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Whats an effective does of Acetyl-l-carnitine?
- Thread starter JoNeS
- Start date
macrophage69alpha
New member
2-4g, some take more
MrMakaveli
New member
macrophage69alpha said:
How does ALC contribute to fat-loss? Very open ended I know but is there a quick answer?
I took this from the Thermorexin.com website.
Acetyl-l-Carnitine:
Acetyl-l-Carnitine is a co-factor and regulator of a number of biological reactions that are important both for lipolysis and neural function including the synthesis of acetylcholine. It has been shown in numerous studies to improve the levels of beneficial neurotransmitters as well as upregulating their receptors. It has positive impact on thyrotropin (thyroid) and growth hormone releasing factors.
Acetyl-l-Carnitine:
Acetyl-l-Carnitine is a co-factor and regulator of a number of biological reactions that are important both for lipolysis and neural function including the synthesis of acetylcholine. It has been shown in numerous studies to improve the levels of beneficial neurotransmitters as well as upregulating their receptors. It has positive impact on thyrotropin (thyroid) and growth hormone releasing factors.
GoldenDelicious
New member
i hear 100g is an effective dose to use to produce the therapeutic goal of relieving people of their money...
BigBlu
New member
That's brilliant 'goldendelicious'. I couldn't have said it better myself!GoldenDelicious said:
I was recommend some AF Store crap to deal with my trenbolone insomnia, and what's more I was told that it 'specifically designed' for tren insomnia...!!! If 1.5mg of Xanax couldn't put me to sleep that night, how the fuck are a bunch berries, vitamins, essential oils or whatever other fashionable natural ingredient is in P Seven gonna put me to sleep, HA?
THE AF STORE PUSHERS PISS ME OFF!!
MrMakaveli
New member
BigBlu said:
I love P-7, I dont think it's designed to PUT you to sleep but to relax you to the point where you can fall asleep naturally. (Designed for tren RAGE, not insomnia...)
Thanks Ulter, I read that I was just wondering if there was anything more to it? I see people talk about injecting the stuff and wondered if it was working through more mechanisms than just that but thanks
BigBlu
New member
Oh no, I was told by Ulter in a reply to my post about Tren insomnia that P-Seven was 'designed' for specifically for 'Tren Insomnia'. I'm South African pal, I'm not that gullible. If you're a mate of Ulter's, then I'm sure you're a 'fan' of P-Seven. You can't treat the side effects of powerful prescription drugs with the likes of P-Seven. I just don't believe it....Whose ass did they kiss to advertise in every second thread?MrMakaveli said:I love P-7, I dont think it's designed to PUT you to sleep but to relax you to the point where you can fall asleep naturally. (Designed for tren RAGE, not insomnia...)
Thanks Ulter, I read that I was just wondering if there was anything more to it? I see people talk about injecting the stuff and wondered if it was working through more mechanisms than just that but thanks
macrophage69alpha
New member
BigBlu said:
pls engage in some form of research before making these type of comments.
Pseven contains pregenenolone a neurosteroid, it and its metabolites effects on mood, sleep and the CNS are steroidal in nature, much in the same way as trenbolone effects are.
Pseven is effective for many people who have difficulty sleeping on trenbolone, but not everyone. as xanax, valium, and even ambien work for many people but not all. take also for example GHB, in most people medium to high doses induce sleep, in others even very high doses cause excitation and sleeplessness (though these people are uncommon, they do in fact exist)
macrophage69alpha
New member
as a note- in south africa and england Pregnenolone is a "powerful" prescription drug.
prescription drug.
BigBlu
New member
I wouldn't make a statement like that without KNOWING what I'm talking about. FYI pregnenolone is sold OTC in South Africa. Pregnenolone is manufactured from cholestrol in the body and is used and converted in the body by enzymatic processes to manufacture endogenous steroids/hormones.. You're correct in saying that it is mainly found in brain tissue. It's effects are harldy sedatory in nature, as I have used this pregnenolone before. I found it to be stimulating. It is hardly a hypnotic and it's hardly "powerful"! What other magical ingredients is P-Seven 'crammed' with? Sasparilla root maybe.....the 'special kind' that blocks 5-HT2 and GABA receptors.....macrophage69alpha said:
My point is that the AF Store products are being PUSHED onto board members by those members who obviously have a financial interest in the company. We're all here to form our own opinions and for newbies and those naive to bodybuilding it is misleading to tout natural 'cure-alls' on a board based on "powerful" physique enhancing drugs
sawastea
Well-known member
Acetyl L-Carnitine
ALC improves both Short-Term Memory and Long-Term Memory.
ALC improves Mood [ALC improves Mood in 53% of healthy subjects].
Acetyl L-Carnitine retards some aspects of the Aging Process in the Skin:
ALC improves the reaction times of people afflicted with Cerebral Insufficiency.
ALC (2-4 grams per day) improves walking distance without Pain in people afflicted with Intermittent Claudication.
ALC prevents the age-related impairment of Eyesight (by protecting the Neurons of the Optic Nerve and the Occipital Cortex of the Brain.
ALC enhances the ability of Macrophages to function as Phagocytes.
ALC improves Athletic Performance [ALC given prior to Exercise increased the maximum running speed of animals].
ALC enhances the function of Cytochrome Oxidase (an essential enzyme of the Electron Transport System (ETS).
ALC improves the Energy metabolism of Neurons (by enhancing the transport of Medium-Chain Saturated Fatty Acids and Short-Chain Saturated Fatty Acids across the Cell Membranes of Neurons into the Mitochondria).
ALC inhibits the damage caused by Hypoxia.
ALC transports Lipids into the Mitochondria of Cells.
ALC improves mood and memory in people with Age Associated Memory Impairment.
ALC improves Mental Function where Alcohol induced cognitive Impairment exists.
ALC increases Alertness.
Acetyl-L-Carnitine inhibits the deterioration in Mental Function associated with Alzheimer’s Disease and slows the progression of Alzheimer’s Disease [people afflicted with Alzheimer’s Disease exhibited significantly less deterioration in Mental Function following the administration of supplemental ALC for 12 months. This finding was verified by using nuclear magnetic resonance on the subjects].
ALC increases Alertness in people afflicted with Alzheimer's Disease - 2,500-3,000 mg per day for 3 months].
ALC inhibits the toxicity of Amyloid-Beta Protein (ABP) to Neurons.
ALC improves Attention Span in people afflicted with Alzheimer's Disease.
ALC improves Short Term Memory in people afflicted with Alzheimer's Disease.
High concentrations of ALC are naturally present in various regions of the Brain.
ALC reverses the age-related decline that occurs in Cholinergic Receptors (i.e. the Receptors that receive Acetylcholine).
ALC improves (eye to hand) Coordination [supplemental ALC @ 1.5 grams per day for 30 days improved eye to hand coordination in healthy, sedentary subjects by a factor of 300-400%].
ALC improves the Interhemispheric Flow of Information across the Corpus Callosum of the Brain.
ALC retards the decline in the number of Dopamine Receptors that occurs in tandem with the Aging Process and (more rapidly) with the onset of Parkinson's Disease.
ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.
ALC can prevent the destruction of Dopamine Receptors by MPTP (a neurotoxin capable of causing Parkinson's Disease via Dopaminergic Receptor death.
ALC improves Attention Span and Memory in people afflicted with Down’s Syndrome.
ALC retards the inevitable decline in the number of Glucocorticoid Receptors that occurs in tandem with the Aging Process.
ALC enhances the recovery of people afflicted with Hemiplegia (Paralysis of one side of the body) and improves their Mood and Attention Span.
ALC retards the age-related deterioration of the Hippocampus [research - rats].
Acetyl-L-Carnitine (ALC) improves Learning ability [women aged 22 - 27 were supplemented with ALC for 30 days. Complex video game tests before and after supplementation concluded that supplemental ALC caused large increases in speed of Learning, speed of reaction and reduction in errors].
ALC inhibits (and possibly reverses) the degeneration of Myelin Sheaths that occurs in tandem with the progression of the Aging Process [scientific research - hyperglycemic mice treated with ALC for 16 weeks exhibited improved nerve conduction velocity and exhibited thicker Myelin Sheaths and larger myelinated Nerve Fibers].
ALC retards the inevitable decline in the number of Nerve Growth Factor (NGF) Receptors that occurs in tandem with the Aging Process.
ALC stimulates and maintains the growth of new Neurons within the Brain (both independently of Nerve Growth Factor (NGF) and as a result of preserving NGF) and helps to prevent the death of existing Neurons [ALC inhibits Neuron death in the Striatal Cortex, Prefrontal Cortex and the Occipital Cortex of the Brain].
ALC inhibits the degeneration of Neurons that is implicit in Neuropathy.
ALC rejuvenates and increases the number of N-Methyl-D-Aspartate Receptors (NMDA Receptors) in the Brain [even a single dose of ALC increases the number of functional NMDA Receptors]:
ALC protects the NMDA Receptors in the Brain from the natural decline that occurs in tandem with the Aging Process [research - animals].
ALC is presently being researched as a treatment for Parkinson's Disease.
ALC inhibits the loss of Vision, degeneration of Neurons and damage to the Retina associated with Retinopathy (including Diabetic Retinopathy).
ALC improves the quality of Sleep and reduces the quantity of Sleep required.
ALC improves Spatial Memory (an aspect of Short Term Memory that involves remembering one’s position in space).
ALC inhibits the excessive release of Cortisol in response to Stress and inhibits the depletion of Luteinising Hormone Releasing Hormone (LHRH) and Testosterone that occurs as a result of excessive Stress.
ALC improves Verbal Fluency.
ALC enhances the function of Cytochrome Oxidase (also called Complex IV) - an essential enzyme of the Electron Transport System.
ALC normalizes Beta-Endorphin levels.
ALC reduces Stress-induced Cortisol release [research - animals].
ALC prevents the depletion of Luteinising Hormone Releasing Hormone (LHRH) caused by exposure to excessive Stress.
ALC retards the decline in the production of Nerve Growth Factor (NGF) that occurs in tandem with the Aging Process.
ALC increases plasma Testosterone levels (via its influence on Acetylcholine neurotransmission in the Striatal Cortex of the Brain) and prevents the depletion of Testosterone caused by exposure to excessive Stress [research - rats].
ALC increases the body's levels of circulating Thyrotrophin.
ALC facilitates the production of Adenosine Triphosphate (ATP) [research - animals].
ALC "shuttles" Long Chain Fatty Acids between the Cytosol and the Mitochondria of Cells.
ALC facilitates both the release and synthesis of Acetylcholine.
ALC's ability to increase the synthesis of Acetylcholine occurs as a result of it donating its Acetyl group towards the production of Acetylcholine.
ALC increases the Brain's levels of Choline Acetylase (which in turn facilities the production of Acetylcholine).
ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.
References
De Falco, F. A., et al. Effect of the chronic treatment with L-acetylcarnitine in Down’s syndrome. Clin Ther. 144:123-127, 1994.
Bowman, B. Acetyl-carnitine and Alzheimer’s disease. Nutr Rev. 50:142-144, 1992.
Bruno, G., et al. Acetyl-L-carnitine in Alzheimer disease: a short-term study on CSF neurotransmitters and neuropeptides. Alzheimer Dis Assoc Disord (USA). 9(3):128-131, 1995.
Calvani, M., et al. Action of acetyl-L-carnitine in neurodegeneration and Alzheimer’s disease. Annals of the New York Academy of Sciences (USA). 663:483-486, 1993.
Carta, A., et al. Acetyl-L-carnitine: a drug able to slow the progress of Alzheimer’s Disease? Annals of the New York Academy of Sciences (USA. 640:228-232, 1991.
Guarnaschelli, C., et al. Pathological brain ageing: evaluation of the efficacy of a pharmacological aid. Drugs under Experimental and Clinical Research. 14(11):715-718, 1988.
Passeri, M., et al. Acetyl-L-carnitine in the treatment of mildly demented elderly patients. International Journal of Clinical Pharmacology Research. 10(1-2):75-79, 1990.
Pettegrew, J. W., et al. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer’s disease. Neurobiol Aging. 16:1-4, 1995.
Rai, G., et al. Double-blind, placebo controlled study of acetyl-L-carnitine in patients with Alzheimer’s dementia. Current Medical Research and Opinion. 11(10):638-647, 1989.
Sano, M., et al. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer’s disease. Arch Neurol. 49:1137-1141, 1992.
Sinforiani, E., et al. Neuropsychological changes in demented patients treated with acetyl-L-carnitine. International Journal of Clinical Pharmacology Research. 10(1-2):69-74, 1990.
Spagnoli, A. U., et al. Long-term acetyl-l-carnitine treatment in Alzheimer’s disease. Neurology. 41(11):1726-1732, 1991.
ALC improves both Short-Term Memory and Long-Term Memory.
ALC improves Mood [ALC improves Mood in 53% of healthy subjects].
Acetyl L-Carnitine retards some aspects of the Aging Process in the Skin:
ALC improves the reaction times of people afflicted with Cerebral Insufficiency.
ALC (2-4 grams per day) improves walking distance without Pain in people afflicted with Intermittent Claudication.
ALC prevents the age-related impairment of Eyesight (by protecting the Neurons of the Optic Nerve and the Occipital Cortex of the Brain.
ALC enhances the ability of Macrophages to function as Phagocytes.
ALC improves Athletic Performance [ALC given prior to Exercise increased the maximum running speed of animals].
ALC enhances the function of Cytochrome Oxidase (an essential enzyme of the Electron Transport System (ETS).
ALC improves the Energy metabolism of Neurons (by enhancing the transport of Medium-Chain Saturated Fatty Acids and Short-Chain Saturated Fatty Acids across the Cell Membranes of Neurons into the Mitochondria).
ALC inhibits the damage caused by Hypoxia.
ALC transports Lipids into the Mitochondria of Cells.
ALC improves mood and memory in people with Age Associated Memory Impairment.
ALC improves Mental Function where Alcohol induced cognitive Impairment exists.
ALC increases Alertness.
Acetyl-L-Carnitine inhibits the deterioration in Mental Function associated with Alzheimer’s Disease and slows the progression of Alzheimer’s Disease [people afflicted with Alzheimer’s Disease exhibited significantly less deterioration in Mental Function following the administration of supplemental ALC for 12 months. This finding was verified by using nuclear magnetic resonance on the subjects].
ALC increases Alertness in people afflicted with Alzheimer's Disease - 2,500-3,000 mg per day for 3 months].
ALC inhibits the toxicity of Amyloid-Beta Protein (ABP) to Neurons.
ALC improves Attention Span in people afflicted with Alzheimer's Disease.
ALC improves Short Term Memory in people afflicted with Alzheimer's Disease.
High concentrations of ALC are naturally present in various regions of the Brain.
ALC reverses the age-related decline that occurs in Cholinergic Receptors (i.e. the Receptors that receive Acetylcholine).
ALC improves (eye to hand) Coordination [supplemental ALC @ 1.5 grams per day for 30 days improved eye to hand coordination in healthy, sedentary subjects by a factor of 300-400%].
ALC improves the Interhemispheric Flow of Information across the Corpus Callosum of the Brain.
ALC retards the decline in the number of Dopamine Receptors that occurs in tandem with the Aging Process and (more rapidly) with the onset of Parkinson's Disease.
ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.
ALC can prevent the destruction of Dopamine Receptors by MPTP (a neurotoxin capable of causing Parkinson's Disease via Dopaminergic Receptor death.
ALC improves Attention Span and Memory in people afflicted with Down’s Syndrome.
ALC retards the inevitable decline in the number of Glucocorticoid Receptors that occurs in tandem with the Aging Process.
ALC enhances the recovery of people afflicted with Hemiplegia (Paralysis of one side of the body) and improves their Mood and Attention Span.
ALC retards the age-related deterioration of the Hippocampus [research - rats].
Acetyl-L-Carnitine (ALC) improves Learning ability [women aged 22 - 27 were supplemented with ALC for 30 days. Complex video game tests before and after supplementation concluded that supplemental ALC caused large increases in speed of Learning, speed of reaction and reduction in errors].
ALC inhibits (and possibly reverses) the degeneration of Myelin Sheaths that occurs in tandem with the progression of the Aging Process [scientific research - hyperglycemic mice treated with ALC for 16 weeks exhibited improved nerve conduction velocity and exhibited thicker Myelin Sheaths and larger myelinated Nerve Fibers].
ALC retards the inevitable decline in the number of Nerve Growth Factor (NGF) Receptors that occurs in tandem with the Aging Process.
ALC stimulates and maintains the growth of new Neurons within the Brain (both independently of Nerve Growth Factor (NGF) and as a result of preserving NGF) and helps to prevent the death of existing Neurons [ALC inhibits Neuron death in the Striatal Cortex, Prefrontal Cortex and the Occipital Cortex of the Brain].
ALC inhibits the degeneration of Neurons that is implicit in Neuropathy.
ALC rejuvenates and increases the number of N-Methyl-D-Aspartate Receptors (NMDA Receptors) in the Brain [even a single dose of ALC increases the number of functional NMDA Receptors]:
ALC protects the NMDA Receptors in the Brain from the natural decline that occurs in tandem with the Aging Process [research - animals].
ALC is presently being researched as a treatment for Parkinson's Disease.
ALC inhibits the loss of Vision, degeneration of Neurons and damage to the Retina associated with Retinopathy (including Diabetic Retinopathy).
ALC improves the quality of Sleep and reduces the quantity of Sleep required.
ALC improves Spatial Memory (an aspect of Short Term Memory that involves remembering one’s position in space).
ALC inhibits the excessive release of Cortisol in response to Stress and inhibits the depletion of Luteinising Hormone Releasing Hormone (LHRH) and Testosterone that occurs as a result of excessive Stress.
ALC improves Verbal Fluency.
ALC enhances the function of Cytochrome Oxidase (also called Complex IV) - an essential enzyme of the Electron Transport System.
ALC normalizes Beta-Endorphin levels.
ALC reduces Stress-induced Cortisol release [research - animals].
ALC prevents the depletion of Luteinising Hormone Releasing Hormone (LHRH) caused by exposure to excessive Stress.
ALC retards the decline in the production of Nerve Growth Factor (NGF) that occurs in tandem with the Aging Process.
ALC increases plasma Testosterone levels (via its influence on Acetylcholine neurotransmission in the Striatal Cortex of the Brain) and prevents the depletion of Testosterone caused by exposure to excessive Stress [research - rats].
ALC increases the body's levels of circulating Thyrotrophin.
ALC facilitates the production of Adenosine Triphosphate (ATP) [research - animals].
ALC "shuttles" Long Chain Fatty Acids between the Cytosol and the Mitochondria of Cells.
ALC facilitates both the release and synthesis of Acetylcholine.
ALC's ability to increase the synthesis of Acetylcholine occurs as a result of it donating its Acetyl group towards the production of Acetylcholine.
ALC increases the Brain's levels of Choline Acetylase (which in turn facilities the production of Acetylcholine).
ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.
References
De Falco, F. A., et al. Effect of the chronic treatment with L-acetylcarnitine in Down’s syndrome. Clin Ther. 144:123-127, 1994.
Bowman, B. Acetyl-carnitine and Alzheimer’s disease. Nutr Rev. 50:142-144, 1992.
Bruno, G., et al. Acetyl-L-carnitine in Alzheimer disease: a short-term study on CSF neurotransmitters and neuropeptides. Alzheimer Dis Assoc Disord (USA). 9(3):128-131, 1995.
Calvani, M., et al. Action of acetyl-L-carnitine in neurodegeneration and Alzheimer’s disease. Annals of the New York Academy of Sciences (USA). 663:483-486, 1993.
Carta, A., et al. Acetyl-L-carnitine: a drug able to slow the progress of Alzheimer’s Disease? Annals of the New York Academy of Sciences (USA. 640:228-232, 1991.
Guarnaschelli, C., et al. Pathological brain ageing: evaluation of the efficacy of a pharmacological aid. Drugs under Experimental and Clinical Research. 14(11):715-718, 1988.
Passeri, M., et al. Acetyl-L-carnitine in the treatment of mildly demented elderly patients. International Journal of Clinical Pharmacology Research. 10(1-2):75-79, 1990.
Pettegrew, J. W., et al. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer’s disease. Neurobiol Aging. 16:1-4, 1995.
Rai, G., et al. Double-blind, placebo controlled study of acetyl-L-carnitine in patients with Alzheimer’s dementia. Current Medical Research and Opinion. 11(10):638-647, 1989.
Sano, M., et al. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer’s disease. Arch Neurol. 49:1137-1141, 1992.
Sinforiani, E., et al. Neuropsychological changes in demented patients treated with acetyl-L-carnitine. International Journal of Clinical Pharmacology Research. 10(1-2):69-74, 1990.
Spagnoli, A. U., et al. Long-term acetyl-l-carnitine treatment in Alzheimer’s disease. Neurology. 41(11):1726-1732, 1991.
macrophage69alpha
New member
BigBlu said:
if you knew what you were talking about you would know the ingredients, you did not know any of them prior to making your assertions that it would not work.
BigBlu
New member
That's an assumption. Here we go son: Contents: Alcohol, glycerin, propylene glycol, oleic acid, peppermint oil, 7-oxo DHEA and pregnenolone. FYI, I knew the ingredients from the time I joined this board. Back to my point. NONE, and I repeat NONE of those ingredients will make you sleep! The Sasparilla Root thing was a joke. I'm not wanting to play tit-for-tat here, mate. We're both man enough to respect each other opinions, but nothing beats hard science when it comes to biochemistry. From what I can gather it seems that you have a vested interest in the AF Store products. I have no problem with that. We all need to make a living.....but it's becoming more and more fashionable in 'Western' society to hype up claims and aim for the placebo and/or psychological effect in product sales.macrophage69alpha said:
macrophage69alpha
New member
pregnenolone and its metabolites (particularly allo-pregnenolone) are anxiolytic
Psychol Med. 2002 Jul;32(5):929-33. Related Articles, Links
Low pregnenolone sulphate plasma concentrations in patients with generalized social phobia.
Heydari B, Le Melledo JM.
Department of Psychiatry, University of Alberta Hospital, Edmonton, Canada.
BACKGROUND: Animal studies have shown that neuroactive steroids modulate the activity of the gamma-aminobutyric acid type A/benzodiazepine receptor complex and that these steroids display anxiolytic or anxiogenic activity depending on their positive (e.g. allopregnanolone) or negative allosteric modulation (e.g. dehydroepiandrosterone sulphate) of this receptor. This study compared plasma levels of allopregnanolone, dehydroepiandrosterone sulphate and pregnenolone sulphate in healthy controls and in patients with generalized social phobia, as assessed with the Mini-International Neuropsychiatric Interview. METHODS: Plasma concentrations of allopregnanolone, pregnenolone sulphate, and dehydroepiandrosterone sulphate were measured in 12 unmedicated male patients with generalized social phobia and 12 matched healthy male volunteers. RESULTS: Concentrations of pregnenolone sulphate were significantly lower in patients with generalized social phobia than in healthy controls. No statistically significant differences were found for the concentrations of allopregnanolone and dehydroepiandrosterone sulphate in plasma. CONCLUSIONS: These results are particularly interesting since we also observed lower pregnenolone sulphate concentrations in male patients suffering from generalized anxiety disorder. Their relevance to the pathophysiology of social anxiety disorder remains to be determined.
Trends Neurosci. 1999 Sep;22(9):410-6. Related Articles, Links
Comment in:
Trends Neurosci. 2000 Feb;23(2):57-8.
Trends Neurosci. 2001 Oct;24(10):570-2.
Neuroactive steroids: mechanisms of action and neuropsychopharmacological perspectives.
Rupprecht R, Holsboer F.
Dept of Psychiatry, Ludwig-Maximilians-University of Munich, 80336 Munich, Germany.
Steroids influence neuronal function by binding to intracellular receptors that can act as transcription factors and regulate gene expression. In addition, some so-called 'neuroactive steroids' are potent modulators of an array of ligand-gated ion channels and of distinct G-protein coupled receptors via nongenomic mechanisms, and they can influence sleep and memory. This article describes how these neuroactive steroids modulate neurotransmitter receptors and addresses the neuropsychopharmacological potential that arises from the intracellular crosstalk between genomic and nongenomic steroid effects. Neuroactive steroids could also have a role in the response to stress and the treatment of psychiatric disorders, such as depression, and, as they affect a broad spectrum of behavioral functions through their unique molecular properties, they could constitute a yet unexploited class of drugs.
etc..etc..
trenbolone, likely through progestenic and androgenic action is anxiogenic...
many problems with sleep are due to anxiety, hence the reason that anxiolytic drugs are often effective.
Psychol Med. 2002 Jul;32(5):929-33. Related Articles, Links
Low pregnenolone sulphate plasma concentrations in patients with generalized social phobia.
Heydari B, Le Melledo JM.
Department of Psychiatry, University of Alberta Hospital, Edmonton, Canada.
BACKGROUND: Animal studies have shown that neuroactive steroids modulate the activity of the gamma-aminobutyric acid type A/benzodiazepine receptor complex and that these steroids display anxiolytic or anxiogenic activity depending on their positive (e.g. allopregnanolone) or negative allosteric modulation (e.g. dehydroepiandrosterone sulphate) of this receptor. This study compared plasma levels of allopregnanolone, dehydroepiandrosterone sulphate and pregnenolone sulphate in healthy controls and in patients with generalized social phobia, as assessed with the Mini-International Neuropsychiatric Interview. METHODS: Plasma concentrations of allopregnanolone, pregnenolone sulphate, and dehydroepiandrosterone sulphate were measured in 12 unmedicated male patients with generalized social phobia and 12 matched healthy male volunteers. RESULTS: Concentrations of pregnenolone sulphate were significantly lower in patients with generalized social phobia than in healthy controls. No statistically significant differences were found for the concentrations of allopregnanolone and dehydroepiandrosterone sulphate in plasma. CONCLUSIONS: These results are particularly interesting since we also observed lower pregnenolone sulphate concentrations in male patients suffering from generalized anxiety disorder. Their relevance to the pathophysiology of social anxiety disorder remains to be determined.
Trends Neurosci. 1999 Sep;22(9):410-6. Related Articles, Links
Comment in:
Trends Neurosci. 2000 Feb;23(2):57-8.
Trends Neurosci. 2001 Oct;24(10):570-2.
Neuroactive steroids: mechanisms of action and neuropsychopharmacological perspectives.
Rupprecht R, Holsboer F.
Dept of Psychiatry, Ludwig-Maximilians-University of Munich, 80336 Munich, Germany.
Steroids influence neuronal function by binding to intracellular receptors that can act as transcription factors and regulate gene expression. In addition, some so-called 'neuroactive steroids' are potent modulators of an array of ligand-gated ion channels and of distinct G-protein coupled receptors via nongenomic mechanisms, and they can influence sleep and memory. This article describes how these neuroactive steroids modulate neurotransmitter receptors and addresses the neuropsychopharmacological potential that arises from the intracellular crosstalk between genomic and nongenomic steroid effects. Neuroactive steroids could also have a role in the response to stress and the treatment of psychiatric disorders, such as depression, and, as they affect a broad spectrum of behavioral functions through their unique molecular properties, they could constitute a yet unexploited class of drugs.
etc..etc..
trenbolone, likely through progestenic and androgenic action is anxiogenic...
many problems with sleep are due to anxiety, hence the reason that anxiolytic drugs are often effective.
macrophage69alpha
New member
the fact of the matter is that many people who have difficulty sleeping while on trenbolone do respond well to Pseven.
It was not specifically designed for this, though it has by way of users reports and Ulters own experience become highly reccomended for it.
It was not specifically designed for this, though it has by way of users reports and Ulters own experience become highly reccomended for it.
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