Nandrolone Effect On Brain

  • Deca-Durabolin May Cause Brain Damage
  • Deca-Durabolin May Cause Brain Damage | IronMag Bodybuilding Blog
  • The Impact of Nandrolone Decanoate on the Central Nervous System
  • Anabolic steroids cause long-standing changes in the brain | Dopinglinkki
  • Nandrolone Decanoate …brain damage and drug dependance |
  • National Geographic

    Deca-Durabolin May Cause Brain Damage

    nandrolone effect on brain It has been approved by the FDA for wasting diseases and for treatment for anemia, since Among athletes it is one of the most favorable steroids for gaining strength and muscle. Its relatively low toxicity assures fewer side-effects with moderate use. Usually users report increased wellbeing after the initiation of nortestosterone treatment. Some doctors even efffct nandrolone has abuse potential similar to narcotic drugs. What I am about to say in this article is how nandrolone affects wellbeing and possibly explains why users dianabol tablets for bodybuilding use wffect drug alone nandrolone effect on brain in combination with psychoactive drugs.

    Deca-Durabolin May Cause Brain Damage | IronMag Bodybuilding Blog

    nandrolone effect on brain

    Most scientifical research towards brain damage and drug dependence is focused on nandrolone; one of the most commonly ab used AAS. Nandrolone is a synthetic modification of the testosterone molecule and lacks a methyl CH3 group at the C19 position. Apart from elite athletes aiming for increased performance during competition, both professional and amateur bodybuilders administer AASs to gain maximal muscle volume. During the past decade their use has spread to colleges and high schools as well.

    Over the last years, several studies examining substance use-patterns have shown an increase in anabolic-androgenic steroids AASs in all user groups, not only in athletes. The use of AASs is no longer limited to professional power training athletes and body builders, but a large number of young adolescents take AASs in high doses with the intention of improving their physical fitness, appearance, increasing of confidence levels, and even pleasure. This trend is alarming because, while the side effects of both anabolic steroids and stimulants have been well documented, very few studies have been performed to assess the potential effects resulting from the concomitant use of these drugs.

    We also know that many bodybuilders, probably the majority, stacks in polypharmacy. Mostly these compounds fit nicely together. Just as oral steroids complete the injectables. Some smoke marihuana to sleep. Do we even think about the fact that some of these recreational drugs could work synergistically on the side effects? I know guys that started as bodybuilders but along the way they visited the gym no more.

    They became lethargic and only wanted to use drugs in their spare time. It has become kind of common. On the discussion-boards we try to warn members for these dangers. Researches try to find answers to these questions and we will discuss some to make you all aware. But what does it do exactly?

    And with Growth hormone? I think I saw to many guys that have debilitating themselves. Nice guys that liked to party, now in their thirties, you can see it in their faces in their eyes. Just like to much alcohol can damage your brain. No one will deny that. The mental side effects associated with AASs have been observed more frequently as the use of AASs has become more widespread.

    Changes in mood, euphoria, delusions, depression and violent behavior, are reported to be associated with the prolonged use of AASs. The neurochemical mechanisms behind AAS-induced mental side effects are not clear. Nevertheless, on the basis of animal studies, it has been suggested that AAS abuse may constitute a risk factor in aggressive behavior, partly by affecting the serotonergic system and drug dependence by affecting the dopaminergic system in the brain.

    No cases of abuse or dependence have been described in men or women who received or self-administered therapeutic doses of AASs for medical indications. However, when used for enhancing physical appearance, AASs can lead to abuse and dependence in both men and women has proposed a two-stage model of AAS dependence. According to this hypothesis, anabolic effects on muscle growth account for the first stage of steroid use.

    Regarding the background literature AASs abusers share personality factors with the abusers of psychotropic substances, such as cannabis, amphetamine and cocaine. Thus, studies in laboratory animals are a useful tool to explore androgen reward. Several experimental models have been developed to study reward in laboratory animals, where conditioned place preference CPP and self-administration are the most important methodologies. Male hamsters preferentially self-administer testosterone orally, and in many studies the testosterone induces conditioned place preference.

    Both hamsters and rats self-administer testosterone intravenously i. Syrian hamsters have also been shown to self-administer nandrolone. As seen, AASs are self-administered by rodents, although the effect is known to be rather modest.

    Still, it is comparable with other mild reinforcers such as benzodiazepines and nicotine. Pre-exposure to AASs has been demonstrated to affect the response to other substances of abuse in experimental animals. Nandrolone decanoate is shown to block CPP induced by food, tetrahydrocannabinol and morphine. Male adult rats have been shown to increase voluntary alcohol intake after cessation of AAS-administration. Recreational drugs like XTC or amphetamines have less effect on steroids users than on non-users.

    Researchers at the Finnish National Public Health Institute concluded this from experiments they did on rats. The researchers wanted to know more about the relationship between steroids and drugs, because studies have shown that drugs use is higher among steroids users than non-users. They wondered whether it had anything to do with the way in which the combination of substances affects the brain.

    The more dopamine released in the nucleus accumbens, the better you feel. And serotonin contributes to feelings of pleasure and enjoyment too. The figure below shows the concentration of serotonin in the nucleus accumbens of rats that had been given XTC [the arrow indicates when this happened, Ed. The Deca-rats received an injection containing 5 or 20 mg nandrolone decanoate per kg bodyweight every other day for 10 days. XTC causes a serotonin peak; Deca does not.

    Deca did, however, cause a dopamine peak, as did amphetamines and nandrolone. Deca flattens off the serotonin peak. And the steroid does the same to the dopamine peak. Rats that have been given XTC are more active than normal. They are high, and this is reflected in their behavioural score. The graph below shows that Deca suppresses that behaviour. They exclude the possibility that steroids speed up the breakdown of dopamine and serotonin. They looked at that, and observed no change. They suspect that steroids have a negative effect on the brain cells that manufacture serotonin and dopamine.

    The potentially harmful effect of steroids on the cells that produce neurotransmitters may explain why steroids users are relatively frequent drugs users. Steroids users feel unwell more often and use recreational drugs as a form of self-medication. The abuse of anabolic androgenic steroids AASs is not only a problem in the world of sports but is associated with the polydrug use of nonathletes.

    Investigations of the neurochemical effects of AAS have focused in part on the monoaminergic systems, involving, among other things, the development of dependence. We have previously shown that pretreatment with nandrolone decanoate attenuates dose-dependently the increase in extracellular dopamine DA concentration evoked by amphetamine and 3,4-methylenedioyxymethamphetamine in the nucleus accumbens NAc. The aim of this study was to investigate whether the nandrolone pre-exposure modulates the acute neurochemical and behavioral effects of cocaine in rats and whether the effects are long lasting.

    DA, 5-hydroxytryptamine 5-HT , and their metabolites were measured from samples collected from the NAc by microdialysis. The behavior of the animals was recorded. Given that accumbal outflow of DA and 5-HT, as well as LMA and stereotyped behavior, is related to gratification of stimulant drugs, this study suggests that nandrolone, at the doses tested, has a significant effect on the pleasurable properties of cocaine.

    Furthermore, because neurochemical and behavioral responses were still attenuated after a fairly long recovery period, it seems that nandrolone may induce long-lasting changes in the brains of rat. The impact of AASs, particularly Nandrolone Decanoate, on the brain dopaminergic systems has been studied to some extent in rodents.

    Similar results were later obtained for mRNA levels. On the other hand, the densities of dopamine D2-like receptors were upregulated in the caudate putamen, VTA and NAc core, while downregulated in the shell. An increase was detected in the D1 —receptor in amygdala and the D4 in the NAc, and a decrease in D 1 receptor in the hippocampus. This reduced metabolism might possibly be a compensation for increased DA uptake, since the DA baseline levels remains unchanged.

    This is in line with earlier findings of DAT up-regulation. Long-term use of anabolic-androgenic steroids AAS appears to severely impact a user's ability to accurately recall the shapes and spatial relationships of objects, say medicos from McLean Hospital and Harvard Medical School.

    Their study, appearing in the journal Drug and Alcohol Dependence, used a variety of tests to determine whether steroid users developed cognitive defects due to their admitted history of abuse. The subjects in the study were aged between 29 and 55 and had been using steroids for an average of seven years. Each participant was asked to complete five cognitive tests that assessed a wide range of brain functions, including memory for shapes and locations of objects, memory for lists of words, reaction time, ability to maintain attention, and speed of information processing.

    Researcher Harrison Pope and his colleagues discovered that those participants who were long-term AAS users did significantly worse than nonusers on a test called "Pattern Recognition Memory," where participants are asked to try to remember a collection of patterns that they have been presented on a computer screen.

    The scores on this test declined noticeably with increasing lifetime AAS use. Importantly, the results remained stable in sensitivity analyses addressing potential confounding factors, indicating that the findings were unlikely to be attributable to some factor other than AAS use. Those deficits directly corresponded to their length of use of anabolic-androgenic steroids," explained Pope. Pope said the visuospatial deficits observed in steroid users were similar to those only previously seen in elderly people with dementia, who can become easily become lost or disoriented.

    Tugyan et all undertook a study in order to investigate the possible neuroprotective and anti-apoptotic role of EPO treatment on Nandrolone Decanoate induced brain injury. Apoptosis is a programmed cell death. In recent years, many experimental studies have examined the relation of apoptosis and AAS usage in different tissues and organs. Other researchers investigated the apoptotic effects of three kinds of AAS on ventricular myositis, and they also demonstrated that these compounds increased apoptotic cell count in a dose dependent manner.

    To our knowledge, there is no study evaluating the effects of Nandrolone Decanoate on brain tissue. Their study demonstrated that Nandrolone Decanoate caused a significant increase in apoptotic cells and a significant decrease in neuronal count in the parietal cortex, prefrontal cortex and hippocampal regions of the brain.

    Because of the high sensitivity of the brain, the ongoing damage and increasing amount of reactive oxygen species ROS lead to pathological changes in brain tissue.

    Previous studies show the antioxidant effect of EPO in different brain regions. The present study shows that Nandrolone Decanoate induced the oxidative stress and apoptotic cell death in several regions of the brain including parietal cortex, prefrontal cortex and hippocampal regions and indicates that EPO decreases the apoptotic and antioxidant stress induced by Nandrolone Decanoate usage in brain tissue in the parietal cortex, prefrontal cortex and hippocampal regions of the brain.

    The present study indicates for the first time that EPO has neuroprotective effects against Nandrolone Decanoate induced-brain injury by its anti-apoptotic and anti-oxidant effects. It has been previously demonstrated that EPO can cross the brain—blood-barrier by active translocation through capillary endothelium. It reaches its peak concentration in the brain 4 h after the first administration and subsequently decays slowly to baseline levels over the next 20—30 h.

    The study of Tugyan et all shows that Nandrolone Decanoate administration led to a decrease in neuronal count and apoptotic cell death as well as an increase in oxidative stress in the brain. Additionally, the improving effects of H-EPO are shown against Nandrolone Decanoate induced brain damage in a dose dependent manner.

    GH improves spatial memory and reverses certain anabolic androgenic steroid-induced effects in intact rats.

    The Impact of Nandrolone Decanoate on the Central Nervous System

    nandrolone effect on brain

    Anabolic steroids cause long-standing changes in the brain | Dopinglinkki

    nandrolone effect on brain

    Nandrolone Decanoate …brain damage and drug dependance |

    nandrolone effect on brain