Back a few weeks ago I had the pleasure of presenting at the Integria Symposium and the even greater pleasure of listening to some of the fabulous speakers …you see I’ve heard my stuff before! 😉 The ‘Mosaic of Autoimmunity’ was delivered by the very funny and knowledgeable Professor Yehuda Shoenfeld, who reiterated the sequence of events now well recognised to precede and precipitate autoimmunity: genetic susceptibility + endocrine context + environmental trigger –>autoimmunity.
Clinicians know that overwhelmingly women dominate when it comes to autoimmune disease epidemiology and most understand that this is a consequence of oestrogen’s immunostimulatory effects. Professor Shoenfeld, described the female, or E2 dominant, immune system as being ‘super charged’ and that increased rates of autoimmune diseases were a reflection of this. Sometimes practitioners do initially great work with a/immune clients – clearing up the diet & gut, ensuring vitamin D adequacy etc and then get ‘stuck’ or plateau with antibody levels that ‘won’t budge’. Going back and checking the hormonal contribution in the case is often indicated. If the patient has an unhealthy E2 dominance and /or impaired detoxification and clearance of this hormone then working on this aspect often kickstarts the next stage of improvement.
A new thing to me (I know I’m a bit slow sometimes 🙁 ) was his mention of the potential link also with high prolactin (PRL). The literature on this is extensive and hyperprolactinemia (HPRL), even just mild elevations, have been correlated with a very long list of both systemic and organ specific diseases including:
- RA, SLE, Systemic Sclerosis, Sjogrens Syndrome
- Coeliac disease
- Grave’s & Hashimoto’s disease
- Addison’s disease
- Psoriasis vulgaris
While PRL is well established as an important immune modulatory hormone which has a bidirectional relationship with cytokines of both the Th1 and Th2 families, the question has been whether the high rates of HPRL in a/immune patients are a consequence or a cause of these a/immune conditions. The current answer to this differs from disease to disease. For example, while no correlation has been demonstrated between PRL levels and disease activity in MS and Uveitis, in Coeliac Disease, PRL levels rise with disease activity and correlate with both mucosal atrophy and the anti-endomysial antibody titres, leading researchers to suspect that PRL plays a modulatory role in the immune response that damages the intestinal lining (Shelley et al 2012).
Probably the most impacting evidence to date have been several studies confirming bromocriptine (a PRL blocking medication) as an effective treatment for SLE, improving clinical parameters and lowering ds-DNA autoantibodies to boot. While this approach is yet to be studied in other a/immune presentations, Kerry Bone also talked about reducing HPRL as a treatment objective in various autoimmune cases and of course recommends using Vitex agnus-castus for this.
So what does this mean for all of us seeing patients suffering from a/immune diseases? Don’t forget the hormonal context! PRL levels need to assessed in each a/immune patient and any client with levels > 400mIU/L would undoubtedly benefit from the inclusion of some Vitex! Oh and while you’re there, in your SLE patients, check out their blood DHEAs and read this interesting review of the 2 hormones and their respective role in both the pathophysiology of the disease & its improved management! 🙂
Do you really know what your patient’s pathology is trying to tell you? Is there more to it than ‘one size fits all’ reference ranges? Rachel’s Master Diagnostics Pack will make sure you get the most detailed understanding out of any testing (mainstream or functional) your patients have had. Rachel presents diagnostics in a fun accessible way that is immediately relevant to the integrative practitioner. For more information on interpreting pathology, click here.