Noon talk in room 301 at NUNM
"Biofilms == What has the last 200-Million Dollars in Research Taught Us"
copyrighted powerpoint--PS anderson
www.consultDrA.com

his presentation:
evaluation of biofilm research
clinical relevance

10 yrs ago involved in cancer research at Bastyr, 5 yr NIH trial
next research--undiagnosable nonhealing illnesses
junk drawer dxs: fibromyalgia, rheumatologic conditions not well differentiated
what were impediments to cure?
nutrigenomics
multiple causes, multiple organ systems involved, often dxd as rheumatologic condition
most had lab verifiable infections, not cleared by usual treatments

research review 20 years later
NIH and CDC have ID'd biofilms as highest threat to human health
but haven't publicized it because they don't know what to do about it

clinically trying things, some worked, some didn't
doing OK
a few years forward--at oncology think tank meeting
met a guy doing biofilm research, 12 million dollars funding, 11 million in Anderson's Q's
last million will be FDA approved interventions for biofilms
government "disappears" some of the research
he got more sources from this guy, looked at the research, is sharing sources with us in his powerpoint

biofilm becomes a resistance factor for the microbe
resistant to antibiotics

lives "anyplace wet": blood vessels, mouth, (me: what about gut, lungs/bronchi, sinuses?)
biofilms start in the gut and get more severe, cause significant immune response when disrupted
sick long enough: more microbes migrate there
it gets bigger, from thin to thick, from low diversity to high
the worst biofilms are "phase 2" become their own microbe
can contain bacteria, parasites, viruses, fungi--they share DNA
treatments don't work: kill one but the rest survive
cure one thing and another thing pops up

clinically relevant in sicker population, chronically ill
lots of suppressive treatments, incomplete treatment
many microbes involved
pseudomonas and gram negatives
mycoplasma
H. pylori (symptomatic)

treatments for phase 1 are enzymes and such
work pretty well
patients usually not that sick

Biofilm summary from Stephen E. Fry MD (in power point)
Biofilms are considered the rule in nature rather than the exceptoin.  If you have chronic infection, biofilms may be an underlying cause.  Many, if not most, ....

testing for biofilms
can't really?

prevention - phase 1 agents
goals: inhibit quorum sensing, initial attachment, organism efflux pump
MORE ON THIS SLIDE
enzymes
aromatics--oregano, garlic, olive, etc (daily consumption of these = best prevention)
tannins
phenolics
xylitol, stevia
nigella = black cumin--can be used for phase 2 as well, plant immune modulators, wedges into biofilms

phase 2 later biofilm
not treatable with phase 1 agents except black cumin
synthetic antimicrobials
direct biofilm disruption--agents - ?? PO, IV
product: biocidin, he likes it, goes to phase 1.5 ish

oral bismuth (ionic)
EDTA, calcium-disodium EDTA and Na2-EDTA as additive to immune and abx IV formulas for pts who may have biofilm
silver nanoparticles, low 23 PPM nasal spray or 200-500ppm for other systems, hydrosol not colloidal
anti-infective: H2o2, HDIVC, Ge, Zn, etc

BEG bactroban, e and gentamycin

thiols (mono-) ALA (Oral or IV), NAC (oral or IV, or nebulized for resp), glutathione (IV or nebulized)
(ala and nac will cause strange gut reactions when added, this indicates that there's a biofilm)
thiols (di-) DMSA (oral, 300-500mg po away from food bid day prior to and of the IV anti-infective), DMPS (IV and oral)

oral bismuth-thiol complex--neither alone, a new molecule (do not use IV bismuth at this time, heavy metal)
combo: the last million he hadn't figured out yet
little to no chelation effect.  dithiol is bound to bismuth so toxicity of bismuth and chelating ability are "negated"
bismuth nontoxic in this form, new mol will show up on heavy metal testing as bismuth
wedges into the biofilm and reacquaints the immune system with what's in there: the "wedge effect"

HIS FORMULA:
DMPS 25mg, ALA 100mg, bismuth subnitrate 200mg per cap
ideally no substitutions
DMSA 100mg can sub for DMPS
bismuth subcitrate can sub for subnitrate (weaker product)
this is the strongest formula that can be made, stronger products have been sequestered by the govt

take for 60 days---more on slide

other supports needed for about a month
many need adrenal support
if on low dose hydrocrotisone and adrenal support they will probably need 2-4x more hydrocorisone
if on non-rx adrenal support they may need 5-10x the dose for "a time"
some need thyroid support

his otc version
Bis-thiol plus buck cumin

support immune system during tx
support healthy microbiome

when biofilm opens up you get an immune response
achy, headache, fever, possible psych sx
can be big crisis if you are not ready for it
very acute
must warn patient ahead of time--if they start feeling terrible that's a good sign
return of early sx is likely: sign of treatment success
if healing crisis does not subside: bugs dying releasing metallotoxins or broad spectrum herbals aren't heavy duty enough
duration of treatment relates to duration of illness, up to 2 years

immune suppressed patient
won't get fever, cytokine storm
treat presumptively, prescription anti-infectives to hedge bets

this article has all the same references as this talk
http://ndnr.com/gastrointestinal/biofilms-what-have-we-learned-from-the-research/
and webinar on priority one

fasting?
get stronger/faster reaction with it

We used to live in a world where people got sick from exposure to feces and lives were saved with antibiotics. Now we live in a world where people are dying from antibiotics and their lives are being saved by feces.
--a colleague

Ursolic acid ameliorates autoimmune arthritis via suppression of Th17 and B cell differentiation.
Baek SY1, Lee J1, Lee DG1, Park MK1, Lee J2, Kwok SK2, Cho ML1, Park SH2.
Abstract

AIM:
Ursolic acid (UA) is a pentacyclic triterpenoid found in most plant species, which has been shown anti-inflammatory and anti-oxidative activities. In this study, we examined the effects of UA on collagen-induced arthritis (CIA) in mice, and to identify the mechanisms underlying the effects.

METHODS:
CIA was induced in mice. Two weeks later, the mice were treated with UA (150 mg/kg, ip, 3 times per week) for 4 weeks. The expression of cytokines and oxidative stress markers in joint tissues was measured with immunohistochemistry. The numbers of CD4+IL-17+, CD4+CD25+Foxp3+ and pSTAT3 cells in spleens were determined using confocal immunostaining or flowcytometric analyses. Serum antibody levels and B cell-associated marker mRNAs were analyzed with ELISAs and qRT-PCR, respectively. CD4+ T cells and CD19+ B cells were purified from mice spleens for in vitro studies.

RESULTS:
UA treatment significantly reduced the incidence and severity of CIA-induced arthritis, accompanied by decreased expression of proinflammatory cytokines (TNF-α, IL-1β, IL-6, IL-21 and IL-17) and oxidative stress markers (nitrotyrosine and iNOS) in arthritic joints. In CIA mice, UA treatment significantly decreased the number of Th17 cells, while increased the number of Treg cells in the spleens, which was consistent with decreased expression of pSTAT3, along with IL-17 and RORγt in the splenocytes. In addition, UA treatment significantly reduced the serum CII-specific IgG levels in CIA mice. The inhibitory effects of UA on Th17 cells were confirmed in an in vitro model of Th17 differentiation. Furthermore, UA dose-dependently suppressed the expression of B cell-associated markers Bcl-6, Blimp1 and AID mRNAs in purified CD19+ B cells pretreated with IL-21 or LPS in vitro.

CONCLUSION:
UA treatment significantly ameliorates CIA in mice via suppression of Th17 and differentiation. By targeting pathogenic Th17 cells and autoantibody production, UA may be useful for the treatment of autoimmune arthritis and other Th17-related diseases.
PMID: 25087995 [PubMed - in process] PMCID: PMC4155530

SOURCE
http://www.ncbi.nlm.nih.gov/pubmed/25087995
Acta Pharmacol Sin. 2014 Sep;35(9):1177-87. doi: 10.1038/aps.2014.58. Epub 2014 Aug 4.

Modulation of autoimmune rheumatic diseases by oestrogen and progesterone
• Grant C. Hughes & Divaker Choubey
Nature Reviews Rheumatology 10, 740–751 (2014) doi:10.1038/nrrheum.2014.144
Published online 26 August 2014
http://www.nature.com/nrrheum/journal/v10/n12/full/nrrheum.2014.144.html
Abstract
Sexual dimorphism is evident in the risk and expression of several human autoimmune diseases. Differences in disease manifestations observed between sexes are likely to involve immunomodulation by sex steroids, nonhormonal factors encoded by genes on the X and Y chromosomes, and immunological phenomena unique to pregnancy. In systemic lupus erythematosus (SLE), and perhaps other autoantibody-mediated diseases, oestrogen seems to increase the risk of disease in genetically predisposed women by targeting key immune pathways, including the type 1 interferon (IFN) response, differentiation of CD4+ T helper cells and survival of autoreactive B cells. By contrast, progesterone seems to reduce the risk of SLE by counteracting the effects of oestrogen on some of these same pathways, which suggests that the balance between oestrogen and progesterone can determine disease expression. In this Review we focus on the roles of the sex steroid hormones oestrogen and progesterone in modulating the risk and expression of SLE and rheumatoid arthritis. Intensive research in this area promises to identify novel therapeutic strategies and improve understanding of the immunological requirements and complications of pregnancy, and is expected to define the mechanisms behind sexual dimorphism in autoimmunity, immunity and other aspects of human health—a newly announced directive of the NIH.

First time I've heard of IgD: 11/26/14. From Dr D'Adamo. =-]

QUICK REFERENCE RANDOM ASSOCIATIONS IN semi-ALPHABETICAL ORDER
( This list is brought forward and updated with new information.Collapse )

The National Institutes of Health, 10 large drug companies and seven nonprofit organizations announced an unconventional partnership on Tuesday intended to speed up development of drugs to treat Alzheimer’s disease, Type 2 diabetes, rheumatoid arthritis and lupus.

During the course of a five-year, $230 million effort, the participants will share data in regular conference calls and meetings, working together to determine which findings are likely to lead to effective treatments. They will make their findings and data publicly available.

...What concerns me about this is the emphasis on drugs. There are better ways to adjust physiology than taking in foreign substances. And there are more useful things we could study. Like food, and exercise, and how to they affect our biochemical and electrical mileau. Sex, we should throw more money at studying sex and how it affects neurotransmitters. On the effects of chewing gum and on understanding the endocrinology of sexual preference. And on why our hearts slow down as we age, and a million other questions. I'm just curious: I really want to know the answers. I wish that the money spent on medical research was directed more by altruism and less by profit motive.

SOURCE
http://www.nytimes.com/2014/02/05/health/nih-joins-drug-makers-and-nonprofits-on-stubborn-diseases.html

This is starting to make sense.
http://www.medpagetoday.com/Rheumatology/GeneralRheumatology/43797?isalert=1
http://www.medpagetoday.com/Rheumatology/GeneralRheumatology/43797?isalert=1

The Russians have known about phages and used them to treat severe infections since the 1930's. New research shows that lots of phages live in mucus. Wherever there is mucus there is likely to be a large population of phages--including mucus produced by other species such as sea coral, plants, etc.

Phages are viruses that use bacterial cells to replicate in. They can also insert new DNA into bacteria, and they are able to evolve quickly enough to keep up with changing resistance patterns. Big Pharma is not putting any money toward phage research because phage therapy would compete with antibiotic sales, and as we know, for them, the bottom line IS the bottom line. They want us to think that phages are dangerous. But according to Dr Mercola a normal human produces approximately a quart of mucus (snot) daily in the upper respiratory tract, most of which we swallow. So we are phage central already.
( notes from Mercola's new article on phagesCollapse )