I have a feeling 19-nor compound mess with the brain somewhat.
That seems to be the case:
There was a recent study published in 2015 in Toxicology and Applied Pharmacology which found that intramuscular (IM) doses of 17β-Hydroxyestra-4,9,11-trien-3-one (trenbolone) in adult rats resulted in neurodegeneration. The study administered IM injections of trenbolone to several groups of male and female rats over the course of 48 hours at time points of 0.5 h, 2 h, 6 h, 12 h, and 48 h. All rat groups with exception of the control group and pregnant females were treated with a solution of 1.0 and 0.2 mg/ml of trenbolone. The largest dose in the experiment was 5 mg/ml and was administered to the pregnant female rats. As such, when a conversion is done to adjust for dose to weight ratio, the equivalent dose in humans is approximately 0.85 mg/kg of body weight which for a 85 kg (187 lb) male translates to 72.25 mg of trenbolone (depending on dosing this is within an average range for a user). The study also cultured primary hippocampal neurons and treated them with trenbolone to assess effects in vitro.1
Anyway, skipping to the results, it was shown that Aβ42 levels were altered both in vivo as well as in vitro in response to trenbolone administration. An increase in Aβ42 concentration in the brain and hippocampus leads to aggregation and deposition, thereby damaging neurons. Of note, the level of Aβ42 concentration was found to be higher in the male rats. Why? Well, one hypothesis is that sex differences in the protein concentration are due to estrogen (E2) levels – estrogen levels are higher in females and estrogen is known to reduce Aβ accumulation.1
What is Aβ42:Well, Aβ (amyloid beta) is a senile plaque Aβ protein that ends in residue 40 or 42 that is critical to the pathogenesis of Alzheimer’s disease. Aβ42 only makes up less that 10% of total AB, however, it aggregates at a much faster rate than Aβ40. It is the initial and major component of senile plaque deposits, and observation of the Aβ42/ Aβ40 ratio is a reliable biomarker for development of Alzheimer’s disease.2
As you can see, increasing the concentration of this protein in the brain isn’t something that we want to do. In the primary hippocampal neuron cultures, the trenbolone induced apoptosis of the hippocampal neurons (apoptosis is programmed cell death) which is the hallmark feature of both acute and chronic neurodegenerative diseases. Keep in mind too that this trial only consisted of two days of treatment, and that most AAS cycles involving trenbolone range anywhere from 8-12 weeks long. I’m not saying that if you use trenbolone you will absolutely end up with Alzheimer’s disease or some form on dementia, however, there is a good chance that you are increasing your risk of heightened Aβ42 aggregation. Damage to neurons often times occurs much earlier than the clinical symptoms of neurodegenerative disorders present themselves, and as such it’s possible that damage has already unknowingly been done.
Just some food for thought..
1http://www.ncbi.nlm.nih.gov/pubmed/25461682
2http://www.ncbi.nlm.nih.gov/pubmed/23571809
