The Aging GABAergic System and Its Nutritional Support

Mito

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Abstract​

Aging is associated with a decline in hormones and an associated decline in GABAergic function and calcium and ion current dysregulation. Neurosteroid hormones act as direct calcium channel blockers, or they can act indirectly on calcium channels through their interaction with GABA receptors. The calcium channel dysfunction associated with hormone loss further leads to an excitatory cell state, which can ultimately lead to cell death. The calcium theory of aging posits that cellular mechanisms, which maintain the homeostasis of cytosol Ca2+ concentration, play a key role in brain aging and that sustained changes in Ca2+ homeostasis provide the final common pathway for age-associated brain changes. There is a link between hormone loss and calcium dysregulation. Loss of calcium regulation associated with aging can lead to an excitatory cell state, primarily in the mitochondria and nerve cells, which can ultimately lead to cell death if not kept in check. A decline in GABAergic function can also be specifically tied to declines in progesterone, allopregnanolone, and DHEA levels associated with aging. This decline in GABAergic function associated with hormone loss ultimately affects GABAergic inhibition or excitement and calcium regulation throughout the body. In addition, declines in GABAergic function can also be tied to vitamin status and to toxic chemicals in the food supply. The decline in GABAergic function associated with aging has an effect on just about every body organ system. Nutritional support of the GABAergic system with supportive foods, vitamins, and GABA or similar GABA receptor ligands may address some of the GABAergic dysfunction associated with aging.
 
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Peatness

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Is there anything GAGA can't do? Great article, supports dr peats ideas on hormones. Useful read for anyone with a metabolic issue. Thanks for sharing
 

shine

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Is there anything GAGA can't do? Great article, supports dr peats ideas on hormones. Useful read for anyone with a metabolic issue. Thanks for sharing

YAAAAAS GAGA SLAAAAY QUEEEEN YAAAS
 
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Peatness

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Abstract​

Aging is associated with a decline in hormones and an associated decline in GABAergic function and calcium and ion current dysregulation. Neurosteroid hormones act as direct calcium channel blockers, or they can act indirectly on calcium channels through their interaction with GABA receptors. The calcium channel dysfunction associated with hormone loss further leads to an excitatory cell state, which can ultimately lead to cell death. The calcium theory of aging posits that cellular mechanisms, which maintain the homeostasis of cytosol Ca2+ concentration, play a key role in brain aging and that sustained changes in Ca2+ homeostasis provide the final common pathway for age-associated brain changes. There is a link between hormone loss and calcium dysregulation. Loss of calcium regulation associated with aging can lead to an excitatory cell state, primarily in the mitochondria and nerve cells, which can ultimately lead to cell death if not kept in check. A decline in GABAergic function can also be specifically tied to declines in progesterone, allopregnanolone, and DHEA levels associated with aging. This decline in GABAergic function associated with hormone loss ultimately affects GABAergic inhibition or excitement and calcium regulation throughout the body. In addition, declines in GABAergic function can also be tied to vitamin status and to toxic chemicals in the food supply. The decline in GABAergic function associated with aging has an effect on just about every body organ system. Nutritional support of the GABAergic system with supportive foods, vitamins, and GABA or similar GABA receptor ligands may address some of the GABAergic dysfunction associated with aging.
Sorry I derailed your thread. Still think the GABA article is a must read for all. Thanks again
 

reality

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2.24.4. Dietary Fructose and γ-Aminobutyric Acid

An excellent study by Hassel et al. measured metabolism of [14C]glucose and [14C]fructose by isolated nerve endings. Isolated nerve terminals (synaptosomes) were prepared from neocortex of Wistar rats and incubated in a Krebs solution containing 1 μCi [U-14C] glucose and [U-14C] fructose [126]. Glucose metabolism in nerve cells produced about half of the glutamate compared to the amount of glutamate produced by the nerve cell metabolism of fructose. Metabolism of fructose in the nerve cells led to a significantly increased production of glutamate as compared to GABA and as compared to glucose metabolic products.

Therefore, dietary fructose may contribute to high glutamate production and decreased GABA production, contributing to GABAergic imbalance and an excitotoxic state.

Thoughts?
 

mostlylurking

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Thoughts?
I think thiamine deficiency ties in to this somehow:
snippet: "Thiamine is needed for glutamate dehydrogenase, an enzyme which breaks down the excitatory neurotransmitter glutamate. Thiamine deficiency has been shown to reduce acetylcholine synthesis in the brain and induce excessive glutamate release, effectively paving the way for neuronal excitotoxicity and dysfunction."

Metabolism of sugars, including fructose, use up thiamine. In a thiamine deficiency, you get increased glutamate because of a lack of glutamate dehydrogenase.

also this: Perinatal thiamine restriction affects central GABA and glutamate concentrations and motor behavior of adult rat offspring
snippet: "These results show that the deficiency of thiamine during an early developmental period affects certain motor behavior parameters and GABA and glutamate levels in specific brain areas."
 
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Peatness

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I think thiamine deficiency ties in to this somehow:
snippet: "Thiamine is needed for glutamate dehydrogenase, an enzyme which breaks down the excitatory neurotransmitter glutamate. Thiamine deficiency has been shown to reduce acetylcholine synthesis in the brain and induce excessive glutamate release, effectively paving the way for neuronal excitotoxicity and dysfunction."

Metabolism of sugars, including fructose, use up thiamine. In a thiamine deficiency, you get increased glutamate because of a lack of glutamate dehydrogenase.

also this: Perinatal thiamine restriction affects central GABA and glutamate concentrations and motor behavior of adult rat offspring
snippet: "These results show that the deficiency of thiamine during an early developmental period affects certain motor behavior parameters and GABA and glutamate levels in specific brain areas."
Great find!
 

reality

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I think thiamine deficiency ties in to this somehow:
snippet: "Thiamine is needed for glutamate dehydrogenase, an enzyme which breaks down the excitatory neurotransmitter glutamate. Thiamine deficiency has been shown to reduce acetylcholine synthesis in the brain and induce excessive glutamate release, effectively paving the way for neuronal excitotoxicity and dysfunction."

Metabolism of sugars, including fructose, use up thiamine. In a thiamine deficiency, you get increased glutamate because of a lack of glutamate dehydrogenase.

also this: Perinatal thiamine restriction affects central GABA and glutamate concentrations and motor behavior of adult rat offspring
snippet: "These results show that the deficiency of thiamine during an early developmental period affects certain motor behavior parameters and GABA and glutamate levels in specific brain areas."

Interesting!

I had a massive improvement in mental health, sleep and digestion with thiamine. It’s a serious game changer
 

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