Targeted support for pelvic pain with high-bioavailability Lacursome® technology, based on PEA, R-ALA, Quercetin, Lactobacillus crispatus SP28 and titrated extract of Undaria.
Cronyra is a dietary supplement formulated to promote pelvic wellness and contribute to the management of chronic pain in the female urogenital area. Its synergistic composition combines substances with anti-inflammatory, antioxidant and vaginal microflora-supportive actions: Palmitoylethanolamide (PEA) and α-lipoic acid (R-ALA) assist the natural control mechanisms of pain, inflammation, and oxidative stress; Quercetin, a plant-derived bioflavonoid, has an anti-inflammatory and stabilizing action at the cellular level; the probiotic Lactobacillus crispatus SP28 contributes to the maintenance ofvaginal flora balance; and finally, the titrated extract of Undaria pinnatifida, protects the activity of PEA.
| Nutritional Information. | Per maximum daily dose (2 tablets) |
| PEA | 600 mg |
| R-ALA | 300 mg |
| Quercetin | 200 mg |
| Undaria E tit. 10% of which fucoxanthin |
200mg 20 mg |
| Lactobacillus crispatus SP28 | 2 billion CFU* |
Micronized PEA (Palmitoylethanolamide); Bulking agent: Hydroxypropylcellulose; R-ALA (R-alpha lipoic acid); Undaria (Undaria pinnatifida (Harvey) Suringar) thallus ES tit. 10% fucoxanthin; Quercetin; Lactobacillus crispatus SP28; Cocoa butter; Anti-caking agents: Silicon dioxide, Magnesium salts of fatty acids.
30 capsules 0.9 g net weight 27 g
Chronic pelvic pain (CPP) in the gynecologic setting is a debilitating condition affecting up to 15-20% of women of childbearing age. It is defined as pain localized to the pelvic district that persists for at least 6 months and significantly affects quality of life, sexuality, psychological well-being, and work activity.
What makes pelvic pain particularly difficult to experience is its continuity: a pain that returns over time, until it becomes chronic, with the feeling that the body requires constant attention. Its persistence eventually alters daily habits, energy levels, and serenity.
The pain can come in different forms. Sometimes it is dull and diffuse, felt as a pressure or heaviness in the lower abdomen; at other times it becomes sharp, like a sudden twinge that forces one to slow down. It may be intermittent or continuous, with phases of respite alternating with flare-ups.
Chronic pelvic pain is often related to menstrual cyclicity, with more intense and prolonged dysmenorrhea accompanied by stiffness and fatigue that may extend to the back. The intimate sphere can also be involved: dyspareunia, i.e., pain during or after intercourse, can generate anticipatory fear and a strong emotional impact.
In some cases, pain also occurs during daily functions such as urination or evacuation, contributing to the perception of a pelvic area in constant tension. When vaginal flora alterations or urogenital dysbiosis are associated, the sensation is that of a fragile intimate balance, with symptoms that tend to recur.
In this context, terms such as pelvic inflammation and neuroinflammation help name a complex experience, promoting recognition of the problem and a greater understanding of what many women experience every day.
The triggering cause of chronic pelvic pain can be multifactorial. The main initial factors include:
Although these factors often represent the initial event, chronic pelvic pain tends to persist because it activates and sustains a number of complex biological mechanisms involving the immune, nervous, and musculoskeletal systems, transforming an initially reversible stimulus into a condition of pain maintained over time. Among these mechanisms we recognize:
One of the first mechanisms involved is the persistence of an inflammatory state at the pelvic level and, in parallel,increased oxidative stress, with excessive production of reactive oxygen species; aspects that contribute to maintaining an irritative and pro-nociceptive environment. The result is hyper-activation of nociceptors, with sensitization of ion channels involved in pain transmission; this leads to increased release of algogenic neuropeptides that further fuelinflammation and the pain signal.
In the presence ofpersistent inflammation, peripheral nerves undergo functional and structural changes that result in lowering the activation threshold of nociceptors, making them hypersensitive even to normally non-painful stimuli. Clinically, this results in allodynia (pain evoked by harmless stimuli) and hyperalgesia (amplified pain response). Associated with this is neuroangiogenesis, or the growth of new nerve fibers in the pelvic area, which increases pain receptor density and amplifies local pain perception.
The continuous bombardment of pain signals from the periphery induces profound changes in the central nervous system as well. In the spinal cord, dorsal horn neurons become hyperexcitable, with further release of pro-inflammatory cytokines within the central nervous system. These changes promote central sensitization, a process whereby pain persists regardless of the initial stimulus.
An additional key element in the maintenance of chronic pelvic pain is urogenital dysbiosis, which acts as a real catalyst for the inflammatory and painful process. It is not just a consequence of the underlying pathology, but an active mechanism capable of promoting and perpetuating the local inflammatory state.
In this context, chronic pelvic pain is no longer just the symptom of a local pathology, but the result of a nervous system that has "learned" the pain, making it autonomous and persistent.
Cronyra represents a nutraceutical support targeted at the mechanisms of chronic pelvic pain; it is formulated with actives that act in a complementary manner on inflammation, sensitization and dysbiosis. The goal is to support a physiological modulation of pain and improve the patient's quality of life.
Palmitoylethanolamide (PEA) exerts a multimodal action on the main mechanisms involved in chronic pain. At the inflammatory level, PEA modulates immune cell activity through activation of PPAR-α receptors, helping to reduce the production of pro-inflammatory mediators. On the level of peripheral nociception, PEA intervenes by reducing hyper-activation of nociceptors. It indirectly modulates CB1 receptors, glutamate activity, and the functionality of ion channels involved in pain transmission, contributing to raising the pain threshold and reducing neuronal hyperexcitability. PEA also exerts a central role in modulating neuroinflammation and central sensitization. Finally, PEA counteracts oxidative stress-related pain amplification through activation of the Nrf2 pathway, promoting endogenous antioxidant mechanisms.
Fucoxanthin from Undaria is converted to fucoxantinol, which can inhibit the enzyme NAAA and thus counteract the physiological reduction in PEA levels, prolonging its action. This is complemented by the patented Lacursome(R), which is useful for increasing the bioavailability of PEA, whereby the active ingredients are granulated into lipid nanoparticles derived from cocoa butter that carry the active ingredients in the intestine, promoting their absorption and availability.
R-α-lipoic acid (R-ALA) plays a relevant role in modulating biological mechanisms that contribute to the persistence and amplification of pain through its antioxidant, anti-inflammatory, and neuroprotective actions. One of the main areas of intervention of R-ALA is oxidative stress, a key factor in the amplification of the pain signal. On the neuroinflammation level, R-ALA modulates the activity of pro-inflammatory transcription factors such as NF-κB, reducing the production of cytokines and inflammatory mediators in the central nervous system. By acting on microglia and the function of ion channels involved in pain signal transmission, it helps to contain central sensitization processes, which are responsible for the persistence of pain even in the absence of active peripheral stimuli. Finally, R-ALA exerts neuroprotective action by regulating the mechanisms of neuronal apoptosis. This support for neuronal health is particularly relevant in chronic pain settings, where neuronal damage and dysfunction contribute to symptom chronification.
Quercetin is a natural flavonoid with a biological profile of particular interest in modulating the processes that sustain inflammation and pain persistence. At the inflammatory level, quercetin exerts a modulating action on the COX-2/prostaglandin axis, reducing the production of PGE₂, a major mediator involved in lowering the pain threshold. In parallel, quercetin plays a relevant role in the containment of oxidative stress, helping to reduce the accumulation of reactive oxygen species, allowing it to limit nociceptor hyper-activation and pain signal propagation along peripheral and central pathways. On the peripheral nociception side, quercetin modulates the function of sodium and calcium channels, which are involved in the generation and propagation of the action potential in sensory neurons. Taken together, these effects make quercetin a biological modulator capable of acting in a coordinated manner on inflammation, oxidative stress, and pain transmission, supporting multimodal strategies geared toward reducing pain chronification.
Alterations in the vaginal microbiota directly correlate with hypersensitivity and pelvic pain, so maintaining a eubiotic microbiota is a protective factor in pelvic pain. In light of this, intervening in the microbiota with L. crispatus SP28 thus enables the reduction of peripheral algogenic stimuli, synergistically complementing the action of PEA, R-ALA, and quercetin on pain signal modulation.
Overall, Cronyra proposes anintegrated action that supports a return to a more physiological functional balance, with positive and perceptible effects on daily life and quality of life.
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