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Summary first published in September 2012, authored by Peter Renner and Markus Horneber
PlexusDx partners exclusively with 503A compounding pharmacies, which are state-licensed facilities regulated more stringently than larger manufacturing operations
Published human and preclinical research GHK-Cu has been investigated in both laboratory and human research for several decades
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
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& Morris, S
