Monosodium Glutamate & Obesity

Julia HumphreyCentral Washington University

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

“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

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

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

What are your thoughts? Questions?