Premature Ejaculation and SSRIs

[BlackJack]

Do u think a safe effect way to treat premature ejaculation is using SRRi?

if so which one would be ideal

[BlackJack]

Dr. M could u ccomment on this i found..

“Chronic over-masturbation results in over-reactive (over-trained) prostate, bulbourethral glands and PC muscles, as a result of nervous plasticity, and alternate the skin neuroendocrine function, in addition to destruction of serotonin and GABA nervous control, exhaustion of the hypothalamus-pituitary-adrenal and -testicular axis and liver system for an unbalanced release of pro-opinomelanocotin (POMC) peptides (such as AdrenoCorticoTropin Hormone or ACTH, endorphins, a-Mmelanocyte-Stimulating Hormone or a-MSH, and Lipotropin Hormone or LPH) , prostate abrasion, excessive inflammatory hormone prostaglandin E2 production, excessive stress hormones cortisol and epinephrine for performance anxiety, parasympathetic and sympathetic erectile nervous disorders, excessive use of PC muscles, and precum/semen leakage. When the serotonin, GABA, endorphrin, cortisol, and/or a-MSH fail to modulate the dopamine-norepinephrine/norepinphrine conversion and the psychological stressors norepinephrine/epinephrine-induced inflammatory hormone prostaglandin E2 production, you may get more than one of the following responses to sexual stimulation: 1. Excessive dopamine-norepinephrine induced excessive prostaglandin E2 for the core temperature rise (over-heating or “sex fever’) in the brain, spine, adrenal glands and prostate- the sympathetic nervous Fight and Flight responses; 2. Prostaglandin E2 over-excited the penile and prostate nerves for penile and prostate hypersensitivity; 3. Excessive prostaglandin E2 induces prostate and bulbourethral inflammatory responses and over-heating for precum/semen leakage and instant ejaculation”

“Over-masturbation/over-ejaculation/excessive-orgasm can castrate your hypothalamus-pituitary-testicular(ovarian) axis by arterial constriction and inflammatory narrowness in your brain and pelvic organs (testicles, prostate, seminal vesicles, penis, ovaries, uterus, vagina and clitoris) due to excessive release of prolactin, norepinephrine, and epinephrine, excessive binding of norepeinephrine/epinephrine on the alpha-adrenergic receptors, the norepinephrine/epinephrine induced excessive prostaglandin E2, and the post-sex deficiency of nitric oxide and prostaglandins E1/E3 production. Once your hypothalamus-pituitary-testicular(ovarian) axis is locked (tightened up), you will lack of androgen hormones (DHEA, testosterone or/and DHT) to unlock it. In the good old days, we castrated animal testicles by mechanically tightening up the arteries to the testicles. Over-masturbation, over-ejaculation, excessive sex or/and excessive orgasm produce the similar castration effects as the mechanical one. To prevent the castration effects, you have to keep your blood flow to your brain and testicles after having sexual activities and experiencing sex-induced stress. The post-sex androgen hormones and oxytocin in your bloodstream or/and residual semen are essential to keep arterial dilation via the nitric oxide and cGMP release from the vegal/parasympathetic nervous endings , as well as the action of the stress hormones norepinephrine and epinephrine on the sympathetic nervous beta-adrenergic receptors where partially blocking the alpha-adrenergic receptors may be required. “

[DrMariano2]

@BlackJack 211 wrote:

Do u think a safe effect way to treat premature ejaculation is using SRRi?

if so which one would be ideal

Norepinephrine is what triggers orgasm.

Premature ejaculation occurs when norepinephrine levels are elevated chronically or rise too quickly, and thus makes it too easy to trigger an orgasm.

Serotonin is one of the signals that reduces norepinephrine signaling – so long as the dose is not too high (where it may instead increase norepinephrine).

Serotonin Reuptake Inhibitors have become one standard treatment for premature ejaculation because they increase serotonin signaling by prolonging existing serotonin signals.

Any of the existing SSRIs may be used since the mechanism of the same. However, each SSRI has different characteristics on the other signals (hormones and neurotransmitters and cytokines, degradative enzymes such as the Cytochrome P450 system, interactions, etc.). Thus, side effects may occur depending on the individual.

Of the SSRIs, Escitalopram (Lexapro) is the cleanest in regard to effects on other signaling systems in my experience. This is why it is a good first choice. However, not everyone fits. Lexapro may be less tolerated by some people due to individual genetic differences in the response to Lexapro’s effects on signaling systems. Thus one has to keep an open mind and consider the others. For example, a recent patient did very well on Zoloft (Sertraline). Zoloft can cause weight gain in some people but it did not with this particular patient. Thus, it worked. And it worked better than Lexapro. Some patients do better on Paxil (Paroxetine). Some function better with Prozac (Fluoxetine).

[chaos]

FWIW, I never had prematue ejaculation, but the first drug doctors used to treat my depression was zoloft.

I literally had to work to have an orgasm. My fiancee was like “enough is enough”.

The only other drug with which I noticed that side effect was prozac, and not to nearly the same extent.

[BlackJack]

i’m just not sure its worth taking an SSRI for PE because of all the sides that could come with the SSRI

[DrMariano2]

If one doesn’t want to use an SSRI for premature ejaculation, then all the causes of high norepinephrine production would have to be assessed and managed. This includes stress management.

[BlackJack]

sometimes i think my weak erections are the main culprit..

when i have sex right after my erection goes a bit limp is when i ejaculate

maybe Cialis would help

i remember one night i took a cialis with 5 shots of vodka and i literally went for 2 hours; Dr M would u think its ok to take cialis with booze?

Dr. M if one addresses the root cause of high norephin. either be low iron, thyroid, adrenal , etc , how long would it take for the neurotranmitters to rebalance (llowering norephin and increasing ones like serotonin and gABA)

[DrMariano2]

@BlackJack 233 wrote:

sometimes i think my weak erections are the main culprit..

when i have sex right after my erection goes a bit limp is when i ejaculate

maybe Cialis would help

i remember one night i took a cialis with 5 shots of vodka and i literally went for 2 hours; Dr M would u think its ok to take cialis with booze?

Dr. M if one addresses the root cause of high norephin. either be low iron, thyroid, adrenal , etc , how long would it take for the neurotranmitters to rebalance (llowering norephin and increasing ones like serotonin and gABA)

I would not recommend drinking 5 shots of vodka at a time with or without cialis. That itself causes enough damage and inflammation in the liver to stop growth hormone from working.

Addressing the nutritional problems a person has generally improves function quickly – say, within 1-3 weeks. However, some nutrients, such as iron take a long time to build up, and thus will take months.

[BlackJack]

I understand the negative of alcohol,, but being able to have2hour of sex is an extreme confidence booster.. its very alpha male. i think its the greats feeling in the world.

i have had PE for the last 10 years and cialis + booze was by far the only thing that work magic.

without it im lucky togo 1 minute.

[DrMariano2]

@BlackJack 259 wrote:

I understand the negative of alcohol,, but being able to have2hour of sex is an extreme confidence booster.. its very alpha male. i think its the greats feeling in the world.

i have had PE for the last 10 years and cialis + booze was by far the only thing that work magic.

without it im lucky togo 1 minute.

Alcohol works by improving GABA Receptor sensitivity.

Benzodiazepines like Xanax or Clonazepam also work by improving GABA Receptor sensitivity. They replaced alcohol in the psychiatry tool kit decades ago. They have additive effects, which is why when taken, patients should avoid alcohol use.

Alcohol has too short a duration of action, whereas Xanax may last 6-8 hours, Clonazepam 12-20 hours.

The benzodiazepines also are much more potent than alcohol. A single drink of an alcoholic beverage contains 13 grams of alcohol. It may last an hour if lucky. A single dose of Xanax is 0.25 mg. It may last 6 hours.

The benzodiazepines do not have the toxicity that alcohol has by far.

[hardasnails1973]

@DrMariano 272 wrote:

Alcohol works by improving GABA Receptor sensitivity.

Benzodiazepines like Xanax or Clonazepam also work by improving GABA Receptor sensitivity. They replaced alcohol in the psychiatry tool kit decades ago. They have additive effects, which is why when taken, patients should avoid alcohol use.

Alcohol has too short a duration of action, whereas Xanax may last 6-8 hours, Clonazepam 12-20 hours.

The benzodiazepines also are much more potent than alcohol. A single drink of an alcoholic beverage contains 13 grams of alcohol. It may last an hour if lucky. A single dose of Xanax is 0.25 mg. It may last 6 hours.

The benzodiazepines do not have the toxicity that alcohol has by far.

Could a person’s past fast pace life style which involved heavy drinking and recreational drug use cause a potential down regulation of GABA and hormone receptors.

[DrMariano2]

@hardasnails1973 276 wrote:

Could a person’s past fast pace life style which involved heavy drinking and recreational drug use cause a potential down regulation of GABA and hormone receptors.

Map out the circuits.

For example: Fast paced life style = high stress = increased norepinephrine. Methamphetamine = increased norepinephrine = increased stress.

Increased stress = increased norepinephrine signaling. To increase norepinephrine, GABA, serotonin, and/or dopamine need to be reduced.

Increased stress/norepinephrine signaling may lead to increased histamine signaling, increased pro-inflammatory cytokine signaling. This also leads to increase insulin resistance/increased insulin signaling.

Increased stress/norepinephrine signaling also results in the renal loss of zinc, iodine – leading to related metabolic problems.

Chronic or extreme stress may lead to dysregulation of hypothalamic-pituitary-adrenal axis. Dysregulation of hypothalamic-pituitary-adrenal axis may lead to impaired cortisol, DHEA, pregnenolone, progesterone, testosterone, estrogen, aldosterone signaling. This may lead to increased stress/norepinephrine, increased pro-inflammatory signaling. This in turn, may reduce T4 to T3 conversion or reduce Free T3.

Alcohol and Marijuana use may be attempts to help reduce excessive norepinephrine signaling. However, they have their own toxicities and downsides.

Alcohol, in particular, negates growth hormone signaling. A single drink of alcohol negates all of a day’s growth hormone. Beer is estrogenic (the hops). This and alcohol toxicity causes gynecomastia, increased abdominal fat (the beer belly), reduced testicular size, and aggressive behavior.

There are a lot of ramifications of a fast paced life-style with drug abuse.

[hardasnails1973]

@DrMariano 278 wrote:

Map out the circuits.

For example: Fast paced life style = high stress = increased norepinephrine. Methamphetamine = increased norepinephrine = increased stress.

Increased stress = increased norepinephrine signaling. To increase norepinephrine, GABA, serotonin, and/or dopamine need to be reduced.

Increased stress/norepinephrine signaling may lead to increased histamine signaling, increased pro-inflammatory cytokine signaling. This also leads to increase insulin resistance/increased insulin signaling.

Increased stress/norepinephrine signaling also results in the renal loss of zinc, iodine – leading to related metabolic problems.

Chronic or extreme stress may lead to dysregulation of hypothalamic-pituitary-adrenal axis. Dysregulation of hypothalamic-pituitary-adrenal axis may lead to impaired cortisol, DHEA, pregnenolone, progesterone, testosterone, estrogen, aldosterone signaling. This may lead to increased stress/norepinephrine, increased pro-inflammatory signaling. This in turn, may reduce T4 to T3 conversion or reduce Free T3.

Alcohol and Marijuana use may be attempts to help reduce excessive norepinephrine signaling. However, they have their own toxicities and downsides.

Alcohol, in particular, negates growth hormone signaling. A single drink of alcohol negates all of a day’s growth hormone. Beer is estrogenic (the hops). This and alcohol toxicity causes gynecomastia, increased abdominal fat (the beer belly), reduced testicular size, and aggressive behavior.

There are a lot of ramifications of a fast paced life-style with drug abuse.

Since in blackjacks case would a fractional catecholamine serum give comparing it to a urinary neurotransmitters give more information to assessing his situation? So there for drug like xanax to help with gaba receptors sensitivity could help to modulate norephipherine signaling. Does cymbalta also help to modulate serotonin and norepinepherine signaling as well? Could theanine be a possible natural alternative to help modulate these neurotransmitters as well? He has tried gaba and 5 htp in the past with out success.

Thanks

[BlackJack]

Thank you, what you say makes so match sense and it matches up with me perfectly…

everyone of my sexual encounters from the ages of 17-21 were under the influence of either alcohol or other drugs.

[DrMariano2]

@hardasnails1973 283 wrote:

Since in blackjacks case would a fractional catecholamine serum give comparing it to a urinary neurotransmitters give more information to assessing his situation?

So there for drug like xanax to help with gaba receptors sensitivity could help to modulate norephipherine signaling.

Does cymbalta also help to modulate serotonin and norepinepherine signaling as well?

Could theanine be a possible natural alternative to help modulate these neurotransmitters as well?

He has tried gaba and 5 htp in the past with out sucess.

Thanks

A fractionated plasma catecholamine tests gives epinephrine, norepinephrine, and dopamine levels. Currently, Quest Diagnostics’ dopamine test is not very sensitive and cannot give a level < 10 or 20. LabCorp does a better job with this. The test is originally aimed for cancer. However, it may be also interpreted for behavior and certain conditions such as diabetes. Epinephrine primarily come from the adrenal medulla. Norepinephrine comes from the adrenal medulla and peripheral sympathetic nervous system cells. So long as the sympathetic nervous system and adrenal medulla are connected, Norepinephrine and epinephrine reflect nervous system sympathetic nervous system activity. The adrenal medulla is essentially a sympathetic nervous system ganglion. Dopamine is problematic. It mostly occurs from leakage from the sympathetic nervous system nerves and adrenals in the process of making norepinephrine.

Serum serotonin levels and its urinary metabolite 5-HIAA can also be measured Much of serotonin comes from the enteric nervous system. When the enteric nervous system and central nervous system correlate in serotonin activity, then this is a useful measure. Often they do. Interpreting when they do and don’t correlate would come with experience. Adjusting serotonin via serotonin reuptake inhibitors changes serotonin simultaneously both in the enteric nervous system and the central nervous system, giving one an idea of the correlated based on responses from both systems.

Urinary neurotransmitter tests give a larger selections of neurotransmitters. Often GABA, Glutamate, Histamine, and others also are measured. Interpretation is complicated since one has to tease apart peripherals sources versus central nervous system sources and then determine whether or not they correlate. I found this difficult to do. Many practitioners also find it hard to correlate these levels with the clinical findings.

Note that when plasma glutamate is tracked repeatedly over time, what is interesting is that plasma glutamate levels decrease during psychotic episodes of schizophrenia, bipolar disorder, and other psychotic illnesses. The problem of doing a single-point glutamate level and trying to find out whether this correlates with illness is difficult since the comparison is among different people rather than a longitudinal view of a single person. Glutamate is released by other non-central nervous system sources such as platelets.

Neurotransmitter testing is thus complicated and problematic. Norepinephrine, Epinephrine, and Serotonin are the most easily interpreted. The others are much more difficult if they at all can be used.

Different labs also vary in their urinary neurotransmitter levels. This further makes it difficult to correlate what level one sees and the clinical picture – making urinary neurotransmitter levels less useful a tool. So far, at least in my experience, I have had the most success in correlating levels with clinical picture using Sanesco’s tests.

I like the fractionated plasma catecholamine test as well as the serum serotonin and urinary 5HIAA tests in that they are standard tests available in major labs and they are also paid for by health insurance. The alternative medicine lab urinary neurotransmitter tests are often not paid for by health insurance, are expensive for most patients to pay out of pocket.

Increasing GABA signaling by increasing GABA receptor sensitivity helps reduce norepinephrine signaling. This route is the most commonly used route to control norepinephrine. And it is effective. The problem is that it is not specific to only the sympathetic nervous system cells (including the locus ceruleus). Increasing GABA signaling affects every brain cell – causing the adverse effects such as memory impairment and oversedation.

Cymbalta prolongs serotonin and norepinephrine signaling.

Theanine helps increase dopamine and serotonin simultaneously. Dopamine and serotonin help reduce norepinephrine.

Increasing serotonin signaling also reduces dopamine signaling. If dopamine is low to begin with, this causes problems such as akathisia, agitation, insomnia, anxiety, other movement disorders, since lowering dopamine excessively will impair control over norepinephrine, causing norepinephrine to rise despite the higher serotonin signal.

I haven’t found using GABA as a supplement useful since the dose needed to have adequate blood-brain barrier penetrance is so high, adverse effects occur such as oversedation. The higher the dose, the longer the substance lasts, causing problems when higher GABA levels are not needed such as in the daytime.

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