenal volume in the pathophysiology of obesity-related type 2 diabetes. J Endocrinol Invest. 2006 Feb;29(2):159-63.
 
Duclos M, Marquez Pereira P, Barat P, Gatta B, Roger P. Increased cortisol bioavailability, abdominal obesity, and the metabolic syndrome in obese women. Obes Res. 2005 Jul;13(7):1157-66.
 
Dimitriou T, Maser-Gluth C, Remer T. Adrenocortical activity in healthy children is associated with fat mass. Am J Clin Nutr. 2003 Mar;77(3):731-6.
 
Marniemi J, Kronholm E, Aunola S, Toikka T, Mattlar CE, Koskenvuo M, Ronnemaa T. Visceral fat and psychosocial stress in identical twins discordant for obesity. J Intern Med. 2002 Jan;251(1):35-43.
 
Alesci S, Ramsey WJ, Bornstein SR, Chrousos GP, Hornsby PJ, Benvenga S, Trimarchi F, Ehrhart-Bornstein M. Adenoviral vectors can impair adrenocortical steroidogenesis: clinical implications for natural infections and gene therapy. Proc Natl Acad Sci U S A. 2002 May 28;99(11):7484-9.
 
Andrew R, Gale CR, Walker BR, Seckl JR, Martyn CN. Glucocorticoid metabolism and the Metabolic Syndrome: associations in an elderly cohort.Exp Clin Endocrinol Diabetes. 2002 Sep;110(6):284-90.
 
Ekesbo R, Nilsson PM, Lindholm LH, Persson K, Wadstrom T. Combined seropositivity for H. pylori and C. pneumoniae is associated with age, obesity and social factors. J Cardiovasc Risk. 2000 Jun;7(3):191-5.
 
Birketvedt GS, Florholmen J, Sundsfjord J, Osterud B, Dinges D, Bilker W, Stunkard A. Behavioral and neuroendocrine characteristics of the night-eating syndrome. JAMA. 1999 Aug 18;282(7):657-63.
 
Andrew R, Phillips DI, Walker BR. Obesity and gender influence cortisol secretion and metabolism in man. J Clin Endocrinol Metab. 1998 May;83(5):1806-9.
 
Toplak H, Haller EM, Lauermann T, Weber K, Bahadori B, Reisinger EC, Tilz GP, Wascher TC. Increased prevalence of IgA-Chlamydia antibodies in NIDDM patients. Diabetes Res Clin Pract. 1996 Apr;32(1-2):97-101.
 
Toplak H, Wascher TC, Weber K, Lauermann T, Reisinger EC, Bahadori B, Tilz GP, Haller EM. [Increased prevalence of serum IgA Chlamydia antibodies in obesity] Acta Med Austriaca. 1995;22(1-2):23-4. German.
 
Pasquali R, Cantobelli S, Casimirri F, Capelli M, Bortoluzzi L, Flamia R, Labate AM, Barbara L. The hypothalamic-pituitary-adrenal axis in obese women with different patterns of body fat distribution. J Clin Endocrinol Metab. 1993 Aug;77(2):341-6.
 

More information on dysphoria

The U.S. National Institute on Alcohol Abuse and Alcoholism defines dysphoria as: "A feeling of emotional and⁄or mental discomfort, restlessness, malaise, and depression." Roughly speaking, its the opposite of euphoria.

         Dysphoria is not exactly the same thing as depression, but the two disorders are often found together. Some studies discussing dysphoria are listed below.

 
Spring B, Schneider K, Smith M, Kendzor D, Appelhans B, Hedeker D, Pagoto S. Abuse potential of carbohydrates for overweight carbohydrate cravers. Psychopharmacology (Berl). 2008 May;197(4):637-47. Epub 2008 Feb 14.
 
Gibson EL. Emotional influences on food choice: sensory, physiological and psychological pathways. Physiol Behav. 2006 Aug 30;89(1):53-61. Epub 2006 Mar 20. Review.
 
Corvera-Tindel T, Doering LV, Gomez T, Dracup K. Predictors of noncompliance to exercise training in heart failure. J Cardiovasc Nurs. 2004 Jul-Aug;19(4):269-77; quiz 278-9.
 
Musselman DL, Betan E, Larsen H, Phillips LS. Relationship of depression to diabetes types 1 and 2: epidemiology, biology, and treatment. Biol Psychiatry. 2003 Aug 1;54(3):317-29. Review.
 
Sexton H, Søgaard AJ, Olstad R. How are mood and exercise related? Results from the Finnmark study. Soc Psychiatry Psychiatr Epidemiol. 2001 Jul;36(7):348-53.
 
Sherwood NE, Jeffery RW, Wing RR. Binge status as a predictor of weight loss treatment outcome. Int J Obes Relat Metab Disord. 1999 May;23(5):485-93.
 
Lloyd HM, Rogers PJ, Hedderley DI, Walker AF. Acute effects on mood and cognitive  performance of breakfasts differing in fat and carbohydrate content. Appetite. 1996 Oct;27(2):151-64.
 
Polivy J. Psychological consequences of food restriction. J Am Diet Assoc. 1996 Jun;96(6):589-92; quiz 593-4. Review.
 
Møller SE. Serotonin, carbohydrates, and atypical depression. Pharmacol Toxicol. 1992;71 Suppl 1:61-71. Review.
 
Wurtman JJ. Carbohydrate craving. Relationship between carbohydrate intake and disorders of mood. Drugs. 1990;39 Suppl 3:49-52. Review.
 
Rodin J, Schank D, Striegel-Moore R. Psychological features of obesity. Med Clin North Am. 1989 Jan;73(1):47-66. Review.
 
Schuman M, Gitlin MJ, Fairbanks L. Sweets, chocolate, and atypical depressive traits. J Nerv Ment Dis. 1987 Aug;175(8):491-5.

 

 

 

 

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