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   **1. Sexual Function Assessment in Brain‑Tumor
   Patients**

   | Domain | What to Evaluate | Why It Matters |
   |——–|——————|—————|
   | **Physical Functioning** | • Erectile function (ED), ejaculatory issues, vaginal
   lubrication
   • Hormonal status: testosterone, estradiol, LH/FSH, prolactin | Tumors or treatment can disrupt neuro‑endocrine pathways → impotence, anorgasmia |
   | **Psychological / Cognitive Impact** | • Mood (depression/anxiety), self‑esteem, body image
   • Cognitive deficits: memory, attention, executive function | Neurocognitive decline affects
   sexual desire and performance; mood disorders further impair libido |
   | **Relationship Dynamics** | • Partner communication, intimacy expectations,
   relational satisfaction | Relationship strain can exacerbate sexual dysfunction or conversely be a
   source of support |
   | **Treatment‑Related Factors** | • Surgical side‑effects (nerve damage), radiotherapy-induced fibrosis, chemotherapy neurotoxicity
   • Hormonal therapies altering testosterone/estrogen levels |
   Physical changes directly influence sexual function; endocrine shifts alter libido
   and erectile capacity |

   —

   ## Practical Clinical Recommendations

   | Step | Action | Key Points |
   |——|——–|————|
   | 1 | **Initial Screening** | • Use brief questionnaires (e.g., PHQ‑2 for
   depression, IIEF‑5 for erectile dysfunction) at each visit.

   • Ask about sexual activity and satisfaction in a non‑judgmental way.
   |
   | 2 | **Detailed History** | • Document frequency, type of intercourse, use of lubricants/condoms, pain or dyspareunia, urinary symptoms, medication side‑effects.
   |
   | 3 | **Physical & Laboratory Review** | • Assess
   prostate size (digital rectal exam), PSA trends.

   • Check testosterone, LH/FSH if erectile dysfunction is persistent despite therapy.

   |
   | 4 | **Address Modifiable Factors** | • Encourage
   weight loss, exercise, smoking cessation.
   • Discuss sexual positioning to reduce pain for the woman. |
   | 5 | **Therapeutic Interventions** | – **Vaginal
   lubricants/creams**: non‑ionic, preservative‑free options.

   – **Topical estrogen (for post‑menopausal)**: short course if symptomatic.

   – **PDE‑5 inhibitors**: titrate dose; start low to assess tolerance.

   – **Pelvic floor physical therapy**: can improve arousal and reduce pain. |
   | 6 | **Follow‑Up Plan** | – Reassess after 4–6 weeks of PDE‑5 inhibitor use and lubricant regimen.
   – If adequate response, maintain current dosing; if insufficient,
   consider dose escalation or alternative agents (e.g., vardenafil).

   – If still inadequate, evaluate for underlying endocrine disorders or psychological factors.
   |

   —

   ## 3. Evaluation & Management of Low Testosterone in the Context of Hirsutism

   | Step | Action | Rationale |
   |——|——–|———–|
   | **Baseline labs** | • Serum total testosterone (morning 7–10 am)
   • SHBG, albumin
   • LH, FSH
   • Estradiol
   • Prostate‑specific antigen (PSA) if >50 yr or risk factors | Confirm androgen excess, rule out secondary causes.
   |
   | **Interpretation** | • Low testosterone with
   normal/low SHBG suggests primary hypogonadism
   • Elevated LH indicates primary testicular failure
   • Normal LH/FSH may indicate secondary hypogonadism (pituitary/hypothalamic) | Tailor therapy accordingly.
   |
   | **Baseline labs before therapy** | • CBC, CMP, lipid panel,
   fasting glucose, HbA1c, testosterone (morning), PSA (if >50 yr) | Establish baseline for monitoring.

   |

   —

   ## 4. Treatment Algorithm

   ### Step‑by‑Step Decision Tree

   «`
   START
   |
   |—> Check eligibility:
   • No contraindications (no severe liver disease, untreated hypertension, etc.)
   • Informed consent obtained.
   |
   |—> Baseline labs:
   • CBC, CMP, fasting lipids, fasting glucose/HbA1c, testosterone (morning), PSA (if >50).

   |
   |—> Select anabolic agent:
   |— Option A: Enobosarm (oral) – 2.5–10 mg daily
   |— Option B: SARMs via injection (e.g., Ostarine 25 mg IM weekly)
   |
   |—> Determine dosing schedule based on product availability and patient’s preference.

   |
   |—> Initiate therapy:
   |— Educate patient on potential side effects:
   • Mild liver enzyme elevations
   • Transient lipid changes (increase LDL, decrease HDL)
   • Mood alterations
   • Possible gynecomastia (rare)
   |
   |—> Monitoring plan:
   |— Baseline labs: LFTs, fasting lipids, CBC,
   testosterone levels.
   |— Repeat labs at 4–6 weeks post-initiation,
   then every 3 months.
   |— Adjust dose or discontinue if AST/ALT > 2× ULN
   or lipid abnormalities exceed thresholds.
   |
   |—> Duration:
   |— Use for the shortest effective period (e.g.,
   12–24 weeks).
   |— After completion, reassess motivation and consider alternative interventions.

   |
   |—> Safety considerations:
   |— Avoid use in individuals with uncontrolled hypertension, active liver disease,
   or those on medications metabolized by CYP3A4
   that could interact with ketone metabolism.
   |— Monitor for signs of ketoacidosis (e.g., nausea,
   vomiting, abdominal pain).
   |
   END
   «`

   **Key Points:**

   – **Ketone supplements may alter brain fuel availability and influence motivation.**
   – **Safety hinges on monitoring metabolic status
   and avoiding high‑dose or prolonged use.**
   – **A structured protocol can help balance potential benefits
   against risks for those seeking to enhance task engagement.**

   This approach offers a systematic way to evaluate whether ketone supplementation could be a viable tool for improving sustained effort in demanding cognitive
   tasks, while ensuring participant safety.

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