JustTheScience

Originally synthesized from kelp by Japanese researchers in 1908, Monosodium Glutamate (MSG) is now a major component of the food industry with 2009 global production levels estimated at 2 million tons (Sano 2009). ¹  The glutamate class of acids including MSG activates taste sensors that are responsible for the savory flavor, also called “umami,” which is considered to be a basic taste along with sweet, sour, salty, and bitter (Rolls 2009) (Kurihara 2009). ^2 3  Americanized Chinese food is widely known for its MSG content, particularly due to the 1960′s MSG related phenomenon dubbed “Chinese Restaurant Syndrome (CRS).”  Afflicted individuals with CRS exhibited symptoms including burning sensations, and facial and chest pain, following eating at Chinese restaurants that used MSG as a food additive (Schaumburg et al 1969). ⁴  Media coverage caused hyper-awareness of the syndrome, as is evident by a 1979 survey by Kerr et al (1979), in which 43% of respondents stated that they had suffered from CRS, despite only 2% of respondents reporting ever having symptoms matching those widely attributed to CRS.⁵

Although public awareness of the symptoms of Chinese Restaurant Syndrome is high, the question remains whether or not there is legitimate scientific evidence for this condition.  A large double blind study by Geha et al (2000) of people who self reported a sensitivity to MSG found that some individuals exhibited reactions to direct ingestion of MSG.  Results were neither consistent upon retesting nor were any of the effects persistent or serious.⁶  Rosenblum et al (1971) found no difference in symptoms between individuals ingesting MSG and a placebo (Sodium Chloride (table salt)) and no symptoms resulting from this study matched those of CRS.⁷  Tarasoff and Kelly (1993) found no difference between a placebo and MSG when the MSG was ingested with food, even at high concentrations. ⁸  Woods et al (1998) and Woessner et al (1999)  found no link between MSG intake and asthma exasperation in asthmatics who self reported a sensitivity to MSG,⁹¹⁰  and Hawkins (2009) found that the blood/brain barrier is impermeable to glutamates.¹¹ Finally, Burrin and Stoll (2009) found that natural and artificial dietary glutamates are metabolized in the same manner and are both a major oxidative fuel for the gut, an important precursor for a key neurotransmitter (glutathione).  ¹²

Key Points

• MSG is a major component of the food industry; 2009 global production levels estimated at 2 million tons.¹³
• MSG activates taste sensors responsible for the savory flavor (called “unami”).^14 15
• MSG was attributed to a phenomenon called “Chinese Restaurant Syndrome.”  Afflicted individuals exhibited symptoms including burning sensations, and facial and chest pain, following eat at Chinese restaurants that used MSG as a food additive.¹⁶
• A 2000 study reported inconsistent results that were neither persistent or serious to direct ingestion of MSG.¹⁷
• 1971 study found no difference in symptoms between individuals ingesting MSG or Sodium Chloride (table salt).¹⁸
• 1993 study found no difference between individuals ingesting a MSG or a placebo with food or drink, even at high concentrations.¹⁹
• 1998 and 1999 studies found no link between MSG intake and asthma exasperation in asthmatics who self-reported a sensitivity to MSG.²⁰²¹
• 2009 study found blood/brain barrier is impermeable by glutamates (including MSG). ²²
• 2009 study found dietary glutamates are both a major oxidative fuel for the gut, and an important precursor for the neurotransmitter glutathione. ²³

1. History of glutamate production [↩]
2. Functional neuroimaging of umami taste: what makes umami pleasant? [↩]
3. Glutamate: from discovery as a food flavor to role as a basic taste (umami) [↩]
4. Monosodium L-Glutamate: Its Pharmacology and Role in the Chinese Restaurant Syndrome [↩]
5. Prevalence of the “Chinese restaurant syndrome” [↩]
6. Multicenter, double-blind, placebo-controlled, multiple-challenge evaluation of reported reactions to monosodium glutamate [↩]
7. Single and double blind studies with oral monosodium glutamate in man [↩]
8. Monosodium L-glutamate: a double-blind study and review [↩]
9. The effects of monosodium glutamate in adults with asthma who perceive themselves to be monosodium glutamate–intolerant [↩]
10. Monosodium glutamate sensitivity in asthma [↩]
11. The blood-brain barrier and glutamate [↩]
12. Metabolic fate and function of dietary glutamate in the gut [↩]
13. History of glutamate production [↩]
14. Functional neuroimaging of umami taste: what makes umami pleasant? [↩]
15. Glutamate: from discovery as a food flavor to role as a basic taste (umami) [↩]
16. Monosodium L-Glutamate: Its Pharmacology and Role in the Chinese Restaurant Syndrome [↩]
17. Multicenter, double-blind, placebo-controlled, multiple-challenge evaluation of reported reactions to monosodium glutamate [↩]
18. Single and double blind studies with oral monosodium glutamate in man [↩]
19. Monosodium L-glutamate: a double-blind study and review [↩]
20. The effects of monosodium glutamate in adults with asthma who perceive themselves to be monosodium glutamate–intolerant [↩]
21. Monosodium glutamate sensitivity in asthma [↩]
22. The blood-brain barrier and glutamate [↩]
23. Metabolic fate and function of dietary glutamate in the gut [↩]

The organic food industry has grown dramatically over the last several years, and it’s a natural assumption that eating organic foods is better for you.  Organic foods are grown in an environment perceived to be free of harmful pesticides and herbicides, and in some instances are deemed to be more nutritional than those grown in a conventional manner.  Are there any significant differences between organic and normally raised agricultural products?

One well known difference between organically and non-organically grown produce are the chemicals, or lack thereof, utilized during the growing process.  Studies have found negative effects resulting from acute exposure to pesticides (Grandjean et al 2006) and herbicides (Kamel et al 2003) on farm workers and their children (if exposed prenatally).¹²  For the consumers of produce from farms that utilize pesticides and herbicides, however, it’s been shown that actual exposure to these chemicals is relatively small.   Leblac et al (2000) determined that an average person’s exposure to pesticides is 4% of an individual’s maximum recommended exposure. ³  Galal-Gorchev H. (1991) found that a person’s exposure to pesticide residue is well below established acceptable daily intake levels in the 21 western countries that supply data on the matter. ⁴   Juhler et al (1999) determined dietary exposure to pesticides does not affect male spermazoa,⁵ and Safe (1995) found an individual’s exposure to estrogenic compounds from organochlorine pesticides is 0.0000025% of the daily intake of estrogenic flavonoids in the diet.⁶  While organic farming has been shown to lower pesticide residues in food by 2/3, much organic produce is not pesticide free due to legacy contamination and drift from other fields (Baker et al 2002). ⁷

As far as differences in nutritional value between organic and conventionally grown produce, much of the current literature is suggesting a need for further research, although some slightly notable differences have been found. A review of 55 articles on the subject found conventionally produced crops had significantly higher nitrogen content, and organically produced crops had significantly higher acidity and phosphorus content.  These differences were attributed to the difference in production methods and none of them had a material impact on the food’s nutritional value (Dangour et al 2009) (Bourne and Prescott 2002). ^8 9  A study by Magkos et al (2003) found higher levels of ascorbic acid in organically grown leafy vegetables and potatoes and lower protein levels in some organic vegetables and cereals, but found this evidence to be inadequate to make a definitive argument.  A study by Caris-Veyrat et al (2004) found that organic tomatoes had higher levels of antioxidants (vitamin C, carotenoids, and polyphenols) than conventionally grown tomatoes, but when both types of tomatoes were fed to people for 3 weeks, no difference was found in antioxidant levels in the bloodstream between those that consumed organic or conventional. ^10 11   Similarly, Tarozzi et al (2005) found that organic red oranges have a greater total antioxidant activity than those grown conventionally, but did not investigate whether or not the organic oranges would alter antioxidant levels in the bloodstream  ¹²

1. Pesticide Exposure and Stunting as Independent Predictors of Neurobehavioral Deficits in Ecuadorian School Children [↩]
2. Neurobehavioral performance and work experience in Florida farmworkers [↩]
3. Estimation of the dietary intake of pesticide residues, lead, cadmium, arsenic and radionuclides in France [↩]
4. Dietary intake of pesticide residues: cadmium, mercury, and lead [↩]
5. Human Semen Quality in Relation to Dietary Pesticide Exposure and Organic Diet [↩]
6. Environmental and Dietary Estrogens and Human Health: Is There a Problem? [↩]
7. Pesticide residues in conventional, IPM-grown and organic foods: Insights from three U.S. data sets [↩]
8. Nutritional quality of organic foods: a systematic review [↩]
9. A Comparison of the Nutritional Value, Sensory Qualities, and Food Safety of Organically and Conventionally Produced Foods [↩]
10. Organic food: nutritious food or food for thought? A review of the evidence [↩]
11. Influence of Organic versus Conventional Agricultural Practice on the Antioxidant Microconstituent Content of Tomatoes and Derived Purees; Consequences on Antioxidant Plasma Status in Humans [↩]
12. Antioxidant effectiveness of organically and non-organically grown red oranges in cell culture systems [↩]

There have been many different theories regarding when and how often an individual should eat, among them: including vs. skipping breakfast, not eating anything before bedtime, and eating several smaller meals vs. fewer concentrated meals.  In this article, we intend to examine whether or not feeding timing and frequency is relevant to metabolism, and/or satiation.

Including breakfast in one’s day has been shown to have myriad effects.  De Castro (2004) found those that skip breakfast are more likely to overeat later. ¹   Additionally, Schlundt et al (1992) and Stubbs et al (1996) found those that eat breakfast eat less fat throughout the day and are less prone to impulsive eating of familiar foods. ²³ However, multiple studies have found that feeding frequency and timing does not have an effect on metabolic performance (Wilhelmine et al 1998) (Dallosso et al 1982) ( Verboeket van de Venne and Westerterp 1998) (Wolfram et al 1987). ^4 5 6 7 In addition, Goldberg et al (1998) found that one’s metabolic rate while sleeping is roughly concurrent with one’s basal metabolic rate (BMR), which in combination with results from the previously mentioned studies suggests that there are no adverse metabolic effects from eating before sleeping.⁸  However, it is important if you are partaking in late night eating that you eat a prepared portion of food, as it’s been demonstrated that it’s common for individuals to overindulge late (Waller et al 2004). ⁹

Eating more frequent smaller meals has been shown to decrease future hunger more effectively than eating few highly concentrated meals (Speechly and Buffenstein 1999).  Johnstone et al (2000) found similar results in their study, and also determined that the nutritional composition of these smaller meals (i.e. high in protein, fat, or carbohydrates) did not affect later decreased hunger, provided they contained a similar caloric composition^10 11

1. The time of day of food intake influences overall intake in humans [↩]
2. The role of breakfast in the treatment of obesity: a randomized clinical trial [↩]
3. Breakfasts high in protein, fat or carbohydrate: effect on within-day appetite and energy balance [↩]
4. Effect of the pattern of food intake on human energy metabolism [↩]
5. Feeding frequency and energy balance in adult males [↩]
6. Frequency of feeding, weight reduction and energy metabolism [↩]
7. Thermogenesis in humans after varying meal time frequency [↩]
8. Overnight and basal metabolic rates in men and women [↩]
9. Evening Ready-to-Eat Cereal Consumption Contributes to Weight Management [↩]
10. Greater Appetite Control Associated with an Increased Frequency of Eating in Lean Males [↩]
11. Altering the temporal distribution of energy intake with isoenergetically dense foods given as snacks does not affect total daily energy intake in normal-weight men [↩]

Stretching prior to, and following exercise is a commonly recommended practice.  Whether or not there are benefits in including this in one’s routine is a controversial subject.  Studies exist that have found little to no benefit of including stretching as part of an athletic regimen (Thacker et al 2004). ¹  Other studies exist that have found stretching before or after athletic activity slightly reduces muscle, ligament, and tendon injuries as well as soreness (Jamtvedt et al 2009). ² In addition, Herbert and Gabriel (2002) found that stretching before or after exercising does not confer protection from muscle soreness and that stretching before exercising does not practically reduce the risk of injury.³ In this article, we intend to examine in more details whether or not there are benefits associated with incorporating the three major types of stretching (static, dynamic, and ballistic) as part of a regular exercise routine.

Static stretching takes place when an individual’s body is at rest, and one holds each stretch for thirty seconds to one minute.  In individuals who are not yet fully involved in a committed athletic program, evidence exists that static stretching can help them ease into a new program without stressing the body (Kokkonen et al 2007).⁴  Static stretching also increases torque in concentric muscle movements (Cramer et al 2006), flexibility (O’Sullivan et al 2009), and range of motion over the long term (LaRoche and Connolly 2006).  Static stretching has otherwise been found have no or negative effects on athletic performance, including a reduction in muscle power endurance, (Yamaguchi et al 2006) (Yamaguchi and Ishii 2005) (Nelson et al 2005) (Brandenburg 2006), sprinting and endurance running performance (Fletcher and Anness 2007) (Wilson et al 2008) (Heyes and Walker 2007), muscle activation (Cramer et al 2004), and jumping height (Holt and Lambourne 2008) (Bradly et al 2007). ^{5 6 7 89 10 11 12 1314 15 16 17}

Dynamic stretching utilizes momentum from form to propel the body beyond in an extended range of motion.  This has been shown to have the greatest positive effect on a range of metrics, including improved muscular power (Yamaguchi and Ishii 2005), sprinting (Fletcher and Anness 2007), and high speed running performance (Little and Williams 2006).^18 19 20 A long-term dynamic stretching program has been positively correlated with sustained muscle power, strength, muscular endurance, anaerobic capacity, and agility performance enhancements (Herman and Smith 2008).²¹  However, it has not been shown to improve running economy (Heyes and Walker 2007). ²²

Ballistic stretching uses bouncing movements to force limbs into an extended range of motion when the muscle has not relaxed enough to enter it.  Studies have shown the existence of some benefits, including improved vertical jump height (Woolstenhulme et al 2006) and general range of motion as a result of ballistic stretching (LaRoche and Connolly 2006).^23 24  Compared to the other two types, there is a dearth of research on ballistic stretching specifically comparisons between ballistic and dynamic stretching.

In short, due to the different benefits of the three types of stretching it is important to make sure that your stretching program will benefit your athletic regimen and not undermine it.

1. The Impact of Stretching on Sports Injury Risk: A Systematic Review of the Literature [↩]
2. A pragmatic randomised trial of stretching before and after physical activity to prevent injury and soreness [↩]
3. Effects of stretching before and after exercising on muscle soreness and risk of injury: systematic review [↩]
4. Chronic Static Stretching Improves Exercise Performance [↩]
5. Acute Effects of Static Stretching on Maximal Eccentric Torque Production in Women [↩]
6. Effects of Static Stretching for 30 Seconds and Dynamic Stretching on Leg Extension Power [↩]
7. Acute Effect of Static Stretching on Power Output During Concentric Dynamic Constant External Resistance Leg Extension [↩]
8. Acute Muscle Stretching Inhibits Muscle Strength Endurance Performance [↩]
9. Duration of stretch does not influence the degree of force loss following static stretching [↩]
10. The Acute Effects of Combined Static and Dynamic Stretch Protocols on Fifty-Meter Sprint Performance in Track-and-Field Athletes [↩]
11. The effect of warm-up, static stretching and dynamic stretching on hamstring flexibility in previously injured subjects [↩]
12. Pre-exercise stretching does not impact upon running economy [↩]
13. The acute effects of static stretching on peak torque, mean power output, electromyography, and mechanomyography [↩]
14. The Effects Of Static Stretching On Energy Cost And Endurance Performance During Treadmill Running [↩]
15. The Effect of Static,Ballistic, and Proprioceptive Neuromuscular Facilitation Stretching on Vertical Jump Performance [↩]
16. The Impact of Different Warm-Up Protocols on Vertical Jump Performance in Male Collegiate Athletes [↩]
17. Effects of Stretching on Passive Muscle Tension and Response to Eccentric Exercise [↩]
18. Effects of Static Stretching for 30 Seconds and Dynamic Stretching on Leg Extension Power [↩]
19. The Acute Effects of Combined Static and Dynamic Stretch Protocols on Fifty-Meter Sprint Performance in Track-and-Field Athletes [↩]
20. Effects of Differential Stretching Protocols During Warm-Ups on High-Speed Motor Capacities in Professional Soccer Players [↩]
21. Four-Week Dynamic Stretching Warm-up Intervention Elicits Longer-Term Performance Benefits [↩]
22. Pre-exercise stretching does not impact upon running economy [↩]
23. Ballistic Stretching Increases Flexibility and Acute Vertical Jump Height When Combined With Basketball Activity [↩]
24. Effects of Stretching on Passive Muscle Tension and Response to Eccentric Exercise [↩]

As levels of diabetes, obesity, and other dietary issues increase (diabetes alone has increased 763% from 1935 to 1996 in the united states (Gross et al 2004)) studies have been conducted to investigate whether the 1,000% rise in the use of High Fructose Corn Syrup (HFCS) from 1967 to 2000 in the American food industry is a major contributor (Bray et al 2004).^{1  2} In this article, we will examine whether or not HFCS is truly a factor in this significant increase.

Early studies found that there were possible clinical explanations for metabolic differences derived from HFCS ingestion and other sweeteners; primarily that it did not trigger insulin creation and thereby was thought to not trigger satiety signals (Reiser et al 1989) (Elliott et al 2002) (Bray et al 2004) (Teff et al 2004) .^3 4 5 6  However, more recent studies have found no difference in resulting satiety in men or women resulting from HFCS, sucrose, or milk, (Soenen and Westerterp-Plantenga 2007) (Melanson et al 2008) (Akhavan and Anderson 2007),^7 8 9 and that HFCS yields similar metabolic responses to other caloric sweeteners. (Angelopoulos et al 2009),¹⁰ Stanhope et al 2008 and Melanson  et al 2007 determined that sucrose and HFCS do not have significantly different short-term metabolic effects,^11 12 and moderate levels (~1.5 grams of fructose per kilogram of body mass) of HFCS intake  does not cause ectopic lipid deposition or insulin resistance in healthy humans (Le et al 2006).¹³

Although HFCS is not itself responsible for the increase in dietary and metabolic disorders, other studies have demonstrated that increasing levels of excess energy consumption in general is a cause (Gross et al 2004).¹⁴  For thousands of years humans consumed fructose amounting to 16–20 grams per day, largely from fresh fruits (Gross et al 2004). ¹⁵ Westernization of diets has resulted in significant increases in food with added fructose, leading to typical daily consumptions amounting to 85–100 grams of fructose per day (Gross et al 2004). ¹⁶  For example, a 12 ounce Coke contains 39 grams of fructose and the USDA Recommended Daily Allowance allots for 32 grams of carbohydrates in a 2,000 calorie diet.¹⁷  A single 12 ounce Coke therefore contains significantly more than an individual’s entire excess dietary energy allowance for a day.  Raben et al 2002 found that people have a very difficult time compensating for increased levels of calories associated with increased sugar intake by lowering caloric intake elsewhere.¹⁸  While moderate ingestion of HFCS will not specifically cause harm to oneself, it is advisable to monitor and limit consumption as much as possible.

1. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity [↩]
2. Fructose, insulin resistance, and metabolic dyslipidemia [↩]
3. Fructose, weight gain, and the insulin resistance syndrome [↩]
4. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity [↩]
5. Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women [↩]
6. Day-long glucose, insulin, and fructose responses of hyperinsulinemic and nonhyperinsulinemic men adapted to diets containing either fructose or high-amylose cornstarch [↩]
7. No differences in satiety or energy intake after high-fructose corn syrup, sucrose, or milk preloads [↩]
8. High-fructose corn syrup, energy intake, and appetite regulation [↩]
9. Effects of glucose-to-fructose ratios in solutions on subjective satiety, food intake, and satiety hormones in young men [↩]
10. The Effect of High-Fructose Corn Syrup Consumption on Triglycerides and Uric Acid [↩]
11. Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals [↩]
12. Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women [↩]
13. A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans [↩]
14. Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment [↩]
15. Fructose, insulin resistance, and metabolic dyslipidemia [↩]
16. Fructose, insulin resistance, and metabolic dyslipidemia [↩]
17. Carbohydrates [↩]
18. Sucrose compared with artificial sweeteners: different effects on ad libitum food intake and body weight after 10 wk of supplementation in overweight subjects [↩]