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[planeta 5553]

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Think:"My urges to watch porn won't go away when I relapse, they'll only get stronger and more frequent"(self.NoFap)

submitted 9 hours ago by weirddudee

The only way to get the urges to go a away is to quit

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[–]Irving_Pichel152 days 10 pontos 8 hours ago 

This is correct. Every single time I've fallen, it's led to a colossal binge. Anywhere from days to months but it's almost non-stop.

[Visitante]

dia 1

[Zaro 12]

103 dias. Acredito que estou livre do fap e do porn.

[Visitante]

dia 2

[Freud F. 4]

dia 3

[Visitante]

6 horas atrás, Zaro disse:

103 dias. Acredito que estou livre do fap e do porn.

Interessante, fala mais...

qts anos?

[planeta 5553]

https://raypeatforum.com/community/threads/masturbation-downregulates-certain-androgenic-receptors-in-the-brain-and-upregulates-certain-estro.6998/

 

Masturbation downregulates certain androgenic receptors [in the brain] and upregulates certain estro

Discussion in 'Articles & Scientific Studies' started by you, Jun 16, 2015.

 

Page 1 of 2 12Next >

A few interesting rat studies.

http://www.ncbi.nlm.nih.gov/pubmed/17239879

Estrogen receptor alpha (ERalpha) participates in the neuroendocrine regulation of male sexual behavior, primarily in brain areas located in the limbic system. Males of many species present a long-term inhibition of sexual behavior after several ejaculations, known as sexual satiety. It has been shown that androgen receptor density is reduced 24 h after a single ejaculation or mating to satiety, in the medial preoptic area, nucleus accumbens and ventromedial hypothalamus. The aim of this study was to analyze if the density of ERalpha was also modified 24 h after a single ejaculation or mating to satiety. Sexual satiety was associated with an increased ERalpha density in the anteromedial bed nucleus of the stria terminalis (BSTMA), ventrolateral septum (LSV), posterodorsal medial amygdala (MePD), medial preoptic area (MPA) and nucleus accumbens core (NAc). A single ejaculation was related to an increase in ERalpha density in the BSTMA and MePD. ERalpha density in the arcuate (Arc) and ventromedial hypothalamic nuclei (VMN), and serum estradiol levels remained unchanged 24 h after one ejaculation or mating to satiety. These data suggest a relationship between sexual activity and an increase in the expression of ERalpha (estrogenic receptor) in specific brain areas, independently of estradiol levels in systemic circulation.

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http://www.ncbi.nlm.nih.gov/pubmed/12689608

Male sexual behavior is regulated by limbic areas like the medial preoptic nucleus (MPN), the bed nucleus of the stria terminalis (BST), the nucleus accumbens (nAcc) and the ventromedial hypothalamic nucleus (VMN). Neurons in these brain areas are rich in androgen receptors (AR) and express FOS-immunoreactivity in response to mating. In many species sexual satiation, a state of sexual behavior inhibition, is attained after multiple ejaculations. The mechanisms underlying sexual satiation are largely unknown. In this study we show that sexual activity reduces androgen receptor immunoreactivity (AR-ir) in some of the brain areas associated with the control of male sexual behavior, but not in others. Thus, one ejaculation reduced the AR-ir in the MPN and nAcc, but not in the BST and VMN. Copulation to satiation, on the other hand, reduced AR-ir in the MPN, nAcc and VMN, and not in the BST. The AR-ir reduction observed in the MPN of sexually satiated rats was drastic when compared to that of animals ejaculating once. Serum androgen levels did not vary after one ejaculation or copulation to exhaustion. These data reveal that sexual activity reduces AR in specific brain areas and suggest the possibility that such a reduction underlies the sexual inhibition that characterizes sexual satiety.

http://www.ncbi.nlm.nih.gov/pubmed/12914589

The present article reviews the current findings on the interesting phenomenon of sexual satiety. Knut Larsson in 1956 reported on the development of sexual exhaustion in the male rat after repeated copulation. We have studied the process and found the following results. (1) One day after 4 hours of ad libitum copulation, two-thirds of the population showed complete inhibition of sexual behavior, while the other third displayed a single ejaculatory series from which they did not recover. (2) Several pharmacological treatments, including 8-OH-DPAT, yohimbine, naloxone and naltrexone, reverse this sexual satiety, indicating that the noradrenergic, serotonergic and opiate systems are involved in this process. Indeed, direct neurochemical determinations showed changes in various neurotransmitters during sexual exhaustion. (3) Given enough stimulation, by changing the stimulus female, sexual satiety was prevented, suggesting that there are motivational components of the sexual inhibition that characterizes sexual exhaustion. (4) The GABA antagonist bicuculline, or the electrical stimulation of the medial preoptic area, did not reverse sexual exhaustion. These data suggest, on the one hand, that sexual exhaustion and the postejaculatory interval (which is shortened by bicuculline administration) are not mediated by similar mechanisms and, on the other, that the medial preoptic area does not regulate sexual satiety. (5) The androgen receptor density in brain areas closely related to the expression of masculine sexual behavior, such as the medial preoptic nucleus, was drastically reduced in sexually exhausted animals. Such reduction was specific to certain brain areas and was not related to changes in the levels of androgens. These results suggest that changes in brain androgen receptors account for the inhibition of sexual behavior present during sexual exhaustion. (6) The recovery process of sexual satiety after 4 hours of ad libitum copulation reveals that, after 4 days, only 63% of the males are able to show sexual behavior while after 7 days all animals display copulatory activity.

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Human study

http://www.ncbi.nlm.nih.gov/pubmed/11760788

This current study examined the effect of a 3-week period of sexual abstinence on the neuroendocrine response to masturbation-induced orgasm. Hormonal and cardiovascular parameters were examined in ten healthy adult men during sexual arousal and masturbation-induced orgasm. Blood was drawn continuously and cardiovascular parameters were constantly monitored. This procedure was conducted for each participant twice, both before and after a 3-week period of sexual abstinence. Plasma was subsequently analysed for concentrations of adrenaline, noradrenaline, cortisol, prolactin, luteinizing hormone and testosterone concentrations. Orgasm increased blood pressure, heart rate, plasma catecholamines and prolactin. These effects were observed both before and after sexual abstinence. In contrast, although plasma testosterone was unaltered by orgasm, higher testosterone concentrations were observed following the period of abstinence. These data demonstrate that acute abstinence does not change the neuroendocrine response to orgasm but does produce elevated levels of testosterone in males.

http://www.ncbi.nlm.nih.gov/pubmed/12659241

The purpose of this study is to gain understanding of the relationship between ejaculation and serum testosterone level in men. The serum testosterone concentrations of 28 volunteers were investigated daily during abstinence periods after ejaculation for two phases. The authors found that the fluctuations of testosterone levels from the 2nd to 5th day of abstinence were minimal. On the 7th day of abstinence, however, a clear peak of serum testosterone appeared, reaching 145.7% of the baseline ( P < 0.01). No regular fluctuation was observed following continuous abstinence after the peak. Ejaculation is the precondition and beginning of the special periodic serum testosterone level variations, which would not occur without ejaculation. The results showed that ejaculation-caused variations were characterized by a peak on the 7th day of abstinence; and that the effective time of an ejaculation is 7 days minimum. These data are the first to document the phenomenon of the periodic change in serum testosterone level; the correlation between ejaculation and periodic change in the serum testosterone level, and the pattern and characteristics of the periodic change.

http://www.ncbi.nlm.nih.gov/pubmed/17196592

Research points to an association between testosterone (T) and partnering in some women and men, and this association has been interpreted as an effect of either relationship status (i.e. differences in relationship status lead to differences in T) or relationship orientation (i.e. T is associated with the likelihood of entering relationships). To address whether physical partner presence was associated with decreased T, we examined T levels in people (72 women; 49 men) who were single, in long-distance relationships, or in same-city relationships. No participants were using exogenous hormones, including hormonal contraceptives. Participants provided a saliva sample and responded to questions about their relationship status. Single men had higher T than long-distance and same-city partnered men, which supports the relationship orientation interpretation. In contrast, same-city partnered women had lower T than single women and women in long-distance relationships, which supports the relationship status interpretation. We conclude that physical partner presence is not necessary to see an association between partnering and hormones in men (since same-city and long-distance partnered men had similar T levels), but may be necessary in women (since same-city partnered women had lower T than long-distance partnered women).

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For long I have thought that masturbation reduces testosterone. While masturbation does very slightly do this through several ways, I've discovered that the feeling of weakness is actually caused by something else.

Masturbation downregulates certain androgenic receptors [in the brain] and upregulates certain estrogenic receptors and this is why we get the feeling of having lost testosterone - being weak, being feminine, etc.
It takes 3-4 days to recover from this receptor change and personally it always takes at least 3 days for me - 3 days of SLEEP.

Prolactin is increased after orgasm which causes a decrease in dopamine. Technically, if prolactin was all there was to it, all you'd need to do to regain the strength you had prior to the orgasm is to consume a strong dopaminergic agent or a prolactin inhibitor such as vitamin B6 (which is a strong inhibitor in 200+mg dosages).
Yet, having tested this myself, taking vitamin B6 does not cause me to feel well again sufficiently, though it slightly does.
This suggests, as mentioned, that the problem is really to do with androgenic receptors in the brain, amongst other things, and sleep really is the best way to recover.

Notice that downregulating of the androgenic receptors leads to "poor confidence," "passivity" and other unwanted side-effects.

 

Editado Julho 3, 2016 às 05:02 por planeta

[Freud F. 4]

Dia 4

[Visitante]

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[NOFAP 89]

Depois que parei de acompanhar o tópico me entreguei ao vicio novamente durante 2 meses. Mas estou de volta:

 

Dia 01