My health insurance rate just went up. Why? Because the company we use was forced by the current health care reform to open their underwriting to accept more high risk clients. In other words, they now must insure unhealthy and/or potentially unhealthy individual which raises this company's medical care payouts. In essence, I now pay to cover the health care costs of others who have chosen to live unhealthy lives. I don't expect anyone else to take care of my health for me. It is my responsibility alone. Esp. when it comes to my lifestyle and lifestyle related disease (which is the leading cause of the top 4 killers in America: heart disease, diabetes, cancer, stroke). Is this fair? No, it is socialized medicine. If Americans lived a healthier lifestyle this wouldn't be such a big deal. But we are a VERY unhealthy country!
In 2008, health care spending in the United States reached $2.4 trillion, and was projected to reach $3.1 trillion in 2012. (Keehan, S. et al. “Health Spending Projections Through 2017, Health Affairs Web Exclusive W146: 21 February 2008.)
Health care spending is projected to reach $4.3 trillion by 2016. (Keehan, S. et al. “Health Spending Projections Through 2017, Health Affairs Web Exclusive W146: 21 February 2008.)
Health care spending is 4.3 times the amount spent on national defense. (California Health Care Foundation. Health Care Costs 101 -- 2005. 02 March 2005)
In 2008, the United States will spend 17 percent of its gross domestic product (GDP) on health care. It is projected that the percentage will reach 20 percent by 2017. (Keehan, S. et al. “Health Spending Projections Through 2017, Health Affairs Web Exclusive W146: 21 February 2008.)
Although nearly 46 million Americans are uninsured, the United States spends more on health care than other industrialized nations, and those countries provide health insurance to all their citizens.
Health care spending accounted for 10.9 percent of the GDP in Switzerland, 10.7 percent in Germany, 9.7 percent in Canada and 9.5 percent in France, according to the Organization for Economic Cooperation and Development.
We know that we are over-utilizing many health care services such as CT, and MRI. We also love our RX drugs. We consume more RX drugs and receive more surgical interventions than ever before in our countries history, but we are sicker than ever.
What does this all lead us to believe? We have very unhealthy lifestyle compared to other industrialized countries. What lifestyle choices are we talking about? It all about what we Americans eat, how we think, and our level of physical activity. I don't want us to be Europe. I love American. But McDonald's, Crispy Cream and Starbucks shouldn't be a staple.
More to come soon . . . We need to Create Wellness
Wednesday, April 8, 2009
Friday, March 27, 2009
Daily Consumption of Diet Soda Linked to Metabolic Syndrome, Type 2 Diabetes
Originally printed online at Medscape
Daily Consumption of Diet Soda Linked to Metabolic Syndrome, Type 2 Diabetes
February 11, 2009 — Drinking diet soda at least daily is associated with significantly greater risks for select incident components of the metabolic syndrome (MetSyn) and type 2 diabetes, according to the results of an observational study reported in the January 16 Online First issue of Diabetes Care.
"Two longitudinal cohort studies have shown positive associations between diet soda consumption and incident MetSyn independent of baseline measures of adiposity," write Jennifer A. Nettleton, PhD, from the University of Texas Health Sciences Center in Houston, and colleagues. "Replication of previously observed diet soda-MetSyn associations in a distinct cohort would bolster their credibility and provide further insight into the nature of the relationship. Previous studies have not addressed associations between diet soda and individual MetSyn components or risk of type 2 diabetes nor have they fully addressed potential longitudinal mediators of these relationships, i.e., changes in adiposity status."
The goal of this study was to evaluate associations between diet soda consumption and the risk for incident MetSyn, its components, and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA).
Initial evaluation was performed from 2000 to 2002, at which time baseline food frequency questionnaires measured diet soda consumption. Three follow-up evaluations were performed from 2002 to 2003, 2004 to 2005, and 2005 to 2007. Incident type 2 diabetes was defined as fasting glucose levels of more than 126 mg/dL, self-reported type 2 diabetes, or use of diabetes medication. National Cholesterol Education Program Adult Treatment Panel 3 criteria were used to define MetSyn and its components. After adjustment for demographic, lifestyle, and dietary confounders, hazard ratios (HRs) were estimated for type 2 diabetes, MetSyn, and MetSyn components.
Compared with participants who did not drink diet soda, those who drank diet soda at least daily had a 36% greater relative risk for incident MetSyn (HR, 1.36; 95% confidence interval [CI], 1.11 - 1.66) and a 67% greater relative risk for incident type 2 diabetes (HR, 1.67; 95% CI, 1.27 - 2.20).
Of the individual components of MetSyn, only high waist circumference (men: ≥ 102 cm; women: ≥ 88 cm) and high fasting glucose levels (≥ 100 mg/dL) were prospectively associated with consumption of diet soda. Associations between diet soda intake and type 2 diabetes were independent of baseline measures of adiposity or changes in these measures. In contrast, associations between diet soda and MetSyn were not independent of these factors.
"Although these observational data cannot establish causality, consumption of diet soda at least daily was associated with significantly greater risks of select incident MetSyn components and type 2 diabetes," the study authors write.
Limitations of this study include observational design, precluding determination of causality; possible confounding by other dietary and lifestyle/behavioral factors; and difficulties in estimating intake of diet soda or artificial sweetener.
"These results corroborate findings from the ARIC [Atherosclerosis Risk in Communities] and Framingham studies and show stronger adverse associations exist between diet soda and type 2 diabetes," the study authors conclude. "Diet soda consumption, either independently or in conjunction with other dietary and lifestyle behaviors, may lead to weight gain, impaired glucose control, and eventual diabetes."
The National Heart, Lung, and Blood Institute supported this study. The study authors have disclosed no relevant financial relationships.
Diabetes Care. Published online January 16, 2009.
Daily Consumption of Diet Soda Linked to Metabolic Syndrome, Type 2 Diabetes
February 11, 2009 — Drinking diet soda at least daily is associated with significantly greater risks for select incident components of the metabolic syndrome (MetSyn) and type 2 diabetes, according to the results of an observational study reported in the January 16 Online First issue of Diabetes Care.
"Two longitudinal cohort studies have shown positive associations between diet soda consumption and incident MetSyn independent of baseline measures of adiposity," write Jennifer A. Nettleton, PhD, from the University of Texas Health Sciences Center in Houston, and colleagues. "Replication of previously observed diet soda-MetSyn associations in a distinct cohort would bolster their credibility and provide further insight into the nature of the relationship. Previous studies have not addressed associations between diet soda and individual MetSyn components or risk of type 2 diabetes nor have they fully addressed potential longitudinal mediators of these relationships, i.e., changes in adiposity status."
The goal of this study was to evaluate associations between diet soda consumption and the risk for incident MetSyn, its components, and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA).
Initial evaluation was performed from 2000 to 2002, at which time baseline food frequency questionnaires measured diet soda consumption. Three follow-up evaluations were performed from 2002 to 2003, 2004 to 2005, and 2005 to 2007. Incident type 2 diabetes was defined as fasting glucose levels of more than 126 mg/dL, self-reported type 2 diabetes, or use of diabetes medication. National Cholesterol Education Program Adult Treatment Panel 3 criteria were used to define MetSyn and its components. After adjustment for demographic, lifestyle, and dietary confounders, hazard ratios (HRs) were estimated for type 2 diabetes, MetSyn, and MetSyn components.
Compared with participants who did not drink diet soda, those who drank diet soda at least daily had a 36% greater relative risk for incident MetSyn (HR, 1.36; 95% confidence interval [CI], 1.11 - 1.66) and a 67% greater relative risk for incident type 2 diabetes (HR, 1.67; 95% CI, 1.27 - 2.20).
Of the individual components of MetSyn, only high waist circumference (men: ≥ 102 cm; women: ≥ 88 cm) and high fasting glucose levels (≥ 100 mg/dL) were prospectively associated with consumption of diet soda. Associations between diet soda intake and type 2 diabetes were independent of baseline measures of adiposity or changes in these measures. In contrast, associations between diet soda and MetSyn were not independent of these factors.
"Although these observational data cannot establish causality, consumption of diet soda at least daily was associated with significantly greater risks of select incident MetSyn components and type 2 diabetes," the study authors write.
Limitations of this study include observational design, precluding determination of causality; possible confounding by other dietary and lifestyle/behavioral factors; and difficulties in estimating intake of diet soda or artificial sweetener.
"These results corroborate findings from the ARIC [Atherosclerosis Risk in Communities] and Framingham studies and show stronger adverse associations exist between diet soda and type 2 diabetes," the study authors conclude. "Diet soda consumption, either independently or in conjunction with other dietary and lifestyle behaviors, may lead to weight gain, impaired glucose control, and eventual diabetes."
The National Heart, Lung, and Blood Institute supported this study. The study authors have disclosed no relevant financial relationships.
Diabetes Care. Published online January 16, 2009.
Sunday, March 15, 2009
More on Coconut Oil
Virgin Coconut Oil is a food, and is one of the best cooking oils you can use. It has been a staple cooking oil for thousands of years in tropical climates. As a cooking oil, its chemical structure is kept in tact and therefore is resistant to mutations of fatty acid chains even when used in higher cooking temperatures, unlike most vegetable oils. Research shows that the medium chain fatty acids found in coconut oil boosts the body’s metabolism, raises body temperatures, and helps provide greater energy which can lead to weight loss.
Virgin Coconut oil is rich in lauric acid, a nutrient that supports the body’s immune system. Lauric acid is also found in human mother’s milk. Dr. Mary Enig (Lipid Chemist) suggests the average adult include about 3.5 tablespoons of coconut oil per day in their diet to take in an equivalent amount of lauric acid that a nursing infant would receive from breast milk.
Virgin Coconut oil is rich in lauric acid, a nutrient that supports the body’s immune system. Lauric acid is also found in human mother’s milk. Dr. Mary Enig (Lipid Chemist) suggests the average adult include about 3.5 tablespoons of coconut oil per day in their diet to take in an equivalent amount of lauric acid that a nursing infant would receive from breast milk.
Sunday, March 8, 2009
Coconut Oil and Weight Loss
I'm often asked about what comprises a good diet and what's better, more carbs, less fat, no carbs etc. The best rule of thumb is to remember that food is intended to be fuel for the body. Looking at calories is good, but also considering the calorie sources is important. For instance; white sugar and flour would be considered simple or refined carbs. These are poor choices for calories. Likewise, calories from heavy saturated animal fat and trans fats are also poor calorie choices. Now there are good fats, though. Unfortunately the 80s were not kind to fats. We were misinformed that because fat has more calories per gram that carbs, then carbs must be better to consume than fat. This is too simplistic. Some fats actually stimulate the metabolism and are healthy. Take coconut oil for instance. It is a saturated plant fat that has very good thermogenic and antimicrobial properties. I added two tables spoons to the smoothie that my wife and I enjoy for breakfast every morning. Within weeks her and I had lost 10 pounds. You actually feel warm after consuming coconut oil. Heat is a byproduct of metabolism. Stay tuned for my smoothie recipe in upcoming blogs.
Friday, February 13, 2009
Cow's Milk and Autoimmune Diseases
Cow's Milk and Autoimmune Diseases
Pedro Bastos
Autoimmune diseases (AD) are the most common illnesses in the U.S., afflicting five to eight percent of the American population,1 especially women.2
AD develop when the body's immune system loses the ability to distinguish between what is "self" and what is "non-self," and attacks healthy tissues and organs as if they were a foreign invader like a bacteria or virus.1
The resulting disease depends on which tissues are involved. For instance, in celiac disease, the targeted tissue is small bowel mucosa. In type 1 diabetes, the insulin producing pancreatic beta cells are involved. The thyroid gland is the affected organ in autoimmune thyroid diseases. In Sjögren's syndrome, the attack is directed to the glands that secrete saliva and tears. The joints are affected in rheumatoid arthritis, and it is the gastrointestinal tract that is affected in Crohn's disease. In psoriasis, the skin is affected, and in Multiple Sclerosis, the target tissue is the myelin sheath surrounding nerves.
Although AD have a genetic predisposition,1,3 the concordance rate between twins is only about 30 %, so the interaction between one's genotype and several environmental factors plays a major role.1-3
In the last 20 years, several dietary factors have been implicated in AD such as drugs,1 heavy metals,1 viral and bacterial infections,1 vitamin D deficiency,4-14 and gluten consumption15-37 (that's a group of water-soluble proteins found in wheat, barley, rye and oats15). It also appears that cow's milk is involved in certain AD, as well.
Various epidemiological studies have associated milk with T1D38-45, especially when the initial exposure begins in the first months of life. This evidence appears to be consistence, since various reviews of the scientific literature published in 199346, 199447,48, 199849, 199950,51, 200252, 200353 and 200554,55 corroborate the association between cow's milk drinking and T1D.
Regarding MS and cow's milk consumption, epidemiological studies have also repeatedly shown a strong correlation56-60.
The most likely mechanism is called molecular mimicry whereby amino acid sequences from milk proteins resemble amino acid sequences in our body's organs and tissues.
Indeed, there is molecular mimicry between bovine insulin (present in cow's milk) and human insulin61-66, which may explain the Cow's Milk-T1D connection.
Molecular mimicry is also a suspected mechanism explaining the MS connection and the implicated milk proteins are:
Butyrophilin(a bovine milk fat globule protein), since there is molecular mimicry between this protein and myelin oligodendrocyte glycoprotein (MOG), an autoantigen involved in MS.67
Bovine serum albumin(one of the proteins in cow's milk whey), as there is structural similarity between this protein and the autoantigen myelin basic protein.68
Finally, there is molecular mimicry between bovine serum albumin and human collagen type 1, which has implications for RA69. Indeed, case studies have shown that elimination of milk and dairy products from the diets of patients with RA improved symptoms, and the disease was markedly exacerbated on re-challenge.69
Bovine Milk is also implicated in other auto-immune diseases, such as Crohn's disease70, Sjögren's syndrome71 and even celiac disease.72
Based on this evidence, it appears that people with an elevated risk for auto-immune diseases or already with the disease would benefit from a dairy free diet, which is one of the characteristics of the Paleo Diet.
References:
References:
1. Progress in Autoimmune Disease Research. The Autoimmune Disease Coordinating Committee Report to Congress. U.S. Department of Health and Human Services, National Institutes of Health, National Institute of Allergy and Infectious Diseases. Bethesda (MD), 2005. http://www3.niaid.nih.gov/topics/autoimmune/PDF/ADCCFinal.pdf
2. Fairweather D, Rose NR. Women and autoimmune disease. Emerg Infect Dis 2004;10:2005-2011. http://www.cdc.gov/ncidod/EID/vol10no11/04-0367.htm
3. Rose N R, Mackay IR. The auto-immune diseases. Academic Press, 2006
4. Mohr SB, Garland CF, Gorham ED, Garland FC. The association between ultraviolet B irradiance, vitamin D status and incidence rates of type 1 diabetes in 51 regions worldwide. Diabetologia. 2008 Jun 12.
5. Cutolo M, Otsa K, Uprus M, Paolino S, Seriolo B. Vitamin D in rheumatoid arthritis. Autoimmun Rev. 2007 Nov;7(1):59-64.
6. Ramagopalan SV, Maugeri NJ, Handunnetthi L, Lincoln MR, Orton SM, Dyment DA, Deluca GC, Herrera BM, Chao MJ, Sadovnick AD, Ebers GC, Knight JC. Expression of the multiple sclerosis-associated MHC class II Allele HLA-DRB1*1501 is regulated by vitamin D. PLoS Genet. 2009 Feb;5(2):e1000369
7. Niino M, Fukazawa T, Kikuchi S, Sasaki H. Therapeutic potential of vitamin D for multiple sclerosis. Curr Med Chem. 2008;15(5):499-505
8. Stefanić M, Papić S, Suver M, Glavas-Obrovac L, Karner I. Association of vitamin D receptor gene 3'-variants with Hashimoto's thyroiditis in the Croatian population. Int J Immunogenet. 2008 Apr;35(2):125-31.
9. Lin WY, Wan L, Tsai CH, Chen RH, Lee CC, Tsai FJ. Vitamin D receptor gene polymorphisms are associated with risk of Hashimoto's thyroiditis in Chinese patients in Taiwan. J Clin Lab Anal. 2006;20(3):109-12.
10. Nancy AL, Yehuda S. Prediction and prevention of autoimmune skin disorders. Arch Dermatol Res. 2009 Jan;301(1):57-64
11. Bang B, Asmussen K, Sørensen OH, Oxholm P. Reduced 25-hydroxyvitamin D levels in primary Sjögren's syndrome. Correlations to disease manifestations. Scand J Rheumatol. 1999;28(3):180-3.
12. Müller K, Oxholm P, Sørensen OH, Thymann M, Høier-Madsen M, Bendtzen K. Abnormal vitamin D3 metabolism in patients with primary Sjögren's syndrome. Ann Rheum Dis. 1990 Sep;49(9):682-4.
13. Naderi N, Farnood A, Habibi M, Derakhshan F, Balaii H, Motahari Z, Agah MR, Firouzi F, Rad MG, Aghazadeh R, Zojaji H, Zali MR. Association of vitamin D receptor gene polymorphisms in Iranian patients with inflammatory bowel disease. J Gastroenterol Hepatol. 2008 Dec;23(12):1816-22.
14. Simmons JD, Mullighan C, Welsh KI, Jewell DP. Vitamin D receptor gene polymorphism: association with Crohn's disease susceptibility. Gut. 2000 Aug;47(2):211-4.
15. McGough N, Cummings JH. Coeliac disease: a diverse clinical syndrome caused by intolerance of wheat, barley and rye. Proc Nutr Soc. 2005 Nov;64(4):434-50
16. Toumi D, Mankai A, Belhadj R, Ghedira-Besbes L, Jeddi M, Ghedira I. Thyroid-related autoantibodies in Tunisian patients with coeliac disease. Clin Chem Lab Med. 2008;46(3):350-3.
17. Spadaccino AC, Basso D, Chiarelli S, Albergoni MP, D'Odorico A, Plebani M, Pedini B, Lazzarotto F, Betterle C. Celiac disease in North Italian patients with autoimmune thyroid diseases. Autoimmunity. 2008 Feb;41(1):116-21.
18. Iuorio R, Mercuri V, Barbarulo F, D'Amico T, Mecca N, Bassotti G, Pietrobono D, Gargiulo P, Picarelli A. Prevalence of celiac disease in patients with autoimmune thyroiditis. Minerva Endocrinol. 2007 Dec;32(4):239-43.
19. Ch'ng CL, Jones MK, Kingham JG. Celiac disease and autoimmune thyroid disease. Clin Med Res. 2007 Oct;5(3):184-92.
20. Maclaurin BP, Matthews N, Kilpatrick JA. Coeliac disease associated with auto-immune thyroiditis, Sjogren's syndrome, and a lymphocytotoxic serum factor. Aust N Z J Med. 1972 Nov;2(4):405-11. No abstract available.
21. Pittman Fe, Holub Da. Sjoegren's Syndrome and Adult Celiac Disease. Gastroenterology. 1965 Jun;48:869-76.
22. Teppo AM, Maury CP. Antibodies to gliadin, gluten and reticulin glycoprotein in rheumatic diseases:elevated levels in Sjögren's syndrome. Clin Exp Immunol. 1984 Jul;57(1):73-8.
23. Szodoray P, Barta Z, Lakos G, Szakáll S, Zeher M. Coeliac disease in Sjögren's syndrome--a study of 111 Hungarian patients. Rheumatol Int. 2004 Sep;24(5):278-82.
24. Lidén M, Kristjánsson G, Valtýsdóttir S, Hällgren R. Gluten sensitivity in patients with primary Sjögren's syndrome. Scand J Gastroenterol. 2007 Aug;42(8):962-7.
25. Paimela L, Kurki P, Leirisalo-Repo M, Piirainen H. Gliadin immune reactivity in patients with rheumatoid arthritis. Clin Exp Rheumatol. 1995 Sep-Oct;13(5):603-7.
26. Cordain L, Toohey L, Smith MJ, Hickey MS. Modulation of immune function by dietary lectins in rheumatoid arthritis. Br J Nutr. 2000 Mar;83(3):207-17.
27. Hafstrom I, Ringertz B, Spangberg A, von Zweigbergk L, Brannemark S, Nylander I, Ronnelid J, Laasonen L, Klareskog L: A vegan diet free of gluten improves the signs and symptoms of rheumatoid arthritis: the effects on arthritis correlate with a reduction in antibodies to food antigens. Rheumatology (Oxford) 2001, 40:1175-1179.
28. Reichelt KL, Jensen D. IgA antibodies against gliadin and gluten in multiple sclerosis. Acta Neurol Scand. 2004 Oct;110(4):239-41
29. Pengiran Tengah CD, Lock RJ, Unsworth DJ, Wills AJ. Multiple sclerosis and occult gluten sensitivity. Neurology. 2004 Jun 22;62(12):2326-7.
30. Michaëlsson G, Gerdén B, Ottosson M, Parra A, Sjöberg O, Hjelmquist G, Lööf L. Patients with psoriasis often have increased serum levels of IgA antibodies to gliadin. Br J Dermatol. 1993 Dec;129(6):667-73.
31. Michaëlsson G, Gerdén B, Hagforsen E, Nilsson B, Pihl-Lundin I, Kraaz W, Hjelmquist G, Lööf L. Psoriasis patients with antibodies to gliadin can be improved by a gluten-free diet. Br J Dermatol. 2000 Jan;142(1):44-51.
32. Hoorfar J, Buschard K, Dagnaes-Hansen F. Prophylactic nutritional modification of the incidence of diabetes in autoimmune non-obese diabetic (NOD) mice. Br J Nutr. 1993 Mar;69(2):597-607.
33. Scott FW. Food-induced type 1 diabetes in the BB rat. Diabetes Metab Rev 1996;12:341-59.
34. Schmid S, Koczwara K, Schwinghammer S, Lampasona V, Ziegler AG, Bonifacio E. Delayed exposure to wheat and barley proteins reduces diabetes incidence in non-obese diabetic mice. Clin Immunol. 2004 Apr;111(1):108-18.
35. Ziegler A-G, Schmid S, Huber D, Hummel M, Bonifacio E. Early infant feeding and risk of developing type 1 diabetes-associated autoantibodies. JAMA 2003;290:1721-8.
36. Pastore M-R, Bazzigaluppi E, Belloni C, Arcovio C, Bonifacio E, Bosi E. Six months of gluten-free diet do not influence antibody titers, but improve insulin secretion in subjects at high risk for type 1 diabetes. J Clin Endocrinol Metab 2003;88:162-5.
37. Banin P, Perretta R, Ravaioli E, De Sanctis V. Regression of autoimmunity and abnormal glucose homeostasis in an adolescent boy with silent coeliac disease. Acta Paediatr 2002;91:1141-3.
Pedro Bastos
Autoimmune diseases (AD) are the most common illnesses in the U.S., afflicting five to eight percent of the American population,1 especially women.2
AD develop when the body's immune system loses the ability to distinguish between what is "self" and what is "non-self," and attacks healthy tissues and organs as if they were a foreign invader like a bacteria or virus.1
The resulting disease depends on which tissues are involved. For instance, in celiac disease, the targeted tissue is small bowel mucosa. In type 1 diabetes, the insulin producing pancreatic beta cells are involved. The thyroid gland is the affected organ in autoimmune thyroid diseases. In Sjögren's syndrome, the attack is directed to the glands that secrete saliva and tears. The joints are affected in rheumatoid arthritis, and it is the gastrointestinal tract that is affected in Crohn's disease. In psoriasis, the skin is affected, and in Multiple Sclerosis, the target tissue is the myelin sheath surrounding nerves.
Although AD have a genetic predisposition,1,3 the concordance rate between twins is only about 30 %, so the interaction between one's genotype and several environmental factors plays a major role.1-3
In the last 20 years, several dietary factors have been implicated in AD such as drugs,1 heavy metals,1 viral and bacterial infections,1 vitamin D deficiency,4-14 and gluten consumption15-37 (that's a group of water-soluble proteins found in wheat, barley, rye and oats15). It also appears that cow's milk is involved in certain AD, as well.
Various epidemiological studies have associated milk with T1D38-45, especially when the initial exposure begins in the first months of life. This evidence appears to be consistence, since various reviews of the scientific literature published in 199346, 199447,48, 199849, 199950,51, 200252, 200353 and 200554,55 corroborate the association between cow's milk drinking and T1D.
Regarding MS and cow's milk consumption, epidemiological studies have also repeatedly shown a strong correlation56-60.
The most likely mechanism is called molecular mimicry whereby amino acid sequences from milk proteins resemble amino acid sequences in our body's organs and tissues.
Indeed, there is molecular mimicry between bovine insulin (present in cow's milk) and human insulin61-66, which may explain the Cow's Milk-T1D connection.
Molecular mimicry is also a suspected mechanism explaining the MS connection and the implicated milk proteins are:
Butyrophilin(a bovine milk fat globule protein), since there is molecular mimicry between this protein and myelin oligodendrocyte glycoprotein (MOG), an autoantigen involved in MS.67
Bovine serum albumin(one of the proteins in cow's milk whey), as there is structural similarity between this protein and the autoantigen myelin basic protein.68
Finally, there is molecular mimicry between bovine serum albumin and human collagen type 1, which has implications for RA69. Indeed, case studies have shown that elimination of milk and dairy products from the diets of patients with RA improved symptoms, and the disease was markedly exacerbated on re-challenge.69
Bovine Milk is also implicated in other auto-immune diseases, such as Crohn's disease70, Sjögren's syndrome71 and even celiac disease.72
Based on this evidence, it appears that people with an elevated risk for auto-immune diseases or already with the disease would benefit from a dairy free diet, which is one of the characteristics of the Paleo Diet.
References:
References:
1. Progress in Autoimmune Disease Research. The Autoimmune Disease Coordinating Committee Report to Congress. U.S. Department of Health and Human Services, National Institutes of Health, National Institute of Allergy and Infectious Diseases. Bethesda (MD), 2005. http://www3.niaid.nih.gov/topics/autoimmune/PDF/ADCCFinal.pdf
2. Fairweather D, Rose NR. Women and autoimmune disease. Emerg Infect Dis 2004;10:2005-2011. http://www.cdc.gov/ncidod/EID/vol10no11/04-0367.htm
3. Rose N R, Mackay IR. The auto-immune diseases. Academic Press, 2006
4. Mohr SB, Garland CF, Gorham ED, Garland FC. The association between ultraviolet B irradiance, vitamin D status and incidence rates of type 1 diabetes in 51 regions worldwide. Diabetologia. 2008 Jun 12.
5. Cutolo M, Otsa K, Uprus M, Paolino S, Seriolo B. Vitamin D in rheumatoid arthritis. Autoimmun Rev. 2007 Nov;7(1):59-64.
6. Ramagopalan SV, Maugeri NJ, Handunnetthi L, Lincoln MR, Orton SM, Dyment DA, Deluca GC, Herrera BM, Chao MJ, Sadovnick AD, Ebers GC, Knight JC. Expression of the multiple sclerosis-associated MHC class II Allele HLA-DRB1*1501 is regulated by vitamin D. PLoS Genet. 2009 Feb;5(2):e1000369
7. Niino M, Fukazawa T, Kikuchi S, Sasaki H. Therapeutic potential of vitamin D for multiple sclerosis. Curr Med Chem. 2008;15(5):499-505
8. Stefanić M, Papić S, Suver M, Glavas-Obrovac L, Karner I. Association of vitamin D receptor gene 3'-variants with Hashimoto's thyroiditis in the Croatian population. Int J Immunogenet. 2008 Apr;35(2):125-31.
9. Lin WY, Wan L, Tsai CH, Chen RH, Lee CC, Tsai FJ. Vitamin D receptor gene polymorphisms are associated with risk of Hashimoto's thyroiditis in Chinese patients in Taiwan. J Clin Lab Anal. 2006;20(3):109-12.
10. Nancy AL, Yehuda S. Prediction and prevention of autoimmune skin disorders. Arch Dermatol Res. 2009 Jan;301(1):57-64
11. Bang B, Asmussen K, Sørensen OH, Oxholm P. Reduced 25-hydroxyvitamin D levels in primary Sjögren's syndrome. Correlations to disease manifestations. Scand J Rheumatol. 1999;28(3):180-3.
12. Müller K, Oxholm P, Sørensen OH, Thymann M, Høier-Madsen M, Bendtzen K. Abnormal vitamin D3 metabolism in patients with primary Sjögren's syndrome. Ann Rheum Dis. 1990 Sep;49(9):682-4.
13. Naderi N, Farnood A, Habibi M, Derakhshan F, Balaii H, Motahari Z, Agah MR, Firouzi F, Rad MG, Aghazadeh R, Zojaji H, Zali MR. Association of vitamin D receptor gene polymorphisms in Iranian patients with inflammatory bowel disease. J Gastroenterol Hepatol. 2008 Dec;23(12):1816-22.
14. Simmons JD, Mullighan C, Welsh KI, Jewell DP. Vitamin D receptor gene polymorphism: association with Crohn's disease susceptibility. Gut. 2000 Aug;47(2):211-4.
15. McGough N, Cummings JH. Coeliac disease: a diverse clinical syndrome caused by intolerance of wheat, barley and rye. Proc Nutr Soc. 2005 Nov;64(4):434-50
16. Toumi D, Mankai A, Belhadj R, Ghedira-Besbes L, Jeddi M, Ghedira I. Thyroid-related autoantibodies in Tunisian patients with coeliac disease. Clin Chem Lab Med. 2008;46(3):350-3.
17. Spadaccino AC, Basso D, Chiarelli S, Albergoni MP, D'Odorico A, Plebani M, Pedini B, Lazzarotto F, Betterle C. Celiac disease in North Italian patients with autoimmune thyroid diseases. Autoimmunity. 2008 Feb;41(1):116-21.
18. Iuorio R, Mercuri V, Barbarulo F, D'Amico T, Mecca N, Bassotti G, Pietrobono D, Gargiulo P, Picarelli A. Prevalence of celiac disease in patients with autoimmune thyroiditis. Minerva Endocrinol. 2007 Dec;32(4):239-43.
19. Ch'ng CL, Jones MK, Kingham JG. Celiac disease and autoimmune thyroid disease. Clin Med Res. 2007 Oct;5(3):184-92.
20. Maclaurin BP, Matthews N, Kilpatrick JA. Coeliac disease associated with auto-immune thyroiditis, Sjogren's syndrome, and a lymphocytotoxic serum factor. Aust N Z J Med. 1972 Nov;2(4):405-11. No abstract available.
21. Pittman Fe, Holub Da. Sjoegren's Syndrome and Adult Celiac Disease. Gastroenterology. 1965 Jun;48:869-76.
22. Teppo AM, Maury CP. Antibodies to gliadin, gluten and reticulin glycoprotein in rheumatic diseases:elevated levels in Sjögren's syndrome. Clin Exp Immunol. 1984 Jul;57(1):73-8.
23. Szodoray P, Barta Z, Lakos G, Szakáll S, Zeher M. Coeliac disease in Sjögren's syndrome--a study of 111 Hungarian patients. Rheumatol Int. 2004 Sep;24(5):278-82.
24. Lidén M, Kristjánsson G, Valtýsdóttir S, Hällgren R. Gluten sensitivity in patients with primary Sjögren's syndrome. Scand J Gastroenterol. 2007 Aug;42(8):962-7.
25. Paimela L, Kurki P, Leirisalo-Repo M, Piirainen H. Gliadin immune reactivity in patients with rheumatoid arthritis. Clin Exp Rheumatol. 1995 Sep-Oct;13(5):603-7.
26. Cordain L, Toohey L, Smith MJ, Hickey MS. Modulation of immune function by dietary lectins in rheumatoid arthritis. Br J Nutr. 2000 Mar;83(3):207-17.
27. Hafstrom I, Ringertz B, Spangberg A, von Zweigbergk L, Brannemark S, Nylander I, Ronnelid J, Laasonen L, Klareskog L: A vegan diet free of gluten improves the signs and symptoms of rheumatoid arthritis: the effects on arthritis correlate with a reduction in antibodies to food antigens. Rheumatology (Oxford) 2001, 40:1175-1179.
28. Reichelt KL, Jensen D. IgA antibodies against gliadin and gluten in multiple sclerosis. Acta Neurol Scand. 2004 Oct;110(4):239-41
29. Pengiran Tengah CD, Lock RJ, Unsworth DJ, Wills AJ. Multiple sclerosis and occult gluten sensitivity. Neurology. 2004 Jun 22;62(12):2326-7.
30. Michaëlsson G, Gerdén B, Ottosson M, Parra A, Sjöberg O, Hjelmquist G, Lööf L. Patients with psoriasis often have increased serum levels of IgA antibodies to gliadin. Br J Dermatol. 1993 Dec;129(6):667-73.
31. Michaëlsson G, Gerdén B, Hagforsen E, Nilsson B, Pihl-Lundin I, Kraaz W, Hjelmquist G, Lööf L. Psoriasis patients with antibodies to gliadin can be improved by a gluten-free diet. Br J Dermatol. 2000 Jan;142(1):44-51.
32. Hoorfar J, Buschard K, Dagnaes-Hansen F. Prophylactic nutritional modification of the incidence of diabetes in autoimmune non-obese diabetic (NOD) mice. Br J Nutr. 1993 Mar;69(2):597-607.
33. Scott FW. Food-induced type 1 diabetes in the BB rat. Diabetes Metab Rev 1996;12:341-59.
34. Schmid S, Koczwara K, Schwinghammer S, Lampasona V, Ziegler AG, Bonifacio E. Delayed exposure to wheat and barley proteins reduces diabetes incidence in non-obese diabetic mice. Clin Immunol. 2004 Apr;111(1):108-18.
35. Ziegler A-G, Schmid S, Huber D, Hummel M, Bonifacio E. Early infant feeding and risk of developing type 1 diabetes-associated autoantibodies. JAMA 2003;290:1721-8.
36. Pastore M-R, Bazzigaluppi E, Belloni C, Arcovio C, Bonifacio E, Bosi E. Six months of gluten-free diet do not influence antibody titers, but improve insulin secretion in subjects at high risk for type 1 diabetes. J Clin Endocrinol Metab 2003;88:162-5.
37. Banin P, Perretta R, Ravaioli E, De Sanctis V. Regression of autoimmunity and abnormal glucose homeostasis in an adolescent boy with silent coeliac disease. Acta Paediatr 2002;91:1141-3.
Wednesday, January 28, 2009
Hallucinations, Other Psychotic Symptoms in Children Linked to Use of ADHD Medications
Hallucinations, Other Psychotic Symptoms in Children Linked to Use of ADHD Medications
Caroline Cassels
January 28, 2009 — Physicians, patients, and parents should be aware that psychotic symptoms or mania arising in children treated with standard, approved drugs for attention-deficit/hyperactivity disorder (ADHD) may constitute an adverse drug reaction and not necessarily an additional psychiatric disorder, Food and Drug Administration (FDA) research suggests.
An analysis of 49 randomized controlled clinical trials as well as postmarketing surveillance data on ADHD drugs shows some children, including those with no identifiable risk factors, developed drug-related symptoms of psychosis or mania, including hallucinations, at usual doses.
"These drugs seem capable of producing this type of adverse psychiatric reaction. If a child receiving 1 of these medications were to develop such symptoms, strong consideration should be given to the idea that it could be a reaction to the medication rather than a separate psychiatric disorder in and of itself," principal investigator Andrew D. Mosholder, MD, from the US FDA, in Silver Spring, Maryland, told Medscape Psychiatry.
The analysis revealed that a total of 11 psychosis/mania adverse events occurred during 743 person-years of double-blind treatment of ADHD medications. Although the number of cases was small, the investigators point out there were no such events reported in 420 person-years of placebo exposure in the same trials. Dr. Mosholder added that such adverse events can occur across the board with all currently approved ADHD medications.
The study is published in the February issue of Pediatrics.
Tip of the Iceberg?
Further, investigators say that the reported incidence in the analysis may represent only the tip of the iceberg. Clinical-trial subjects undergo careful selection to ensure high likelihood of treatment success and a low probability of intolerance to these medications — a situation that does not generally reflect everyday clinical practice. Therefore, they point out, the findings likely underestimate the incidence of such adverse effects in the general population.
"One of the things we would like to call attention to is that such reactions are probably not rare. The other point is that these drugs are increasingly being used in younger children who, if they do experience hallucinations, may have difficulty understanding what's happening to them or describing it to an adult. So, if a child says 'I don't want to go to bed because it is covered with ants,' there should be consideration given that this may be an adverse drug reaction," study coauthor Kate Gelperin, MD, also from the FDA, told Medscape Psychiatry.
A 2003 survey conducted by the US Centers for Disease Control and Prevention estimated that 7.8% of children in the United States aged 14 to 17 years, or more than 4 million, have received a diagnosis of ADHD. Of these individuals, 4.3% were taking medication for the disorder.
According to Dr. Mosholder, the current analysis was prompted by a 2005 review examining postmarketing surveillance data of 1 of the methylphenidate products, which turned up reports of adverse psychiatric events in children.
Based on these reports, the FDA investigated whether such events were also associated with other ADHD agents used in pediatric populations. In March 2006, the investigators presented the current findings to an FDA pediatric advisory committee.
Subsequently, he said, these findings prompted changes to medication labeling and medication guides for ADHD products. However, he added, the current paper marks the first time the findings have been published in the peer-reviewed medical literature.
Half of Cases in Young Children
The study was 2-pronged and examined data from 49 placebo-controlled clinical trials of various ADHD agents in pediatric development programs for the products as well as postmarketing spontaneous reports of psychosis or mania gleaned from the FDA Adverse Event Reporting System (AERS).
The drugs included in the study included 8 agents that are either approved or proposed for the treatment of ADHD. These included Adderall XR extended-release tablets (amphetamine/dextroamphetamine, Shire US) , Focalin XR extended-release capsules (dexmethylphenidate, Novartis Pharmaceuticals), Concerta extended-release tablets (methylphenidate, ALZA Corp), Metadate CD extended-release capsules (methylphenidate, Celltech Pharmaceuticals), Ritalin LA extended-release capsules (methylphenidate, Novartis Pharmaceuticals), Strattera (atomoxetine, Eli Lilly), Daytrana transdermal system (methylphenidate, Shire US), and Provigil (modafinil, Cephalon), which is not approved for the treatment of ADHD.
Analysis of the data from the clinical trial revealed psychosis/mania events occurred during double-blind treatment with every compound except Adderall XR, although the researchers note there were psychosis/mania events reported with open-label Adderall XR treatment. The rate per 100-person years in the pooled active-drug group was 1.48. No such adverse events were reported in patients in the placebo-treatment groups.
Overall, the postmarketing findings revealed a total of 865 unique postmarketing case reports describing signs and/or symptoms of psychosis or mania. The majority of these were pediatric cases, with nearly half reported in children aged 10 years or younger.
No Identifiable Risk Factors
Resolution of symptoms after stopping the medication was reported in 25% to 59%, depending on the drug. Interestingly, no risk factors were identified that could account for the majority of reports of psychosis- or mania-related events.
"It was surprising to us is that in the postmarketing spontaneous reports we were not able to identify a clear risk factor that predicted the occurrence of the hallucinations or other psychotic events. Going into this analysis, I thought that we would have found more situations where there was a very high dose of the drug or overdose or drug-abuse situation or other psychiatric illness, but this was not the case," said Dr. Gelperin.
It is important, say the investigators, that clinicians, patients, and parents, particularly those with very young children, are aware of the possibility of such adverse reactions.
Prescribers need to sit down with the patient and/or the parents if the patient is a young child and let them know what the safety profile of the ADHD medication is before starting treatment, said Dr. Gelperin.
Second, if a hallucination or other type of adverse psychiatric event does occur, as a first step the drug should be stopped or the dose reduced before any other medication is added or diagnosis made.
"If symptoms of psychosis or mania are overlooked as a drug reaction, the worst-case scenario is that the child is given an additional new diagnosis and an additional new medication, which would be very unfortunate," said Dr. Gelperin.
The authors report no conflicts of interest.
Pediatrics. 2009;123:611-616. Abstract
Caroline Cassels
January 28, 2009 — Physicians, patients, and parents should be aware that psychotic symptoms or mania arising in children treated with standard, approved drugs for attention-deficit/hyperactivity disorder (ADHD) may constitute an adverse drug reaction and not necessarily an additional psychiatric disorder, Food and Drug Administration (FDA) research suggests.
An analysis of 49 randomized controlled clinical trials as well as postmarketing surveillance data on ADHD drugs shows some children, including those with no identifiable risk factors, developed drug-related symptoms of psychosis or mania, including hallucinations, at usual doses.
"These drugs seem capable of producing this type of adverse psychiatric reaction. If a child receiving 1 of these medications were to develop such symptoms, strong consideration should be given to the idea that it could be a reaction to the medication rather than a separate psychiatric disorder in and of itself," principal investigator Andrew D. Mosholder, MD, from the US FDA, in Silver Spring, Maryland, told Medscape Psychiatry.
The analysis revealed that a total of 11 psychosis/mania adverse events occurred during 743 person-years of double-blind treatment of ADHD medications. Although the number of cases was small, the investigators point out there were no such events reported in 420 person-years of placebo exposure in the same trials. Dr. Mosholder added that such adverse events can occur across the board with all currently approved ADHD medications.
The study is published in the February issue of Pediatrics.
Tip of the Iceberg?
Further, investigators say that the reported incidence in the analysis may represent only the tip of the iceberg. Clinical-trial subjects undergo careful selection to ensure high likelihood of treatment success and a low probability of intolerance to these medications — a situation that does not generally reflect everyday clinical practice. Therefore, they point out, the findings likely underestimate the incidence of such adverse effects in the general population.
"One of the things we would like to call attention to is that such reactions are probably not rare. The other point is that these drugs are increasingly being used in younger children who, if they do experience hallucinations, may have difficulty understanding what's happening to them or describing it to an adult. So, if a child says 'I don't want to go to bed because it is covered with ants,' there should be consideration given that this may be an adverse drug reaction," study coauthor Kate Gelperin, MD, also from the FDA, told Medscape Psychiatry.
A 2003 survey conducted by the US Centers for Disease Control and Prevention estimated that 7.8% of children in the United States aged 14 to 17 years, or more than 4 million, have received a diagnosis of ADHD. Of these individuals, 4.3% were taking medication for the disorder.
According to Dr. Mosholder, the current analysis was prompted by a 2005 review examining postmarketing surveillance data of 1 of the methylphenidate products, which turned up reports of adverse psychiatric events in children.
Based on these reports, the FDA investigated whether such events were also associated with other ADHD agents used in pediatric populations. In March 2006, the investigators presented the current findings to an FDA pediatric advisory committee.
Subsequently, he said, these findings prompted changes to medication labeling and medication guides for ADHD products. However, he added, the current paper marks the first time the findings have been published in the peer-reviewed medical literature.
Half of Cases in Young Children
The study was 2-pronged and examined data from 49 placebo-controlled clinical trials of various ADHD agents in pediatric development programs for the products as well as postmarketing spontaneous reports of psychosis or mania gleaned from the FDA Adverse Event Reporting System (AERS).
The drugs included in the study included 8 agents that are either approved or proposed for the treatment of ADHD. These included Adderall XR extended-release tablets (amphetamine/dextroamphetamine, Shire US) , Focalin XR extended-release capsules (dexmethylphenidate, Novartis Pharmaceuticals), Concerta extended-release tablets (methylphenidate, ALZA Corp), Metadate CD extended-release capsules (methylphenidate, Celltech Pharmaceuticals), Ritalin LA extended-release capsules (methylphenidate, Novartis Pharmaceuticals), Strattera (atomoxetine, Eli Lilly), Daytrana transdermal system (methylphenidate, Shire US), and Provigil (modafinil, Cephalon), which is not approved for the treatment of ADHD.
Analysis of the data from the clinical trial revealed psychosis/mania events occurred during double-blind treatment with every compound except Adderall XR, although the researchers note there were psychosis/mania events reported with open-label Adderall XR treatment. The rate per 100-person years in the pooled active-drug group was 1.48. No such adverse events were reported in patients in the placebo-treatment groups.
Overall, the postmarketing findings revealed a total of 865 unique postmarketing case reports describing signs and/or symptoms of psychosis or mania. The majority of these were pediatric cases, with nearly half reported in children aged 10 years or younger.
No Identifiable Risk Factors
Resolution of symptoms after stopping the medication was reported in 25% to 59%, depending on the drug. Interestingly, no risk factors were identified that could account for the majority of reports of psychosis- or mania-related events.
"It was surprising to us is that in the postmarketing spontaneous reports we were not able to identify a clear risk factor that predicted the occurrence of the hallucinations or other psychotic events. Going into this analysis, I thought that we would have found more situations where there was a very high dose of the drug or overdose or drug-abuse situation or other psychiatric illness, but this was not the case," said Dr. Gelperin.
It is important, say the investigators, that clinicians, patients, and parents, particularly those with very young children, are aware of the possibility of such adverse reactions.
Prescribers need to sit down with the patient and/or the parents if the patient is a young child and let them know what the safety profile of the ADHD medication is before starting treatment, said Dr. Gelperin.
Second, if a hallucination or other type of adverse psychiatric event does occur, as a first step the drug should be stopped or the dose reduced before any other medication is added or diagnosis made.
"If symptoms of psychosis or mania are overlooked as a drug reaction, the worst-case scenario is that the child is given an additional new diagnosis and an additional new medication, which would be very unfortunate," said Dr. Gelperin.
The authors report no conflicts of interest.
Pediatrics. 2009;123:611-616. Abstract
Mercury in High-Fructose Corn Syrup?
Mercury in High-Fructose Corn Syrup?
Miranda Hitti
January 27, 2009 — Some foods and drinks rich in high-fructose corn syrup may contain detectable levels of mercury, a new report shows.
The report, published on the web site of the Minneapolis-based nonprofit Institute for Agriculture and Trade Policy (IATP), shows detectable levels of mercury in 17 out of 55 tested products rich in high-fructose corn syrup.
But the researchers aren't telling people to avoid those products or other items containing high-fructose corn syrup, and they aren't sure what form of mercury those products contained.
The Corn Refiners Association stands by high-fructose corn syrup, calling it "safe."
Mercury and High-Fructose Corn Syrup
The new report comes from researchers including David Wallinga, MD, director of the IATP's food and health program. They bought 55 products that list high-fructose corn syrup first or second on their list of ingredients, which means high-fructose corn syrup was a leading ingredient in those products.
Wallinga's team sent samples of those products to a commercial lab, which checked the levels of total mercury in each sample.
"Overall, we found detectable mercury in 17 of 55 samples, or around 31%," write Wallinga and colleagues.
Here is the list of those products:
Quaker Oatmeal to Go bars
Jack Daniel's Barbecue Sauce
Hershey's Chocolate Syrup
Kraft Original Barbecue Sauce
Nutri-Grain Strawberry Cereal Bars
Manwich Gold Sloppy Joe
Market Pantry Grape Jelly
Smucker's Strawberry Jelly
Pop-Tarts Frosted Blueberry
Hunt's Tomato Ketchup
Wish-Bone Western Sweet & Smooth Dressing
Coca-Cola Classic: no mercury found on a second test
Yoplait Strawberry Yogurt
Minute Maid Berry Punch
Yoo-hoo Chocolate Drink
Nesquik Chocolate Milk
Kemps Fat Free Chocolate Milk
Wallinga and colleagues caution that their list was "just a snapshot in time; we only tested one sample of each product. That clearly is not sufficient grounds to give definitive advice to consumers."
Mercury exposure at high levels can harm the brain, heart, kidneys, lungs, and immune system. A form of mercury called methylmercury is particularly risky to a baby's developing brain and nervous system, according to background information from the Environmental Protection Agency (EPA).
Wallinga points out that the lab only tested for total mercury levels, not methylmercury or other types of mercury. He also notes that the EPA has a "reference dose," or upper limit, for methylmercury intake but not for other forms of mercury.
Where Did the Mercury Come From?
Wallinga's report doesn't prove that the mercury in the tested products came from high-fructose corn syrup, but "I'm hard pressed to say where else it would come from," Wallinga tells WebMD.
Wallinga explains that mercury can be used to make caustic soda, which is one of the products used to make high-fructose corn syrup. That's outdated technology; mercury isn't needed to make caustic soda, notes Audrae Erickson, president of the Corn Refiners Association, in a statement emailed to WebMD.
Erickson didn't comment specifically on Wallinga's study. Instead, her statement focuses on a new study published online in Environmental Health, which shows mercury in some samples of commercial high-fructose corn syrup tested in 2005.
"This study appears to be based on outdated information of dubious significance," Erickson states. "Our industry has used mercury-free versions of the two re-agents mentioned in the study, hydrochloric acid and caustic soda, for several years."
Wallinga agrees about the technological shift away from mercury. "If you just look within the confines of the U.S., yes, about 90% of production now is not using mercury," says Wallinga. "The problem is that we don't actually know where our companies are buying their high-fructose corn syrup from ... it's a global industry."
"For me, the take-home message is really that this is a totally avoidable, unnecessary exposure to mercury," says Wallinga. "We've got a safer, more efficient technology for making these chemicals that are part of the ingredients used to manufacture high-fructose corn syrup."
Mercury's Form Unknown
Like Wallinga's report, the study published in Environmental Health doesn't specify the form of mercury present in the high-fructose corn syrup.
"I would imagine that a good majority of the mercury that is detected would have been in the form of elemental mercury," not methylmercury, toxicologist Carl Winter, PhD, tells WebMD. Winter, who directs the FoodSafe Program at the University of California, Davis, says that methylmercury is "by far the most toxic form of mercury" because methylmercury is better absorbed by the body than other forms of mercury.
"We have a principle in toxicology, which is the dose makes the poison," says Winter. "It's the amount of a chemical, not its presence or absence, that determines the potential for harm, and frankly, I don't see based on their findings that they've made much of a case that this is something that consumers need to worry about." Besides his academic work, Winter is a volunteer spokesman for the Institute of Food Technologists, a nonprofit scientific society that includes food science and technology professionals in industry, academia, and government. Winter says his work has never been funded by food or chemical industries.
Companies Respond
WebMD contacted the makers of all 17 products that tested positive for mercury in Wallinga's report.
ConAgra Foods, which makes Manwich Bold Sloppy Joe and Hunt's Tomato Ketchup, is "absolutely confident in the safety of our products," ConAgra Foods spokeswoman Stephanie Childs tells WebMD.
Childs notes that "the levels of mercury reported in our ketchup are well below the EPA's safe exposure level. In fact, we estimate that you'd have to eat more than 100 pounds of ketchup per day to even come anywhere near the EPA's safe exposure level in terms of mercury.
A spokeswoman for Kraft Foods, Adrienne Dimopoulos, tells WebMD that Kraft has not had time to review the study's findings. However, "Kraft Foods' highest priority is the safety and quality of our products and the safety of our consumers. All of the ingredients we use are approved and deemed safe for food use by regulatory agencies, including the US FDA."
Amy Reilly, a spokeswoman for Target, which makes Market Pantry Grape Jelly, tells WebMD that Target is carefully evaluating the information and that "Target looks to the Food and Drug Administration to provide guidance on the safety of food additives and ingredients."
An FDA spokesperson wasn't immediately available to comment on Wallinga's report or the study published in Environmental Health.
SOURCES:
Dufault, R. Environmental Health, Jan. 26, 2009; online edition.
Wallinga, D. "Not So Sweet: Missing Mercury and High Fructose Corn Syrup."
David Wallinga, MD, director, Food and Health Program, Institute for Agriculture and Trade Policy.
Statement from Audrae Erickson, president, Corn Refiners Association.
Carl Winter, PhD, director, FoodSafe Program and Extension Food Toxicologist, department of food science and technology, University of California, Davis.
Adrienne Dimopoulos, spokeswoman, Kraft Foods.
Amy Reilly, spokeswoman, Target.
Miranda Hitti
January 27, 2009 — Some foods and drinks rich in high-fructose corn syrup may contain detectable levels of mercury, a new report shows.
The report, published on the web site of the Minneapolis-based nonprofit Institute for Agriculture and Trade Policy (IATP), shows detectable levels of mercury in 17 out of 55 tested products rich in high-fructose corn syrup.
But the researchers aren't telling people to avoid those products or other items containing high-fructose corn syrup, and they aren't sure what form of mercury those products contained.
The Corn Refiners Association stands by high-fructose corn syrup, calling it "safe."
Mercury and High-Fructose Corn Syrup
The new report comes from researchers including David Wallinga, MD, director of the IATP's food and health program. They bought 55 products that list high-fructose corn syrup first or second on their list of ingredients, which means high-fructose corn syrup was a leading ingredient in those products.
Wallinga's team sent samples of those products to a commercial lab, which checked the levels of total mercury in each sample.
"Overall, we found detectable mercury in 17 of 55 samples, or around 31%," write Wallinga and colleagues.
Here is the list of those products:
Quaker Oatmeal to Go bars
Jack Daniel's Barbecue Sauce
Hershey's Chocolate Syrup
Kraft Original Barbecue Sauce
Nutri-Grain Strawberry Cereal Bars
Manwich Gold Sloppy Joe
Market Pantry Grape Jelly
Smucker's Strawberry Jelly
Pop-Tarts Frosted Blueberry
Hunt's Tomato Ketchup
Wish-Bone Western Sweet & Smooth Dressing
Coca-Cola Classic: no mercury found on a second test
Yoplait Strawberry Yogurt
Minute Maid Berry Punch
Yoo-hoo Chocolate Drink
Nesquik Chocolate Milk
Kemps Fat Free Chocolate Milk
Wallinga and colleagues caution that their list was "just a snapshot in time; we only tested one sample of each product. That clearly is not sufficient grounds to give definitive advice to consumers."
Mercury exposure at high levels can harm the brain, heart, kidneys, lungs, and immune system. A form of mercury called methylmercury is particularly risky to a baby's developing brain and nervous system, according to background information from the Environmental Protection Agency (EPA).
Wallinga points out that the lab only tested for total mercury levels, not methylmercury or other types of mercury. He also notes that the EPA has a "reference dose," or upper limit, for methylmercury intake but not for other forms of mercury.
Where Did the Mercury Come From?
Wallinga's report doesn't prove that the mercury in the tested products came from high-fructose corn syrup, but "I'm hard pressed to say where else it would come from," Wallinga tells WebMD.
Wallinga explains that mercury can be used to make caustic soda, which is one of the products used to make high-fructose corn syrup. That's outdated technology; mercury isn't needed to make caustic soda, notes Audrae Erickson, president of the Corn Refiners Association, in a statement emailed to WebMD.
Erickson didn't comment specifically on Wallinga's study. Instead, her statement focuses on a new study published online in Environmental Health, which shows mercury in some samples of commercial high-fructose corn syrup tested in 2005.
"This study appears to be based on outdated information of dubious significance," Erickson states. "Our industry has used mercury-free versions of the two re-agents mentioned in the study, hydrochloric acid and caustic soda, for several years."
Wallinga agrees about the technological shift away from mercury. "If you just look within the confines of the U.S., yes, about 90% of production now is not using mercury," says Wallinga. "The problem is that we don't actually know where our companies are buying their high-fructose corn syrup from ... it's a global industry."
"For me, the take-home message is really that this is a totally avoidable, unnecessary exposure to mercury," says Wallinga. "We've got a safer, more efficient technology for making these chemicals that are part of the ingredients used to manufacture high-fructose corn syrup."
Mercury's Form Unknown
Like Wallinga's report, the study published in Environmental Health doesn't specify the form of mercury present in the high-fructose corn syrup.
"I would imagine that a good majority of the mercury that is detected would have been in the form of elemental mercury," not methylmercury, toxicologist Carl Winter, PhD, tells WebMD. Winter, who directs the FoodSafe Program at the University of California, Davis, says that methylmercury is "by far the most toxic form of mercury" because methylmercury is better absorbed by the body than other forms of mercury.
"We have a principle in toxicology, which is the dose makes the poison," says Winter. "It's the amount of a chemical, not its presence or absence, that determines the potential for harm, and frankly, I don't see based on their findings that they've made much of a case that this is something that consumers need to worry about." Besides his academic work, Winter is a volunteer spokesman for the Institute of Food Technologists, a nonprofit scientific society that includes food science and technology professionals in industry, academia, and government. Winter says his work has never been funded by food or chemical industries.
Companies Respond
WebMD contacted the makers of all 17 products that tested positive for mercury in Wallinga's report.
ConAgra Foods, which makes Manwich Bold Sloppy Joe and Hunt's Tomato Ketchup, is "absolutely confident in the safety of our products," ConAgra Foods spokeswoman Stephanie Childs tells WebMD.
Childs notes that "the levels of mercury reported in our ketchup are well below the EPA's safe exposure level. In fact, we estimate that you'd have to eat more than 100 pounds of ketchup per day to even come anywhere near the EPA's safe exposure level in terms of mercury.
A spokeswoman for Kraft Foods, Adrienne Dimopoulos, tells WebMD that Kraft has not had time to review the study's findings. However, "Kraft Foods' highest priority is the safety and quality of our products and the safety of our consumers. All of the ingredients we use are approved and deemed safe for food use by regulatory agencies, including the US FDA."
Amy Reilly, a spokeswoman for Target, which makes Market Pantry Grape Jelly, tells WebMD that Target is carefully evaluating the information and that "Target looks to the Food and Drug Administration to provide guidance on the safety of food additives and ingredients."
An FDA spokesperson wasn't immediately available to comment on Wallinga's report or the study published in Environmental Health.
SOURCES:
Dufault, R. Environmental Health, Jan. 26, 2009; online edition.
Wallinga, D. "Not So Sweet: Missing Mercury and High Fructose Corn Syrup."
David Wallinga, MD, director, Food and Health Program, Institute for Agriculture and Trade Policy.
Statement from Audrae Erickson, president, Corn Refiners Association.
Carl Winter, PhD, director, FoodSafe Program and Extension Food Toxicologist, department of food science and technology, University of California, Davis.
Adrienne Dimopoulos, spokeswoman, Kraft Foods.
Amy Reilly, spokeswoman, Target.
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