Posted on 11/19/2025 9:31:20 PM PST by ConservativeMind
Degenerative joint diseases like osteoarthritis and intervertebral disk degeneration are conditions that affect millions of people worldwide, leading to pain and reduced mobility.
A study found that cytosolic phospholipase A2 (cPLA2) is an important enzyme. It plays a key role in inflammation and cartilage breakdown. The study suggests that cPLA2 could be a possible target for treating joint diseases.
Osteoarthritis and intervertebral disk degeneration are conditions that slowly break down cartilage in joints and disks in the spine. This leads to pain, inflammation, and impaired function that worsens over time.
Members used advanced methods to examine the relationship between cPLA2 and joint degeneration. Notably, they investigated a common antihistamine, fexofenadine, as a potential cPLA2 inhibitor.
Cytosolic phospholipase A2: regulator of degenerative joint diseases The study revealed several critical insights:
—Role in damaged cartilage cells: cPLA2 is the main driver of cartilage decay. This enzyme becomes too active in certain cartilage cells. These cells are already likely to break down and show signs of aging.
—Keeping cartilage healthy: Removing cPLA2 through genetics and blocking it with drugs greatly lowered inflammation. This also stopped cartilage cells from breaking down and aging. This means this gene is crucial for keeping cartilage cells healthy, and stopping its action could protect the cartilage from damage.
—Potential of fexofenadine: Fexofenadine blocked cPLA2 effectively by reducing inflammation and prevented cartilage cells from aging.
These findings underscore the potential of targeting cPLA2 as a disease-modifying treatment strategy for degenerative joint diseases. The researchers believe that blocking cPLA2 can help with inflammation and chondrocyte aging—the main causes of cartilage damage.
Pharmacological studies using fexofenadine further supported the genetic findings. Fexofenadine treatment reduced cartilage degradation as well as both inflammation and age-related deterioration.
(Excerpt) Read more at medicalxpress.com ...
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If you need such a drug and have these other issues, consider switching.
It apparently made a big difference with degenerative back and joint cell tests.
bkmk
Why take an antihistamine that blocks histamine receptors when you can take diamine oxidase enzyme that actually degrades the histamines in the body?
Cytosolic phospholipase A2 (cPLA2) is an enzyme involved in inflammation by releasing arachidonic acid, a precursor for inflammatory mediators.
Arachidonic acid is an omega-6 polyunsaturated fatty acid found in cell membranes that is involved in cell signaling, inflammation, and neurological functions. It is a precursor in the formation of leukotrienes, prostaglandins, and thromboxanes.
Arachidonic acid is a key inflammatory intermediate and can also act as a vasodilator.
Bookmark
Okay missy.
What do you know about this?!?
🤔
Your alt stack is powders
MSM
Glucosamine CL
Sodium ascorbate
2x teaspoon daily
Add 10000-20000-30000 units D3 daily, depending on how bold you are. Your D3 “calcium problem” counterweight is magnesium glycinate and its ascorbate form. K2 for good lucks.
Whats in a name? LOL.
“Pharmacological studies using fexofenadine further supported the genetic findings. Fexofenadine treatment reduced cartilage degradation as well as both inflammation and age-related deterioration”
Fexofenadine = Allegra, allergy antihistamine.
In my youth I was very active with organized Baseball and later softball. That along with tossing around a football I must have rotated my right Glenohumeral joint (ball and docket) half a million times. Plus the day to day wear and tear. When I hit 60 I couldn’t raise my arm above my shoulder without shooting pain. This was going on for a year. The typical OTC Chondroitin Glucosamine supplements
did little to help.
About five years ago I was reading about UC-II which is a chicken cartilage derived supplement. In combination with Hyaluronic acid and Boron a pill was marketed. Sams Club and Costco have their version and they call it Triple action Joint health. About $25 for 110 pills for the Costco version and Sams comes in a 125 count bottle.
When I first started taking it I did two pills a day (1 is the recommendation) for 60 days then backed off to one. By month four / five I was pain free and have maintained that for five years. I have since added to the daily intake a turmeric and egg shell membrane supplement. I also have an arthritic lower spine which my regiment has helped but not to the degree of my shoulder. I lived with a heating pad in bed and my desk chair for many months. I haven’t had to turned them on this entire year since I added the turmeric and Egg shell membrane.
“Ball and socket”
Antihistamines seem to give me premature ventricular contractions. And one night when I was miserably sick and taking multiple drugs, I went from vagalling down to rebound V tach degrading into A fib with ventricular response. No fun at all.
So careful if you take it. PVCs give a sensation of skipped beats or a extra big beat. Mostly they’re benign. But nor always.
My sacroiliac joint would like to give it a try. Heart says no way.
I can’t find anything pointing to diamine oxidase degrading or affecting cytosolic phospholipase A2 (cPLA2).
Cytosolic phospholipase A2 (cPLA2) is an enzyme that plays a role in the release of arachidonic acid from phospholipids, which can lead to the production of inflammatory mediators, including histamines.
Upon activation, cPLA2 releases arachidonic acid from membrane phospholipids. Arachidonic acid is then converted into eicosanoids, which can enhance the effects of histamine and promote inflammation.
Diamine oxidase (DAO) is an enzyme that helps break down histamine.
The article is about the antihistamine Fexofenadine (Allegra) blocking cPLA2 effectively by reducing inflammation (by blocking histamine receptors) and preventing cartilage cells from aging.
My joint pain and inflammation was gone immediately when I began taking diamine oxidase enzyme. Why take a selective peripheral H₁ blocker when you can decrease histamines with diamine oxidase enzyme in the entire body and have no need for the histamine blocker?
Fexofenadine is a selective peripheral H₁ blocker. It is classified as a second-generation antihistamine because it is less able to pass the blood–brain barrier and cause sedation, compared to first-generation antihistamines like diphenhydramine (Benadryl).
Why block the histamines released by Cytosolic phospholipase A2 (cPLA2) through arachidonic acid in a selective area rather than degrade them in the entire body?
“Cytosolic phospholipase A2 (cPLA2) is an enzyme that plays a role in the release of arachidonic acid from phospholipids, which can lead to the production of inflammatory mediators, including histamines.”
You seem to think cPLA2 only produces histamines, but it doesn't—even by your own quote. Histamines are just a part of what it influences.
Your histamine degraders can't touch the other products made. Heck, they don't even stop the histamines from being made, either.
Your solution doesn't touch this problem.
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