on July 28, 2026
The semiotic observation of the patient reveals a complex network of correlations between peripheral manifestations and alterations in visceral or endocrine homeostasis. Chromatic and structural variations in the periocular region, skin, and subcutaneous tissue do not represent mere aesthetic issues, but true biological markers.
Hyperpigmentations and swellings of the periorbital area, commonly referred to as deep dark circles, may be caused by fluid retention due to impaired glomerular filtration or systemic sensitization phenomena related to intestinal parasites [1]. Similarly, marked skin pallor points toward blood count alterations of a martial basis (iron-deficiency anemia), while acneiform lesions reflect the response of the pilosebaceous unit to androgen fluctuations or conditions of ovarian dysfunction, such as Polycystic Ovary Syndrome (PCOS) [2].
Extending the analysis to anthropometry and the distribution of adiposity, the morphological picture directly reflects the prevailing metabolic and neuroendocrine setup. Mapping adipose deposits allows for the identification of specific functional biomorphotypes related to the hypothalamus-pituitary-adrenal axis or hepatic clearance.
The Hypercortisolic Biomorphotype ("Cocomero"): HPA Axis Pathophysiology and Integrated Modulation
The biomorphotype characterized by central abdominal fat accumulation and concomitant muscle atrophy of the limbs reproduces the clinical phenotype of chronic hypercortisolism or Cushing's Syndrome [3]. Within the framework of integrated constitutional systems, such as the Rimodrena system, this conformation is identified as the "Cocomero" type.
Endocrine-Metabolic Mechanisms
Prolonged cortisol secretion by the adrenal cortex alters the regulation of the hypothalamus-pituitary-adrenal (HPA) axis. Cortisol stimulates hepatic gluconeogenesis and proteolysis in skeletal muscle tissue, depriving the body of amino acids for glucose synthesis [4]. This protein catabolism leads to the progressive thinning of the lower limbs.
The resulting state of hyperglycemia stimulates compensatory hypersecretion of insulin. The combination of high cortisol levels and hyperinsulinemia activates lipogenesis specifically in visceral adipose tissue, which is rich in glucocorticoid receptors, resulting in a conformation with a protruding abdomen, increased neck fat ("buffalo hump"), and moon face [5].
Prolonged hypercortisolism also involves:
· Arterial hypertension due to enhanced vascular sensitivity to catecholamines and residual mineralocorticoid activity [6];
· Dyslipidemia, with increased triglycerides and VLDL;
· Fluid retention and a tendency toward periungual and periorbital edema;
· Immunosuppression due to the inhibition of NF-kB transcription and pro-inflammatory cytokines [7];
· Alteration of the appetite center with hyperphagia secondary to the physiological need to replenish depleted glycogen stores.
Interventional Strategies: Targeted Phytotherapy and Nutraceuticals
The management of the hypercortisolic type requires interventions aimed at remodulating the HPA axis, countering oxidative stress, and improving insulin sensitivity.
Neurovegetative and Vascular Modulation
· Crataegus oxyacantha (Hawthorn): The flavonoids and triterpenes contained in the extract exert a positive inotropic and negative chronotropic action, associated with the relaxation of vascular smooth muscle through the inhibition of the angiotensin-converting enzyme (ACE) and the modulation of calcium channels [8].
· Melissa officinalis: Rosmarinic acid acts as a GABA transaminase inhibitor, increasing brain GABA availability and consequently sedating the central nervous system [9].
· Citrus sinensis (Sweet Orange Essential Oil): The d-limonene present in the essential oil exerts a muscle-relaxing and anxiolytic action, working synergistically with lemon balm and hawthorn extracts.
Mineral and Carbohydrate Metabolism Support
· Magnesium: It acts as a natural NMDA receptor antagonist and calcium channel blocker, reducing neuromuscular hyperexcitability and promoting intestinal peristalsis in cases of constipation [10].
· Picolinate Chromium, Berberine, Banaba (Lagerstroemia speciosa) and Cinnamomum verum: Chromium constitutes the functional core of the glucose tolerance factor (GTF), enhancing the receptor's affinity for insulin [11]. Berberine activates AMP-activated protein kinase (AMPK), stimulating the translocation of GLUT4 transporters independently of insulin [12].
Neuroendocrine Modulation of the HPA Axis
· Phosphatidylserine: This membrane phospholipid, administered at therapeutic doses (400-800 mg/day), attenuates the serum peak of ACTH and cortisol induced by physical and psychological stress, preserving neuronal plasticity and mnemonic functions [13].
· Target Microbiota (Psychobiotics): The administration of Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 has demonstrated, in controlled clinical trials, the ability to reduce the proportion of free urinary cortisol (by up to 13%) and attenuate systemic stress-related manifestations through the modulation of the gut-brain axis [14].
The Biomorphotype with Hepatic Inefficiency ("Avocado"): Estrogenic Dysfunction and Allergic Reactivity
The "Avocado" biomorphotype is characterized by a quantitative disproportion between the lower part of the body (marked adipose and edematous accumulation on the thighs, hips, and buttocks) and the upper district (narrow shoulders, mammary hypotrophy). This picture presents overlaps with the gynoid constitution or with the traits of endomorphism according to Sheldon [15].
Metabolic-Constitutional Pathogenesis
Unlike pure visceral accumulation, this conformation recognizes as a primary cause a dysfunction in hepatic homeostasis and the clearance of steroid hormones.
· Altered Estrogen Catabolism: The liver is the primary site of phase I (hydroxylation via cytochrome P450) and phase II (glucuronidation, sulfation) of estrogen metabolism. Inefficiency in these pathways causes the recirculation of intermediate metabolites with high estrogenic activity [16]. The density of ER- and ER- receptors at the trochanteric and femoral regions directs the deposition of adipose tissue in these areas.
· Glycemic Dysregulation and Hyper-reactivity: Hepatic load compromises the capacity for glycogen storage and release, inducing glycemic fluctuations that influence mood (irritability, anxiety) and sleep quality. The detoxification deficit also increases the bioavailability of pro-inflammatory substances and allergens, stimulating immune responses and systemic allergic symptoms.
Detoxification and Modulation Phytotherapeutic Protocol
Hepatoprotection and Biliary Drainage
· Taraxacum officinale (Dandelion): Contains triterpenic alcohols including taraxasterol. It acts through a dual mechanism: choleretic (increased bile secretion by hepatocytes) and cholagogue (stimulation of gallbladder contraction) [17]. This action optimizes the clearance of steroid metabolites and the elimination of liposoluble toxins.
· Silybum marianum (Milk Thistle) and Cynara scolymus (Artichoke): Silymarin exerts a protective effect on the hepatocyte membrane and stimulates RNA polymerase I, increasing protein synthesis and parenchyma regeneration [18]. Artichoke cynarin supports bile flow and the blood lipid profile.
· General Diuretic Support: Arctium lappa (burdock), Equisetum arvense, Achillea millefolium and Betula verrucosa complete the picture by promoting diuresis and reducing the extracellular matrix load.
Estrogen Receptor Modulation
The use of phytoestrogens (soy and red clover isoflavones, flaxseed lignans, coumestans) and extracts of Salvia officinalis or Angelica sinensis exploits their action of selective estrogen receptor modulation (SERM) [19]:
· In the presence of hypoestrogenism, phytoestrogens bind to receptors, delivering a weak but functional pro-estrogenic signal;
· In the presence of hyperestrogenism, they occupy high-affinity receptors, preventing the action of the more potent endogenous estradiol, rebalancing the hormonal signal.
Dioscorea villosa provides diosgenin, a steroid-structured molecule with a progesterone-like action, essential for balancing estrogen dominance in the second phase of the cycle [20]. The picture is complemented by myo-inositol and pyridoxine (Vitamin B6), essential cofactors in insulin signal transduction and neurotransmitter synthesis.
Allergy Prophylaxis and Immunomodulation
· Ribes nigrum (Blackcurrant): Fresh blackcurrant meristem directly stimulates the adrenal cortex to produce endogenous glucocorticoids (physiological cortisone-like action). Unlike the administration of exogenous steroids, which causes HPA axis suppression through negative feedback, the embryonic extract promotes a physiological and balanced activation of the adrenal glands, leaving the body's self-regulatory capacity unaltered [21]. The flavonoid fraction and anthocyanosides simultaneously exert a vasoprotective and antioxidant action.
· Trace Elements and Microbiota: The combination of Manganese-Copper or Zinc-Selenium modulates the activity of superoxide dismutase (SOD) and glutathione peroxidase. Supplementation with Lactobacillus and Bifidobacterium restores the barrier function of the intestinal epithelium, preventing the trans-epithelial passage of allergenic macromolecules (gut leakiness) [22].
Exercise Endocrinology: Myokines and Metabolic Reprogramming
The prescription of physical exercise in biotypes with reduced glucose tolerance or high neuroendocrine stress should not be limited to the calculation of acute energy expenditure. The therapeutic value of movement lies in metabolic induction and the secretion of humoral myokine signals by contracting skeletal muscle [23].
Therapeutic Myokines: Irisin and Adiponectin
· Irisin: Derived from the proteolytic cleavage of the FNDC5 membrane protein in response to the activation of the transcriptional coactivator PGC-1$\alpha$, irisin is released into the bloodstream during muscle activity [24]. It acts on white adipocytes, inducing their trans-differentiation into brown adipocytes (browning). Irisin stimulates the expression of uncoupling protein 1 (UCP-1) at the mitochondrial level, dissipating the proton gradient as heat instead of producing ATP. Furthermore, it improves GLUT4 translocation into muscle cells, reducing insulin resistance.
· Adiponectin: Secreted by adipose tissue in response to muscle contraction and the reduction of fat mass (in the presence of adequate leptin levels), adiponectin activates the AMPK and PPAR- receptor cascade [25]. It increases fatty acid oxidation in skeletal muscle, reduces hepatic gluconeogenesis, and increases the transcription of uncoupling proteins (UCP), creating a virtuous cycle of metabolic acceleration that persists beyond the duration of the training session.
· Growth Hormone (GH): Training with appropriate loads under normocaloric conditions stimulates the pulsatile secretion of GH through the hypothalamus-pituitary axis. GH exerts a powerful direct lipolytic effect on visceral adipocytes and supports muscle protein synthesis, counteracting the catabolic action of cortisol [26].
Bibliographic References
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