LETTERS TO THE EDITOR
High fructose corn syrupAdam Truax, R-PAC
Drexel University, Philadelphia, PA, USAAmanda K. Bliss, RD, CDN
Kenmore Mercy Hospital, Kenmore, NY, USASanjay Gupta, MD
BryLin Hospital at Buffalo, Buffalo, NY, USA, State University of New York Upstate Medical University, Syracuse, NY, USA
KEYWORDS: high fructose corn syrup, obesity, mentally ill, metabolic abnormalities
ANNALS OF CLINICAL PSYCHIATRY 2011;23(3):228-229
TO THE EDITOR:
The ingestion of fructose in the form of high fructose corn syrup (HFCS) via soft drinks and pre-packaged foods has risen dramatically in the United States. There has been a significant increase in the prevalence of obesity (in both children and adults) and diabetes. From 1977 to 2007, the amount of HFCS consumed per capita annually increased from 9.6 lbs to 56.3 lbs.1 The presence of HFCS in the American food supply is ubiquitous, with fructose representing more than 40% of sweeteners added to prepared foods and beverages, such as non-diet soft drinks.2 Type 2 diabetes, or non-insulin-dependent diabetes mellitus (NIDDM), affects 23.6 million people in the United States, or 8% of the population. The prevalence of NIDDM increased 13.5% from 2005 to 2007.3,4 Patients with schizophrenia and other chronic psychiatric disorders are at particularly high risk for developing NIDDM.5
Although the exact mechanisms underlying fructose-induced metabolic disturbances are still under debate, several unique characteristics of fructose metabolism implicate HFCS as a contributor to the rise in obesity, NIDDM, and the associated cardiovascular sequelae. In contrast to glucose metabolism, fructose undergoes rapid uptake into the liver and avoids regulation by phosphofructokinase, the main regulatory enzyme in glycolysis. Therefore, fructose continuously enters the glycolytic pathway. By circumventing the major regulatory step in glycolysis, fructose up-regulates the lipogenic substrates acetyl-CoA and glycerol-3-phosphate, leading to the overproduction of triglycerides.6-8 Although fructose metabolism may lead to dyslipidemia—which contributes to insulin resistance and impaired glucose tolerance—fructose fails to induce the production of leptin, a key hormone involved with appetite suppression.9-11 Another unique consequence of fructose metabolism is increased plasma uric acid levels, which are associated with obesity and hypertension.12,13 The metabolic disturbances resulting from HFCS ingestion and subsequent metabolism of fructose contribute to the development of dyslipidemia, weight gain, insulin resistance, and hypertension, all of which are components of metabolic syndrome.14
The relationship between HFCS and metabolic syndrome is of acute relevance to the psychiatric community. The administration of psychotropic medications, such as atypical antipsychotics, can lead to increased appetite, especially for carbohydrates, resulting in increased consumption of foods and beverages sweetened with HFCS.15,16 There also is increased thirst as a result of consumption of carbohydrates, psychotropic medications, and sweetened drinks. Increased thirst often leads to further consumption of beverages, such as soda, which have a high HFCS content. It is known that many chronically psychiatrically ill patients may consume as many as 2 to 4 liters of soda a day. Often, individuals use these drinks as a substitute for water because they “don’t like the taste of water.”
Satiety is regulated largely in the brain by serotonin. Serotonin’s effect on curtailing appetite can be amplified by consumption of carbohydrates, except fructose.16 The consumption of fructose—the only sugar that does not turn off appetite—is likely a major cause of obesity compounded by the effect of psychotropic medications and lifestyle issues.
There is a high prevalence of obesity, hypertriglyceridemia, and hyperglycemia among psychiatric patients, who are at increased risk for acquiring metabolic syndrome. These factors ultimately decrease life expectancy for these patients.15-17 Psychiatrists can reduce the pernicious effects of fructose metabolism by discouraging the consumption of products made with HFCS, such as soft drinks and prepackaged foods, and by recommending consumption of balanced meals and decreased portion sizes, increased water intake to maintain hydration and curb appetite, and increased intake of fresh fruits and vegetables. Physical activity, at least 30 minutes daily, also should be emphasized.
Educate patients on the use of artificial sweeteners as a means to decrease HFCS consumption. Artificial sweeteners can be chemical and/or natural compounds.18 These products offer the same sweetening ability as regular sucrose (table sugar) with fewer calories.18 Use of these alternative sweeteners is popular as part of weight loss/weight maintenance programs and by individuals with diabetes.18
Much of the controversy surrounding artificial sweeteners concerns their questionable association with cancer. The American Cancer Society reports that multiple carcinogenicity studies have yet to provide a strong association between using FDA-approved sweeteners and developing cancer.19 The FDA provides a list of approved sweeteners, which are generally recognized as safe, and the recommended acceptable daily intake.18,19 If patients remain hesitant to consume artificial sweeteners, encourage them to decrease their caloric consumption by consuming sucrose in controlled and limited amounts.
Practitioners can provide a great benefit to their patients through education. There is an unmet need for further multidisciplinary studies to better assess the connection between elevated HFCS consumption and health disparities that plague psychiatric patients. In conclusion, focusing on a comprehensive approach to treatment that includes behavior modification (diet and exercise) and continued reinforcement may be of most benefit to this patient population.
DISCLOSURE: The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
- United States Department of Agriculture. U.S. per capita caloric sweeteners estimated deliveries for domestic food and beverage use by calendar year. 2008. Available at: http://www.ers.usda.gov/Briefing/Sugar/data/table50.xls. Accessed September 29, 2008.
- Bray GA, Nielsen SJ, Popkin BM. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr. 2004;79:537–543.
- American Diabetes Association. Total prevalence of diabetes and pre-diabetes. Available at: http://www.diabetesarchive.net/diabetes-statistics/prevalence.jsp. Accessed September 29 2008.
- Centers for Disease Control and Prevention. Number (in millions) of persons with diagnosed diabetes United States, 1980-2003. Available at: http://www.cdc.gov/diabetes/statistics/prev/national/figpersons.htm. Accessed September 29, 2008.
- Mukherjee S, Decina P, Bocola V, et al. Diabetes mellitus in schizophrenic patients. Compr Psychiatry. 1996;37:68–73.
- Mayes PA. Intermediary metabolism of fructose. Am J Clin Nutr. 1993;58:7545–7655.
- Rutledge AC, Adeli K. Fructose and the metabolic syndrome: pathophysiology and molecular mechanisms. Nutr Rev. 2007;65:S13–S23.
- Fried SK, Rao SP. Sugars hypertriglyceridemia, and cardiovascular disease. Am J Clin Nutr. 2003;78:873S–880S.
- Basciano H, Federico L, Adeli K. Fructose insulin resistance, and metabolic dyslipidemia. Nutr Metab (Lond). 2005;2:5.
- Havel PJ. Control of energy homeostasis and insulin action by adipocyte hormones: leptin acylation stimulating protein, and adiponectin. Curr Opin Lipidol. 2002;13:51–59.
- Havel PJ. Peripheral signals conveying metabolic information to the brain: short-term and long-term regulation of food intake and energy homeostasis. Exp Biol Med. 2001;226:963–977.
- Heinig M, Johnson RJ. Role of uric acid in hypertension renal disease, and metabolic syndrome. Cleve Clin J Med. 2006;73:1059–1064.
- Nakagawa T, Tuttle KR, Short RA, et al. Hypothesis: fructose-induced hyperuricemia as a causal mechanism for the epidemic of the metabolic syndrome. Nat Clin Pract Nephrol. 2005;1:80–86.
- Grundy SM, Brewer HB, Cleeman JI, et al. Definition of metabolic syndrome: report of the National, Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Circulation. 2004;109:433–438.
- McEvoy JP, Meyer JM, Goff DC, et al. Prevalence of the metabolic syndrome in patients with schizophrenia: baseline results from the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) schizophrenia trial and comparison with national estimates from NHANES III. Schizophr Res. 2005;80:19–32.
- Bermudes RA, Keck PE, Welge JA. The prevalence of the metabolic syndrome in psychiatric inpatients with primary psychotic and mood disorders. Psychosomatics. 2006;47:491–497.
- Rassman J, Gupta S. The metabolic syndrome: Modify root causes and treat risk factors. JAAPA. 2005;18:30–36.
- Mayo Clinic. Artificial sweeteners: a safe alternative to sugar? 2008. Available at: http://www.mayoclinic.com/health/artificialsweeteners/MY00073. Accessed September 28 2009.
- National Cancer Institute. Artificial sweeteners: understanding these and other sugar substitutes. 2009. Available at: http://www.cancer.gov/cancertopics/factsheet/Risk/artificial-sweeteners. Accessed September 28 2009.
CORRESPONDENCE: Sanjay Gupta, MD, 230 Bewley Building, Lockport, NY 14094 USA; E-MAIL: email@example.com
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