goomoonryong9
New Member
I was under the impression that LVH is not permanent or are there anything that makes the LVH irreversible that you know of when on nandrolone?
MESO-Rx
Anabolic Steroids
MESO-Rx Exclusive What Makes Nandrolone Different? Unique Benefits for Joints, Muscles, and Blood
- Thread starter MESO-Rx Administrator
- Start date
Type-IIx
Well-known Member
By coming off, cessation, withdrawal
Good to know
Would something like NPP be beneficial for recovery from something like an Achilles tear (of course after surgery) ?
Type-IIx
Well-known Member
There is evidence that it can help prevent against fatty infiltration after rotator cuff surgeries and perhaps also Achilles tendon repair, but I cannot give medical advice
Fair enough, but that sounds good.
readalot
Member
Week 7 after ramping up to 280 mg/week of ND with 70 mg/week TC. Do not recommend. Anhedonia, nihilistic thoughts. Joint pain still there? Absolutely. Joint lubrication and relief ... absolutely not.
Two prior 16 week stints with ND. Same thing.
N=1.
Two prior 16 week stints with ND. Same thing.
N=1.
iris
Well-known Member
Even at the starting/lowest dose all this happened, all 3 times you have tried taking it?
That it affected you mentally so badly whilst also not benefitting your joints is a pity.
readalot
Member
rexy
Member
I get the same issues with nandrolone at any dose, and from the first week. Just cannot tolerate it whatsoever. Sadly I've written it off completely. It really is like a switch for depression and instant ED for me.
I also have the same physical/mental reactions (43yo male). I have tried on many occasions to implement nandrolone for joint pain reduction at varying doses (25mg/50mg/100mg per week) but after a few days I always start feeling terrible mentally. Depression/demotivation/anhedonia creep in. This was in addition to 210mg test c and 200mg Masteron e all times. I just don’t react well to nandrolone.
readalot
Member
Now up to 280 mg/week ND with the 70 mg/week TC.
View: https://youtu.be/qrO4YZeyl0I?si=a3V1aJn6YLxB2Fv0
Break on through to the other side?
7.5 weeks in. Probably just ain't running it high enough
.
View: https://youtu.be/qrO4YZeyl0I?si=a3V1aJn6YLxB2Fv0
Break on through to the other side?
7.5 weeks in. Probably just ain't running it high enough
.That sucks. I’m 44 running 300npp
300dhb
300test cyp.
Never had a single problem from NPP. Always ran 300-600
How long before that subsides? Is it tied to the Ester length or does it take some time to recover?
DugPrime
Member
No, you won't benefit from one of the most toxic compounds.
Mr_Fusion
New Member
In what respect is NPP "one of the most toxic compounds"?
For me it took about a week of stopping the NPP to start feeling like myself again (return of well-being and normal sex drive) It was tied to ester length for me because when I was using decanoate at same dose (100mg/wk) before, it took proportionally longer (about two weeks) for me to feel like myself again. Hope that is helpful.
Very helpful, thank you! A whole lot more concerning to me if it lasted longer. I will definitely wait to include npp off cycle to test the waters now.
DugPrime
Member
These studies are related to the harmful effect of anabolic steroids to the body organs , especially with these related to the brain because that the one thing that you can't really monitor especially in the long term , so i discovered some interesting things and almost none of them is known ( some are based on new studies and some are based on old studies ) and some are good news and some are bad news .
It is rare to find a study that experimenting with a group of AAS and decide which one of them is the worst for the body .
Fortunately I found some studies , a big one comparing the most common AAS (Tren,Test,Winny,Deca) and their effect to the body organs and the brain , the other one only compared the effect of (Tren,Test,Winny,Deca) to Brain cells ( Neurotoxicity ) .
Here is the first one published in 2022 :
Anabolic Androgenic Steroids: Neurobiological Effects of Nandrolone, Testosterone, Trenbolone, and Stanozolol
So from this study , which one was the worst for body organs and the brain ?
it was Deca .
Here it is from the conclusion from the study , then will go into the details :
Here are the details and the most important things from the full study ( you have to download it to see the full study ) :
First thing the effect of Nandrolone,Test,Tren to the body organs weight ( which indicates to alteration or intoxication ) .
So which one was the worst for the Liver , and the Kidney ?
It was Deca .
Here it is image from the study compared the harmful effect of different AAS on body organs : Capture hosted at ImgBB
Highest increasing of the weight of the kidney was caused by Nandrolone decanoate then was tren ( which indicate renal intoxication ) .
In addition, nandrolone decanoate was the only AAS that reduced the weight of the liver ( which indicate liver damage) .
Although hepatic alterations are primarily associated with 17a-alkylated AAS .
It has been reported before that deca is hepatotoxic 1.
Which also confirmed by this study .
Surprisingly testosterone decanoate was the only AAS that reduced the weight of the testicles , Maybe we should avoid using it in very high dosages ?
The second important thing from the study is the effect of Test,Tren,Deca on Cognitive functions :
Deca was also the worst , it was the only AAS that impaired memory , Tren actually didn't impair cognitive function at all , even this amazed the researchers .
Here is the quotation from the study :
The second study compared the toxicity of Test,Tren,Winny,Deca on neuronal cortical cell (neurons) which also the previous study quoted this study to indicate which one of them is the worst for the brain cells .
Here is the study :
Toxic Impact of Anabolic Androgenic Steroids in Primary Rat Cortical Cell Cultures
The cellular toxicity induced by AAS was determined by measuring mitochondrial activity, lactate dehydrogenase (LDH) release, and caspase-3/7 activity .
Testosterone, Trenbolone ,Nandrolone induce cell death by apoptosis to cortical neurons but to different extents , while stanozolol induce cell death by necrosis.
But which one was the most toxic to the brain cells ?
Also it was Deca .
Here it is from the conclusion of the study :
Also this study confirmed the neurotoxic effect of supraphysiological level of testosterone on brain cells , which was reported before (1) .
The cortical cell death detected herein could be one explanation for the smaller cortical volume and less grey matter seen among long term AAS users (1) .
Clarification : primary cell cultures from rodents are useful in vitro models to study drug induced effects on cell viability, and other cellular functions, as well as investigating the underlying mechanisms of these effects. the advantage with primary cell cultures compared to immortalized cell lines is that they are more similar to the in vivo state, as they exhibit several physiological and biochemical features .
But there is another important thing , and i see here a lot in reddit : " trenbolone and the accumulation of amyloid plaques " .
First of all how many of you guys know that supraphysiological testosterone levels also increase *amyloid plaques* (Aβ) levels (1) ?
And here the abstract from the study , then i will explain :
Explanation :
And with Alcohol,Tobacco ( the most widely used recreational drugs ) , how many of you guys know that smoking also accumulate amyloid plaques (Aβ42,Aβ40) in the hippocampus and cortex in the brain of "Humans" and Animals 1,2,3,4,5 .
Even "Moderate" amount of alcohol accumulate amyloid plaques in the brain 1,2,3 .
Alcohol also increase the toxicity induced by amyloid plaques on neurons 1 , and prevent brain from clearing out the plaques 2 3 .
Regardless of the other neurotoxic effects of alcohol and smoking on the cns like ( excessive oxidative stress in the brain and the body , neuroinflammation, impaired neuroprotection, and inhibiting neurogenesis ) .
High Sugar Diet "elevated blood glucose" independently of any health condition like (Obesity, Metabolic Syndrome,Type 2 Diabetes) also accumulate amyloid plaques in the brain (in the Cortex and Hippocampus) 1,2,3 .
(So in a healthy person , even high sugar consumption can accumulate amyloid plaques)
High Cholesterol, and higher levels of LDL and lower levels of HDL ( which are caused by All AAS ) also accumulate amyloid plaques in brain (1,2,3,4) Cholesterol also increase the toxicity of the plaques on neurons (5) .
Also lack of sleep for one day can accumulate amyloid plaques (1) .
Dianabol and Deca also increase neuronal susceptibility to the apoptotic stimulus provided by amyloid plaques (like Alcohol) (1) ( which is worse than accumulation of the plaque because the accumulation can happen by manyways ) .
Never seen anyone before cites these studies like we see with tren ( regardless it was a single study and it was on rats ) because people think tren is the only drug that can accumulate amyloid plaques , anyway the Demonization Propaganda of PEDs will never tell you that .
But the big question here is Amyloid Plaques really cause Alzheimer's ?
There is a a lot of people in the AAS community didn't know that the amyloid hypothesis was based on study which was discovered to be a Scandal and it was one of of the biggest scandals in the history of science , this has been known in 2022 after knowing the hypothesis was based on a fake study published in 2006 .
Even before 2022 the amyloid hypothesis was subject of criticism in a lot of studies
Like these studies :
1 - Alzheimer's Disease (AD) therapeutics based on the amyloid hypothesis have repeatedly failed in clinical trials. Together with numerous reports that amyloid is present in brains from aged individuals without cognitive dysfunction, this suggests that the association of amyloid with AD is collateral rather than causal 1
2 - Normal cognition and hippocampal volume are associated with preservation of high soluble Aβ42 levels despite increasing brain amyloidosis 1 .
Explanation of the study :
3 - A lot of nondemented older adults were found to have amyloid plaques during autopsy examination 1 .
4 - Intriguingly, just as there are brain amyloid plaques without Alzheimer's disease , there is also Alzheimer's disease without brain amyloid plaques 1 .
5- Alzheimer's disease (AD) is a biologically complex neurodegenerative dementia. Nearly 20 years ago, with the combination of observations from biochemistry, neuropathology and genetics, a compelling hypothesis known as the amyloid cascade hypothesis was formulated. The core of this hypothesis is that it is pathological accumulations of amyloid-β, a peptide fragment of a membrane protein called amyloid precursor protein, that act as the root cause of AD and initiate its pathogenesis. Yet, with the passage of time, growing amounts of data have accumulated that are inconsistent with the basically linear structure of this hypothesis. And while there is fear in the field over the consequences of rejecting it outright, clinging to an inaccurate disease model is the option we should fear most. This Perspective explores the proposition that we are over-reliant on amyloid to define and diagnose AD and that the time has come to face our fears and reject the amyloid cascade hypothesis 5 .
6- Amyloid beta (Aβ) and its extracellular aggregates amyloid plaques are another pathological hallmark of AD. In contrast to NFT, reports regarding the correlation of amyloid plaques with clinical symptoms and neuronal loss were inconsistent, as most studies suggested that the correlation is weak [83,98,99]. An examination of postmortem brains revealed significant Aβ depositions in certain brain regions for both AD patients and healthy elderly individuals [100]. Furthermore, using PET imaging, it was found that the hippocampal burden of Aβ in patients is similar to that of age-matched individuals [101]. However, immunoblotting results showed that the types of Aβ in normal individuals and in patients can be different [102]. Thus, pathological evidence for the connection of Aβ deposition to neuron death is scarce.
You can find a lot more studies , just search in google scholar .
Even the drugs that targets the removing of the plaques has failed to show any cognitive benefits even it worsen the patients 1,2,https://www.reuters.com/business/healthcare-pharmaceuticals/roche-shutters-most-trials-alzheimers-drug-after-failed-trials-2022-12-01/ (3),4,5 .
And with the frequent presence of amyloid plaques in the brains of cognitively healthy older people even without a single neurological problem 1,2,3,4,5
With also the publication of recent studies that's falsifying the amyloid hypothesis like these studies :
1 - Several observations and experimental studies are against the hypothesis. The natural history of AD progression does not correlate with brain amyloid formation, therefore amyloid cannot be causally linked to AD [35,36]. Brain amyloid PET scans of cognitively unimpaired people often look the same as the PET scans of people with AD [37]. At brain autopsy, 30% of people without AD had typical amyloid formation characteristics of AD brains [38,39]. In short, as David Snowdon put it in his great ‘Nun Study’ in 1997: “Brain amyloid is not synonymous with dementia” [40].
2 - High Soluble Amyloid-β42 Predicts Normal Cognition in Amyloid-Positive Individuals with Alzheimer’s Disease-Causing Mutations
3 - In Alzheimer's disease, amyloid beta accumulation is a protective mechanism that ultimately fails
4- Most amyloid-positive individuals do not develop dementia within a normal life span (Brookmeyer and Abdalla, 2018). The population-based amyloid-and-dementia prevalence curves diverge for most of the seventh and eighth decades of life, becoming parallel only by the age of 85 years, when the amyloid-to-dementia ratio reaches 5:1 (Jack et al., 2019). That is, four-fifths of amyloid-positive individuals remain cognitively normal within a normal lifetime. Conversely, the ratio between low soluble Aβ42 and dementia is close to 1:1, as most individuals with cerebrospinal fluid (CSF) levels of Aβ42 below 800 pg/ml by ELISA (INNOTEST Aβ42; Innogenetics) are clinically demented (Andreasen et al., 2001). In short, high brain amyloid is compatible with normal neurological function whereas low soluble Aβ42 is not. No patient with Alzheimer’s disease has high Aβ42 levels but most amyloid-positive individuals remain normal throughout their lifespan .
5- Previous failures and recent modest results indicate that the Amyloid Cascade Hypothesis is no longer tenable , Sadly, disappointment was predicted over two decades ago, but the warning has been disregarded (Smith et al., 2002). Persisting in pursuing a miraculous cure will continue to drain ideas, resources, and enthusiasm.
All of these studies make it obvious that amyloid plaque hypothesis "amyloid plaques cause alzheimer's " is false , the amyloid hypothesis has not never been proven , on the contrary, it was refuted in too many scientific studies, therefore it's just still a "Hypothesis" .
Only a correlation between the plaques and alzheimer's that explains a little to us so far .
Anyway in case you're worried , you can stack neuroprotective supplements that prevent and reduce amyloid plaques accumulation in the brain like ( Melatonin , Milk thistle , Omega 3 , Curcumin , Caffeine , Vitamin D ) most of us take these supplements anyway .
Of course tren is not safe for the brain or the whole body ( as it is the case with all AAS ) but the "amyloid hypothesis" is not that thing you should fear from .
One last thing there is study published in 2022 linked supraphysiological doses of Deca and Test to cause neuronal degeneration in locus coeruleus and the degeneration occurs at any supraphysiological dose .
The locus coeruleus is the main noradrenergic nucleus of the brain and the degeneration of neurons in the locus coeruleus has been postulated as a contributor to the development of neurodegenerative diseases such as alzheimer's disease and parkinson's disease .
No one is talking about this study , and the result of this study is much worse than the tren fake hypothesis study , but because it's not about Demonizing tren so no one will care .
Boldenone one of the most widely used AAS , induced neurodegeneration and impairment in memory and cognitive functions by increasing oxidative stress in the brain ,and by increasing neuroinflammation and nitrosative stress 1 .
Stanozolol also impair memory and kill neurons in the hippocampus 1.2 .
So the neurotoxicity of PEDs are not limited to tren and tren isn't also the worst .
Tren now is scapegoat for everything harmful in aas community .
So be aware guys of the Demonizing Propaganda that targeting PEDs and tren in particular .
Anyway guys , professional bodybuilders uses tons of PEDs throughout their lives and for decades ( including tren and what more a lot worse than tren ) none of them developed dementia and alot of them in their 60s and 70s now ) , but the only thing you should really avoid for the sake of your brain is recreational drugs and aas at the same time , even alcohol and tobacco you should avoid them , aas and drugs should never be mixed together .
stay safe guys and sorry for my weird english , english is not my primary language .
DugPrime
Member
Fortunately I found some studies , a big one comparing the most common AAS (Tren,Test,Winny,Deca) and their effect to the body organs and the brain , the other one only compared the effect of (Tren,Test,Winny,Deca) to Brain cells ( Neurotoxicity ) .
Here is the first one published in 2022 :
Anabolic Androgenic Steroids: Neurobiological Effects of Nandrolone, Testosterone, Trenbolone, and Stanozolol
So from this study , which one was the worst for body organs and the brain ?
it was Deca .
Here it is from the conclusion from the study , then will go into the details :
Here are the details and the most important things from the full study ( you have to download it to see the full study ) :
First thing the effect of Nandrolone,Test,Tren to the body organs weight ( which indicates to alteration or intoxication ) .
So which one was the worst for the Liver , and the Kidney ?
It was Deca .
Here it is image from the study compared the harmful effect of different AAS on body organs : Capture hosted at ImgBB
Highest increasing of the weight of the kidney was caused by Nandrolone decanoate then was tren ( which indicate renal intoxication ) .
In addition, nandrolone decanoate was the only AAS that reduced the weight of the liver ( which indicate liver damage) .
Although hepatic alterations are primarily associated with 17a-alkylated AAS .
It has been reported before that deca is hepatotoxic 1.
Which also confirmed by this study .
Surprisingly testosterone decanoate was the only AAS that reduced the weight of the testicles , Maybe we should avoid using it in very high dosages ?
The second important thing from the study is the effect of Test,Tren,Deca on Cognitive functions :
Deca was also the worst , it was the only AAS that impaired memory , Tren actually didn't impair cognitive function at all , even this amazed the researchers .
Here is the quotation from the study :
The second study compared the toxicity of Test,Tren,Winny,Deca on neuronal cortical cell (neurons) which also the previous study quoted this study to indicate which one of them is the worst for the brain cells .
Here is the study :
Toxic Impact of Anabolic Androgenic Steroids in Primary Rat Cortical Cell Cultures
The cellular toxicity induced by AAS was determined by measuring mitochondrial activity, lactate dehydrogenase (LDH) release, and caspase-3/7 activity .
Testosterone, Trenbolone ,Nandrolone induce cell death by apoptosis to cortical neurons but to different extents , while stanozolol induce cell death by necrosis.
But which one was the most toxic to the brain cells ?
Also it was Deca .
Here it is from the conclusion of the study :
Also this study confirmed the neurotoxic effect of supraphysiological level of testosterone on brain cells , which was reported before (1) .
The cortical cell death detected herein could be one explanation for the smaller cortical volume and less grey matter seen among long term AAS users (1) .
Clarification : primary cell cultures from rodents are useful in vitro models to study drug induced effects on cell viability, and other cellular functions, as well as investigating the underlying mechanisms of these effects. the advantage with primary cell cultures compared to immortalized cell lines is that they are more similar to the in vivo state, as they exhibit several physiological and biochemical features .
But there is another important thing , and i see here a lot in reddit : " trenbolone and the accumulation of amyloid plaques " .
First of all how many of you guys know that supraphysiological testosterone levels also increase *amyloid plaques* (Aβ) levels (1) ?
And here the abstract from the study , then i will explain :
Explanation :
And with Alcohol,Tobacco ( the most widely used recreational drugs ) , how many of you guys know that smoking also accumulate amyloid plaques (Aβ42,Aβ40) in the hippocampus and cortex in the brain of "Humans" and Animals 1,2,3,4,5 .
Even "Moderate" amount of alcohol accumulate amyloid plaques in the brain 1,2,3 .
Alcohol also increase the toxicity induced by amyloid plaques on neurons 1 , and prevent brain from clearing out the plaques 2 3 .
Regardless of the other neurotoxic effects of alcohol and smoking on the cns like ( excessive oxidative stress in the brain and the body , neuroinflammation, impaired neuroprotection, and inhibiting neurogenesis ) .
High Sugar Diet "elevated blood glucose" independently of any health condition like (Obesity, Metabolic Syndrome,Type 2 Diabetes) also accumulate amyloid plaques in the brain (in the Cortex and Hippocampus) 1,2,3 .
(So in a healthy person , even high sugar consumption can accumulate amyloid plaques)
High Cholesterol, and higher levels of LDL and lower levels of HDL ( which are caused by All AAS ) also accumulate amyloid plaques in brain (1,2,3,4) Cholesterol also increase the toxicity of the plaques on neurons (5) .
Also lack of sleep for one day can accumulate amyloid plaques (1) .
Dianabol and Deca also increase neuronal susceptibility to the apoptotic stimulus provided by amyloid plaques (like Alcohol) (1) ( which is worse than accumulation of the plaque because the accumulation can happen by manyways ) .
Never seen anyone before cites these studies like we see with tren ( regardless it was a single study and it was on rats ) because people think tren is the only drug that can accumulate amyloid plaques , anyway the Demonization Propaganda of PEDs will never tell you that .
But the big question here is Amyloid Plaques really cause Alzheimer's ?
There is a a lot of people in the AAS community didn't know that the amyloid hypothesis was based on study which was discovered to be a Scandal and it was one of of the biggest scandals in the history of science , this has been known in 2022 after knowing the hypothesis was based on a fake study published in 2006 .
Even before 2022 the amyloid hypothesis was subject of criticism in a lot of studies
Like these studies :
1 - Alzheimer's Disease (AD) therapeutics based on the amyloid hypothesis have repeatedly failed in clinical trials. Together with numerous reports that amyloid is present in brains from aged individuals without cognitive dysfunction, this suggests that the association of amyloid with AD is collateral rather than causal 1
2 - Normal cognition and hippocampal volume are associated with preservation of high soluble Aβ42 levels despite increasing brain amyloidosis 1 .
Explanation of the study :
3 - A lot of nondemented older adults were found to have amyloid plaques during autopsy examination 1 .
4 - Intriguingly, just as there are brain amyloid plaques without Alzheimer's disease , there is also Alzheimer's disease without brain amyloid plaques 1 .
5- Alzheimer's disease (AD) is a biologically complex neurodegenerative dementia. Nearly 20 years ago, with the combination of observations from biochemistry, neuropathology and genetics, a compelling hypothesis known as the amyloid cascade hypothesis was formulated. The core of this hypothesis is that it is pathological accumulations of amyloid-β, a peptide fragment of a membrane protein called amyloid precursor protein, that act as the root cause of AD and initiate its pathogenesis. Yet, with the passage of time, growing amounts of data have accumulated that are inconsistent with the basically linear structure of this hypothesis. And while there is fear in the field over the consequences of rejecting it outright, clinging to an inaccurate disease model is the option we should fear most. This Perspective explores the proposition that we are over-reliant on amyloid to define and diagnose AD and that the time has come to face our fears and reject the amyloid cascade hypothesis 5 .
6- Amyloid beta (Aβ) and its extracellular aggregates amyloid plaques are another pathological hallmark of AD. In contrast to NFT, reports regarding the correlation of amyloid plaques with clinical symptoms and neuronal loss were inconsistent, as most studies suggested that the correlation is weak [83,98,99]. An examination of postmortem brains revealed significant Aβ depositions in certain brain regions for both AD patients and healthy elderly individuals [100]. Furthermore, using PET imaging, it was found that the hippocampal burden of Aβ in patients is similar to that of age-matched individuals [101]. However, immunoblotting results showed that the types of Aβ in normal individuals and in patients can be different [102]. Thus, pathological evidence for the connection of Aβ deposition to neuron death is scarce.
You can find a lot more studies , just search in google scholar .
Even the drugs that targets the removing of the plaques has failed to show any cognitive benefits even it worsen the patients 1,2,https://www.reuters.com/business/healthcare-pharmaceuticals/roche-shutters-most-trials-alzheimers-drug-after-failed-trials-2022-12-01/ (3),4,5 .
And with the frequent presence of amyloid plaques in the brains of cognitively healthy older people even without a single neurological problem 1,2,3,4,5
With also the publication of recent studies that's falsifying the amyloid hypothesis like these studies :
1 - Several observations and experimental studies are against the hypothesis. The natural history of AD progression does not correlate with brain amyloid formation, therefore amyloid cannot be causally linked to AD [35,36]. Brain amyloid PET scans of cognitively unimpaired people often look the same as the PET scans of people with AD [37]. At brain autopsy, 30% of people without AD had typical amyloid formation characteristics of AD brains [38,39]. In short, as David Snowdon put it in his great ‘Nun Study’ in 1997: “Brain amyloid is not synonymous with dementia” [40].
2 - High Soluble Amyloid-β42 Predicts Normal Cognition in Amyloid-Positive Individuals with Alzheimer’s Disease-Causing Mutations
3 - In Alzheimer's disease, amyloid beta accumulation is a protective mechanism that ultimately fails
4- Most amyloid-positive individuals do not develop dementia within a normal life span (Brookmeyer and Abdalla, 2018). The population-based amyloid-and-dementia prevalence curves diverge for most of the seventh and eighth decades of life, becoming parallel only by the age of 85 years, when the amyloid-to-dementia ratio reaches 5:1 (Jack et al., 2019). That is, four-fifths of amyloid-positive individuals remain cognitively normal within a normal lifetime. Conversely, the ratio between low soluble Aβ42 and dementia is close to 1:1, as most individuals with cerebrospinal fluid (CSF) levels of Aβ42 below 800 pg/ml by ELISA (INNOTEST Aβ42; Innogenetics) are clinically demented (Andreasen et al., 2001). In short, high brain amyloid is compatible with normal neurological function whereas low soluble Aβ42 is not. No patient with Alzheimer’s disease has high Aβ42 levels but most amyloid-positive individuals remain normal throughout their lifespan .
5- Previous failures and recent modest results indicate that the Amyloid Cascade Hypothesis is no longer tenable , Sadly, disappointment was predicted over two decades ago, but the warning has been disregarded (Smith et al., 2002). Persisting in pursuing a miraculous cure will continue to drain ideas, resources, and enthusiasm.
All of these studies make it obvious that amyloid plaque hypothesis "amyloid plaques cause alzheimer's " is false , the amyloid hypothesis has not never been proven , on the contrary, it was refuted in too many scientific studies, therefore it's just still a "Hypothesis" .
Only a correlation between the plaques and alzheimer's that explains a little to us so far .
Anyway in case you're worried , you can stack neuroprotective supplements that prevent and reduce amyloid plaques accumulation in the brain like ( Melatonin , Milk thistle , Omega 3 , Curcumin , Caffeine , Vitamin D ) most of us take these supplements anyway .
Of course tren is not safe for the brain or the whole body ( as it is the case with all AAS ) but the "amyloid hypothesis" is not that thing you should fear from .
One last thing there is study published in 2022 linked supraphysiological doses of Deca and Test to cause neuronal degeneration in locus coeruleus and the degeneration occurs at any supraphysiological dose .
The locus coeruleus is the main noradrenergic nucleus of the brain and the degeneration of neurons in the locus coeruleus has been postulated as a contributor to the development of neurodegenerative diseases such as alzheimer's disease and parkinson's disease .
No one is talking about this study , and the result of this study is much worse than the tren fake hypothesis study , but because it's not about Demonizing tren so no one will care .
took me 5 seconds of research.
