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If you put this altogether, most people in industrial countries are eating hundreds of grams of excitotoxins, including MSG, on a yearly basis. And a bunch of it is going to get snatched up the neuronal tissue of the hypothalamus, where, if in sufficient quantities, will do significantly damage, especially over the years and decades.
So is there really any evidence for all that I am saying. Yes! One recent study shows that this is going with much more prevalence that scientists initially anticipated. Before we go into this study, though, I have to make the observation that many animal studies have shown that MSG consumption can lead to obesity later in life. [1] A 2011 study on a Chinese population verified this in adults: the more MSG consumed, the more weight gain experienced by the participants. [2] The authors of the study noted that “influences energy balance through the disruption of the hypothalamic signaling cascade of leptin action.” In other words, the researchers believed that MSG was negatively impacting hormonal leptin levels through the hypothalamus.
The reason that researchers were so sure that this could be an issue is that animals studies showed that there were leptin receptors in a region of the hypothalamus called the arcuate nucleus. Of course, the question is if MSG could reach and damage these receptors enough to make a negative impact. Several animal studies showed that this could definitely occur and that the arcuate nucleus could be damaged permanently by MSG. [3] And, so yes, one should be asking, “Why on God’s green earth would we put this in our food supply?”
Common sense tells you that you do not want to damage a key endocrine gland for ANY reason and yet this is exactly what we are doing by consuming these kind of nasty excitotoxins. MSG literally overexcites – thus the name “excitotoxin” – neurons and can lead to synaptic miswiring and hormonal death.
A similar analogy could be Vitamin D. Vitamin D is good and used for a host of metabolic processes, because it controls calcium processing in the body. Calcium is used for many things, including neuronal signaling, bone building and many other functions. However, too much Vitamin D can actually lead to hypercalcemia, which, of course, too much calcium can lead to pain, fatigue and, ironically, bone damage. This is similar to consuming too many glutamates: it literally chokes one’s neuronal systems with “too much of a good thing.”
Now the evidence is out that MSG from food likely effects one hormone (leptin) influenced by the hypothalamus. Is it really that much of a stretch to assume it does the same with testosterone through GnRH when there is abundant animal evidence of just such a phenomenon? Many animal studies have shown that MSG in relatively small dosages can lead to hypogonadism. [5] Is it really prudent to wait for another study to directly show this on humans?
By the way, it is important to remember that the hypothalamus is also involved in signaling the thyroid. Recent animal studies show that excitotoxins can take out the hypothalamus and lead to hypothyroidism. [4] What is the significance to us men? Remember: hypothyroidism is associated with low testosterone. This means that the risks to your testosterone from MSG are actually multiple: 1) by damaging GnRH signaling and 2) by inducing or exacerbating hypothyroidism.
The bottom line is that your poor hypothalamus is sitting vulnerable and exposed to MSG that you consume and that this is a huge risk to your testosterone and general endocrine function. Study after study is showing issues: read also my link on Excitotoxin Syndrome for another example. The bottom line is that there is simply no compelling reason to risk the negative impact and potential damage of MSG consumptions.
REFERENCES:
1) Neuroendocrinology, 1992, 56(3), "Monosodium Glutamate-lnduced Reductions in Hypothalamic Beta-Endorphin Content Result in Mu-Opioid Receptor Upregulation in the Medial Preoptic Area"
2) Am J Clin Nutr 2011 94: 958-960, "A lack of epidemiologic evidence to link consumption of monosodium L-glutamate and obesity in China"
3) AJP - Endo, July 1 1997, 273(1):E202-E206, "Attenuation of leptin-mediated effects by monosodium glutamate-induced arcuate nucleus damage"
4) Endocrinology, Jul 1 2010, 151(7):3267-3276, "Developmental Hypothyroidism Increases the Expression of Kainate Receptors in the Hippocampus and the Sensitivity to Kainic Acid-Induced Seizures in the Rat"
5) African Journal of Biotechnology, Jul 2009, 8(13):3031-3035, "Hepatotoxic effects of low dose oral administration of monosodium glutamate in male albino rats"
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