Sexual wellbeing is part of overall wellbeing. It is not a luxury or frivolous and the fact that it is routinely left out of medication counseling, or left somewhere in the fine print, in that tiny font nobody reads, is really a failure of care.
If your desire has shifted, your arousal has changed, your body isn’t responding the way it used to, or intimacy has become uncomfortable or emotionally flat since starting a medication, you are not imagining it. And the odds are good that nobody told you this might happen!
Research confirms that medications play a significant and frequently underacknowledged role in sexual function, and understanding the mechanisms by which they affect sexual health is essential for improving quality of life. Yet fewer than a quarter of patients are ever proactively asked about sexual side effects by their prescribing provider.
This post is the start of that conversation you should have been offered. We’re going to cover a wide range of medications, prescription and over-the-counter, looking at what they are, why they affect sexual wellbeing physiologically, and what can actually be done about it. We’ll cover everything from the commonly discussed (SSRIs, beta blockers) to the ones that almost never come up in these conversations (antihistamines, proton pump inhibitors, hair loss medications, and more), but may be prescribed to manage chronic conditions.
An important note before we begin: I am not a physician or pharmacist. Everything in this post is educational information, not medical advice. Please do not adjust or discontinue any medication based on this post alone. Please have that conversation with your prescribing provider. What I hope this post gives you is the language, knowledge, and confidence to have it.
Before we get into specific medications, it helps to understand the main ways that drugs can impact sexual function. Most medication-related sexual side effects fall into one or more of these categories:
Hormonal disruption: Many medications suppress, mimic, or compete with sex hormones, including testosterone, estrogen, and progesterone. Since these hormones play central roles in desire, arousal, tissue health, and physical response, disrupting them has downstream effects.
Neurotransmitter interference: Sexual desire and arousal are regulated significantly by dopamine (associated with wanting and motivation) and modulated by serotonin. Medications that increase serotonin or decrease dopamine availability can dampen desire and delay or prevent orgasm. Histamine also plays a role in sexual arousal, lubrication, and erection.
Vascular and circulatory effects: Arousal in all bodies depends on increased blood flow to the genital tissue. Medications that affect circulation, blood pressure, or vascular tone can impair this process, affecting arousal, erection, lubrication, and sensation.
Anticholinergic effects: Some medications block acetylcholine, a neurotransmitter involved in the nervous system’s “rest and digest” functions, which includes the parasympathetic response that drives physical arousal. These drugs also cause systemic dryness throughout the body, including in the intimate tissue.
Central nervous system depression: Medications that slow the CNS can blunt the physiological and psychological responsiveness that arousal requires.
Elevated prolactin: Some medications increase prolactin (the hormone associated with milk production). Elevated prolactin directly suppresses testosterone and estrogen, reducing desire and impairing sexual function across all genders.
With that framework in place, let’s get into the medications!
Selective serotonin reuptake inhibitors, SSRIs, and their close relatives, serotonin-norepinephrine reuptake inhibitors (SNRIs), are among the most frequently prescribed medications and among the most thoroughly documented causes of sexual dysfunction.
A 2024 study analyzing data from the WHO’s global database of individual case safety reports confirmed high disproportional reporting of sexual dysfunction, particularly with SSRIs and SNRIs, across the categories of desire, arousal, and orgasm.
How they affect sexual well-being: SSRIs work by increasing serotonin availability. While this is beneficial for depression and anxiety, elevated serotonin has an inhibitory (dampening) effect on dopamine pathways. Dopamine is critically involved in desire, motivation, and the reward experience of sexual pleasure. Elevated serotonin can also stimulate prolactin production, further suppressing testosterone and estrogen, compounding the effect. Additionally, SSRIs affect peripheral nervous system function in ways that can impair genital sensitivity and the orgasmic response. Also, some SSRIs inhibit nitric oxide which aids in relaxing the muscles and promoting genital blood flow.
What this looks like: Decreased libido (sometimes dramatically so), difficulty with physical arousal, reduced genital sensation, delayed orgasm, absent orgasm (anorgasmia), and what many describe as emotional or sexual “flatness,” feeling present but not particularly interested or responsive. This is sometimes called SSRI anorgasmia or Post-SSRI Sexual Dysfunction (PSSD) when it persists after discontinuation. PSSD can last for years or be permanent.
Common culprits: Fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), escitalopram (Lexapro), citalopram (Celexa), venlafaxine (Effexor), duloxetine (Cymbalta).
Lower-risk alternatives: Bupropion (Wellbutrin), Viibryd (vilazodone), and mirtazapine (Remeron) are consistently noted in the literature as having significantly lower rates of sexual side effects. Bupropion/Wellbutrin in particular is sometimes added alongside an SSRI specifically to counteract sexual side effects.
The relational impacts: This side effect carries a particular relational cost. When someone’s desire disappears after starting an antidepressant and nobody told them it might, they often internalize it as a personal failure, and their partner may interpret the withdrawal as rejection.
Older classes of antidepressants, tricyclics like amitriptyline (Elavil), imipramine (Tofranil), and nortriptyline (Pamelor), and monoamine oxidase inhibitors (MAOIs) like phenelzine (Nardil), also carry significant sexual side effects through similar serotonergic mechanisms. Moreover, some antidepressants have anticholinergic effects, meaning they disrupt the neurotransmitter acetylcholine. This interferes with the parasympathetic nervous system, which aids in arousal, blood flow, and lubrication, sometimes causing erectile dysfunction, vaginal dryness, and reduced sexual desire. The overall sexual side effect burden with TCAs can be similar to or greater than SSRIs.
Antipsychotics are strongly associated with sexual dysfunction as well.
How they affect sexual well-being: Antipsychotics primarily work by blocking dopamine receptors, and as established above, dopamine is central to desire and pleasure of sexual experience. Block dopamine and you blunt wanting. Additionally, by suppressing dopamine, antipsychotics significantly raise prolactin levels, which in turn suppresses testosterone and estrogen across all genders. Research published in multiple reviews confirms that psychiatric medications alone account for nearly 40% of all reported erectile dysfunction cases.
What this looks like: Significantly decreased libido, difficulty with arousal, erectile dysfunction, delayed or absent orgasm, reduced genital sensation, and vaginal dryness.
Common culprits: Haloperidol (Haldol), risperidone (Risperdal), olanzapine (Zyprexa), quetiapine (Seroquel), aripiprazole (Abilify — tends to have a lower prolactin-raising profile), thioridazine (Mellaril).
Second-generation vs. first-generation: Atypical antipsychotics generally have a more balanced neurotransmitter profile and may cause less severe sexual side effects, but they are not free of them. Aripiprazole and quetiapine tend to have lower rates of sexual dysfunction relative to risperidone.
Beta blockers are widely used for hypertension, POTS, dysautonomia, migraines, heart conditions, and anxiety. They work by blocking the body’s adrenaline response, slowing heart rate and reducing blood pressure.
How they affect sexual well-being: The same mechanism that makes beta blockers therapeutically useful, calming the cardiovascular response, also dampens the physiological arousal response. Physical sexual arousal involves increased heart rate, elevated blood pressure, and increased blood flow to genital tissue. Beta blockers can reduce all of these. Older, non-selective beta blockers also affect hormone levels and may reduce testosterone. Additionally, the fatigue and emotional blunting that some people experience on beta blockers can indirectly reduce interest in intimacy.
What this looks like: Reduced physical arousal response, erectile dysfunction, reduced lubrication, decreased desire, and sometimes a general feeling of emotional flatness and fatigue that affects intimacy.
Common culprits: Propranolol (Inderal), metoprolol (Lopressor), atenolol. Newer medications like nebivolol may have a more favorable sexual side effect profile due to their nitric oxide-releasing properties.
Thiazide diuretics (like hydrochlorothiazide) show mixed evidence regarding sexual function but have been associated with erectile dysfunction (particularly at higher doses). Spironolactone, a diuretic with anti-androgenic properties, can significantly reduce testosterone levels in all bodies, affecting desire and function. This is also why it’s used in gender-affirming hormone therapy for trans women, and conditions like PCOS.
Centrally acting antihypertensives like methyldopa (less commonly used today) have documented associations with sexual dysfunction through central nervous system effects.
What this looks like: Reduced testosterone, decreased libido, erectile dysfunction, reduced lubrication, fatigue affecting sexual interest.
Chronic opioid use is associated with opioid-induced endocrinopathy, a disruption of the hormonal system caused by opioids’ effect on the Hypothalamic-Pituitary-Gonadal (HPG) axis.
How they affect sexual well-being: Opioids suppress the release of gonadotropin-releasing hormone (GnRH), which cascades into reduced production of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which in turn suppresses testosterone and estrogen production in the gonads. The result can be low sex hormone levels across all genders, with predictable effects on desire, arousal, and physical responses. Opioids also affect central dopamine signaling, the pleasure pathways, and can cause fatigue and sedation that further reduces sexual interest.
What this looks like: Decreased libido, reduced arousal, erectile dysfunction, anorgasmia or delayed orgasm, vaginal dryness, reduced genital sensitivity, and fatigue.
Common culprits: Oxycodone (OxyContin, Percocet), hydrocodone (Vicodin), codeine, tramadol, morphine, fentanyl. Even lower-dose opioids used for chronic pain management can affect the HPG axis over time.
For many people with chronic pain, opioids are necessary for managing conditions that themselves interfere with intimacy. The medication adds another layer to an already complex picture.
This category deserves particular attention because the sexual side effects of hormonal birth control are both well-documented in research and dramatically underreported in clinical conversations, particularly with people being prescribed these medications at young ages without any discussion of potential impact on desire or sexual function.
How they affect sexual wellbeing: Combined oral contraceptives (COCs) affect sexual function through two primary mechanisms. First, the synthetic estrogen in oral contraceptives significantly increases production of sex hormone-binding globulin (SHBG), a protein that binds testosterone and renders it biologically unavailable. Second, the hormones in oral contraceptives suppress ovarian androgen production. The combined effect is a significant reduction in free testosterone in all bodies with ovaries.
Research is nuanced. While most people taking combined oral contraceptives (COCs) do not experience changes in sex drive, a notable minority report a decline.
A concerning finding from research published in The Journal of Sexual Medicine: in people with sexual dysfunction who had used oral contraceptives, elevated SHBG levels did not return to normal after discontinuing the pill, suggesting that for some individuals, effects on hormones may persist after stopping the medication.
Beyond libido, the estrogen-dominant hormonal environment of some contraceptives can reduce blood flow to genital tissue, decrease nerve sensitivity, cause vaginal dryness, and affect arousal response.
What this looks like: Decreased desire, reduced genital sensitivity, vaginal dryness, reduced arousal, and in some cases pain during sex due to tissue changes.
Common culprits: Combined oral contraceptive pills (all brands using synthetic estrogen + progestin), hormonal patches (Xulane), vaginal ring (NuvaRing). Progestin-only options (mini pill, Depo-Provera, Nexplanon implant) have less impact on SHBG and free testosterone, though Depo-Provera and some progestin-only pills can reduce estrogen levels by suppressing ovulation, which affects lubrication and tissue health.
What about IUDs: Hormonal IUDs (Mirena, Kyleena, etc.) deliver progestin locally to the uterus with minimal systemic absorption, meaning their effect on overall hormone levels and sexual function is significantly lower than systemic hormonal methods.
This is one of the most overlooked categories of medications that impact sexual functioning. Medications like diphenhydramine (Benadryl), loratadine (Claritin), cetirizine (Zyrtec), and fexofenadine (Allegra) are taken by millions of people, often daily, for allergy management, but it’s not very well known that they might affect sexual function.
How they affect sexual well-being: Histamine plays a role in sexual arousal, erection, and genital vasodilation. When antihistamines block histamine receptors throughout the body, they interfere with this process. Some antihistamines also reduce testosterone levels and raise prolactin. First-generation antihistamines (diphenhydramine, chlorpheniramine, hydroxyzine) have significant anticholinergic effects, causing systemic dryness, including dryness of mucous membranes in intimate tissue, and sedation that reduces responsiveness. Cimetidine (Tagamet), an H2 receptor blocker used for heartburn, has anti-androgenic properties and has been linked to reduced testosterone and sexual dysfunction.
What this looks like: Vaginal dryness causing painful sex, reduced arousal response, decreased desire, drowsiness reducing interest in intimacy, and in people with penises, erectile difficulties.
Common culprits: Diphenhydramine (Benadryl, Unisom, ZzzQuil), chlorpheniramine (Chlor-Trimeton), hydroxyzine (Vistaril, Atarax), cimetidine (Tagamet), ranitidine (Zantac), loratadine (Claritin), cetirizine (Zyrtec), dimenhydrinate (Dramamine), meclizine (Antivert/Bonine). Fexofenadine (Allegra) is generally noted as having the least impact on sexual function among the second-generation antihistamines, as it does not cross the blood-brain barrier and has fewer anticholinergic effects.
Gabapentin (Neurontin) and pregabalin (Lyrica) are used for neuropathic pain, fibromyalgia, epilepsy, anxiety, and frequently prescribed off-label for a wide range of pain and psychiatric conditions.
How they affect sexual well-being: Gabapentin is hypothesized to cause sexual dysfunction through central inhibitory effects on neurotransmission, effectively dampening the neural signaling involved in arousal and orgasm.
For pregabalin, a clinical study found that sexual dysfunctions occurred in 41.33% of patients, including erectile dysfunction (51.61% of those affected), anorgasmia (32.26%), and loss of libido (35.48%). Notably, these effects were not dose-dependent and occurred even at low therapeutic doses.
What this looks like: Anorgasmia or significantly delayed orgasm (particularly in people with vulvas), loss of libido, erectile dysfunction, anejaculation (inability to ejaculate), and reduced genital sensation. These effects are generally reversible upon discontinuation, but can be distressing while occurring.
Common culprits: Gabapentin (Neurontin, Gralise, Horizant), pregabalin (Lyrica).
Benzodiazepines, used for anxiety, sleep, seizures, and muscle relaxation, are associated with sexual dysfunction through CNS depression and their effects on hormone production.
How they affect sexual well-being: Benzodiazepines enhance GABA, an inhibitory neurotransmitter, producing sedation and anxiolytic effects throughout the nervous system. This same CNS depression can blunt arousal responsiveness, reduce desire, and impair physical sexual function. Research has also linked benzodiazepines to decreased libido and erectile dysfunction. The sedation and emotional blunting associated with benzos can also reduce relational engagement and interest in intimacy.
What this looks like: Reduced desire, difficulty with arousal, erectile dysfunction, anorgasmia, general fatigue, and sedation reducing interest in intimacy.
Common culprits: Diazepam (Valium), lorazepam (Ativan), clonazepam (Klonopin), alprazolam (Xanax), temazepam (Restoril).
How they affect sexual well-being: Finasteride (Propecia, Proscar) and dutasteride (Avodart) work by inhibiting the enzyme that converts testosterone to dihydrotestosterone (DHT). DHT plays important roles in sexual function, genital tissue sensitivity, and libido. Blocking its production can have significant downstream effects on sexual function and neurological response.
A study published in the Journal of Sexual Medicine by Dr. Michael Irwig of George Washington University documented striking findings in otherwise healthy men aged 21–46 who took finasteride for hair loss: 94% developed low libido, 92% developed erectile dysfunction, 92% experienced decreased arousal, and 69% had problems with orgasm. Perhaps most concerning, the mean duration of sexual side effects was 40 months after discontinuation of the drug.
It is important to note that the research on finasteride’s sexual side effects is genuinely mixed; some large controlled surveys find no significant difference in sexual dysfunction between finasteride users and non-users. The nocebo effect (experiencing symptoms because you expect them) may explain some reported cases. However, given the severity of effects reported in a subset of users, particularly the persistence after discontinuation, this is a conversation worth having proactively before starting the medication.
What this looks like: Decreased libido, erectile dysfunction, reduced arousal, anorgasmia, ejaculatory dysfunction, and in some cases depression and cognitive changes. In a subset of users, effects may persist long after stopping the medication (sometimes referred to as Post-Finasteride Syndrome, though this remains an area of ongoing research).
Widely used for autoimmune conditions including lupus, multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, and chronic inflammatory conditions, corticosteroids and immunosuppressants carry several mechanisms of impact on sexual well-being.
How they affect sexual wellbeing: Long-term corticosteroid use (like prednisone) can suppress the hypothalamic-pituitary-adrenal axis, affecting sex hormone production. Steroids also cause significant body changes over time that can profoundly affect body image and how someone feels about intimacy. Immunosuppressants used in transplant or autoimmune management can cause fatigue, hormonal disruption, and mood effects that ripple into intimate life.
What this looks like: Decreased libido, body image distress affecting desire for intimacy, fatigue reducing interest in and capacity for intimacy, mood changes (including irritability, depression) that create relational strain, and in some cases direct hormonal effects on desire and arousal.
Chemotherapy agents can affect sexual well-being through multiple simultaneous mechanisms, yet are frequently under-addressed in oncology care. Research notes that decreased libido is a frequent complication of chemotherapy, along with impaired arousal (frequently due to vaginal dryness), dyspareunia (painful sex), and difficulties reaching orgasm.
How they affect sexual wellbeing: Chemotherapy drugs can damage ovarian and testicular function, leading to premature menopause or hypogonadism and the associated hormonal changes. They can cause peripheral nerve damage affecting genital sensation. They cause profound fatigue. Radiation therapy can damage vascular and nerve tissue. Hormonal cancer treatments work directly by suppressing sex hormone production, with significant effects on desire, tissue health, lubrication, arousal, and function.
What this looks like: Vaginal dryness and atrophy causing painful sex, erectile dysfunction, loss of desire, anorgasmia, fatigue, body image changes from cancer treatment, and the psychological weight of a life-altering diagnosis.
While antibiotics don’t directly cause sexual dysfunction through hormonal or neurological mechanisms, they carry an indirect impact.
How they affect sexual well-being: Antibiotics disrupt the microbiome throughout the body, including the vaginal microbiome. This disruption may result in vaginal yeast infections or bacterial vaginosis, both of which cause discomfort, odor, discharge, and pain that can make intimacy uncomfortable or impossible during treatment and recovery. Frequent antibiotic use can create a cycle of recurrent infections that may affect intimate life. Some people experience mood and physical changes with certain antibiotics (metronidazole, for example, can cause nausea, metallic taste, and mood effects) that indirectly affect intimacy.
Proton pump inhibitors, like omeprazole (Prilosec), pantoprazole (Protonix), lansoprazole (Prevacid), and esomeprazole (Nexium), are among the most commonly used medications in the world for acid reflux and GERD.
How they affect sexual well-being: Long-term PPI use has been associated with magnesium deficiency, which affects muscle function, mood, and energy. PPIs can also reduce the absorption of zinc, which plays a role in testosterone production. Some research has noted associations between long-term PPI use and reduced testosterone levels, though this is an emerging rather than fully established area. Additionally, PPIs interact with the H2 receptor system, and as noted in the antihistamine section, H2 receptor activity is involved in sexual arousal.
Lithium (used for bipolar disorder) and anticonvulsant medications used as mood stabilizers, including valproate (Depakote), carbamazepine (Tegretol), and lamotrigine (Lamictal), have varying effects on sexual function.
Lithium has been associated with decreased libido, erectile dysfunction, and delayed orgasm. Valproate and carbamazepine affect sex hormone metabolism through cytochrome P450 pathways, which can alter testosterone and estrogen levels. Lamotrigine generally has a more favorable sexual side effect profile relative to other anticonvulsants.
Non-steroidal anti-inflammatory drugs, ibuprofen (Advil, Motrin), naproxen (Aleve), aspirin, and prescription NSAIDs are taken by enormous numbers of people for pain and inflammation.
How they affect sexual well-being: NSAIDs inhibit prostaglandin synthesis and prostaglandins play a role in penile erection and vaginal lubrication. Research confirms a possible link that NSAIDs can contribute to erectile dysfunction through vascular effects and hormonal pathways. Chronic NSAID use has been associated with reduced testosterone production.
What this looks like: Reduced arousal, erectile difficulties, decreased libido, and potentially reduced lubrication.
Decongestants like pseudoephedrine (Sudafed) and phenylephrine work by constricting blood vessels to reduce nasal congestion. This same vasoconstrictive mechanism reduces blood flow to genital tissue, which is the opposite of what arousal requires.
How they affect sexual well-being: By narrowing blood vessels systemically, decongestants can impair the engorgement and lubrication responses that are part of physical arousal. In people with penises, this can contribute to erectile difficulties. This is generally a short-term effect during active use rather than a long-term concern with occasional use.
Many people worry about being dismissed or seeming like they’re complaining about something trivial compared to the condition being treated. It is not trivial! Your sexual well-being is part of your quality of life, and prescribers who are doing their jobs well want to know about this.
Useful language: “Since starting [medication], I’ve noticed a significant change in my [desire/ability to become aroused / ability to orgasm/comfort during intimacy]. It’s affecting my quality of life and my relationship. I’d like to talk about my options.”
Options your provider might explore include: dose adjustment (sometimes a lower dose maintains therapeutic benefit with fewer sexual side effects), switching to a similar medication that has a more favorable sexual side effect profile, adding an adjunctive medication (such as bupropion to counteract SSRI-induced sexual dysfunction), or exploring whether a different treatment modality is appropriate.
Please do not stop or reduce a medication without discussing it with your prescriber first.
If you’re experiencing dryness, it is treatable! Vaginal dryness caused by antihistamines, hormonal contraceptives, chemotherapy, or other medications doesn’t have to be pushed through. Pushing through painful intimacy creates avoidance and relational strain. Quality lubricants, both water-based and silicone-based, are legitimate medical and pleasure tools. For longer-term vaginal dryness from hormonal causes, vaginal moisturizers used regularly (not just during intimacy) can help maintain tissue health. Localized vaginal estrogen (available by prescription) is another option for those experiencing tissue atrophy, including people who cannot use systemic estrogen.
For reduced sensation, extending the time spent in arousal, exploring different kinds of stimulation, and using adaptive tools can all help find pleasure pathways that are still available even when medication has altered the usual response.
In the absence of information, partners often interpret changes in desire, withdrawal from intimacy, or altered responsiveness as personal rejection. Naming what’s happening, like “I think my medication is affecting my desire,” can fundamentally change the relational dynamic.
This conversation is often easier with some preparation and support. If you’re not sure how to start it, that’s exactly the kind of thing I can help with. Get in contact here or check out my FREE Communication E-book here.
When certain kinds of intimacy are off the table, temporarily or for a longer stretch, this doesn’t mean intimacy itself is gone. Connection, closeness, pleasure, and physical affection can take many forms that don’t depend on the same desire baseline or physical response that medication may be affecting. It can be life-changing to build an intimate life that is accessible to the body and nervous system you have right now. My Everything But: The Redefining Intimacy Menu exists specifically for this. Check it out here!
While medication effects are physiological and not always fixable by lifestyle alone, certain practices can support the overall environment: regular physical activity as able, adequate sleep, stress management, nutrition, and avoiding excess alcohol and tobacco.
Finding a practitioner who genuinely understands the intersection of medication, chronic illness, disability, and sexuality is worth the search.
Sometimes the medication that affects your sexual well-being is also the medication that is giving you your life back.
You cannot have a vibrant, intimate life if you are in the depths of a depressive episode that makes getting out of bed feel impossible. You cannot experience desire if untreated anxiety is keeping your nervous system in a constant state of threat response. You cannot be present with a partner when unmanaged pain is consuming you. You cannot sustain relationships when an autoimmune flare has you bedridden.
The antidepressant that has flattened your libido may also be the thing that got you back to yourself. The pain medication that affects your desire may be the only thing making your daily life livable. The hormonal treatment that’s causing dryness may be managing a condition that would otherwise be disabling.
This is not a reason to accept sexual side effects without exploration; there are often options, adjustments, and supportive strategies that can help, but it is a reason to hold this conversation with compassion for yourself and the complex reality of managing health with imperfect tools.
Here is a quick reference for the medication categories covered in this guide and their primary mechanisms of sexual impact:
| Medication Category | Primary Sexual Impact |
|---|---|
| SSRIs / SNRIs | ↓ Libido, delayed/absent orgasm, ↓ arousal via serotonin-dopamine balance |
| Tricyclics / MAOIs | ↓ Libido, anorgasmia, dryness, ↓ arousal |
| Antipsychotics | ↓ Testosterone, ↓ libido, and erectile difficulties |
| Beta blockers | ↓ Physical arousal response, erectile difficulties, fatigue |
| Diuretics (esp. spironolactone) | ↓ Testosterone, ↓ libido, erectile difficulties |
| Opioids | ↓ Testosterone/estrogen, ↓ libido, anorgasmia |
| Hormonal contraceptives | ↑ SHBG → ↓ free testosterone, dryness, ↓ sensitivity |
| Antihistamines (H1 + H2) | Dryness, ↓ arousal, sedation |
| Gabapentin / Pregabalin | ↓ Libido, ↓ arousal, sedation, and erectile difficulties |
| Benzodiazepines | ↓ Sex hormones, body image effects, fatigue, and mood changes |
| Finasteride / Dutasteride | ↓ DHT → ↓ libido, erectile dysfunction, ↓ sensitivity |
| Corticosteroids | ↓ Sex hormones, body image effects, fatigue, mood changes |
| Chemotherapy | Premature menopause/hypogonadism, nerve damage, dryness, fatigue |
| NSAIDs | ↓ Prostaglandins → ↓ arousal/lubrication, possible ↓ testosterone |
| Decongestants | Vasoconstriction → ↓ engorgement, erectile difficulties |
| Antibiotics | Microbiome disruption → infections causing pain with intimacy |
| Mood stabilizers/anticonvulsants | ↓ DHEA and sex hormone metabolism (carbamazepine, valproate) |
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About the Author: Byrd from Inclusive Intimacy with Byrd
Byrd is a certified sexuality educator and sex and relationship practitioner specializing in inclusive intimacy for diverse individuals and partnerships, including disabled, chronically ill, neurodivergent, and LGBTQIA2S+ communities. Byrd is the founder of Inclusive Intimacy with Byrd, a sex and relationship virtual, international practice.
Byrd holds professional training and credentials from the American Association of Sexuality Educators, Counselors and Therapists (AASECT), the Gottman Institute, the Sexual Health Alliance (SHA), the Institute for Sexuality Education and Enlightenment (ISEE), and the American Board of Sexology (ABS). Their work is rooted in disability justice, neurodiversity affirmation, queer and trans liberation, and trauma-informed care.
Byrd works with individuals and partnerships navigating intimacy and relationships across a wide range of experiences, including chronic illness and disability like ME/CFS, long covid, POTS, and hEDS, neurodivergence like ADHD and autism, LGBTQIA+ identities, non-monogamy, and more. Their approach draws on sex positivity, the Gottman method, CBT, DBT, somatic work, parts work, mindfulness, and attachment theory.
🌿 Learn more at InclusiveIntimacyWithByrd.com | Follow on Instagram @InclusiveIntimacyWithByrd
