I’ve answered this question in a response to one of the most popular misconceptions about why we inflate a balloon in the jugular veins as part of the Combination Therapy Protocol (CTP). Our protocol was developed as a result of applying evidence from many different clinical trials in different areas of medical research. I won’t get into other phases of CTP, but instead focus specifically on balloon angioplasty of the cervical veins with autologous stem cell infusion in the first phase in the sequence. Venous angioplasty is the first part of the protocol and it’s performed for a different primary purpose than it is for Zamboni’s CCSVI treatment. It has been demonstrated in various studies that in MS there is pathology (state of disease, in this case anatomical pathology in venous tissue) in both neck veins and in the veins deep within the brain. Franz Schelling’s (and others’) studies showed that in MS there are abnormal widenings similar to varicose veins in the cranium in the transition between the sigmoid sinus and the internal jugular vein (these are specific points in the veins deep in the brain). 80% of people with this pathology also have a diagnosis of MS and the lesions that are a hallmark of the disease as seen in MRIs, are always seen as developing around THE VEINS!
For the researchers conducting this study, this is the most often asked question of all. When we started this research study a number of years ago, we didn’t know the answer because information on how chemical medications and supplements would affect the function of stem cells just wasn’t available. At the time, we knew of a few medications that would definitely be harmful to stem cell activity and we thought the list was fairly short. But research sheds light on new discoveries over time and in many instances serendipitously uncovers information that is unexpected and or different from the hypothesis or expected outcome. In research this is known as a ‘paradoxical effect’; a reaction opposite to that which was predicted or anticipated. So it is with this study. Since much of what we are doing in this study is being done for the first time in history, this is not surprising. As a result of this research, there are a great number of ‘medical firsts’ in the queue to be published. For example, for the first time in history we have seen the transition of skeletal muscle from spastic to flaccid tissue once the neural pathways begin to re-establish signalling. This is because no patient with the type of paralysis left by a chronic debilitating disease such as MS has ever gone far enough into a healing recovery to experience these changes. We have also seen imaging changes post-therapy in lesions within the brain, so significant that these bright white appearing foci have actually vanished without a trace, as reported by neurologists. In order to study this area more completely, we have now engaged a top neuroscientist in this area of research.
Stimulus-triggered acquisition of pluripotency or STAP was supposed to be the new medical breakthrough based on the science of stimulating any old human cells to become pluripotent stem cells by treating them with certain growth factors, acidic baths, or other manipulation. This technological leap forward would mean that ordinary blood cells for instance, could be treated to become neurons in the brain, etc, and such a discovery could lead to cures for Alzheimer’s and MS among many other diseases. STAP would have been a much easier way to produce stem cells than current methods as neither nuclear transfer nor transcription factors would have been necessary in their growth. But the ‘science of STAP’ is turning out to be the present day equivalency of alchemy, the notion that lead can be turned into gold.
To provide some background here for David Echt’s post, 6 months after treatment in March of 2014, David wasn’t experiencing the recovery we are seeing in other patient/subjects over the same time period, post-therapy. Although there were some important improvements, there was no functional difference in his affected right leg whatsoever; it was still as paralyzed as it had been for the past 6 years. This didn’t make a lot of sense to us. We knew he was on Metformin for his diabetes, but as far as we knew, that shouldn’t have interfered with the activity of the stem cells…OR SO WE THOUGHT. Then we came across a new article entitled ‘The paradoxical effect of metformin on endothelial cells and angiogenesis’. The research concluded that the drug Metformin would have precisely the OPPOSITE effect of what would be expected. Instead of fostering stem cell activity and endothelial growth, it INHIBITED these growth activities, which was a stunning surprise to the researchers. Metformin would therefore inhibit the formation of capillary networks, negate the trophic effect of stem cells in the brain, and likely disrupt endothelial, myelin and neuronal growth. So despite what we THOUGHT WE KNEW, many drug interactions with stem cells are difficult to make recommendations about these drugs because there has not been enough work done in this area of study. It really requires a deep dive into medical journals. What we are witnessing with David’s dramatic demonstration is real medical pioneering stuff. And now we know a couple more things. Because David’s recovery has now resumed, we have a good demonstration of the lasting effect of the ‘type’ of stem cells (mesenchymal neural progenitor cells or ‘true stem cells’) we’re typing, isolating, and colonizing for reinfusion.
Someone asked me the other day what exactly causes the neurotoxic leakage of fibrinogen across the blood brain barrier in the MS central nervous system leading to lesions in the brain and subsequent neurologic symptoms. They meant, WHY are these vessels in the MS brain so prone to injury? If you’ve been reading my blogs here, you know that I’ve been heavily promoting that this leakage of fluids sets off the cascade of events that incites an immune response in the brain (CNS) and subsequent inflammation. This is where the research is taking us (although neurologists do not generally know of this research because it’s in the area of vascular medicine). We can also turn that question around to ask why that same type of injury and subsequent leakage doesn’t occur in the vast majority of the population. The Davalos UCSF study (among other studies) has shown that this leakage is most certainly ‘the cause’ of MS in those patients who are predisposed to disease development. We have seen thinner walled veins and strange valvular anomalies in most if not all MS patients. Zamboni based his hypothesis around weakened jugular veins but didn’t carry his observations, nor his treatment far enough. He had to look further upstream to find the real problem. So what is really going on here that is causing these venous lesions in the MS brain?
Finding a treatment for MS has been a powerful allure for many medical entities. Investigations into treatment strategies originate from pharma-sponsored academic researchers all the way through to pseudo-scientists and esoteric holistic healers who practise on the edges of medicine. MS is a compelling target for research not only because of its fast-growing patient population, but because of the ability to easily affect the symptoms of MS by applying considerably different therapeutic strategies to treatment modalities. The success in reducing MS symptoms as a result of applying so many different approaches leads many researchers down rabbit holes that ultimately do not direct us towards a cure. Dreadful side-effects sometimes accompany these therapies, especially the pharma-based medications. Incredible financial rewards await a cure, but the drug companies are doing their best to maintain the status quo. They are no longer even pretending to look for a cure. As the entrenched incumbents who control the entire medical system world-wide, they privately and secretly argue behind board room doors that whether they can or not, it’s financial folly to do so. It’s much more profitable to keep patients on medications for decades while they fend off, and attempt to discredit other promising therapeutic strategies from other clinical investigators that might actually work. In this respect, the slow-moving disease process of MS makes for their ‘dream disease’, and the drug companies own the entire domain.
Muscle spasticity becomes muscle flaccidity in virtually all patients receiving the Stem cell Combination Therapy Protocol (CTP). The following is a description of what is happening within the body and why individual patient response to therapy is highly variable. Muscle spasticity is defined as an increase in muscle tone (resistance or tension) secondary to a central nervous system (CNS, brain and spinal cord) disorder or trauma. It refers to involuntary muscle stiffness or spasms. In the normal human body, in any coordinated movement, muscles on one side of the joint relax while those on the other side contract. Spasticity occurs when this coordination is impaired and muscles on both sides of the joint contract at the same time as a result of an imbalance of signals. This results in very awkward movements. MS-related spasticity can occur with active movement, or can be present at rest. Although not completely understood, spasticity is thought to be caused by increased sensitivity in the parts of the muscles responsible for tightening, relaxing and stretching. This is currently understood to occur as a result of the demyelination of the nerves connected to these muscles leading to a loss of inhibitory function of the affected nerves leading to an imbalance of excitatory impulses resulting in muscle contraction.
As part of the subject qualification process for our clinical trial, I include questions to candidates regarding trauma or stressors that preceded the patient’s symptoms of MS. My interest in this is more than mere curiosity. Clinical trials that are intended to evaluate the efficacy of a particular therapeutic protocol in patients with a particular disease need to be properly evaluated with a view to treating or preventing the disease along with determining side effects (if any) and risks associated with the protocol. If a new indication (valid reason to use an intervention) for a disease or medical condition is discovered during any part of the investigational process, it is appropriate to make note, collect data and analyze that particular aspect of the disease within the parameters of the trial. From the outset of our research, I noticed that a preponderance of MS patients (over 90%) independently reported a significant traumatic ‘event’ in their lives prior to their diagnosis of MS that we have called the ‘primary antecedent’; a premorbid risk factor that may have induced the subject’s first MS symptoms leading to their subsequent diagnosis.
I’ve been asked what the differences are between our protocol and the Tisch MS protocol in NY, being made famous by Richard Cohen, the husband of TV celebrity Meredith Vieira.
There are several major differences that make our protocol’s results far more enduring and successful in the long-term: 1) repair and revascularization of the micro-vessels deep in the central nervous system to halt disease process. 2) type and number of cells used for replacement of dead neurons within the sclerotic tissue in the CNS. By cell count, there is not the population of appropriate cell types within a natural, centrifugated marrow-derived sample that, once infused back into the patient, will create enough neurons for recovery of lost neuronal tissue in the CNS as a result of the MS disease process. The population of ‘true stem cells’ (mesenchymal/telomerase positive cells) will simply be too diffuse once interspersed within the CNS by whatever delivery method is used.
The cost to an MS patient is between $60,000 in the US and $70,000 per year in Canada…and Biogen claims it’s effective for inhibiting MS symptoms…but they don’t quite know how it works…by their own admission (the medical research equivalent of throwing crap at the wall to see what sticks). Formerly it was only prescribed for symptoms of psoriasis. So how did dimethyl fumarate qualify to become the leading candidate for the treatment of MS?
With self-imposed funding caps for research, drug companies are performing big data searches on thousands of old clinical trials to look for unintended side-effects of molecules that can be interpreted to mean ‘efficacy’ for different diseases. Biogen found dimethylfumaric acid (BG-12), which demonstrated inhibition of immune cells by stimulating the expression of anti-inflammatory cytokines within the central nervous system, in previous trials. Theoretically, this old finding made it effective for the treatment of MS, and expensive-looking but short duration trials of only two years were performed to re-purpose and dress up a drug they already knew they were going to release for the treatment of Relapsing/Remitting MS. But where is Biogen’s conclusive proof that this relatively short period of clinical experimentation justifies the use of this method of disease treatment, and how solid is their data?
In 2009 when Paolo Zamboni came up with an original idea and clinical evidence to associate abnormal pathology in the jugular veins of MS patients to the disease process itself as a possible cause (chronic cerebrospinal venous insufficiency or CCSVI), it was a shot heard around the medical world. Could a simple two hour non-invasive medical procedure to expand neck veins really ‘cure’ a chronic, often fatal neurodegenerative disease and avoid a lifetime of misery for many MS patients? In 150 years of attempting to treat MS, could this pathophysiological abnormality and its relationship to the disease have been missed? After all, this Italian doctor Zamboni published a study that showed evidence of neurologic improvements and increased function after MS patients underwent the jugular vein-expanding procedure. And what do doctors really know about veins anyway? Not even vascular surgeons work in the veins very much. It all seemed plausible.
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