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pii
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Onlty

Unread post by pii »

Hu
Last edited by pii on Tue Jun 23, 2020 2:51 pm, edited 1 time in total.
arahant
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Re: Only erect before orgasm

Unread post by arahant »

Is it a joke?
Having erection before orgasm is the expected response.
After orgasm, there something called refractory period that finish the erection for a while.

https://en.wikipedia.org/wiki/Refractory_period_(sex)
Last edited by arahant on Sat Jan 04, 2020 1:08 pm, edited 1 time in total.
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kpavel
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Re: Only erect before orgasm

Unread post by kpavel »

it is not a joke, I had this for about half a year, then I got rather a delayed problem
arahant
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Re: Only erect before orgasm

Unread post by arahant »

kpavel wrote:it is not a joke, I had this for about half a year, then I got rather a delayed problem
From the link about the refractory period which happens after an orgasm:

"most men cannot achieve or maintain an erection during this time, and many perceive a psychological feeling of satisfaction and are temporarily uninterested in further sexual activity; the penis may be hypersensitive and further sexual stimulation may feel painful during this time frame."

That is why it is difficult to stay erect after orgasm.

Ref:

Rosenthal, Martha (2012). Human Sexuality: From Cells to Society. Cengage Learning. pp. 134–135. ISBN 9780618755714. Retrieved September 17, 2012.

Irving B. Weiner, W. Edward Craighead (2010). The Corsini Encyclopedia of Psychology, Volume 2. John Wiley & Sons. p. 761. ISBN 978-0470170267. Retrieved November 10, 2012.
Wellbutrin (2007 - 2018)
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R3m3dy
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Re: Only erect before orgasm

Unread post by R3m3dy »

arahant, I think that what he means is that he will be stimulating himself and be unable to achieve an erection. If he continues stimulation, he will become erect immediately before orgasm. Something about the “peak stimulation” of orgasm seems to cause at least a partial erection at that moment. This is something that I have experienced.
arahant
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Re: Only erect before orgasm

Unread post by arahant »

R3m3dy wrote:arahant, I think that what he means is that he will be stimulating himself and be unable to achieve an erection. If he continues stimulation, he will become erect immediately before orgasm. Something about the “peak stimulation” of orgasm seems to cause at least a partial erection at that moment. This is something that I have experienced.

I had something similar before take SSRI, I got ED from performance anxiety, I was so obsessed with my erection that lots of tension messed with it...it required extreme stimulation to keep it a bit erect and reach orgasm.
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pii
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Re: Only erect before orgasm

Unread post by pii »

R3m3dy wrote:arahant, I think that what he means is that he will be stimulating himself and be unable to achieve an erection. If he continues stimulation, he will become erect immediately before orgasm. Something about the “peak stimulation” of orgasm seems to cause at least a partial erection at that moment. This is something that I have experienced.
Yes bro This is what i mean i dont know what the other Guy dont understand
pii
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Re: Only erect before orgasm

Unread post by pii »

kpavel wrote:it is not a joke, I had this for about half a year, then I got rather a delayed problem
How u got rid of this bro ?
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kpavel
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Re: Only erect before orgasm

Unread post by kpavel »

piwomocne wrote:
kpavel wrote:it is not a joke, I had this for about half a year, then I got rather a delayed problem
How u got rid of this bro ?
I don't know exactly. I looked my iherb shopping at close months and digged some theory for ya. At that time 3 experiments I would say can be notable from theory. 1) In June I finished GInkgo Biloba (had some success in libido) and began betahistine. After GB I 100% had this problem. 2) In August I added d-aspartic acid, this increases nmda signalling, I also tried some vitex. I stopped that after 3 weeks for following reasons. Had nipple sensations. Hair became very dry. I measured prolactin (which is classically mentioned for refractory period) and it was 33 which is too high. 3) I noticed in my shops that I got 1 bottle of resveratrol by Autumn.
Now theory.
Generally premature ejaculation treatment includes ssri like dapoxetine and pdei like cialis. Serotonin can delay or facilitate ejaculatoin. But you have a long absence of normal erectile size. It could be because of nitric oxide lack. Here's how it's possible: you have low endothelial nitric oxide synthase (eNOS).

Relevance of serum nitric oxide levels and the efficacy of selective serotonin reuptake inhibitors treatment on premature ejaculation: decreased nitric oxide is associated with premature ejaculation.
https://www.ncbi.nlm.nih.gov/pubmed/24118023
The aim of the present study was to determine the relevance of serum nitric oxide levels and the efficacy of selective serotonin reuptake inhibitors (SSRI) treatment on premature ejaculation. Sixty married men (aged 20-50) with lifelong premature ejaculation and forty healthy men (aged 24-48) as control group were included in this study. The patients were evaluated by intravaginal ejaculation latency time (IELT) for premature ejaculation (PE). IELT<1 min is accepted PE. Patients with diabetes mellitus, chronic disorders or erectile dysfunction and heavy smokers were excluded. All patients were evaluated with history, physical examination, International Index of Erectile Dysfunction-5 (IIEF-5) score and IELT by stopwatch method. Nitric oxide levels were measured by Griess reaction, and all samples were frozen at -80 °C. Patients were randomly categorised 4 group to receive fluoxetine 20 mg day(-1) (Group 1), paroxetine 20 mg day(-1) (Group 2), sertraline 50 mg day(-1) (Group 3) and healthy control (Group 4) for 4 weeks. Baseline and post-treatment findings were compared between the four groups. At the end of 4 weeks, in fluoxetine, paroxetine, sertraline groups mean IELT values showed a statistically significant improvement from the baseline values (P < 0.001, P < 0.001, P = 0.03; respectively). Baseline and 1st month follow-up mean IIEF scores were 24.5 and 23.05, 24.70 and 23.60 (P < 0.05) in group 1 and group 3 respectively; also 23.09 and 23.32 (P > 0.05) in group 2. Baseline serum NO levels were 31.8, 30.44, 30.8 and 42.84 in fluoxetine, paroxetine, sertraline and healthy control groups respectively. NO levels were statistically lower in patients with PE. After treatment of fluoxetine, paroxetine and sertraline, NO levels were increased baseline (35.8, 36.4, 38.08) (P < 0.05). Our findings indicated that PE is associated with decreased serum NO levels. After the SSRI treatment increased, NO may retard ejaculation presumably by central peripheral mechanism. Further studies are needed to confirm this suggestion and the role of NO in pathophysiology and treatment for premature ejaculation.

Ejaculatory abnormalities in mice lacking the gene for endothelial nitric oxide synthase (eNOS-/-).
https://www.ncbi.nlm.nih.gov/pubmed/10549894
Nitric oxide (NO) has been established as a neurotransmitter in both the central and peripheral nervous systems. Three isoforms of its synthetic enzyme, NO synthase (NOS), have been identified: 1) in the endothelial lining of blood vessels (eNOS), 2) an inducible form found in macrophages (iNOS), and 3) in neurons (nNOS). Previous studies using pharmacological agents that block all three isoforms of NOS have revealed that NO mediates several aspects of reproductive physiology and behavior, including anomalies in male sexual behavior and erectile function. To determine the specific contribution of the endothelial isoform of NOS in male reproductive behavior, we studied mice missing the gene for only eNOS (eNOS-/-). Wild-type (WT) and eNOS-/- animals were placed with an estrous WT female and observed for 45 min. Both WT and eNOS-/- mice displayed equivalent motivation to mount the stimulus female. However, eNOS-/- mice exhibited striking anomalies in ejaculatory function. A higher percentage of eNOS-/- than WT mice ejaculated during the testing period (p < 0.001). This increased propensity to ejaculate was apparently due to reduced stimulation required to elicit ejaculation; eNOS-/- mice required significantly fewer mounts (p < 0.003) and intromissions (p < 0.001) to ejaculate compared to WT mice. Taken together, these results suggest that NO synthesized by eNOS may be involved in ejaculatory physiology, but not sexual motivation.

eNOS can be regulated by many factors, for example low folate leads to to low nitric oxide.
A new potential risk factor in patients with erectile dysfunction and premature ejaculation: folate deficiency.
https://www.ncbi.nlm.nih.gov/pubmed/25080932
We investigated serum folic acid (FA) levels in patients with erectile dysfunction (ED) and/or premature ejaculation (PE). Fasting serum samples were obtained from 42 patients with ED, 36 with PE, 25 ED patients with PE, and 30 healthy men; the mean intravaginal ejaculation latency time (IELT) was measured during a 4 weeks baseline period. Levels of sex hormones (follicle-stimulating hormone, luteinizing hormone, total testosterone), homocysteine (Hcys), and FA were measured using chemiluminescent immunoassays. The sexual functions of PE patients and normal control men were evaluated using the Chinese Index of Premature Ejaculation (CIPE). The abridged International Index of Erectile Function-5 (IIEF-5) questionnaire was used to gauge erectile quality for ED patients and for normal controls. Serum FA concentrations were lower in ED (7.61 ± 3.97 ng ml⁻¹), PE (9.37 ± 3.40 ng ml⁻¹), and ED/PE (8.84 ± 4.28 ng ml⁻¹) patients than in healthy men (12.23 ± 5.76 ng ml -1 , P < 0.05). No significant differences in sex hormone levels were found between patients with sexual dysfunction and healthy controls (P > 0.05). There were positive correlations between serum FA concentrations and CIPE scores (r = 0.530, P < 0.01), IIEF-5 scores (r = 0.589, P < 0.01), and IELT (r = 0.445, P < 0.01); negative correlations with Hcys concentrations (r = -0.487, P < 0.01) were found in all participants. These findings showed a strong relationship between serum FA levels and sexual dysfunction, possibly due to an effect of FA on the metabolism of nitric oxide, Hcys, and 5-hydroxytryptamine.

If you suspect high homocysteine you can measure it in a lab.
Hyperhomocysteinemia and Endothelial Dysfunction.
https://www.ncbi.nlm.nih.gov/pubmed/20495681/
Hyperhomocysteinemia (HHcy) is a significant and independent risk factor for cardiovascular diseases. Endothelial dysfunction (ED) is the earliest indicator of atherosclerosis and vascular diseases. We and others have shown that HHcy induced ED in human and in animal models of HHcy induced by either high-methionine load or genetic deficiency. Six mechanisms have been suggested explaining HHcy-induced ED. These include 1) nitric oxide inhibition, 2) prostanoids regulation, 3) endothelium-derived hyperpolarizing factors suppression, 4) angiotensin II receptor-1 activation, 5) endothelin-1 induction, and 6) oxidative stress. The goal of this review is to elaborate these mechanisms and to discuss biological and molecular events related to HHcy-induced ED.

Now about resveratrol. Resveratrol can increase eNOS, I found a relevant study. l-citrulline helps to fuel nitric oxide.
Oral L-citrulline and Transresveratrol Supplementation Improves Erectile Function in Men With Phosphodiesterase 5 Inhibitors: A Randomized, Double-Blind, Placebo-Controlled Crossover Pilot Study
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6302103/
Introduction
Phosphodiesterase type 5 inhibitors (PDE5i) are first-line therapy for most men with erectile dysfunction (ED). If ineffective, vacuum erection devices, intracavernous injections, and penile prosthesis implantation are suitable as second- or third-line therapies. However, very few patients select these therapies. It is critically important to improve erectile function with oral administration of effective agents. Administration of L-citrulline or transresveratrol in animal experiments has been reported to improve erectile function, but few such experiments have been performed on humans with ED.
Aim
We aimed to investigate the efficacy of combination therapy of L-citrulline and transresveratrol in patients with ED despite their use of PDE5i.
Methods
In this randomized, double-blind, placebo-controlled crossover pilot study, men with ED (Sexual Health Inventory for Men [SHIM] score below 16) despite on-demand use of PDE5i received a placebo for 1 month or the active treatment (L-citrulline 800 mg/day and transresveratrol 300 mg/day) for another month. Patients continued on-demand use of PDE5i.
Main Outcome Measure
The SHIM score, Erection Hardness Score (EHS), Aging Male Symptoms Scale-sexual domain (AMS-SD), and adverse events were examined.
Results
20 patients ages 29–78 years were enrolled, and after 6 men withdrew, 13 concluded the study without adverse events. Mean SHIM score for the active treatment increased significantly (10.96 ± 1.21) compared with baseline (8.32 ± 1.21) and placebo (8.31 ± 1.23) (both P < .05). Mean EHS score for the active treatment (2.56 ± 0.26) also increased from baseline (2.31 ± 0.26), but not significantly (P = .79). Mean AMS-SD score was not significantly different in either group.
Conclusion
To our knowledge, this is the first study to show that combination therapy of L-citrulline and transresveratrol is effective for ED treatment in men with added on-demand use of PDE5i. This combination supplement may be added if PDE5i is insufficient.

Additionally you can try Prelox formula (citrulline, pycnogenol, oak). I also recommend omega3 fats, like flaxseed oil, really helpful.

In short: check homocysteine, try folate/methylfolate, try citrulline (800 mg/day)+transresveratrol (300 mg/day)+-cialis, Prelox, omega3.
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