DNP and the brain?

[GeorgeWBush]

The brain uses a large amount of the daily energy requirements just to function normally, and a third of that is used to maintain brain cells.

Now, since DNP interferes with the election transport chain, preventing ATP production, and because the brain uses ATP for energy to function keep brain cells alive you can see where a problem would arise and its given me a cause for concern.

Whether there is appreciable brain damage would be difficult to determine because there aren't many ways to accurately gauge deterioration without the use of expensive brain scans, which I don't think anyone has done, pre and post cycle of DNP (though if there are I would love to see them). Also small amounts of cognitive or memory loss would be completely unnoticeable to a person using DNP simply due to the nature of how the brain works.

It should be noted that I'm not purporting that common DNP dosages will turn you into a drooling vegetable or anything of the sort. I have seen people after taking DNP and they remain functional. However, if DNP can pass through the blood brain barrier, and interfere with the brains production and utilization of ATP, then it will undoubtedly have adverse effects that may or may not be permanent. As someone who is interested in taking DNP, and has read a decent amount of conjecture regarding its use, the impact on the brain is one area I have never seen discussed! Yet it is a completely logical conclusion to draw and the implications, if true, would be huge and extremely important in determining the drugs use.

 

[dfein]

I don't know for certain, but what I'm guessing is that the body just hoards energy for the heart and vital organs, however some can still be expended at a cost, kind of like the situation of how testosterone can "magically" increase protein in the body in just about any situation. Of course if you abuse it, you'll probably die from burning on the inside out.

 

[NYHomeboy]

Conciliator? What's your input on this? This kind of worries me... since my memory has gone to shit in the last 3 years that I've used DNP, haha.

 

[bigollie2006]

Conciliator? What's your input on this? This kind of worries me... since my memory has gone to shit in the last 3 years that I've used DNP, haha.

Highly doubt it has anything to do with DNP
Cyclic AMP enhancers and Abeta oligomerization blo... [Curr Alzheimer Res. 2007] - PubMed result

If I read this right, its is actually saying DNP may actually help prevent Alzheimer's Disease.


"One of the earliest manifestations of Alzheimer's disease (AD) is the characteristic inability of affected individuals to form new memories. Memory impairment appears to significantly predate the death of nerve cells, implying that neuronal dysfunction is responsible for the pathophysiology of early stage AD. Mounting evidence now indicates that soluble oligomers of the amyloid-beta peptide (Abeta) are the main neurotoxins that lead to early neuronal dysfunction and memory deficits in AD. Cyclic AMP (cAMP) is a central component of intracellular signaling pathways that regulate a wide range of biological functions, including memory. Among other actions, cAMP triggers the phosphorylation and activation of the cAMP responsive element binding protein (CREB), a transcription factor that regulates the expression of genes that are important for long-term memory. Here, we discuss recent evidence suggesting that cAMP enhancing compounds may find applications as neurocognitive enhancers in AD and in other neurological disorders, as well as possible roles of cAMP in the regulation of neuronal regeneration. In particular, we review recent results showing that low concentrations of 2,4-dinitrophenol (DNP) upregulate neuronal cAMP and tau levels, promote neurite outgrowth and neuronal differentiation and block the oligomerization and neurotoxicity of Abeta. Possible implications of these findings in the development of novel therapeutic approaches in AD are discussed."


Im not very good at reading abstracts but I am pretty sure thats what it is saying in the last few sentences

 

[bigollie2006]

Mapping of cerebral oxidative metabolism with MRI. [Proc Natl Acad Sci U S A. 2010] - PubMed result
another good article
"Using a T(1rho) MRI based indirect detection method, we demonstrate the detection of cerebral oxidative metabolism and its modulation by administration of the mitochondrial uncoupling agent 2,4-dinitrophenol (DNP) in a large animal model with minimum utilization of gas. The study was performed by inhalation in swine during imaging on clinical MRI scanners. Metabolic changes in swine were determined by two methods. First, in a series of animals, increased metabolism caused by DNP injection was measured by exhaled gas analysis. The average whole-body metabolic increase in seven swine was 11.9% + or - 2.5% per mg/kg, stable over three hours. Secondly, hemispheric brain measurements of oxygen consumption stimulated by DNP injection were made in five swine using T(1rho) MRI following administration of gas. Metabolism was calculated from the change in the T(1rho) weighted MRI signal due to H(2)(17)O generated from inhalation before and after doubling of metabolism by DNP. These results were confirmed by direct oxygen-17 MR spectroscopy, a gold standard for in vivo H(2)(17)O measurement. Overall, this work underscores the ability of indirect oxygen-17 imaging to detect oxygen metabolism in an animal model with a lung capacity comparable to the human with minimal utilization of expensive gas. Given the demonstrated high efficiency in use of and the proven feasibility of performing such measurements on standard clinical MRI scanners, this work enables the adaption of this technique for human studies dealing with a broad array of metabolic derangements."

 

[captshiner]

Parkinson's disease: diagnosis and ... - Google Books

the authors of the book and just a 'couple pages worth of doctors would likely see it differently

 

[Michael Scally MD]

Editor—There are only a few cases in the literature of 2,4-dinitrophenol (DNP) poisoning in adults resulting in death.1 We describe the first case of multiorgan failure and widespread rigidity secondary to DNP poisoning 8 h after presentation.

The prevalence of non-prescription weight loss measures is increasing.2 The internet is commonly being used as a low cost alternative of acquiring advice and prescriptions. DNP (C6H4N2O5) first gained popularity for weight loss in the 1930s with studies showing that a daily dose of 300–400 mg for 2 weeks resulted in 36–95% increase in an individual's basal metabolic rate.3 It was soon taken off the market due to adverse effects including cataracts, liver failure, agranulocytosis, and death. DNP has also been used as a herbicide and also as a photographic developing chemical. Its use has now resurfaced via the internet.

Continue . . . Tewari A, Ali A, O'Donnell A, Butt MS. Weight loss and 2,4-dinitrophenol poisoning. British Journal of Anaesthesia 2009;102(4):566-7. http://bja.oxfordjournals.org/content/102/4/566.full

 

[captshiner]

https://thinksteroids.com/community/posts/665334

oh wait, isn't DNP supposed to HELP regenerate and protect nerves!?? dumb as hell to continue taking this stuff

 

[Michael Scally MD]

Sebollela A, Freitas-Correa L, Oliveira FF, et al. Expression profile of rat hippocampal neurons treated with the neuroprotective compound 2,4-dinitrophenol: up-regulation of cAMP signaling genes. Neurotox Res 2010;18(2):112-23. Expression profile of rat hippocampal neurons trea... [Neurotox Res. 2010] - PubMed result

2,4-Dinitrophenol (DNP) is classically known as a mitochondrial uncoupler and, at high concentrations, is toxic to a variety of cells. However, it has recently been shown that, at subtoxic concentrations, DNP protects neurons against a variety of insults and promotes neuronal differentiation and neuritogenesis. The molecular and cellular mechanisms underlying the beneficial neuroactive properties of DNP are still largely unknown. We have now used DNA microarray analysis to investigate changes in gene expression in rat hippocampal neurons in culture treated with low micromolar concentrations of DNP. Under conditions that did not affect neuronal viability, high-energy phosphate levels or mitochondrial oxygen consumption, DNP induced up-regulation of 275 genes and down-regulation of 231 genes. Significantly, several up-regulated genes were linked to intracellular cAMP signaling, known to be involved in neurite outgrowth, synaptic plasticity, and neuronal survival. Differential expression of specific genes was validated by quantitative RT-PCR using independent samples. Results shed light on molecular mechanisms underlying neuroprotection by DNP and point to possible targets for development of novel therapeutics for neurodegenerative disorders.

 

[Michael Scally MD]

Highly doubt it has anything to do with DNP
Cyclic AMP enhancers and Abeta oligomerization blo... [Curr Alzheimer Res. 2007] - PubMed result

If I read this right, its is actually saying DNP may actually help prevent Alzheimer's Disease.


"One of the earliest manifestations of Alzheimer's disease (AD) is the characteristic inability of affected individuals to form new memories. Memory impairment appears to significantly predate the death of nerve cells, implying that neuronal dysfunction is responsible for the pathophysiology of early stage AD. Mounting evidence now indicates that soluble oligomers of the amyloid-beta peptide (Abeta) are the main neurotoxins that lead to early neuronal dysfunction and memory deficits in AD. Cyclic AMP (cAMP) is a central component of intracellular signaling pathways that regulate a wide range of biological functions, including memory. Among other actions, cAMP triggers the phosphorylation and activation of the cAMP responsive element binding protein (CREB), a transcription factor that regulates the expression of genes that are important for long-term memory. Here, we discuss recent evidence suggesting that cAMP enhancing compounds may find applications as neurocognitive enhancers in AD and in other neurological disorders, as well as possible roles of cAMP in the regulation of neuronal regeneration. In particular, we review recent results showing that low concentrations of 2,4-dinitrophenol (DNP) upregulate neuronal cAMP and tau levels, promote neurite outgrowth and neuronal differentiation and block the oligomerization and neurotoxicity of Abeta. Possible implications of these findings in the development of novel therapeutic approaches in AD are discussed."

The author sent me the full text paper: De Felice FG, Wasilewska-Sampaio AP, Barbosa AC, Gomes FC, Klein WL, Ferreira ST. Cyclic AMP enhancers and Abeta oligomerization blockers as potential therapeutic agents in Alzheimer's disease. Curr Alzheimer Res 2007;4(3):263-71. Cyclic AMP enhancers and Abeta oligomerization blo... [Curr Alzheimer Res. 2007] - PubMed result

 

[Fate]

Sebollela A, Freitas-Correa L, Oliveira FF, et al. Expression profile of rat hippocampal neurons treated with the neuroprotective compound 2,4-dinitrophenol: up-regulation of cAMP signaling genes. Neurotox Res 2010;18(2):112-23. Expression profile of rat hippocampal neurons trea... [Neurotox Res. 2010] - PubMed result

2,4-Dinitrophenol (DNP) is classically known as a mitochondrial uncoupler and, at high concentrations, is toxic to a variety of cells. However, it has recently been shown that, at subtoxic concentrations, DNP protects neurons against a variety of insults and promotes neuronal differentiation and neuritogenesis. The molecular and cellular mechanisms underlying the beneficial neuroactive properties of DNP are still largely unknown. We have now used DNA microarray analysis to investigate changes in gene expression in rat hippocampal neurons in culture treated with low micromolar concentrations of DNP. Under conditions that did not affect neuronal viability, high-energy phosphate levels or mitochondrial oxygen consumption, DNP induced up-regulation of 275 genes and down-regulation of 231 genes. Significantly, several up-regulated genes were linked to intracellular cAMP signaling, known to be involved in neurite outgrowth, synaptic plasticity, and neuronal survival. Differential expression of specific genes was validated by quantitative RT-PCR using independent samples. Results shed light on molecular mechanisms underlying neuroprotection by DNP and point to possible targets for development of novel therapeutics for neurodegenerative disorders.

DNP protects neurons against a variety of insults
Just learned neurons have feelings [)]