On MSG and Genetically Modified plants

LabRat529

Here... from a very quick search and a very quick skim-through:

http://www.jlr.org/content/44/11/2127.full.pdf

On DNL in rats vs. humans. I hope that answers your question. If not, I can do more digging, but for now I've got to get back to work. My lunch break is over.

LabRat529

Oh... doh.. someone beat me to it Good!

RonSwanson66

Here... I'll counter the study that says MSG promotes obesity in rats with one that says it reduces weight gain:

http://www.ncbi.nlm.nih.gov/pubmed/19587084

CRAP.

Now I don't know whether or not I should feed MSG to my rat.

cabaray

I only avoid MSG because it triggers horrible migraines for me. I certainly wouldn't avoid it otherwise!

A perfectly good reason to avoid it

Sorry about the migraines. Those suck.

Thanks...haven't had one since I found the connection.

LabRat529

If there was no reason to test this out on rats in the first place, not sure why they are doing so many studies.

You test things out in rats 'cause you can open up their heads and take out their brains and look at them. Humans tend to get grumpy when you try that with them

And now I'm REALLY gonna get to work.

Acg67

In conclusion, we found that that the lipogenic capacity
of adipose tissue is reduced in humans compared with
rats. This is not explained by differences in the CHO-to-fat
ratio in the diet and appears to be related to a reduced
amount of SREBP-1c protein. Differences in the expression
of ChREBP could also play a role. Finally, this finding
of low lipogenic activity in adipose tissue in humans confirms
that most of the TGs stored in adipose tissue are provided
by diet and delivered to adipocytes by circulating lipoproteins.

Murlin54

In conclusion, we found that that the lipogenic capacity
of adipose tissue is reduced in humans compared with
rats. This is not explained by differences in the CHO-to-fat
ratio in the diet and appears to be related to a reduced
amount of SREBP-1c protein. Differences in the expression
of ChREBP could also play a role. Finally, this finding
of low lipogenic activity in adipose tissue in humans confirms
that most of the TGs stored in adipose tissue are provided
by diet and delivered to adipocytes by circulating lipoproteins.

AND this same article

"This situation appears
different from that in rats, in which DNL is considered
to occur to a similar extent in the liver and in adipose
tissue and to be more active than in humans (12).
However, this view of a large difference in the lipogenic
activity of adipose tissue between humans and rats has
been challenged. First, the usual diet of rats in animal facilities
is an HCHO diet, contrary to the usual diet of humans,
which is much more rich in fat, at least in Western
countries. This could play a role in the difference between
the two species, given the well-known stimulatory effect of
carbohydrate (CHO) and the inhibitory action of fat on lipogenesis
(18, 19). Actually, Swierczynski et al. (20) concluded
that the difference between the lipogenic potential
of human and rat adipose tissue was only moderate
when humans and rats were studied while receiving comparable
diets."

Murlin54

If there was no reason to test this out on rats in the first place, not sure why they are doing so many studies.

You test things out in rats 'cause you can open up their heads and take out their brains and look at them. Humans tend to get grumpy when you try that with them

And now I'm REALLY gonna get to work.

\

yeah, my only point here was why do studies on the effect of MSG in rats in the first place. They are trying to prove/disprove something. They have not ten studies but hundreds. And I am NOT volunteering to have my brain removed.

tigersword

The problem with labeling MSG in general as "crap" and trying to have it removed from the diet is the fact that MSG is a naturally occurring substance in many foods, and as another poster mentioned, if MSG caused such weight gain, why are Asian countries, who eat far more MSG than we do, not more obese?

M3CH4N1C

BANKER: David Rockefeller Sept. 23, 1994 "This present window of opportunity, during which a truly peaceful and interdependent world order might be built, will not be open for too long — We are on the verge of a global transformation. All we need is the right major crisis and the nations will accept the New World Order."


How To Wake UP Your Sheople Friends & Family

www.youtube.com/watch?v=Q84_RZcscJE

Do you know the difference between "quote mining" and "evidence"?

Do you know the difference between critical thinking and unrealistic optimism?

M3CH4N1C

If there was no reason to test this out on rats in the first place, not sure why they are doing so many studies.

You test things out in rats 'cause you can open up their heads and take out their brains and look at them. Humans tend to get grumpy when you try that with them

And now I'm REALLY gonna get to work.

If things continue like they have been in the world, humans won't resist anymore, just like rats. What's that song by Smashing Pumpkins where the lyrics state "despite all my rage I am still just a rat in a cage." In retrospect that song's lyrics appear to show evidence of psychological conditioning.

RonSwanson66

If there was no reason to test this out on rats in the first place, not sure why they are doing so many studies.

You test things out in rats 'cause you can open up their heads and take out their brains and look at them. Humans tend to get grumpy when you try that with them

And now I'm REALLY gonna get to work.

\

yeah, my only point here was why do studies on the effect of MSG in rats in the first place. They are trying to prove/disprove something. They have not ten studies but hundreds. And I am NOT volunteering to have my brain removed.

The study you posted wasn't studying the effects of MSG, it was studying the effect of exercise on blood and tissue markers. They needed obese rats and megadosed the rats with MSG to make them fat.

Without seeing the other studies, it's impossible to know if this is the case with them as well. But generally, human trials are very expensive. So before getting funding for human trials, scientists must use other methods to determine whether the phenomena they wish to study warrants the investment. These can be in vitro, in situ or in vivo rodent trials.

Good scientists know that the results of these trials are not directly applicable to humans. Unfortunately, lay press can't seem to grasp this point.

Murlin54

the point I was trying to make is they are continuing to study the effects of MSG and yes, using rats. I don't think they are really worried about the effect MSG has on rats. If there were no concerns for the human factor, I don't think there would be so many tests out there. Let's see how much MSG it takes to get a fat rat? Overweight rats or chemically compromised rats are certainly not the concern.

RonSwanson66

the point I was trying to make is they are continuing to study the effects of MSG and yes, using rats. I don't think they are really worried about the effect MSG has on rats. If there were no concerns for the human factor, I don't think there would be so many tests out there. Let's see how much MSG it takes to get a fat rat? Overweight rats or chemically compromised rats are certainly not the concern.

Please point to these "hundreds of studies" you're referring to. I highly doubt that they're studying the effect of MSG on rats.

More likely, they're doing something else (like the study above).

M3CH4N1C

Good scientists know that the results of these trials are not directly applicable to humans. Unfortunately, lay press can't seem to grasp this point.

Good scientist?? What facilitates a good scientist? The way I see it, scientists are becoming like lawyers, repugnant with the word good.

RonSwanson66

Good scientists know that the results of these trials are not directly applicable to humans. Unfortunately, lay press can't seem to grasp this point.

Good scientist?? What facilitates a good scientist? The way I see it, scientists are becoming like lawyers, repugnant with the word good.

Go away troll, I'm not feeding you anymore.

Bring something relevant to the conversation or GTFO.

M3CH4N1C

Good scientists know that the results of these trials are not directly applicable to humans. Unfortunately, lay press can't seem to grasp this point.

Good scientist?? What facilitates a good scientist? The way I see it, scientists are becoming like lawyers, repugnant with the word good.

Go away troll, I'm not feeding you anymore.

Bring something relevant to the conversation or GTFO.

Your definitely the weaker mind. LOL. I suggest you heed your own advice. If you can't stand the heat then stay out of the kitchen.

Murlin54

the point I was trying to make is they are continuing to study the effects of MSG and yes, using rats. I don't think they are really worried about the effect MSG has on rats. If there were no concerns for the human factor, I don't think there would be so many tests out there. Let's see how much MSG it takes to get a fat rat? Overweight rats or chemically compromised rats are certainly not the concern.

Please point to these "hundreds of studies" you're referring to. I highly doubt that they're studying the effect of MSG on rats.

More likely, they're doing something else (like the study above).

On MSG
"Scientists have known about the MSG problem for quite a while. They frequently study obesity by poisoning rats with MSG until they become obese. Naturally, this is called the MSG obese rat. There are over 100 studies on this rat in scientific literature.
MSG causes glutamate neurotoxicity. It causes an obese rat because the glutamate toxicity destroys the leptin message written on the blackboard in the subsconscious brain that directly controls appetite or it destroys the blackboard so no message can be written". "Children and adults consuming MSG, especially in large amounts, can create a neurotoxic brain response in the appetite control center that could easily tilt them toward obesity. MSG should be completely avoided by everyone". from "Mastering Leptin" by Byron J. Richards, CCN

quoting myself quoting from the book Mastering Leptin. The author says "there are over 100 studies on this rat in scientific literature". I tend to believe him since he has pages upon pages of research credits in this book. So no, it wasn't me who said there were over 100 studies, but rather Byron J. Richards. I don't have time right now to go through the book and see if he has a list of the studies he is referring to. I'll take a look later if you are really interested.

RonSwanson66

I tend to believe him since he has pages upon pages of research credits in this book

This is a mistake. Quoting volumes of research is common practice among authors with an agenda, even if the research doesn't support their claims.

Read the statement carefully:

They frequently study obesity by poisoning rats with MSG until they become obese. Naturally, this is called the MSG obese rat. There are over 100 studies on this rat in scientific literature.

The statement is technically true, but misleading. A quick search brought up several studies, none of which was studying the effects of MSG on obesity, but rather using MSG obese rats to study other factors.


http://scholar.google.com/scholar?hl=en&q="msg+obese+rats"&btnG=Search&as_sdt=1,38&as_ylo=&as_vis=1

LabRat529

References that might be of interest:

In ADULT rats showing dietary glutamate had no effect on glutamate concentration in the brain:

Neurosci Lett. 1995 Jun 23;193(1):45-8.
Extracellular glutamate levels in the hypothalamus and hippocampus of rats after acute or chronic oral intake of monosodium glutamate.
Monno A, Vezzani A, Bastone A, Salmona M, Garattini S.
Source
Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy.
Abstract
Using brain microdialysis we studied the effect of high doses of monosodium glutamate (MSG) on the extracellular concentration of glutamate in the hypothalamus and in the hippocampus of freely moving rats. MSG at 4 g/kg (40% solution) given by gavage caused a significant increase in plasma (5.3 +/- 0.4-fold, P < 0.01) and extracellular glutamate in the hippocampus (4.2 +/- 0.6-fold, P < 0.01) and in the hypothalamus (8.9 +/- 1.7-fold, P < 0.01) compared to control rats receiving a 40% sucrose solution (10 ml/kg). The peak increase was found within 40 min after MSG administration then declining to baseline in the next 80 min. No changes were found in glutamate tissue concentrations. Twenty-one days after ad libitum MSG intake with the diet (approximately 4 g/kg) no changes were found, in plasma, in extracellular and tissue concentration of glutamate in the hypothalamus compared to rats fed with a normal diet. Glutamate release induced by 200 mM KCl was not modified as well. Histological analysis of Nissl-stained brain tissue slices did not reveal any obvious cell loss in the hippocampus after acute or chronic MSG administration.

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Brain Res. 1994 Oct 17;660(2):337-40.
Effects of systemic or oral ad libitum monosodium glutamate administration on striatal glutamate release, as measured using microdialysis in freely moving rats.
Bogdanov MB, Wurtman RJ.
Source
Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, Cambridge 02142.
Abstract
We examined effects of high doses of monosodium glutamate (MSG) on extracellular glutamate levels in rat striata, using in vivo microdialysis. Parenteral doses (0.5, 1.0 and 2.0, but not 0.25, g/kg, i.p.) caused dose- and time-dependent increases, peaking after 40 min (at 174 +/- 47%, 485 +/- 99% and 1021 +/- 301% of basal levels, respectively). In contrast, dietary MSG (1.49 +/- 0.10 g/kg/h) was ineffective.

PMID: 7820703 [PubMed - indexed for MEDLINE]

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Brain Res. 1996 Oct 14;736(1-2):76-81.
Consumption of a high dietary dose of monosodium glutamate fails to affect extracellular glutamate levels in the hypothalamic arcuate nucleus of adult rats.
Bogdanov MB, Tjurmina OA, Wurtman RJ.
Source
Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology 02139, USA.
Abstract
We examined the effects of systemic or oral ad libitum monosodium glutamate (MSG) administration on glutamate levels in plasma, and on glutamate release from the arcuate nucleus of the hypothalamus (estimated using brain microdialysis). Systemic MSG administration (0.25, 0.5, 1 or 2 g/kg, i.p.) to adult rats caused dose-dependent increases in glutamate levels within arcuate nucleus dialysates. These levels increased during the initial 20 min after systemic MSG administration, and peaked during the second 20-min interval (maximally to 116 +/- 7%, 146 +/- 15%, 790 +/- 191% and 1230 +/- 676% of basal values, respectively). Plasma glutamate levels, measured simultaneously, were increased maximally during the initial 20 min after MSG administration. These increases were 10-, 13-, 76- and 163-fold after doses of 0.25, 0.5, 1 and 2 g/kg, i.p., respectively. In feeding experiments, consumption of 2.3 g/kg of MSG by previously-trained rats during an 1-h period increased plasma glutamate levels to 352 +/- 61% of basal values 140 min after the start of the feeding period. No changes were observed in glutamate levels of arcuate nucleus dialysates. These findings may explain why ad libitum dietary consumption of MSG apparently lacks neurotoxic potential.

PMID: 8930311 [PubMed - indexed for MEDLINE]
Publication Types, MeSH Terms, Substances

LinkOut - more resources

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In ADULT rats showing dietary amino acids including glutamate DID increase glutamate levels in the brain (shared in the spirit of being fair and as unbiased as possible)


Life Sci. 1995;57(21):1911-23.
Microdialysis as a tool to measure dietary and regional effects on the complete profile of extracellular amino acids in the hypothalamus of rats.
Currie PJ, Chang N, Luo S, Anderson GH.
Source
Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, ON, Canada.
Abstract
Regional and dietary-induced changes in hypothalamic extracellular amino acid concentrations were examined. Microdialysis probes were simultaneously implanted in the hypothalamic paraventricular nucleus (PVN) and the lateral hypothalamus (LH) of anesthetized rats and perfused at a rate of 2 microliters/min. Dialysates were collected every 20 min for 1 h prior to gavage of a balanced amino acid mixture (0.85 g patterned after 1 g of chicken egg albumin) and then every 20 min for 3 h after treatment. Tail vein blood samples were also collected. Marked changes in plasma levels of most amino acids were evident immediately following the amino acid gavage. In the PVN, concentrations of isoleucine, leucine, methionine and valine all increased within 40 min, whereas significant decreases in glutamine, histidine and taurine were observed in the LH. In a separate study, PVN extracellular amino acid concentrations were examined in awake, freely-behaving rats following gavage of equicaloric loads of a balanced amino acid mixture, glucose (0.89 g) or water. Dialysate levels of glutamate, isoleucine, leucine, methionine, threonine, tyrosine and valine showed reliable increases after amino acid treatment, although the overall time course of these effects differed somewhat. The amino acid profile of the PVN was, in general, unaffected by glucose administration. These findings suggest that specific brain regions may respond uniquely to amino acid ingestion and further imply that dietary composition may influence the amino acid profiles of the extracellular fluid in brain.

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Here's another that looks at the obesity MSG link in rats again


Here's another one that looks at the MSG and obesity link

Physiol Behav. 2008 Sep 3;95(1-2):135-44. Epub 2008 May 16.
MSG intake suppresses weight gain, fat deposition, and plasma leptin levels in male Sprague-Dawley rats.
Kondoh T, Torii K.
Source
Institute of Life Sciences, Ajinomoto Co., Inc., Suzuki-cho 1-1, Kawasaki-ku, Kawasaki 210-8681, Japan.
Abstract
Monosodium l-glutamate (MSG), an umami taste substance, may be a key molecule coupled to a food intake signaling pathway, possibly mediated through a specific l-glutamate (GLU) sensing mechanism in the gastrointestinal tract. Here we investigated the effect of the spontaneous ingestion of a 1% MSG solution and water on food intake and body weight in male Sprague-Dawley rats fed diets of varying caloric density, fat and carbohydrate contents. Fat mass and lean mass in the abdomen, blood pressure, and several blood metabolic markers were also measured. Rats given free access to MSG and water showed a high preference (93-97%) for the MSG solution, regardless of the diet they consumed. Rats ingesting MSG had a significantly smaller weight gain, reduced abdominal fat mass, and lower plasma leptin levels, compared to rats ingesting water alone. Naso-anal length, lean mass, food and energy intakes, blood pressure, blood glucose, and plasma levels of insulin, triglyceride, total cholesterol, albumin, and GLU were not influenced by the ingestion of the MSG solution. These same effects were observed in a study of adult rats. Together, these results suggest that MSG ingestion reduces weight gain, body fat mass, and plasma leptin levels. Moreover, these changes are likely to be mediated by increased energy expenditure, not reduced energy intake or delayed development. Conceivably, these effects of MSG might be mediated via gut GLU receptors functionally linked to afferent branches of the vagus nerve in the gut, or the afferent sensory nerves in the oral cavity.

And in HUMANS (These are review articles because I'm lazy and don't feel like tracking down the original references right now. The review articles reference their claims, so if you want original sources, you can go look at their references. Also, yes, I'm including articles that don't align with my personal bias too... because that's only fair):

>>>>>>>>>>>> http://jn.nutrition.org.libproxy.usc.edu/content/130/4/1049.long <<<<<<<<<<<

The Safety Evaluation of Monosodium Glutamate1
Ronald Walker2 and John R. Lupien*
School of Biological Sciences, University of Surrey, Guildford GU2 5XH, Surrey, UK and
*Food and Nutrition Division, FAO, 00100 Roma, Italy
ABSTRACT L-Glutamic acid and its ammonium, calcium, monosodium and potassium salts were evaluated by
the Joint FAO/WHO Expert Committee on Food Additives (JECFA) in 1988. The Committee noted that intestinal and
hepatic metabolism results in elevation of levels in systemic circulation only after extremely high doses given by
gavage (.30mg/kg body weight). Ingestion of monosodium glutamate (MSG) was not associated with elevated
levels in maternal milk, and glutamate did not readily pass the placental barrier. Human infants metabolized
glutamate similarly to adults. Conventional toxicity studies using dietary administration of MSG in several species
did not reveal any specific toxic or carcinogenic effects nor were there any adverse outcomes in reproduction and
teratology studies. Attention was paid to central nervous system lesions produced in several species after
parenteral administration of MSG or as a consequence of very high doses by gavage. Comparative studies
indicated that the neonatal mouse was most sensitive to neuronal injury; older animals and other species (including
primates) were less so. Blood levels of glutamate associated with lesions of the hypothalamus in the neonatal
mouse were not approached in humans even after bolus doses of 10 g MSG in drinking water. Because human
studies failed to confirm an involvement of MSG in “Chinese Restaurant Syndrome” or other idiosyncratic
intolerance, the JECFA allocated an “acceptable daily intake (ADI) not specified” to glutamic acid and its salts. No
additional risk to infants was indicated. The Scientific Committee for Food (SCF) of the European Commission
reached a similar evaluation in 1991. The conclusions of a subsequent review by the Federation of American
Societies for Experimental Biology (FASEB) and the Federal Drug Administration (FDA) did not discount the
existence of a sensitive subpopulation but otherwise concurred with the safety evaluation of JECFA and the
SCF. J. Nutr. 130: 1049S–1052S, 2000.

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Nutrition. 2005 Jun;21(6):749-55.
Monosodium glutamate in standard and high-fiber diets: metabolic syndrome and oxidative stress in rats.
Diniz YS, Faine LA, Galhardi CM, Rodrigues HG, Ebaid GX, Burneiko RC, Cicogna AC, Novelli EL.
Source
Department of Clinical Cardiology, Faculty of Medicine, University of São Paulo State, Botucatu, Brazil.
Abstract
OBJECTIVE:
This study determined the effects of adding monosodium glutamate (MSG) to a standard diet and a fiber-enriched diet on glucose metabolism, lipid profile, and oxidative stress in rats.

METHODS:
Male Wistar rats (65 +/- 5 g, n = 8) were fed a standard diet (control), a standard diet supplemented with 100 g of MSG per kilogram of rat body weight, a diet rich in fiber, or a diet rich in fiber supplemented with 100 g of MSG per kilogram of body weight. After 45 d of treatment, sera were analyzed for concentrations of insulin, leptin, glucose, triacylglycerol, lipid hydroperoxide, and total antioxidant substances. A homeostasis model assessment index was estimated to characterize insulin resistance.

RESULTS:
Voluntary food intake was higher and feed efficiency was lower in animals fed the standard diet supplemented with MSG than in those fed the control, fiber-enriched, or fiber- and MSG-enriched diet. The MSG group had metabolic dysfunction characterized by increased levels of glucose, triacylglycerol, insulin, leptin, and homeostasis model assessment index. The adverse effects of MSG were related to an imbalance between the oxidant and antioxidant systems. The MSG group had increased levels of lipid hydroperoxide and decreased levels of total antioxidant substances. Levels of triacylglycerol and lipid hydroperoxide were decreased in rats fed the fiber-enriched and fiber- and MSG-enriched diets, whereas levels of total antioxidant substances were increased in these animals.

CONCLUSIONS:
MSG added to a standard diet increased food intake. Overfeeding induced metabolic disorders associated with oxidative stress in the absence of obesity. The fiber-enriched diet prevented changes in glucose, insulin, leptin, and triacylglycerol levels that were seen in the MSG group. Because the deleterious effects of MSG, i.e., induced overfeeding, were not seen in the animals fed the fiber-enriched diets, it can be concluded that fiber supplementation is beneficial by discouraging overfeeding and improving oxidative stress that is induced by an MSG diet.

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J Allergy Clin Immunol. 1997 Jun;99(6 Pt 1):757-62.
The monosodium glutamate symptom complex: assessment in a double-blind, placebo-controlled, randomized study.
Yang WH, Drouin MA, Herbert M, Mao Y, Karsh J.
Source
Department of Medicine, University of Ottawa, Ontario, Canada.
Abstract
BACKGROUND:
Considerable debate swirls about the validity of symptoms described by many people after ingestion of monosodium glutamate (MSG), and the question has remained unresolved largely because of a paucity of well-designed challenge studies.

METHODS:
We conducted oral challenge studies in self-identified MSG-sensitive subjects to determine whether they had a statistically significant difference in the incidence of their specific symptoms after ingestion of MSG compared with placebo. First, 5 gm MSG or placebo was administered in random sequence in a double-blind fashion. Subjects who reacted only to a single test agent then underwent rechallenge in random sequence in a double-blind fashion with placebo and 1.25, 2.5, and 5 gm MSG. A positive response to challenge was defined as the reproduction of > of 2 of the specific symptoms in a subject ascertained on prechallenge interview.

RESULTS:
Sixty-one subjects entered the study. On initial challenge, 18 (29.5%) responded to neither MSG nor placebo, 6 (9.8%) to both, 15 (24.6%) to placebo, and 22 (36.1%) to MSG (p = 0.324). Total and average severity of symptoms after ingestion of MSG (374 and 80) were greater than respective values after placebo ingestion (232 and 56; p = 0.026 and 0.018, respectively). Rechallenge revealed an apparent threshold dose for reactivity of 2.5 gm MSG. Headache (p < 0.023), muscle tightness (p < 0.004), numbness/tingling (p < 0.007), general weakness (p < 0.040), and flushing (p < 0.016) occurred more frequently after MSG than placebo ingestion.

CONCLUSIONS:
Oral challenge with MSG reproduced symptoms in alleged sensitive persons. The mechanism of the reaction remains unknown, but symptom characteristics do not support an IgE-mediated mechanism. According to Food and Drug Administration recommendations, the symptoms, originally called the Chinese restaurant syndrome, are better referred to as the MSG symptom complex.

NOTE: that one is interesting because it supports the idea that some people are sensitive to MSG.

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And I'm bored, so I'm done. But you can do all this yourself. Go to pubmed. Type in dietary glutamate toxicity. Hit the limits and select humans. It still doesn't read out all the rat studies. I don't know why. It's annoying.