The study explores the impacts of both genetic and environmental factors on neurodegenerative disorders such as Alzheimer’s disease (AD). It specifically focuses on the effects of Trenbolone, as an environmental hormone, on the onset and progression of AD. Yes, brother, you read that right; Trenbolone is an “environmental hormone” Basically, Trenbolone has become a pollutant due to all of those cows with Trenbolone pellets in their ears and their excretions entering the water supply.
Ma F, Liu D. 17β-trenbolone, an anabolic-androgenic steroid as well as an environmental hormone, contributes to neurodegeneration. Toxicol Appl Pharmacol. 2015 Jan 1;282(1):68-76. doi: 10.1016/j.taap.2014.11.007. Epub 2014 Nov 25. PMID: 25461682
Alzheimer’s disease is caused by an irreversible, progressive degeneration of brain cells. It is marked by β-amyloid peptide (Aβ) plaques and neurofibrillary tangles (NFTs) in the brain. Genetic factors such as mutations in presenilin (PS-1 and PS-2) and amyloid precursor protein (APP) genes have been linked to familial Alzheimer’s disease (FAD). However, many AD patients do not carry these mutations, suggesting a role for other genetic and environmental factors. In the case of this study, the researchers focused on Trenbolone itself.
As I explained earlier, it has become an environmental contaminant due to its rampant use in the cattle industry. So many people and wild animals are exposed to it that it made sense for researchers to study it.
There are two common diagnoses for AD: Familial Alzheimer’s Disease (FAD) and sporadic (also known as late-onset) Alzheimer’s disease. These two main forms of Alzheimer’s disease differ primarily in their onset and cause. I broke it down real simple here:
**Familial Alzheimer’s Disease (FAD)**
FAD is an autosomal dominant genetic condition, which means an affected person has a 50% chance of passing the disease to their children. It’s typically associated with mutations in one of three genes: the APP gene or the presenilin genes PSEN1 or PSEN2. These mutations cause changes in the way the amyloid precursor protein is processed, leading to the formation of beta-amyloid (β-amyloid) plaques, a hallmark of Alzheimer’s disease.
FAD is less common, accounting for less than 1% of all Alzheimer’s cases. However, it’s characterized by an earlier onset, often affecting people in their 30s, 40s, or 50s. The progression of FAD is typically more rapid than in the late-onset form of the disease.
**Sporadic (non-genetic) Alzheimer’s Disease**
This is the type of concern to you, the Trenbolone user without any family history of Alzheimer’s. Most Alzheimer’s disease cases are sporadic (late-onset), typically developing after age 65. While certain genes (like the APOE4 gene) have been identified as risk factors, they do not directly cause the disease but rather increase the likelihood of its development.
In sporadic Alzheimer’s disease, symptoms progress slowly over several years. Initial symptoms may include mild memory loss, confusion, and mood changes… Sound familiar, bro?
The symptoms do get progressively worse to more severe memory loss, disorientation, and changes in behavior and personality.
It’s important to note that both forms of Alzheimer’s disease share common pathological features, such as the presence of β-amyloid plaques and neurofibrillary tangles in the brain. The section below explains what these are.
Beta-amyloid plaques and neurofibrillary tangles are the two key microscopic brain abnormalities identified in patients with Alzheimer’s disease. Both these features disrupt the normal functioning of neurons, eventually leading to the death of these brain cells. Let’s examine each of them in more detail:
Beta-amyloid is a fragment of a larger protein called amyloid precursor protein (APP), normally found in neurons. In Alzheimer’s disease, APP is abnormally processed, leading to the production of a short fragment called beta-amyloid. These beta-amyloid fragments have a tendency to clump together to form insoluble plaques between neurons. These plaques block communication among nerve cells and trigger inflammation, leading to cell death.
The production and accumulation of β-amyloid peptide (Aβ) in the brain are the central cause of AD development, specifically Aβ42, or Amyloid beta (Aβ) 42. This is a peptide composed of 42 amino acids. It is a specific form of amyloid beta that is associated with Alzheimer’s disease (AD). Many current experimental treatments for Alzheimer’s disease focus on reducing levels of Aβ42 in the brain.
The presence of these plaques is currently one of the definitive markers for the diagnosis of Alzheimer’s disease during an autopsy.
Neurofibrillary tangles are twisted strands of a protein called tau that accumulate inside neurons. Tau’s normal function is to help maintain the structure of neurons, specifically the microtubules, which are part of the cell’s transport system.
In Alzheimer’s disease, tau is abnormally modified, which causes it to form twisted fibers or tangles. These tangles disrupt the normal functioning of tau and lead to the collapse of the neuron’s transport system. This disruption prevents nutrients and other critical supplies from moving through the cells, eventually leading to cell death.
Both beta-amyloid plaques and neurofibrillary tangles spread in a predictable pattern in Alzheimer’s disease, usually starting in areas of the brain associated with memory before advancing to other regions.
While these two pathological features are most commonly associated with Alzheimer’s disease, they can also be found in other neurodegenerative diseases, often in different patterns or concentrations. This indicates a complex relationship between these features and neurodegeneration.
So now we get to the part of the study that explains the specific mechanism via which Trenbolone increases the risk of sporadic Alzheimer’s disease.
The study investigates the beloved anabolic–androgenic steroid Trenbolone, used as a growth promoter for livestock and for increasing muscle size and strength in athletes. As you already know, Tren is a potent agonist of mammalian androgen receptors. When the pellets are implanted in the cow’s ears and hit their blood system, Trenbolone will eventually be excreted into the environment, where it is stable and can be absorbed by humans and wild animals through various channels, such as the food chains. Now those are minuscule amounts compared to the dosages you get from injecting it, so keep that in mind as you read on.
The researchers in this study used two ways of testing the effects: they administered Trenbolone to adult and pregnant rats and also to primary hippocampal neurons. Neurons are usually grown in a dish or a well plate. The substance (in this case, Trenbolone) would be added directly to the medium in which the neurons are growing. The neurons would then absorb the substance over time.
They found that Trenbolone could cross the blood-brain barrier, something all of us that use it already knew. They also found it could cross the placental barrier, accumulating in the brain (especially in the hippocampus) and even in the fetus’s brain. Trenbolone in the brain was found to increase Aβ42 accumulation, which we already know is a major causing factor of Alzheimer’s.
Trenbolone also induced early apoptosis or programmed cell death of primary hippocampal neurons. Apoptosis is a normal cellular process, but excessive apoptosis can lead to neurodegeneration. Trenbolone causes apoptosis at an abnormal rate killing your brain cells well before their time.
Most shocking of all, the researcher found that Trenbolone also resists the neuroprotective function of Testosterone. You see, bro, good clinical research suggests that Testosterone regulates apoptosis and inhibits the creation of Beta-Amyloid Plaques. (PMID: 10655508). In this study, the researchers found that Trenbolone negated these positive effects of Testosterone.
So the research suggests that your favorite anabolic–androgenic steroid Trenbolone plays a significant role in neurodegeneration, potentially contributing to the development of Alzheimer’s disease by influencing Aβ42 accumulation, apoptosis, and other crucial processes. This raises health concerns for athletes who include Trenbolone in their steroid cycles.
This is just one study on the potential permanent side effects of Trenbolone. Keep reading these pages; I have more to show you.
My decision to never again use Tren and to exclude it from my list of S.A.F.E.Rx Protocol-approved drugs was not made in haste. It took me decades of trial and error, researching the clinical literature and the anecdotal evidence from friends and clients that I have been able to follow throughout the years. While many people love Trenbolone and will still use it, I will never use it or recommend any of my clients ever use it.
However, if you want to use this drug and need my help, I will still work with you and advise you on the best practices to minimize any possible damage. There is just no really safe way to use steroids; we are all at risk. We can only hope to make the use “safer” by applying the proper drug protocols. To contact me if you want my personalized help just drop me an email here: firstname.lastname@example.org