ResaPura

ResaPura Lavorazione Canapa per conto terzi. Cosmetici cbd/cbg

09/04/2026

Autoimmune disease is the body staying stuck in a bad inflammatory conversation, where immune signals keep firing when they should be standing down. In “Cannabinoids and autoimmune diseases: A systematic review” (2016), Katchan and colleagues reviewed how cannabinoids influence immune signaling across autoimmune conditions and found that these compounds can modulate neurotransmitter and cytokine release, suppress leukocyte proliferation, induce apoptosis in T cells and macrophages, and reduce pro inflammatory cytokine output.

The review also notes preclinical benefits in models of arthritis, multiple sclerosis, and type 1 diabetes, while acknowledging that human evidence remains limited and inconclusive.

That’s what makes cannabinoids important in autoimmune inflammation. They are not just being discussed as pain relievers. They are being studied as immune modulators that may help calm part of the inflammatory machinery itself.

This review specifically describes cannabinoids as having immunosuppressive and anti-fibrotic promise in autoimmune disorders, which matters because autoimmune damage is often driven by cells remaining activated too long, releasing excess inflammatory signals, and perpetuating tissue injury over time.

The honest part is just as important - this is not proof that every cannabinoid helps every autoimmune disease, and it is not a license to overstate the science. The review makes clear that most of the stronger evidence was preclinical, while human trials were still scarce.

But the reason this lane keeps growing is simple. Cannabinoids appear capable of dialing down parts of the immune overreaction that drive autoimmune inflammation, and that puts them in a serious conversation about restoring balance where the body has lost it.

-Mike Robinson, The Researcher OG
Study Link: https://doi.org/10.1016/j.autrev.2016.02.008

09/04/2026

Bone pain is one of the hardest pains to shut down because it is not just pain signaling; it is inflammation, nerve irritation, tumor or injury-driven remodeling, and structural breakdown all feeding each other at once. In “A cannabinoid 2 receptor agonist attenuates bone cancer-induced pain and bone loss” (2010), Lozano-Ondoua and colleagues showed that activating CB2 reduced spontaneous and evoked bone pain in a murine model, while also reducing bone loss.

That matters because this was not just a blunt force numbing effect. It pointed to cannabinoid biology working deeper in the disease process that helps generate the pain in the first place.

What separates this from many standard approaches is that many conventional pain care approaches mainly try to quiet the perception of pain after the signal is already firing. In this study, the CB2 agonist AM1241 did more than reduce pain behavior.

Sustained treatment also reduced bone loss and lowered the incidence of cancer-induced bone fractures, suggesting an effect on the destructive environment driving the pain, not only on the sensation itself. That is a serious distinction in bone pain, where the source is often ongoing tissue destruction and inflammatory signaling that keeps reloading the pathway.

That does not mean every cannabinoid product will act like a targeted CB2 agonist, and this study was in a bone cancer model, not every form of orthopedic or degenerative bone pain. But it gives a strong mechanistic reason why cannabinoids stay in the bone pain conversation.

Some cannabinoid pathways may help dull pain by interrupting the biology feeding the signal, while other methods often chase the signal after it is already screaming. That is a very different kind of pain control, and it is one worth paying attention to.

-Mike Robinson, The Researcher OG
Study Link: https://doi.org/10.1016/j.lfs.2010.02.014

08/03/2026

Cannabis For Chronic Pain

Chronic Pain Affects Nearly Half the Population. Science Is Looking Back to a Plant Humans Have Used for Thousands of Years.

New research examining Cannabis sativa and the body’s endocannabinoid system is helping explain why cannabinoids may help manage pain when many conventional treatments fail.

Chronic pain affects roughly 30–50 percent of people worldwide, and about 10–15 percent of patients do not respond well to existing therapies such as opioids or antidepressants.

These drugs can also cause serious side effects including dependence, tolerance, and sedation.

Researchers are increasingly studying how cannabis compounds interact with the endocannabinoid system, a natural biological network that helps regulate pain and inflammation.

After injury, the body produces signaling molecules such as anandamide (AEA) and 2-AG, which help reduce pain signals and inflammatory responses.

Compounds from cannabis appear to strengthen or mimic this system.

Cannabinoids like THC and CBD influence two major receptor systems

• CB1 receptors in the brain and spinal cord that regulate how pain signals travel through the nervous system

• CB2 receptors in immune cells and peripheral tissues that help reduce inflammation and neuroimmune activity

Scientists also discovered cannabinoids affect additional biological pathways involved in pain signaling, including TRPV1, TRPA1, TRPM8, PPAR, and GPR55 receptors.

Because cannabis interacts with multiple pain pathways at once, researchers are investigating its potential role in conditions such as

• Neuropathic pain
• Inflammatory pain
• Migraine
• Cancer related pain
• Endometriosis pain

A major focus now is the development of CB2 targeted therapies, which may reduce pain and inflammation without the strong brain effects seen with some traditional drugs.

As modern science continues to study the plant’s chemistry and mechanisms, cannabis is increasingly being explored as a multi pathway approach to chronic pain management.

Research is still ongoing, but understanding how cannabinoids interact with the body’s own pain control system may help open the door to safer and more effective treatments for millions of people living with chronic pain.

March 2026
SOURCE HERE ⬇️ & In Comments

https://www.sciencedirect.com/science/article/abs/pii/S2950199726001023

01/03/2026

For a long time, acidic cannabinoids were dismissed as unstable precursors. The assumption was simple - heat them, activate them, move on. But biology is rarely that shallow.
When we talk about THCa, CBDa, and CBGa, we mean molecules that occur in the plant in their native, biologically arranged state. They are not damaged versions of THC or CBD. They are the plant’s native chemistry, built with a carboxylic acid group that changes how they interact with enzymes, receptors, and transcription factors.
That extra molecular group matters.
It alters polarity, binding preference, and metabolic fate. Acidic cannabinoids do not chase CB1 in the same way neutral THC does. Instead, many of them interact with nuclear receptors such as PPARγ, inflammatory mediators such as COX enzymes, serotonin receptors such as 5-HT1A, and transient receptor channels, including TRPV1. That means they influence gene expression, inflammatory tone, and cellular signaling without driving intoxication.
In their acidic state, they often show strong anti-inflammatory and anti-proliferative activity in preclinical models. CBDa has demonstrated potent COX-2 modulation. THCa has shown activity at PPARγ and anti-nausea pathways. CBGa interacts with metabolic and inflammatory signaling networks that tie directly into the regulatory balance.
Here is where it gets powerful.
When used alone, acidic cannabinoids can exert targeted regulatory effects. When combined, they create layered modulation. One may influence serotonin signaling, another metabolic transcription, another inflammatory cascades. That stacking effect is not chaos - it is orchestration.
The ECS is designed for modulation, not overload. Acidic cannabinoids fit that design because they tend to regulate rather than overwhelm. They operate upstream and downstream of classical cannabinoid receptors, shaping tone rather than forcing outcome.
In their natural, biologically arranged form, these molecules are not incomplete. They are precise. Alone, they can influence key pathways. Combined, they can create broader regulatory harmony.
The future conversation is not about activating them through heat. It is about understanding how the acidic architecture itself contributes to restoring balance at the cellular and neuronal levels.
-Mike Robinson, The Researcher OG

11/02/2026

Sometimes “there’s nothing we can do” is just code for we’re not allowed to try.

Drayk didn’t get a hopeful prognosis. He got dismissed.

Nasal cancer. Visible lesion. Antibiotics that did nothing. The vet was clear: no conventional options.

So Drayk’s owners went rogue.

They used THC FECO mixed with coconut oil—applied directly in the nose, with small amounts swallowed—alongside serrapeptase, yunnan baiyao, and turmeric (with black pepper + ginger).

The response was fast.
The vet wasn’t optimistic… until two weeks later when he was shocked by the progress and told them not to stop.

By one month, the cancer was gone. Completely.

Drayk was groggy at first from the THC. That passed. The results didn’t.

The cancer never came back. He lived another 10 months cancer-free until he unfortunately passed from an unrelated issue (bloat).

This is a patient-reported outcome. Not a promise. Not a pitch. Just proof that the standard playbook isn’t the only one.

10/02/2026

Nel 2023 abbiamo stipulato una convenzione con l’UNIVERSITA' degli Studi di Messina – Dipartimento di Scienze Veterinarie 🏛️🐾 per la RICERCA sui nostri prodotti e sul ruolo dei fitocannabinoidi 🌱 nei processi di infiammazione e neuroinfiammazione negli animali da compagnia🐾.

https://www.frontiersin.org/journals/veterinary-science/articles/10.3389/fvets.2024.1341396/full

Visti gli ottimi risultati ottenuti, la collaborazione è stata rinnovata dopo 10 mesi per avviare un nuovo studio sulla modulazione del dolore nell’osteoartrite cronica 🧪💚

https://www.frontiersin.org/journals/veterinary-science/articles/10.3389/fvets.2024.1496473/full

Questo percorso rappresenta per noi uno dei principali motivi di orgoglio e ci spinge a guardare al futuro con maggiore fiducia 🚀✨

18/01/2026

A new study published by Pharmaceutics finds that the cannabis compound cannabidiol, better known as CBD, could enhance the effectiveness of certain chemotherapy drugs against glioblastoma multiforme, one of the most aggressive and difficult-to-treat forms of brain cancer. The research was conducted...

10/01/2026

Introducing CBGa into my AM routine became the inflection point. CBGA doesn’t directly activate CB1 or CB2 receptors; instead, it acts upstream, influencing enzyme signaling and receptor tone, which can allow CB1 receptors to repopulate and regain sensitivity over time. That biochemical shift matched what I noticed in my own system: the THC oil that had felt muted for months suddenly felt effective again at lower doses. The tolerance wall didn’t vanish instantly, but it softened enough that dosing became more efficient, more predictable, and, finally, worth the effort again.

Lowering tolerance meant I could use less THC while feeling more of the intended effects, getting the most out of the oil without constantly escalating the dose just to reach baseline symptom control. For someone balancing seizures and cancer, that kind of dose efficiency isn’t a luxury; it’s a lifeline. The unexpected twist was that Genevieve’s need for CBGA research didn’t just help her; it recalibrated me. That shift allowed the THC oil to act more meaningfully, especially for sleep and symptom relief, because the receptors were finally in a state to respond again.

What saved me wasn’t a new oil formula; it was restoring receptor tone so the old one could finally work like it was supposed to. Genevieve needed the science, but I needed the alignment, and both pointed to the same truth: when the ECS regains balance, tolerance lowers naturally, endogenous modulators increase, and plant-derived bioactives finally hit their stride again without fighting upstream friction.

That moment in 2016 didn’t just shape a protocol; it validated a principle. If the Master Regulator is out of tune, nothing downstream performs correctly. When it finds its tone, everything else follows suit. Genevieve may have needed CBGA, but the Master Regulator made sure I needed it too, and that shared need rewrote the outcome entirely.

And that’s the quiet revolution of acidic precursors in real time: restoring ECS Balance so the therapies you already trust can finally work at their best again.

-Mike Robinson, The Researcher OG

03/01/2026

Holding CBGa concentrate on top of THC Distillate with terps helps show the world what ECS Balance looks like with cannabinoids. If we’re going to use the ultra-strong natural plant THC, we need to offset that with ingestion of cannabinoids like CBGa and CBDa that help our Endocannabinoid System (ECS) to regain it’s equillibrium. This causes numbed receptors to fire up again, new ones to replace the old, and circulates our bodies' cannabinoids, aka endocannabinoids, throughout our bodies, allowing our own fuel to mix with that of the plants. Now that’s a dynamic duo if I’ve ever heard of one, plant and endocannabinoids working together to calm the storms of life.

CBGa - everyday! Let’s talk more about why you should be using it now.

-Mike Robinson, The Researcher OG

Indirizzo

Viale 1 Maggio 5
Corinaldo

Orario di apertura

Lunedì 08:00 - 18:00
Mercoledì 08:00 - 18:00
Giovedì 08:00 - 18:00
Venerdì 08:00 - 18:00
Sabato 08:00 - 13:00

Telefono

+393287492711

Notifiche

Lasciando la tua email puoi essere il primo a sapere quando ResaPura pubblica notizie e promozioni. Il tuo indirizzo email non verrà utilizzato per nessun altro scopo e potrai annullare l'iscrizione in qualsiasi momento.

Contatta Lo Studio

Invia un messaggio a ResaPura:

Condividi

Share on Facebook Share on Twitter Share on LinkedIn
Share on Pinterest Share on Reddit Share via Email
Share on WhatsApp Share on Instagram Share on Telegram