why do most people say "test is best broo"? as if its fact?

[CaptainAll]

No bloat on deca? What's next, no bloat on dbol?!

On real pharmaceutical grade Nandrolone, if not used with test, no bloat. Read Dr. Kerr

 

[dinfar1337]

No bloat on deca? What's next, no bloat on dbol?!

this motherfucker didnt do his bloodtest and now he is the eddie abbew of steriods. no test only deca!

 

[BigTomJ]

Fair enough. But what if test does not work for me?!

Then you arent a human male.

I tried any dose of pharma grade test: 250,500, 750 mg. Puffy red face, libido shattered, ED,

You didnt properly manage estrogen

gains subpar.

Training and nutrition subpar*

500mg nandrolone Decanoate solo and I have 0 issues.

N=1 Personal anecdote.

Why would I go for test?!

Because its what your body knows how to use better than any other alternative and is the foundation of every cycle of every high level bodybuilder of the last 30 years.

 

[BigDadd7]

What is wrong with nandrolone? Nandrolone is far safer than testosterone. Prostate issues zero. Hair issues zero. Estrogen issues zero.

Have you ever run real nandrolone? Not UGL?! You are just parroting

Leaky titties, ed and bloat

 

[BigDadd7]

On real pharmaceutical grade Nandrolone, if not used with test, no bloat. Read Dr. Kerr

You keep using an appeal to authority. "Someone else said...."
I've ran a pharma deca only cycle. Bloat to high heaven. ED. All of it. I swelled up like a balloon and lost most of it afterward. You need test. I don't care what ChatGPT told you about a rodent scrotum study, or what some scam artist on YouTube said to get views. Some of you guys would eat a dog turd if someone on YouTube told you to.

 

[CaptainAll]

Then you arent a human male.


You didnt properly manage estrogen


Training and nutrition subpar*


N=1 Personal anecdote.


Because its what your body knows how to use better than any other alternative and is the foundation of every cycle of every high level bodybuilder of the last 30 years.

You see, you have mentioned managing estrogen. Why would I need to bother with that if Nandrolone only does not require managing estrogen. You just proved inferiority of testosterone

 

[CaptainAll]

Fair enough. But what if test does not work for me?!

I tried any dose of pharma grade test: 250,500, 750 mg. Puffy red face, libido shattered, ED, gains subpar.

500mg nandrolone Decanoate solo and I have 0 issues.

Why would I go for test?!

 

[CaptainAll]

You keep using an appeal to authority. "Someone else said...."
I've ran a pharma deca only cycle. Bloat to high heaven. ED. All of it. I swelled up like a balloon and lost most of it afterward. You need test. I don't care what ChatGPT told you about a rodent scrotum study, or what some scam artist on YouTube said to get views. Some of you guys would eat a dog turd if someone on YouTube told you to.

Just look at a random study I have posted. No water retention. What you have used was not Nandrolone then

 

[DugPrime]

You see, you have mentioned managing estrogen. Why would I need to bother with that if Nandrolone only does not require managing estrogen. You just proved inferiority of testosterone

Now I'll show you inferiority of nandrolone, the most toxic AAs.

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 :

Overall, nandrolone decanoate was identified as the most harmful steroid investigated due to its prominent impact on body weight development, affecting multiple organs, and being the only AAS causing impaired cognitive function.

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 results obtained are in line with previous published findings, where nandrolone decanoate has been described to impair memory in other types of memory tests. For example, both spatial memory function in the Morris water maze task (Magnusson et al., 2009, Pieretti et al., 2013, Tanehkar et al., 2013), as well as olfactory social memory (Kouvelas et al., 2008) are reported to be altered following nandrolone decanoate treatment. Testosterone, on the other hand, has previously been described not to affect memory (Clark et al., 1995, Wood and Serpa, 2020), which also is in accordance with the results from paper IV. Surprisingly, trenbolone decanoate did not induce an impairment in the NOR-test. Trenbolone display several pharmacological similarities with nandrolone decanoate, including the ability to cause neurodegeneration (Ma and Liu, 2015). Furthermore, trenbolone has been described by AAS-users to cause particular harm (Scarth and Bjørnebekk, 2021). In our studies, trenbolone however did not have an impact on cognitive function.

Click to expand...

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 :

With respect to the parameters assessed, nandrolone appeared to be the most toxic AAS, while testosterone, stanozolol, and trenbolone disposed similar effects but to a lesser extent. According to the present results, the order of the examined AASs regarding their toxicity was found to be nandrolone > trenbolone > testosterone > stanozolol .

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 :

The effect of testosterone on the levels of the Alzheimer's disease amyloid-beta peptide (Abeta) was investigated in guinea pigs. Castrated guinea pigs (GPX) were administered testosterone at two different dosages, following which plasma and cerebrospinal fluid (CSF) Abeta_{40} levels were measured. Plasma Abeta_{40} levels were reduced in GPX in the early stages of low-dose testosterone treatment, whereas CSF Abeta_{40} levels were only reduced by the time circulating testosterone had returned to untreated GPX levels. The supraphysiological testosterone dose did not reduce CSF Abeta_{40} levels significantly until circulating testosterone was back to uncastrated levels, whereas plasma Abeta_{40} levels significantly increased over time in these animals. These results indicate that the extent of testosterone-induced changes to Abeta_{40} levels and their response rates depend on both the tissue examined and testosterone dosage.

Click to expand...

Explanation :

High plasma Aβ40 indicates to high accumulation of the plaques in the brain of these animals , on day 18, plasma Aβ40 levels of the supraphysiological testosterone animals were similar to levels found in the plasma of untreated castrated animals ( low testosterone also increase plaques in the brain ) while with supraphysiological testosterone animals Aβ40 levels increased over time significantly above castrated or uncastrated guinea pig .

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 .

( This study literally means that people with plaques in their hippocampus ( the same region that trenbolone accumulate the plaques ) and plaques in their whole brain are had normal cognition and brain volumes regardless of (and despite increasing) brain amyloid .

Explanation of the study :

"It's not the plaques that are causing impaired cognition,'' says Alberto Espay, the new study's senior author and professor of neurology at UC. "Amyloid plaques are a consequence, not a cause," of Alzheimer's disease, says Espay, who is also a member of the UC Gardner Neuroscience Institute. Since then, Espay says that scientists have focused on treatments to eliminate the plaques. But the UC team, he says, saw it differently: Cognitive impairment could be due to a decline in soluble amyloid-beta peptide instead of the corresponding accumulation of amyloid plaques. To test their hypothesis, they analyzed the brain scans and spinal fluid from 600 individuals enrolled in the Alzheimer's Disease Neuroimaging Initiative study, who all had amyloid plaques. From there, they compared the amount of plaques and levels of the peptide in the individuals with normal cognition to those with cognitive impairment. They found that, regardless of the amount of plaques in the brain, the individuals with high levels of the peptide were cognitively normal. According to the authors, as we age most people develop amyloid plaques, but few people develop dementia. In fact, by the age of 85, 60% of people will have these plaques, but only 10% develop dementia, so that’s prevalence five times lower than predicted if amyloid were toxic, they say 1 .

Click to expand...

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 1,2,3,4,5 .

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 .


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 .

 

[Benf15harp]

Whoa

 

[BigDadd7]

Just look at a random study I have posted. No water retention. What you have used was not Nandrolone then

More studies. No actual experience.

 

[BigTomJ]

You see, you have mentioned managing estrogen. Why would I need to bother with that if Nandrolone only does not require managing estrogen. You just proved inferiority of testosterone

Nandrolone only does require the management of estrogen.....

Nandrolone is subject to conversion via aromatase, but only in small amounts.

Without running enough nandrolone in a nandrolone only model you will have incredibly low estrogen.

If your goal is to stay small, and something as basic as getting bloodwork done or doing even a tiny bit of research outside of your bias is too much trouble for you, by all means go deca only.

Have fun

 

[DinoBB76]

low medium test like 1g max 2.5g medium dose + low tren 800/1G a week + medium dose EQ 2.5/3G

 

[Spaceman Spiff]

Then you arent a human male.


You didnt properly manage estrogen


Training and nutrition subpar*


N=1 Personal anecdote.


Because its what your body knows how to use better than any other alternative and is the foundation of every cycle of every high level bodybuilder of the last 30 years.

Tren solo will be the next craze.

 

[ComancheChief]

Tren solo will be the next craze.

That was like 2015 lol

 

[CaptainAll]

Now I'll show you inferiority of nandrolone, the most toxic AAs.

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 1,2,3,4,5 .

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 .


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 .

Rats?

 

[CaptainAll]

Nandrolone only does require the management of estrogen.....

Nandrolone is subject to conversion via aromatase, but only in small amounts.

Without running enough nandrolone in a nandrolone only model you will have incredibly low estrogen.

If your goal is to stay small, and something as basic as getting bloodwork done or doing even a tiny bit of research outside of your bias is too much trouble for you, by all means go deca only.

Have fun

There is no free ride with AAS. But you have to down AI’s to keep up with your test doses.

 

[BigTomJ]

There is no free ride with AAS. But you have to down AI’s to keep up with your test doses.

and? your point?

Taking an AI with your test is objectively healthier than the neurotoxicity of running deca only.

I feel like youre some kid on his first cycle, or just trolling.

 

[Spaceman Spiff]

There is no free ride with AAS. But you have to down AI’s to keep up with your test doses.

I don't take AI even at 700 test

 

[hellogre2]

Ive never discussed with anyone weighting more than 220-250 lbs lean that hasn't used test at absurd dose. NO ONE. The lowest common dose people use is 1g. The average is 1.5 to 2g, and those that really love the stuff will pin 2.5g of test. I've never been that high, but im pretty sure diminish returns increases heavily around that ballpark.

Test isn't only cheap, widely available, suitable for any kind of schedule (testosterone has more ester available than there are injectables steroids), it does everything a man need : estradiol, DHT, increased IGF1, increased insulin sensitivity, predictable AND managable side effect. It gives confidence but don't make you arrogant and dumb like tren, it gives motivation and drive because the dopamine hit is clean, UNLIKE tren. it The only stuff where test isn't the best (but not the worst still) is the look. Its not an instagram compound. Thats why some nerds find a way to shit on the thing that built ALL the pros bodybuilders those last 2 or 3 decades.