IAGIM - Drug Development Association

(Ongoing 2010 -2025)
Prof. J. D. BLOCK - Epidemiologist (N.I.E.) - Chief Scientist IAGIM ASSOCIATION and CEO LIGroup

ALTERNATIVE MORE ADVANCED M/S Article - ; Ref: "Article of the Month".

Neuro-Immuno-Epidemiologist Prof. J. D. Block, Chief Scientist of IAGIM Institute, Founder member and CEO of Locum International (Research) Group are beginning, via the International GLIMER I, II, and III Multiple Sclerosis (M/S) epidemiological, etiology and epigenetic international research study, to unravel the past epidemiology research that could overturn the prevailing wisdom on the cause and progression of multiple sclerosis (M/S) in men and particular women who get it so much more (3:1).

Multiple Sclerosis in not only a debilitating neuro-degenerative disease that strikes predominately females at the peak of their childbearing life but significantly, earlier in the lives, starting literally from birth as their auto-immune system starts to develop during the critical pre-puberity ages of 1-3 and 3-6 years and onwards to puberty and then to child bearing and final to menopause. Although this disease strikes men as well, the incidence is significantly lower than females which is generally 2.5:1 and as high as 3:1 in the Atlantic Region of Canada (450+ per 100 000)and growing, compared to Cape Town or South Florida which are well under 10 or 50:100 000. Men normally get MS later (39-40 years) but more severely as PPMS (Primary Progressive MS).
The question is why are the Canadian and South New-Zealand numbers so high, when compared to the rest of the world. That conundrum is being unraveled by the intensive epidemiological and geographical study covering most countries of the world. The answers are slowly unraveling and the results are both surprising, unexpected and require a total rethink of just exactly what multiple sclerosis really is, today in 2015... Most of us got it badly wrong.

Cascading effects and serial triggers from birth. - MS is a lifelong disease. It starts silently, almost 'benign' in very early childhood age with the auto-immune system at birth and remains unseen and benign for close to two/three decades. This displays, as a two/three decade, cascade of triggering events that eventually culminate in the mid-twenties and early thirties in women with the second significant clinical event of MS. The first significant clinical event of MS is difficult to detect and identify as positive MS, as it is brief (only about 24 hours plus) and the etiology is not clearly understood by the patient and equally poorly by the treating physician, who generally would not recognize the clinical event (exacerbation /attack) as RRMS. In men its more aggressive and SPMS (secondary progressive) and rapidity moves to PPMS (primary progressive within a decade or so - give and take a few years here and there.)

This first attack, at early child bearing age, will pass unnoticed as possibly an optical neuritis (remember the optic nerve is part of the CNS) not the PNS, as the other 11 cranial nerves are classified. Alternatively, the young female in her prime will suffer a 24 hour plus gait or muscle problem, which could start as young as 18 - which few physicians are able to recognize as a clinical significant event. It is only at the second significant clinical event that both the patient, now in the early stages of MS can recognize that something seriously is wrong, and an astute physician would concur. The dormant or sub-clinical phase of MS has now passed, all the triggers have all fallen, and the neuro-degenerative CNS brain, optic and spinal cord disease has displayed its "first, but really second" clinical life long debilitating symptoms. All the triggers in the two to three decade process or cascade have now tripped and the patient is truly sclerotic as per MRI/MRS normal white and gray matter scans show and the presence of oligoclonal bodies in the spinal fluid...

So the question remains; What are these triggers and how do they fit into the almost three decade cascade or "domino effect" to use a well understood cliché'. There are several triggers in this early stage, but really its mid to late stage RRMS that will, with added decades i.e. as time progresses, progress to SMS (Secondary MS) and then PMS (Primary), but luckily only less than 15% of RRMS will progress upwards - unlike in men. Their fate, when it starts, is significantly worse. It generally is faster, quicker and it is diagnosed as PMS at age 40 or a smidgen later. This PMS goes upwards, it's fairly constant and degeneration is faster and much more problematic.

The GLIMER Study has separated the triggers over the life long decades up to the seventh or eight decade into a series of tipping points such as, and in no particular order here - that comes later - the layered autoimmune development, GIT (70%), the GIT microbiota patient lifelong role, Bone Marrow B Cells and Thyroid, T cells, The faulty thyroid QC producing a range of passing and just passing B and T-cells (a whole group of them CD4+ CD8+ NKS and a whole group of other white cells and phagocytes (macrophages) that we will come to later).
The bottom line is that the thyroid gland rejects 90% of the lymphocytes and leukocyte that it examines. Most of them are faulty, in fact almost all of them have deficiencies in one way or the other, they are layered, flawed and have different multiple faults - and the question to ask, - is why?
That's a big question to answer and it has a lot of epigenetic background, as highlighted by a 150 years of epidemiology especially unwrapping, teasing out and sorting the confounding conclusions reached, over the so many decades of wrong conclusions. Confounding statistics a very special type of mathematics, like fractal math's, here too, plays an important role in understanding the big MS picture..

In net effect, the thyroid only passes 10% of the presented white cells. And that 10% that pass are much layered. Now that's an unusual medical term - these lymphocytes and leukocyte, white cells, have varying recognition abilities - all passing lymphocytes and leukocyte are not equal, they have different recognition abilities and some of them are poor and they flag badly, in fact they flag proteins, very poorly indeed. These white blood cells are improperly trained - really the dropouts of the thyroid gland and they cannot really recognize their own body protein (that's because they are bored - modern science has taken their job away and to get vengeance they have a little bit of deadly fun - they attack own body proteins not because they are evil, but because they have become lazy and they have have not been properly trained and educated and that's our fault, yes, modern man and modern medicine with disinfectants, anti-viral and antibiotics, clean sheets, the full nine yards and no real immune system challenges, like the good old days used to be when lymphocytes and leukocyte actually worked for their money - "and didn't get no free ride")- and that starts the ball rolling and initiates and then causes an auto-immune disease, first inflammation and subsequent own-protein attack and the lymphocytes and leukocyte can't help it - they are not trained to do their job effectively, just bored. They are kind of 'protein blind' in specific cases. (Much more of this later).

Now the question arises why are some of these lymphocytes and leukocyte (say 10% of those who pass, that's 1%) are so badly trained and how did they get to this point and why do they do their job so badly, i.e. attack normal basic myelin protein and other insulating proteins (lipoproteins) in a host of other autoimmune diseases (+/-81 in all). In order to answer this question we need to look at epigenetic, epidemiology, etiology and a smidgen of genetics and a large portion of the GIT Microbiota over an extended period of time (the early and second childhood decades) and later to mid childbearing and finally up to menopause. Men don't really have 'menopause', but mid-life crisis's - However around 40 onwards, they have all the other tipping points in this extended, developing, ongoing persistent cascade, with all the same triggers.

Now the balance of the triggers that cause the cascade must be highlighted - early child viral immunization by mother (EBV and others), glandular fever, mononucleosis (kissing's disease), ancient adhesion proteins, (crossing the BBB), NWM casual proximity, Oligodendrites and "their 40 feet" (one podium/many podia), DNA indels, (insertions deletions and repetitions, these are mutation types), default-protein-folding-small-errors (affecting basic myelin protein in MS) - "the pea in the bed" analogy, MHC, random wrong site inflammation, B and T cells 'gone wild', (Trigger the dog, "digging up the garden") chemokines and cytokines production, messenger proteins - "don't kill the messenger syndrome", scaring and lesions, nodes of ranvier (and the axon t0 node ratio), axon degradation and eventually final or part cleavage, and finally comparative autopsies of MS and non-MS patients and their very surprising findings. This end Part One

Part two of this ongoing review - will deal with the epigenetics and epidemiology triggers, such as early EBV immunization, Vit D3 (24-25 dihydroxy cholcalciferol), Normal sunlight exposure, combination food symbiosis of Vit D3 and Sunlight to produce 2000+ IU's of equivalent D3 every day. The right foods. Not 400 IU's but 2000+ IU's of intrinsic and extrinsic Vit. D3 daily and the proper daily ratios. The number of minutes of sunshine a young auto-immune developing child must be exposed to, is in the region of 22-35 min at day (weather depending), but not 8 min a day as is normal in Canada and much less in the Canadian Atlantic Region - eventually we will end with Oligodendrites and their fatal unavoidable mistakes (it's just a statistics game) together with the DNA indels and the statistical probability of DNA mutations (and their surprising causes) affecting the 3.2 billion lines of DNA code per global geographic region as a function of epigenetic and epidemiology. MS like polio, is a preventable disease, not through vaccinations, (not yet, but is coming, a new branch of medicine called retrospective-prospective didactic vaccines. RPDV's are just three to five years away, maybe eight at maximum but in that overall ball game.) Yes, preventable with RPDV's to the pre-pubic age groups or very significantly reducible through RPDV's, with added proper educated lifestyles and seriously educated nutrition to avoid relapses of the immune system. The emergence of the RPDV's are a new class of lymphocytes and leukocytes simulating vaccines. Stopping the boredom and mischief in the emerging white blood cells. This new class of RPDV's are going to be revolutionary and quite extraordinary - much like the emergence of the antibiotic arena but without the resistance as we can modify the training. It's really a bit like Glatiramer Acetate in a way - which is a red-herring vaccination but the upcoming RPDV's are the real McCoy, a new generation of teaching vaccines, without the undesirable side-effects of red-herring physiological chemistry (mimicry). The epigenics are getting quite clear now. We are getting closer to the light. We need to take care of the developing first three/six years of life, and develop a healthy immune system and keep it active and healthy for decades. Diet, sunlight and early EBV inoculating by "Mom method" are three early important triggers, but there are many more triggers we need to protect. We almost know the basic, underlying cascading etiology, how and when it all starts - that's no 'biggy' now- so many years ago in early child hood and definitely for quite sometime now - how it all is going to end...

Jeremy David Block.
B.Sc.. (Eng.), M.Sc.(WCU), (Micro/Stats), D.Pharm (Wits)., PHD (Neuro IAGIM. U.)
Part Two /-2019/22. - Total Parts: 20 - Pages 110 and growing)

ALTERNATIVE MORE ADVANCED MS Article - ; Ref: "Article of the Month"
Prof. J. D. Block - Neuro-Immuno-Epidemiologist (N.I.E.)

Background: Prof. J. D. Block served for the duration of the development of COP 1 as a senior medical/pharmaceutical researcher and part of the Teva COP 1 innovative research team in the early nineties that rapidly developed Teva's first MS immuno-modulating drug Glatiramer Acetate (CopaxoneTM). As Chief Scientist as well as Teva's Group Scientific Research Auditor, and by touching each and every part of the Teva's Organization and the overall scientific team, Teva rapidly attained New Drug Registration with the FDA under J. D. Block scientific and technical guidance and regulatory department training, GRP, GMP GLP, SOPs, Analytical audits and global organization overview (from early active material synthesis to manufacture and then final freeze dried packaging and NDA Registration).

Epidemiology Note * ISRAEL Israeli Jews have a prevalence of up to 62 per 100,000, but Christians (35 per 100,000), Moslem Arabs (15), Druze (11), and Bedouins (17) have lower rates (Alter et al 2006). Genetically similar immigrants have half the rate of native-born Jews, suggesting an environmental factor. Other groups also have a significantly lower incidence of multiple sclerosis (Caucasians Hispanics Latino's black African Americans, Asians African Natives, Inuits, SWA bushman, and Romani Gypsies (almost zero)).

ALTERNATIVE MORE ADVANCED MS Article - ; Ref: "Article of the Month"
Prof. J. D. Block - Neuro-Immuno-Epidemiologist (N.I.E.)

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