18 replies to this topic

[metabrain]

I find that I cannot fall in love while on an antidepressant, research backs this up. I might be able to get a script for Modafinil for my sleep apnea and was wondering does Modafinil allow you to fall in love?

[maximum411]

Modafinil definitely increases my libido- I'm not sure if this would help you fall in love, but increased dopamine certainly could help.

[Junk Master]

Don't think it would help you fall in love but it wouldn't STOP you.  Also, it might give you more energy to get out there and meet new people.

 

I do think using it on a regular basis might be disruptive of sleep architecture, cause you to use more, then raise your level of anxiety, if you are prone to it, to the point where you wouldn't feel as social.

[metabrain]

I asked the question because I have been on SSRIs before and they don't allow you to fall in love since I might be perscribed Modafinil I was worried that I could not fall in love.

[Junk Master]

Long term use of SSRI'S will flatten emotions in some (most) people, and most likely will cause some sexual disfunction, like increased difficulty achieving orgasm;  but, SSRI'S really shouldn't be taken long term, or in high doses (IMO), and short term use of SSRI'S won't stop you from falling in love IF you find the right person.

[metabrain]

I have taken SSRIs for a very long time, is there any way to unflatten the emotions? I am very flat right now.

[jaiho]

Try psilocybin, LSD or MDMA to feel again.

thats the controversial way...

 

NSI-189 and moclobemide was good for emotions

[Junk Master]

In my case the emotional blunting/flattening over time caused by SSRI and SNRI drugs was reversed once I stopped taking them.  Now, I'm not suggesting anyone stop taking medication!

 

I was also luck enough to have little or no side effects upon cessation.  

[Area-1255]

I asked the question because I have been on SSRIs before and they don't allow you to fall in love since I might be perscribed Modafinil I was worried that I could not fall in love.

SSRI's generally kill your ability to feel almost all emotions - especially at high doses..long-term use is associated with deficits in amygdala function and altered limbic function...thus negatively affecting both emotional capacity and creativity...as well as cognitive function...which is why They have found that another reinforcement to this biological paradigm could theoretically be the amount of mass-shooters and other erratic incidents correlated with ONLY SSRI's and not other anti-depressants...although, some opioid analogues may indeed alter personality traits...as does Ambien and Xanax.

 

I would try adding modafanil with a combination of Aswagandha day and night. 

Also using N-Acetyl-L-Tyrosine may help.

[A Better World]

It is only possible to fall in love on Modafinil if both of you are on Modafinil at the time. :-)

[BetelgeuseA]

Yes, it's possible to fall in love when on Modafinil, but it would be harder/rarer than falling in love when sober. As your body is almost in a fight-or-flight condition.

Modafinil does work as a weak Dopamine Reputake Inhibitor, it's harder to fall in love when on DRI's because you wont be as rewardseeking as you would've been if you weren't on them.
But Modafinils main mechanism of action is thought to be on Histamine, which is a important neurotransmitter in the Sleep-Wake regulation, which explains its eugeroic effects.
Histamine is also released during stress, along with epinephrine, which is also a transmitter which Modafinil works on. And logically, the eugeroic effects might alleviate the stress-response from the body even more.

 

[jaiho]

I was under the impression that you need dopamine to fall in love.
I haven't been able to have strong emotions ever since i went on an ssri, which tells me excess serotonin kills love, since it's suppressing dopamine

[Area-1255]

I was under the impression that you need dopamine to fall in love.
I haven't been able to have strong emotions ever since i went on an ssri, which tells me excess serotonin kills love, since it's suppressing dopamine

Excess serotonin not only suppresses feelings of love, but also pretty much all other emotions - including, empathy, motivation, desire, fear and etc

Elevated serotonin turns you into an obsessive-compulsive delirious bastard if you don't watch. 

Also too much serotonin tends to mess with your heart rate; dropping it through the floor or raising it through the roof..both of which cause issues with oxygen saturation and delivery.. which explains why serial murder's have been found to have either high or low serotonin; depending on the type...impulsive aggressors fit the former whereas calculating, cold-blooded offenders fit the latter (elevated serotonin).

Also those with erotomania / obsessive love disorders tend to have either very high or very low serotonin...with more emphasis on the former.

This may seem controversial but even though serotonin DULLS emotions it also reformulates them into repetitive thoughts...so as a result they are less balanced. 

 

Erotomania induced by venlafaxine: a case study

 

Social Anxiety Disorder Linked to High Serotonin Levels, Throwing Treatment with SSRIs into Serious Question
Symptoms / Signs of Too Much Serotonin / Excess Serotonin

 

Eat Weight Disord. 2002 Sep;7(3):221-31.

Is there a common mechanism of serotonin dysregulation in anorexia nervosa and obsessive compulsive disorder?

Barbarich N1.

Author information

 

Abstract

Numerous studies have documented increased rates of comorbidity in patients with anorexia nervosa (AN) or obsessive compulsive disorder (OCD). The interaction of many possible factors influences this comorbidity, but one possible explanation involves the neurotransmitter serotonin, which is widely distributed in the brain and has been implicated in a number of psychological behaviours. Although low serotonin levels have been found in patients with impulsive and aggressive behaviour, high levels have been correlated with obsessive and compulsive behaviour. In an attempt to further our understanding of this relationship, a large number of studies have measured serotonin levels throughout different stages of illness in both AN and OCD; furthermore, serotonin challenge studies and drug treatment trials have provided further support for this theory. This paper discusses the evidence supporting the view that the obsessive behaviour characteristic of AN and OCD may be partially due to a dysregulation in the serotonergic system.

PMID:   12452254   [PubMed - indexed for MEDLINE]  

 

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Edited by Area-1255, 19 September 2015 - 03:41 AM.

[jaiho]

What i don't get with that high serotonin theory, is that, while on an SSRI, such as fluoxetine, i feel better.

But when i come off the SSRI, my baseline has changed. Before i ever touched an SSRI, i could feel sad/happy etc. My depression was more sadness than numbness.

 

After SSRIs, i can never get back to that happy/sad state.

 

It's like SSRI's have permanently done something to my brain where it's stuck in some feedback loop, like the presynaptic 5HT1A auto receptor perhaps.

 

I wish i would have never touched an SSRI and just tried to resolve the depression another way.

[metabrain]

What i don't get with that high serotonin theory, is that, while on an SSRI, such as fluoxetine, i feel better.

But when i come off the SSRI, my baseline has changed. Before i ever touched an SSRI, i could feel sad/happy etc. My depression was more sadness than numbness.

 

After SSRIs, i can never get back to that happy/sad state.

 

It's like SSRI's have permanently done something to my brain where it's stuck in some feedback loop, like the presynaptic 5HT1A auto receptor perhaps.

 

I wish i would have never touched an SSRI and just tried to resolve the depression another way.

 

I got that recently with Lexapro and I get that with almost every SSRI but when I took the SNRI Venlafaxine for 1 day I only the next day my emotions were all back to normal in fact I started crying and started getting anxious the way I used to, I notice that I get the same way on green tea pills so I have to stay away from them, my guess is that my Norepinephrine levels get down regulated when I take an SSRI. My psychiatrists said to me that most people who feel flat on an SSRI feel more normal on an SNRI, we could probably ask around to see do other peoples emotions also return to normal like mine did switching from the SSRI to SNRI.

 

I am betting most people who get like that would benefit from a Triple Reuptake Inhibitor which would balance everything out a little better but that is just my guess.

[Area-1255]

What i don't get with that high serotonin theory, is that, while on an SSRI, such as fluoxetine, i feel better.

But when i come off the SSRI, my baseline has changed. Before i ever touched an SSRI, i could feel sad/happy etc. My depression was more sadness than numbness.

 

After SSRIs, i can never get back to that happy/sad state.

 

It's like SSRI's have permanently done something to my brain where it's stuck in some feedback loop, like the presynaptic 5HT1A auto receptor perhaps.

 

I wish i would have never touched an SSRI and just tried to resolve the depression another way.

When serotonin's autoreceptors are desensitized - it leads to floods of serotonin to other receptors; inhibiting a plethora of other neurotransmitters which then equates to anhedonia, lack of emotional capacity, pleasure etc... additionally, excess serotonin leads to cortisol excess so going off an SSRI - your first step should be to immediately get on both an anti-cortisol and anti-prolactin agent. Next, one should resensitize DA systems and the autoreceptors...so Curcumin/Turmeric extract plus Ginkgo biloba would be a good idea.

[jaiho]

Do you think those herbs will be strong enough to reverse damage? Most substances i take don't touch the issue at all. Getting any kind of euphoria is impossible, the closest would be taking hallucinogens for some kind of pre anhedonia feeling

[Area-1255]

Do you think those herbs will be strong enough to reverse damage? Most substances i take don't touch the issue at all. Getting any kind of euphoria is impossible, the closest would be taking hallucinogens for some kind of pre anhedonia feeling

It's gonna take a while to reverse the damage - it took me about 3 months to feel right again. And that was after hardcore augmentation. Mianserin could help. If you can get your hands on a legitimate source of it - that would tip the scale in the best direction. 

 

Then use that with a dopamine reuptake inhibitor; preferably something pure DRI. 

9-methyl-beta-carboline can help regenerate dopamine networks in addition to the above.

[gamesguru]

Area, are you suggesting ginkgo/ginseng/shilajit/yohimbe are selective to autoreceptors?

 

for various reasons, most selective 5-HT_1A agonists developed so far have failed to demonstrate clinical effectiveness. Indeed, the clinical effectiveness and use of the only marketed compound of this class (buspirone) is very far from that of other antidepressants, despite claims in favour of the use of 5-HT_1A agonists.⁵ On the other hand, presynaptic 5-HT_1A autoreceptors are a primary target of several types of antidepressant drug that enhance extracellular 5-HT (SSRIs, MAOIs) or act directly on such receptors.Ideally, new antidepressant drugs should be targeted at the postsynaptic receptor(s) or intracellular signalling pathways responsible for the therapeutic effects of existing drugs. In this way, they would overcome the neuronal adaptive mechanisms (both presynaptic and postsynaptic) that delay and limit their therapeutic action.

 

Ginkgo also antagonizes glycine, NMDA, and GABA_A.^[1]

"Of the three main Ginkgo biloba extract constituents, the PP (flavonoid) fraction caused a significant (and most pronounced) increase in brain dopamine levels, whereas ginkgolides had only a moderate and bilobalides no effect (Yoshitake et al. 2010). The observed effects appear not to depend on the activity of monoamine oxidases (MAO-A and MAO-B)"

"flavonol glycosides and, to a lesser extent, the ginkgolide fractions were the main components contributing to the observed effects of the EGb 761 extract on the [PFC] dopamine levels"

---

also Area, this study isn't on your website, afaik

Stress-induced 5-HT1A receptor desensitization: protective effects of Ginkgo biloba extract (EGb 761).

 

 Effect of modafinil on learning performance and neocortical long-term potentiation in rats.
Modafinil is a novel wake-promoting agent whose effects on cognitive performance have begun to be addressed at both preclinical and clinical level. The present study was designed to investigate in rats the effects of chronic modafinil administration on cognitive performance by evaluating: (i) working and reference memories in an Olton 4×4 maze, and (ii) learning of a complex operant conditioning task in a Skinner box. In addition, the effect of modafinil on the ability of the rat frontal cortex to develop long-term potentiation (LTP) was also studied. Chronic modafinil did not significantly modify working memory errors but decreased long-term memory errors on the Olton 4×4 maze, meaning that the drug may have a favourable profile on performance of visuo-spatial tasks (typically, a hippocampus-dependent task) when chronically administered. On the other hand, chronic modafinil resulted in a marked decrease of successful responses in a complex operant conditioning learning, which means that repeated administration of the drug influences negatively problem-solving abilities when confronting the rat to a sequencing task (typically, a prefrontal cortex-dependent task). In addition, in vivo electrophysiology showed that modafinil resulted in impaired capacity of the rat prefrontal cortex to develop LTP following tetanization. It is concluded that modafinil can improve the performance of spatial tasks that depend almost exclusively on hippocampal functioning, but not the performance in tasks including a temporal factor where the prefrontal cortex plays an important role. The fact that modafinil together with preventing operant conditioning learning was also able to block LTP induction in the prefrontal cortex, suggests that the drug could interfere some critical component required for LTP can be developed, thereby altering neuroplastic capabilities of the prefrontal cortex.