HYPERSENSITIVITY IDENTIFIED
As I have been saying there are 4 specific b12 and cofactor deficiencies. I have pinned down one of them that hadnt been identified before as a separate thing.
This specific pattern, of neurological mitochondria shutdown, has some specific characteristics. There is an extreme hypersensitivity to adenosylb12 and/or l-carnitine fumarate and sometimes methylfolate if the person converts to adb12 well enough. The first one in may have no effect or may be hyper responsive. The second one taken often causes a huge response. So, in one case, l-carnitine fumarate, perhaps 50mg, as first taken, has no effect. A week later after that was out of the system, adenosylb12 was taken and had no effect and was established. After a few day of adenosylb12 the response to < 1mg of l-Carnitine fumarate is out of this world intense. After that an increase in methylb12 is also extreme, but not the nominal 500mcg already established as that is rolled into the l-carnitine response. So we see the dependence of the nerves on adb12-LCF activating the mitochondria in order to have a response to mb12. The specific mix of these responses depends on the person being extremely deficient of all 3 items in the CNS. The person however didnt have the symptoms of stalled methylation that one often sees in the epithelial tissues of the body. Body does not have much in the way of symptoms compared to the neurological and neuro-psyc. It is mostly neurological.
The mood characteristics show a great deal of anxiety as a base condition. Sudden emotional changes or storms, can look bipolar. Sudden rage, panic attacks etc all are very much worsened by adb12, mb12, LCF once the mutual dependencies are no longer blocking each other. Often risk sports or pseudo risk entertainments, roller coasters, bungee jumping, parachute jumping, fast boats, fast cars, fast anything are too much and too scary. OCD or elements of it may be present. These have to do typically with neural dopamine processing. These symptoms, as well as others including certain neuromuscular, may be present or caused or worsened by benzo usage, especially in those who are experiencing what is commonly called tolerance withdrawal which appears to be more a late or slow onset side effect. There are a lot more characteristics to really pin it down. However, those just clarify how it manifests. Low dopamine symptoms have to appear for Parkinsons to be diagnosed. Recent research has shown that Parkinsons has low CSF cobalamin, elevated CSF MMA and hypothesis that 20 years or more of damage from mal or non functioning neural mitochondria causes Parkinsons and here we have damaged neurons from low adb12-LCF and the beginning of the emotional/personality characteristics often found in Parkinsons (or some forms of Parkinsons) from these damaged neurons. The question comes down to:
HOW SOON BEFORE PARKINSONS DIAGNOSIS CAN CORRECTING THE DEFICIENCIES CORRECT THE DAMAGE AND/OR PREVENT MORE DAMAGE?
Most of these neuro-psyc symptoms appear to be linked to limbic system damage. The hypothesis is that 20 years or more of neurological damage from non-functioning neuro-mitochondria with low CSF cobalamin and elevated CSF MMA (non-functioning mitochondria by virtue of CSF adenosylb12/l-carnitine-fumarate deficiency as indicated by elevated CSF MMA) which has these symptoms is Parkinsons disease. Furthermore, Parkinsons disease is associated with limbic system damage.
It is these extreme deficiencies that appear to damage the neurons and causes the extreme hyper responsiveness. A micro titration of mb12, adb12 and l-carnitine fumarate can build the levels up, eventually to levels that according to the Japanese studies, up-regulates neurological healing. As the damaged neurons are reactivated they are extremely irritable and there is an increase in symptoms. Tapering the benzos may be helpful for turning down the secondary low dopamine symptoms. The benzos can cause a change in the dopamine receptors which appears to cause these Parkinsons type symptoms when a person has the adb12/carnitine deficiency damaged neurons.
This one subgroup, with hypersensitivity to at least adenosylb12 and/or l
carnitine fumarate and possibly mb12, with lots of anxiety, possibly with emotional outbursts, possible instant rage or killing rage, OCD or OCD like, doesn't get a thrill from thrilling activities, fear instead. Then adb12, mb12 or l-carnitine fumarate can, in tiny quantities trigger any or all in succession of the emotional responses. Also, benzos are frequently prescribed for the deficiency symptoms, and when the dose is large enough, it has an effect on the dopamine receptors causing the above emotional responses which are mostly part of the "Parkinson's personality" and in benzo-board lingo is "tolerance withdrawal" rather than "late onset side effects". Tolerance withdrawal is a far scarier term than "side effects". This deficiency appears to damage the limbic system. Then, when the neurons that are now hypersensitive are exposed to anything that starts them producing ATP and transmitting signals they have painfully intense responses, just as different damage can produce intense pain or bodywide pain sensitivity. When looking up the limbic system the disease mentioned that is at least in part caused by damage to the limbic system specifically is Parkinson's.
It appears that the damage appears to keep increasing for years and years until it becomes PARKINSONS, ALS, MS, SUPRA NUCLEAR PALSY and ALZHEIMERS, probably depending upon the exact mix of deficiencies, the exact neurological areas damaged or other factors. Until methylb12, adenosylb12 and l-carnitine fumarate are all brought up to the level that prevents further damage and then to a level that can heal the damage if possible, it is likely that the damage just keeps on going.
This specific aspect is not a methylation problem but that may also be a cofactor. This can be limited to the brain and cord with little or no body involvement. Hydroxycbl does not replace the adnenosylb12 but some people can convert the methylb12 to adenosylb12 to some extent. Further the double or triple deficiency with the l-carnitine fumarate and mb12 assures that no single substance can repair this. It HAS to be a complicated (many substances) protocol with careful titration.
If a person is going to heal from this, assuming that is even possible, its only going to happen with the Active B12 Protocol. That a person can take hydroxcbl for years and it never touches it should be ample demonstration that it doesnt work as it is easily demonstrated that adb12, mb12 and l-carnitine fumarate plus cofactors starts working in minutes to hours. The extreme response demonstrates the extreme deficiency and resulting damage.
A few people taking this from the b12 deficiency end of things who performed some of the titrations of adb12 of injections from 1 to 25mg or so and various ratios of adb12:mb12 discovered this increase in irritability. This irritability is at the heart of the Mr. Hyde transformation in b12 deficiency (mb12 fades first and fastest) and an overbalance of adb12 to mb12 which occasionally shows up when adb12 injections are in the 10-25mg range. Is this an early Parkinsons indicator? With only 2 people doing this series and only 1 person experiencing the mood/personality change, and others having exactly the opposite effect with high oral doses of both adb12 and LCF.
Im still working out the details. I will have a micro-titration set of instructions posted shortly. And of course everybody is free to choose whatever hypothesis they want to work from.
Choosing a strategy
1 Avoiding everything that attempts to restore the neurons and mitochondria to a non-deficient state as that is too irritating and anxiety provoking. Unfortunately that appears unlikely to change the course of the disease progression.
2 Rapid titration of the obviously active and effective substances to limit the number of days that have to be endured until the neuron startup effects are over. This will allow the doses to climb towards those needed to allow the body to restore the nervous system to normality (hopefully) with the up-regulated neurological healing the Japanese research speaks of. The accepted therapy doses of l-carnitine for restoration from technical deficiency is 3,000mg IV. A daily oral dose of l-carnitine in the 1000mg range is a quite normal supplement dose. Higher doses restores normality quicker or so goes the theories and actual results with all the items shown to have dose related effects produces more rapid and/or complete healing. LOTS OF UNKNOWNS.
3 Slow titration of all the active and effective substances bringing them all into balance at each level before increasing to the next step. It may take a year to get the levels up to the usually effective healing levels which may or may not slow down healing. By slow titration the length of onset may be an entire year or more. Feathering it to get things increasing enough to give some adaptation, healing and recovery of function without making it intolerable is not always possible to do when the difference between tolerable results and intolerable may come down to a difference of 10mcg of LCF. LOTS OF UNKNOWNS,
UNKNOWNS:
1 Can the damage be reversed
2 How many years of damage can be reversed
3 Can damage be stopped from proceeding all the way to Parkinsons (MS, ALS, Alzheimers, SNP etc)
4 How to reverse the damage and prevent it from continuing.
Step right up and place your bets ladies and gentlemen, who is going to get sicker and who is going to heal? For that matter who can heal? Who hasnt yet crossed the line of no return into outright irreversible neurological disease. My experience with Subacute Combined Degeneration is that it can be partially reversed and many of the symptoms alleviated and progression very much slowed down. So in SACD some of the demyelization lesions do heal, just as they can in MS. As the limbic system becomes hyper irritable it seems reasonable to expect the same kind of lesions there and to expect them to heal in the same way requiring the same cofactors. We are all in the same boat much more so than many think. We just each are sitting by a different set of leaks.
