Monosodium Glutamate & Obesity Julia Humphrey Central Washington University.
Monosodium Glutamate & Obesity
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Monosodium Glutamate & Obesity
Julia HumphreyCentral Washington University
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Objectives
Understand the difference between natural and manufactured glutamate
Acknowledge the potential relationship between MSG & appetite
Learn the effects of MSG during pregnancy & in offspring
Know how much MSG is consumed & where it is hidden
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What is Monosodium Glutamate (MSG)
Favor enhancer/food additive largely used in the food industry Responsible for umami/savory
taste When detected by taste buds, it
signals the protein presence in the diet
Thought to mainly be in Asian cuisine
Hidden in many processed foods Used in place of sodium
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Natural vs. Processed Glutamate
MSG is the manufactured salt of glutamic acid
Glutamate is the sodium salt of glutamic acid Key to the savory umami taste
Glutamate in nature L-glutamic acid Exists as part of proteins Broken down as a part of protein digestion Natural constituent to fermented foods
MSG D-glutamic acid Refined, can be readily absorbed into
circulation Not bound to proteins, levels spike upon
consumption Possibility of “toxicity” = MSG sensitivity
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MSG & Obesity History
1960s Debons et al. Systemically administered
MSG in mice found a pattern of obesity & hypothalamic damage
This lead to MSG admin. as the most widely used model to induce obesity in rats
Induces a lesion of arcuate nucleus in hypothalamus
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MSG & Obesity
Experimental studies in rats The arcuate nucleus proposed as
an important site of leptin action Leptin produced by adipose cells Essential in maintenance of
appetite, energy homeostasis, & body weight
MSG administered subcutaneously in newborns Lesion of the hypothalamic nucleus Leptin action reduced likely as a
result of lack of leptin receptors in arcuate nucleus
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Obesity, voracity, and short stature: the impact of glutamate on the regulation of appetite
Hermanussen et al. 2006
Purpose Effects of oral administration of MSG in
pregnant rats and offspring Subjects/Methods
32 pregnant rats, day 14 of pregnancy divided into 4 groups Group 1 (n=8): no extra MSG Group 2 (n=8): 2.5 g MSG per day Group 3 (n=8): 5.0 g MSG per day Group 4 (n=8): no extra MSG during pregnancy offspring injected with 4mg/g MSG
Offspring killed half at day 30 and rest at day 90
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Results Maternal feeding with 5 g/d
resulted in severe birth weight reduction (p < 0.01)
Leptin levels reduced in MSG-fed groups (p < 0.05)
MSG-fed animals contained more body fat at day 30 and 90 than controls (p < 0.05) • Impaired glucose tolerance• Insulin resistance
Obesity, voracity, and short stature: the impact of glutamate on the regulation of appetite
Hermanussen et al. 2006
2.5 and 5 g/day MSG consumption showed marked
voracity
Appetite
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Monosodium glutamate versus diet induced obesity in pregnant rats and their offspring
Afifi and Abbas 2011
Purpose Compare oral administration of large
doses of MSG with high calorie diet in pregnant rats & offspring
Subjects/Methods 90 female rats randomly divided into 3
groups Group 1 (n=30): normal chow 4.5% fat Group 2 (n=30): normal chow + 100 g/kg
MSG Group 3 (n=30): high fat chow 31% fat
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Subjects/Methods Female rats allowed to mate and further divided into
groups C10 (n=10): control preg sacrificed on 10th day MSG10 (n=10): MSG treated preg sacrificed on 10th day HC10 (n=10): high calorie preg sacrificed 10th day
C20 (n=10): control preg sacrificed on 20th day MSG20 (n=10): MSG treated preg sacrificed 20th day HC20 (n=10): high calorie preg sacrificed 20th day
Offspring of female rats CO (n=10): control preg offspring sacrificed 10th day MSGO (n=10): MSG preg offspring sacrificed 10th day HC (n=10): high calorie preg offspring sacrificed 10th day
Monosodium glutamate versus diet induced obesity in pregnant rats and their offspring
Afifi and Abbas 2011
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C10 C20 HC10 HC20 MSG10 MSG20
Body weight (g)
236.4 ± 6.5 255.6 ± 7.4 301.6 ± 5.9 309.6 ± 8.0 237.4 ± 6.0 245.4 ± 5.3
Abdominal fat (g)
13.6 ± 0.05 13.6 ± 0.04 44.6 ± 0.49 45.0 ± 0.56 57.6 ± 0.39 58.0 ± 0.5
Blood glucose (mg/dl)
84.2 ± 1.2
79.2 ± 1.0 118.2 ± 3.2 122.6 ± 2.9 120.0 ± 2.2 125.0 ± 2.5
TAG (mg/dl)
147.4 ± 13.0 163.7 ± 15.0 210.6 ± 4.0 221.4 ± 5.0 200.3 ± 5.0 223.3 ± 3.0
TC (mg/dl) 85.2 ± 3.0 86.5 ± 2.0 102.7 ± 2.0 107.5 ± 3.0 103.2 ± 1.0 108.6 ± 2.0
Number of offspring
4.5 ± 0.6 4.7 ± 1.0 3.3 ± 0.5 3.3 ± 0.5 2.0 ± 0.8 1.8 ± 1.0
Monosodium glutamate versus diet induced obesity in pregnant rats and their offspring
Afifi and Abbas 2011
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MSG Consumption
FDA Considers MSG as a food additive “generally
recognized as safe” Not required to list amount of MSG in Nutrition
Facts panel Large variation in MSG consumption
UK (1991): 580 mg/d general 4.68 g/d in extreme users China (2010): 3.8 g/d Thailand (2012): 4.0 g/d Japan & Korea (1990’s): 1.2-1.7 g/d
Speculated intake is up to 10 g/d
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Consumption of MSG in relation to incidence of overweight in chinese adults: China Health and
Nutrition SurveyHe et al. 2011
Subjects Longitudinal open-cohort, ongoing, nationwide survey
1991-2006 10,095 Chinese men and women 18-65 yr
Methods MSG consumption dietary data both in the household &
individual All food purchases, home production, and processed
snack foods were weighed and recorded 24-hour recall for 3 consecutive days MSG intake for each household member estimated
based on the proportion of each individual’s food consumption
MSG intake separated into quintiles Chi square test
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Results Mean cumulative MSG intake 1.8 g/d MSG positively associated with BMI in dose-response
manner (p < 0.01) Highest MSG quintile 33% more likely to be
overweight Higher BMI, income, lower physical activity
Pilot Study Examine association between MSG and serum leptin MSG intake positively related to serum leptin
concentrations Serum leptin concentration increased by 0.45 ng/mL
with every 1-g increase in MSG intake
Consumption of MSG in relation to incidence of overweight in chinese adults: China Health and
Nutrition SurveyHe et al. 2011
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Limitations to Studies
Majority on pregnancy & neonatal outcome is in rodents
Not ethical to perform on humans
MSG dose is very large compared to actual consumption in humans
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Is MSG Safe During Pregnancy?
Animal studies Result of maternal MSG consumption
Low birth weight in offspring Increased insulin resistance in offspring Leptin levels reduced in offspring Leptin resistance in pregnant rat Increased abdominal fat in pregnant rat
Placental barrier Controls the passage of glutamate from maternal
plasma to fetus, metabolizing it before it reaches the fetal circulation
MSG-sensitivity Headaches, nausea, numbness, weakness when
consuming MSG containing foods Want to consume fresh unprocessed as much as
possible during pregnancy Consult doctor
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“Hidden” MSG
Not labeled as MSG Hydrolyzed (anything), glutamate, glutamic acid,
yeast extract, soy sauce, soy protein, gelatin, flavors, flavoring, bouillon, broth, seasonings, etc
Found in common food items Processed cheese, salad dressings, meat &
vegetable stocks/broth, soups, vegetable dips, condiments, chips, pasta sauce
Fast food: KFC Increase in MSG production
Increase in processed foods = increased consumption
200 tons per year in 1969 800 tons per year in 2001
Possible that exposure in utero could be a contributing factor to increasing obesity rates
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Conclusion
Obesity is a multifactorial disease Related to diet, physical
activity, genetics, environment
Like sugar and fat consumption MSG may simply be one factor in the mix
Would like to see national study in U.S Difficult since NHANES does
not provide MSG info
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Resources Afifi MM, Abbas AM. Monosodium glutamate versus diet induced obesity in pregnant rats and
their offspring. Acta Physiologica Hungarica 2011;98;2:177-188 Collison K, Makhoul N, Zaidi M, Inglis A, Andres B, Ubungen R, Shoukri M, Al-Mohanna A.
Interactive effects of neonatal exposure to monosodium glutamate and aspartame on glucose homeostasis. Nutrition & Metabolism 2012;5;58:1-13
Diemen V, Trindade M. Effect of the oral administration of monosodium glutamate during pregnancy and breast-feeding in the offspring of pregnant Wistar rats. Acta Cirurgica Brasileria 2010;25;1:37-42
Friedler B, Grimm V. Prenatal monosodium glutamate (MSG) treatment given through the mother’s diet causes behavioral deficits in rat offspring. International Journal of Neuroscience 1984;23:117-126
He K, Du S, Xun P, Sharma S, Wang H, Zhai F, Popkin B. Consumption of monosodium glutamate in relation to incidence of overweight in Chinese adults: China Health and Nutrition Survey (CHNS). American Journal of Clinical Nutrition 2011;93:1328-36
Hermanussen M, Garcia AP, Voigt M, Salazar V, Tresguerres JAF. Obesity, voracity, and short stature: the impact of glutamate on the regulation of appetite. European Journal of Clinical Nutrition 2006;60:25-31
Insawang T, Selmi C, Cha’on U, Pethlert S, Yongvanit P, Areejitanusorn P, Boonsiri P, Khampitak T, Tangrassmeeprasert R, Pinitsoontorn C, Prasongwattana V, Gershwin M, Hammock B. Monosodium glutamate (MSG) intake is associated with the prevalence of metabolic syndrome in a rural Thai population. Nutrition & Metabolism 2012;9;50:1-6
Yu T, Zhao Y, Shi W, Ma R, Yu L. Effects of maternal oral administration of monosodium glutamate at a late stage of pregnancy on developing mouse fetal brain. Brain Research 1997:195-206
MSG Truth website http://www.msgtruth.org/avoid.htm. Accessed July 12, 2013 Names of ingredients that contain processed free glutamic acid (MSG)
http://www.truthinlabeling.org/hiddensources.html . Accessed July 12, 2013 Glutamic Acid - It Is Not MSG or Monosodium Glutamate http://
www.edenfoods.com/articles/view.php?articles_id=207. Accessed July 12, 2013
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What are your thoughts? Questions?