Common Causes and Contributors: From Vascular to Medication Effects When I assess ED, I use a structured framework: Vascular (vasculogenic) Atherosclerosis, endothelial dysfunction, impaired NO signaling Diabetes-related microvascular disease Hypertension-related vascular remodeling Neurogenic Peripheral neuropathy (diabetes, B12 deficiency, chemotherapy) Post-surgical or post-radiation nerve injury (e.g., radical prostatectomy) Spinal stenosis, discopathy, or pelvic nerve entrapment Hormonal Low testosterone (hypogonadism): impacts libido and PDE5 responsiveness Thyroid dysfunction, hyperprolactinemia, cortisol dysregulation Aromatization and unfavorable T:E2 ratios Psychogenic Depression, anxiety, relationship stress, sexual trauma history Performance anxiety and maladaptive autonomic patterns Drug-induced Antihypertensives (e.g., beta blockers, thiazides) SSRIs/SNRIs, antipsychotics Opioids and androgen suppression Iatrogenic and trauma-related Pelvic surgeries, radiation fibrosis Pelvic fractures, lumbar/pelvic injuries Lifestyle and sleep Sedentary behavior, obesity, poor diet, alcohol use Sleep apnea (major factor in testosterone and endothelial dysfunction) Biomechanics and pain Pelvic floor hypertonicity or dyssynergia SI joint dysfunction, lumbar facet syndromes, hip pathology This framework helps us prioritize diagnostics and personalize treatment
It prevents potential tolerance development, allows your bodys natural sleep regulation to reassert itself, and helps you assess whether DSIP provided genuine benefits
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GHK-Cu may accelerate wound healing by 33%, based on preclinical wound chamber models in which the peptide produced concentration-dependent increases in dry weight, total protein, collagen, DNA, and glycosaminoglycan content
Clinical data is sparse and inconsistent
