- 12-12-2006, 04:14 PM
I was thinking of running the classic bulker for my next cycle--Test/Deca with a Dbol jumpstart.
The thing I'm worried about is the fact that Deca is progestenic and could therefore cause prolactin gyno.
Should any precautions be taken if I decide to go this route? Some people use cabergoline (dostinex) for prolactin. Its kind of scary to me so I was thinking about opting for EQ but I really want to try Deca.
- 12-22-2006, 09:46 PM
- 12-23-2006, 03:20 AM
If you really want to try it then run it at 400mg and keep Dostinex on hand. You don't know how your body will react until you use it. You may not have any issues at 400mg. Deca is obviously widely used - so don't freak out that much about it. Just have some on hand.
12-23-2006, 03:28 AM
You could always use the cheap effective vit. b6 at like 200mgs a day.
E-Pharm Rep... PM me with any questions or concerns
12-23-2006, 04:07 AM
That might work for prevention and prevention is the key to battling sides.Originally Posted by 3clipseGT
Keep Cabergoline by your side. I have prolactin gyno in my left nip right now and let me tell you it is a b1cth, id take estrogen induced gyno over this anyday! Bromocryptine is also used to control prolactin when taking a nandrolone.
12-23-2006, 04:22 AM
easiest way to see how you react to Nandrolone is by taking NPP (nandrolone phenylpropionate) for a few weeks...
12-23-2006, 11:57 AM
Good advice. That way if you react adversely it's only in your body for a few days after cessation of use - instead of 2 weeks.Originally Posted by Ubiquitous
12-23-2006, 01:16 PM
12-23-2006, 02:51 PM
I have heard Ubi saying how cabergoline actually changes your brain function in some way. maybe he will drop in to clear this up but I dont want to have to take any drugs that arent necessary.
I think I should be fine at 400mg...I mean people have been running Deca with no caber for decades.
12-23-2006, 03:49 PM
Yeah Matt, Caber is a Dopamine Agonist selective to the D-2 receptor. Dopamine is an important neurotransmitter/neurohormone that plays a role in quite a few complex mechanisms in the body. Dopamine inhibits Lactotroph secretion (Prolactin is a Lactotroph). We of course use it for this purpose, but it can affect a great many other things if taken haphazardly I feel. I think it's good to be cautious with YOUR BRAIN CHEMISTRY.
It works, I've taken it quite a few times before.. and will take it again... but I don't "take it lightly".
here is an excerpt from Wikipidia for example
Functions in the brain
Dopamine has many functions in the brain. Most importantly, dopamine is central to the reward system. Dopamine neurons are activated when an unexpected reward is presented. In nature, we learn to repeat behaviors that lead to unexpected rewards. Dopamine is therefore believed by many to provide a teaching signal to parts of the brain responsible for acquiring new motor sequences, i.e., behaviors.
Dopamine affects the basal ganglia motor loop which in turn affects the way the brain controls our movements. Shortage of dopamine, particularly the death of dopamine neurons in the nigrostriatal pathway, causes Parkinson's disease, in which a person loses the ability to execute smooth, controlled movements.
Cognition and frontal cortex
In the frontal lobes, dopamine controls the flow of information from other areas of the brain. Dopamine disorders in this region of the brain can cause a decline in neurocognitive functions, especially memory, attention and problem-solving. Reduced dopamine concentrations in the prefrontal cortex are thought to contribute to attention deficit disorder and negative schizophrenia. Conversely, anti-psychotic medications rely on their inhibition of dopamine uptake and are used in the treatment of positive symptoms in schizophrenia.
Regulating prolactin secretion
Dopamine is the primary neuroendocrine regulator of the secretion of prolactin from the anterior pituitary gland. Dopamine produced by neurons in the arcuate nucleus of the hypothalamus is secreted into the hypothalamo-hypophysial blood vessels of the median eminence, which supply the pituitary gland. The lactotrope cells that produce prolactin, in the absence of dopamine, secrete prolactin continuously; dopamine inhibits this secretion.
Motivation and pleasure
Dopamine is commonly associated with the pleasure system of the brain, providing feelings of enjoyment and reinforcement to motivate a person proactively to perform certain activities. Dopamine is released (particularly in areas such as the nucleus accumbens and striatum) by naturally rewarding experiences such as food, sex, use of certain drugs and neutral stimuli that become associated with them. This theory is often discussed in terms of drugs (such as cocaine and amphetamines), which seem to be directly or indirectly related to the increase of dopamine in these areas, and in relation to neurobiological theories of chemical addiction, arguing that these dopamine pathways are pathologically altered in addicted persons. However, cocaine and amphetamine influence separate mechanisms of action.
Cocaine is a dopamine transporter blocker that competitively inhibits dopamine uptake to increase the lifetime of dopamine and augments an overabundance of dopamine (an increase of up to 150%) within the parameters of the dopamine neurotransmitters. Like cocaine, amphetamines increase the concentration of dopamine in the synaptic gap, but by a different mechanism. Amphetamines are similar in structure to dopamine, and so can enter the terminal button of the presynaptic neuron via its dopamine transporters as well as by diffusing through the neural membrane directly. When entering inside the presynaptic neuron, amphetamines force the dopamine molecules out of their storage vesicles and expel them into the synaptic gap by making the dopamine transporters work in reverse. Dopamine's role in experiencing pleasure has been questioned by several researchers. It has been argued that dopamine is more associated with anticipatory desire and motivation (commonly referred to as "wanting") as opposed to actual consummatory pleasure (commonly referred to as "liking"). Dopamine is not released when unpleasant or aversive stimuli are encountered, and so motivates towards the pleasure of avoiding or removing the unpleasant stimuli.
Recent research suggests that the firing of dopamine neurons is a motivational chemical as a result of reward-anticipation. This is based on evidence that, when a reward is perceived to be greater than expected, the firing of certain dopamine neurons increases, which correspondingly increases desire or motivation toward the reward.
Clues to dopamine's role in motivation, desire and pleasure have come from studies performed on animals. In one such study rats were depleted of dopamine by up to 99% in the nucleus accumbens and neostriatum using 6-hydroxydopamine. With this large reduction in dopamine, the rats would no longer eat by their own volition. The researchers then force fed the rats food and noted whether they had the proper facial expressions indicating whether they liked or disliked it. The researchers of this study concluded that the reduction in dopamine did not reduce the rat's consummatory pleasure, only the desire to actually eat. In another study, mutant hyperdopaminergic (increased dopamine) mice show higher "wanting" but not "liking" of sweet rewards.
In humans, though, drugs that reduce dopamine activity (neuroleptics, [eg. some antipsychotics) have been shown to reduce motivation as well as cause anhedonia (the inability to experience pleasure). Conversely the selective D2/D3 agonists pramipexole and ropinirole have anti-anhedonic properties as measured by the Snaith-Hamilton Pleasure Scale. (The Snaith-Hamilton-Pleasure-Scale (SHAPS), introduced in English in 1995, assesses self-reported anhedonia in psychiatric patients.)
Opioid and cannabinoid transmission instead of dopamine may modulate consummatory pleasure and food palatability(liking). This could explain why animals "liking" of food is independent of brain dopamine concentration. Other consummatory pleasures, however, may be more associated with dopamine. One study found that both anticipatory and consummatory measures of sexual behavior (male rats) were disrupted by DA receptor antagonists. Libido can be increased by drugs that affect dopamine but not by drugs that affect opioid peptides or other neurotransmitters.
Sociability is also closely tied to dopamine neurotransmission. Low D2 receptor binding is found in people with social anxiety. Traits common to negative schizophrenia (social withdrawal, apathy, anhedonia) are thought to be related to a hypodopaminergic state in certain areas of the brain. In instances of bipolar, manic subjects can become hypersocial as well as hypersexual. This is also credited to an increase in dopamine, because mania alleviates from dopamine blocking antipsychotics.
Other theories reinforce that the crucial role of dopamine may be in desire, or anticipating pleasurable activity. Related theories  argue that dopamine function may be involved in the salience ('noticeableness') of perceived objects and events, with potentially important stimuli such as: 1) rewarding things or 2) dangerous or threatening things seeming more noticeable or important. This hypothesis argues that dopamine assists decision-making by influencing the priority, or level of desire, of such stimuli to the person concerned.
Pharmacological blockade of brain dopamine receptors increases rather than decreases drug-taking behavior. Since blocking dopamine decreases desire, the increase in drug taking behavior may be seen as not a chemical desire but as a deeply psychological desire to just 'feel something'.
Deficits in dopamine levels are implicated as one of several possible causes for Adult attention-deficit disorder (AADD), and some types of medications used to treat Attention-deficit hyperactivity disorder (ADHD/ADD) such as Methylphenidate are theorized to help stimulate dopaminergic systems, leading to potentially heightened sensation, for those afflicted by it and receiving treatment for it. Other classes of drugs for ADD however, can also interact with other neurotransmitter systems, and some types of heightened sensation can often lead to distorted perception.
Links to psychosis
Main article: dopamine hypothesis of psychosis
Disruption to the dopamine system has also been strongly linked to psychosis and schizophrenia. Dopamine neurons in the mesolimbic pathway are particularly associated with these conditions. This is partly due to the discovery of a class of drugs called the phenothiazines (which block D2 dopamine receptors) that can reduce psychotic symptoms, and partly due to the finding that drugs such as amphetamine and cocaine (which are known to greatly increase dopamine levels) can cause psychosis. Because of this, most modern antipsychotic medication is designed to block dopamine function to varying degrees.
Dopamine is a neurotransmitter that is involved in depression. Amphetamines and dopamine reuptake blockers have potent anti-depressant effects but these drugs quickly lose their benefit after they deplete dopamine levels in the brain. Antidepressants appear to primarily enhance serotonergic neurotransmission during preliminary drug administration but it takes several weeks for the antidepressant effect to be noticed. The late effect of antidepressants is thought to involve the indirect serotonergic modulation of dopaminergic neurotransmission. Blocking the D2 dopamine receptor is known to cause relapse in patients that have achieved remission from depression, and such blocking also counteracts the effectiveness of SSRI medication. However, there are Dopamine reuptake inhibitors that are used to treat depression such as bupropion (Wellbutrin) and amineptine Maneon/Servector.
^ Berridge K, Robinson T (1998). "What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience?". Brain Res Brain Res Rev 28 (3): 309-69. PMID 9858756.
^ Peciña S, Cagniard B, Berridge K, Aldridge J, Zhuang X (2003). "Hyperdopaminergic mutant mice have higher "wanting" but not "liking" for sweet rewards.". J Neurosci 23 (28): 9395-402. PMID 14561867.
^ Lambert M, Schimmelmann B, Karow A, Naber D (2003). "Subjective well-being and initial dysphoric reaction under antipsychotic drugs - concepts, measurement and clinical relevance.". Pharmacopsychiatry 36 Suppl 3: S181-90. PMID 14677077.
^ Lemke M, Brecht H, Koester J, Kraus P, Reichmann H (2005). "Anhedonia, depression, and motor functioning in Parkinson's disease during treatment with pramipexole.". J Neuropsychiatry Clin Neurosci 17 (2): 214-20. PMID 15939976.
^ Peciña S, Berridge K (2005). "Hedonic hot spot in nucleus accumbens shell: where do mu-opioids cause increased hedonic impact of sweetness?". J Neurosci 25 (50): 11777-86. PMID 16354936.
^ Pfaus J, Phillips A (1991). "Role of dopamine in anticipatory and consummatory aspects of sexual behavior in the male rat.". Behav Neurosci 105 (5): 727-43. PMID 1840012.
^ Schultz W (2002). "Getting formal with dopamine and reward". Neuron 36 (2): 241-263. PMID 12383780.
^ Disruption of gene interaction linked to schizophrenia. St. Jude Children's Research Hospital. Retrieved on 2006-07-06.
12-26-2006, 02:16 PM
You must spread some Reputation around before giving it to Ubiquitous again.
So in your personal opinion, should I even worry about using caber with Deca?
12-26-2006, 05:38 PM
See how you react to Deca (or Nandrolone in general) with Test beforehand.. People have been on the Nandrolone bandwagon for years before using Bromo or Caber. If you are using Dbol and high Test dose, more than likely the high aromatization will cause the problem well before Progestins come into play to usher it on.
Sometimes all gyno needs is Dbol added to the stack for it to rear it's ugly head.
12-26-2006, 05:56 PM
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