I have Sjogrens, Lupus, Fibromyalgia & Raynauds. When I first contacted you I was desperate for relief. My pains were almost completely gone after one month of using Banjo, and only came back (rather quickly) in a very “muted” state after I stopped using it. Meaning to say, that I know they are there but…
On cytokines, inflammation, pain and fibromyalgia Cytokines are inter-cellular chemical messengers produced mostly by white blood cells. Some are generally pro-inflammatory (inflammatory cytokines turn inflammation ‘on’) while others are generally anti-inflammatory (they turn inflammation ‘off’). High levels of inflammatory cytokines indicate an ongoing inflammatory process. There might not be the appearance of ‘inflammation’ as we…
Inflammatory cytokines impair memory and learning: Fibro fog. Cytokines are inter-cellular chemical messengers produced mostly by white blood cells. Some are generally pro-inflammatory (inflammatory cytokines turn inflammation ‘on’) while others are generally anti-inflammatory (they turn inflammation ‘off’.) Inflammatory cytokines, which are often elevated during sickness, are believed responsible for many of the common symptoms…
Because of Banjo: I have more energy. My migraines are so under control, I feel ‘cured’. My herniated discs in my neck are pain free enough that I’m able to turn my head from side to side.
Since the onslaught of lupus, I have had the energy of a sloth. I not only have more energy, but I made it through my daughter’s cheer leading camp… AND, I suffered no ill effects from it.
I am weeping as I tell you all this. Thank you for changing my life.
Results In each of the two Phase 3 trials, patients were randomized to one of three treatment groups: there was a 10mg/kg group, a 1 mg/kg group and a placebo group. Patients received an intravenous dose on days 0, 14 and 28, then every 28 days thereafter for the duration of the study. All patients…
Among other symptoms, lupus is often characterized by pain and fatigue. The fatigue may be debilitating, and is often reported to cause greater impairment and greater loss of quality of life than does the pain.
Like most auto-immune conditions, lupus patients generally experience times of remission – times when disease activity is reduced. Among those lupus patients for whom pain is an issue, the severity of pain will generally diminish during remission and may cease altogether.
However, fatigue generally remains, even during an extended period of remission. Given that fatigue accounts for a substantial portion of the disability of lupus, this is of great concern.
Dendritic cells stimulate the immune system by presenting antigens (foreign particles) to other immune cells and by causing the release of pro-inflammatory cytokines. It is believed that dendritic cells may play an important role in autoimmune disease.
The serum from patients with lupus causes monocytes to transform into dendritic cells and is associated with increased NF-kB activation.
The serum from patients with asthma also causes monocytes to transform into dendritic cells and is associated with increased NF-kB activation.
Inhibition of NF-kB contributes to T cell tolerance – by which is meant tolerance to self. When “tolerant” T cells do not attack self. T cell intolerance may lead to autoimmune disease.
High levels of different auto-antibodies are commonly found in lupus, as well as other autoimmune disease. One type of auto-antibody is directed against double-stranded DNA.
In the study below, researchers looked at four variations of that auto-antibody and found that all four resulted in an increase in TNF – a pro-inflammatory mediator.
Two of the four variants were found to activate NF-kB, suggesting that at least some of the damage caused by these auto-antibodies results from their ability to turn on NF-kB.
This is a very significant finding, and furthers the theory that inhibition of NF-kB might be of value in lupus, as well as other autoimmune disease.
Studies have suggested involvement of interleukin 17 (IL-17) in autoimmune diseases, although its effect on B cell biology has not been clearly established.
Here we demonstrate that IL-17 alone or in combination with B cell-activating factor controlled the survival and proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. This effect was mediated mainly through the nuclear factor-kappaB-regulated transcription factor Twist-1.
NF-kB is the master regulator – the primary means by which inflammation is ‘adjusted’ – turned on and off. Many, many different molecules interact with NF-kB – some stimulating it (increasing inflammation) and others inhibiting it (decreasing inflammation.) The balance between these positive and negative forces determines the extent of inflammation at any given time.
BENLYSTA inhibits the biological activity of B-lymphocyte stimulator, or BLyS. BLyS is a naturally occurring protein which is required for the survival and development of B-lymphocyte cells into mature plasma B cells.
Plasma B cells produce antibodies, the body’s first line of defense against infection. In lupus and certain other autoimmune diseases, elevated levels of BLyS are believed to contribute to the production of autoantibodies – antibodies that attack and destroy the body’s own healthy tissues. The results of prospective observational studies show a significant correlation of elevated levels of BLyS with SLE disease activity.
