Sunday, October 16, 2016

ALS testing guide to finding and treating problems

Extremely valuable time is lost waiting for a medical system that fails to test and treat problems that can be found in the body early.  Even more valuable time is lost to the uncertainty about what to do.

The more time that is wasted, the further the body gets out of balance.  At the very least, get started on the first two tests.

Methylation - this test is ordered online and is a genetic spit test.  It takes about a month to get your results, but then you can feed your results in a number of different sites that give you information about your genetics.  Absent GSTM1 results in impaired ability to eliminate mercury, but I do not think it can be found here.  Methylation is important and can be supported.  Your genetic reports may help to point at other problems.  You take your 23andme results and upload them to these sites to get reports:

  • - there is a small fee to use their site, but once you upload your data from 23 and me, there is lots of information about health problems associated with your genes.
  • - this site will give you valuable information about your methylation pathways.  This is about how your body detoxifies.
  • - This is Dr Yasko's program and her program is complicated, however, working to follow it teaches you about methylation and where your body has methylation problems, and supplement recommendations.  There is also a forum to ask questions about the program.
Gut dysbiosis
There are a few options.  
  1. Ubiome is the most cost effective, however, it may be a lot of work to try and figure out what to do with their information,  From their site:

    What kind of results will I get?
    After your sample has been analyzed, you get to be an explorer and learn about the vast rainforest of bacteria in your body. Logging in to, you'll see detailed information on each of these bacteria - what their names are, how many of each kind there are, what their functions are in the body. 
    You may find yourself curious to compare your results with the aggregate results of everyone who's done the test, and with specific groups of people. Say you want to look at how your microbiome compares to vegans, or smokers, or people on antibiotics. You can do that!
    It’s important to be aware that uBiome is designed to be a tool for personal research, NOT a diagnostic tool. You won't find any predictions about your future health. And your results will not diagnose any medical condition.
  2. GI Effects is more expense, but it does give a good break down for gut issues,  It does come with some recommendations for how to correct, and that can be a start, but it helps you to know what problems you may have and generally you can work on these problems. You may be missing enzymes to go from one product to another, so the recommendations may not be fixing that problem.
  3. Great Plains Organic acids test,  This test gives a good report and some recommendations.  It also measures for some neurotoxins from yeast and bacterial overgrowths.
Here is a fantastic interview that connects liver, bile, dysbiosis and methylation,

To be continued...

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Saturday, July 30, 2016

Protect your Shikimate pathway - eat organic, take probiotics

This is huge, and it is where I've come to focus with ALS and the microbiome shift that the leaky gut study found, and then finding other ALS studies about amino acids as biomarkers for ALS.
"A third very serious consequence of this kind of microbiome shift is reduced nutrition. Instead of having microbes that give nutrients to the body, there are microbes that compete with the body for nutrients. ALS patients have an amino acid profile that has shifted to the point that it has been considered as a biomarker. The amino acid shift suggests the gut microbiota have a compromised shikimate pathway. Humans do not have this pathway, however, we depend on this pathway in our gut. The essential amino acids tryptophan, tyrosine, and phenylalanine come from the shikimate pathway and then methionine production is also compromised. Without sufficient nutrients from this pathway, serotonin, melatonin, melanin, epinephrine, dopamine, thyroid hormone, folate, coenzyme Q10, vitamin K and vitamin E are insufficient."
So, then I've been looking at lactobacillus rhamnosus and these are all of the things that it helps with:
-respiratory infections
-urinary track infections
-reduces intestinal permeability (found to be a problem prior to ALS symptoms in ALS mouse model and continuous leaky gut has huge health consequences as well)
-secretion of biosurfactants which prevents pathogenic microbial adhesion to intestinal walls
-improves GABA
Because these are all problems I see ALS patients utterly suffering with, it looks to me that a probiotic with this species would be helpful, however, there is a precaution with a weakened immune system.
The implications of this kind of nutrition problem is enormous. It means that where ever you have a genetic weakness, this disease is going to hit and complicate what is happening and we are all genetically different, so, researchers are going to be going in many directions.
Lactobacillus species are manganese oxidizing and my research kept pointing to a problem with manganese and I knew that mitochondria, lyme, and cyanobacteria are all manganese oxidizing, and all seem to have some kind of association with ALS. So I was researching manganese oxidizing microbes trying to find a link. Then a conversation I had with an independent health researcher went like this:
"Manganese builds up to toxic levels in the liver and then in the brain stem via transport along the vagus nerve, following an inability for the liver to ship the manganese out via the bile acids."
I ask a few more questions and an hour later I get a reply:
"J Neurol Sci. 1983 Oct;61(2):283-93.
Increased manganese level in spinal cords of amyotrophic lateral sclerosis determined by radiochemical neutron activation analysis.
Miyata S, Nakamura S, Nagata H, Kameyama M.
The manganese distribution in the cross-section of the cervical, thoracic and lumbar portion of the spinal cords from 7 autopsied cases with amyotrophic lateral sclerosis (ALS) and 6 control subjects were determined by radiochemical neutron activation analysis. It was possible to determine 1 ng levels of manganese content accurately in the small tissues about 1 mg of dried weight using wet ashing and chemical separation after neutron activation. The dried weight of spinal cord was about 1/3 of the wet weight. Manganese concentration in the wet tissue was calculated from the ratio of dried to wet weight. In the anterior horn of the cervical cords of ALS, manganese concentration was the highest; 1.75 +/- 0.39 ng/mg of dried weight and 0.59 +/- 0.09 ng/mg of wet weight, respectively. These were significantly higher (P less than 0.01) compared to those in controls; 1.02 +/- 0.12 ng/mg of dried weight and 0.35 +/- 0.04 ng/mg of wet weight, respectively. The elevation of manganese level in the spinal cords of ALS was more prominent in the anterior horn and lateral column than in the posterior column both in dried and wet tissues. Since manganese inhibits neuronal transmission, it is likely that neurological degenerative changes occur as a result of local disturbances of manganese metabolism in the spinal cord of ALS.
So to me this sounds like a potential mechanism of disease that contributes to ALS. It also helps to explain to me why chelating and supplementing minerals seems to help, or at least some people swear it helps and I know that my cousins that had serious neurological issues found a doctor experienced in how to chelate early and they've been stable and healthy for 5 years now, yet prior to finding this doctor they were declining.
Another mechanism mentioned was about sulphate transfer and when that is impaired, things get "thick" and don't flow properly. I haven't researched this area to reasonably understanding it at this point, but my understand is that it would affect bile and lymphatic flow, so that would be a mechanical crippling of distribution of some nutrients, as with the manganese to the microbes in the gut that need, but also detoxification as the lymphatic system delivers toxins for disposal.
So, I am sharing this with people to share with their doctors and neurologist and for preventative reasons for the families of ALS patients.
One other point, glyphosate kills weeds by making them prone to disease by interfering with the shikimate pathway. It chelates minerals from the plants, and GMO plants have been modified to survive with reduced minerals and the amino acid deficiencies, so these foods do not help with the ALS nutritional problems. The amino acid deficiency of these plants match the amino acid deficiencies found in ALS patients. The paper for ALS is "Amino Acids as biomarkers in the SOD1G93A mouse model of ALS."
It just so happened very much by accident that I was looking at my sister's amino acid deficiencies from the nutraeval test that she had and I had just been reading about the amino acid deficiencies from the shikimate pathway and I stopped and looked again, and they matched and my sister eats organic, so GMO foods are not contributing to this problem in her, however, the nutritional deficiencies are still showing up, so the belief that we only get essential amino acids from our foods is likely wrong, we probably also get supplemented from out gut microbes, or perhaps compete with gut microbes for some nutrients.

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Saturday, July 23, 2016

Update to the anti-pathogen and nutrition enhancement approach to ALS

The cluster data from Guam on ALS shows the disease is linked to toxic cyanobacteria.  Mounting other evidence links the disease to viral response.  Additionally, there are links to fungal infections where they don't belong with ALS.  Even Lyme disease has strong links with ALS.

Both the cyanobacteria and Lyme disease play out with the same kind progressive loss of motor function it leaves the question as to whether the high levels of viral and fungal infections found in ALS patients are also producing toxins that follow the same disease pathway.  Additionally, it is known with ALS that the immune system appears to working overtime.

Additionally, ALS patients appear deficient in essential amino acids from the shikimate pathway, including tryptophan, tyrosine and phenylalanine and methionine production is also compromised.  Without sufficient nutrients from this pathway, serotonin, melatonin, melanin, epinephrine, dopamine, thyroid hormone, folate, coenzyme Q10, vitamin K and vitamin E production are compromised.

So, given these common links in ALS patients, it makes sense to fight back against this disease with an anti-pathogen, nutritionally enhancement approach to help the immune system that is working overtime to fight back.

Eat organic

Glyphosate chelates out essential minerals your liver requires to help your body eliminate toxins.  It also harms the gut microbiota and GMO foods are deficient in the same amino acids as ALS patients so everything about glyphosate and GMO foods amplifies known nutritional deficiencies in ALS patients.  Glyphosate soils have the same kind of reduced microbiome diversity as is seen in the guts of ALS patients.  Many ALS patients have gut issues that precede their ALS diagnosis and supplementation with glycine is often recommended to help with leaky gut, however, glyphosate may substitute in for glycine and compound health issues.

For more information on the hazards of GMO search "glyphosate pathways to modern disease."

Alternative energy - Coconut oil

By the time ALS symptoms show up mitochondria and ATP production is damaged.  An ALS mouse model study found that at 65 days the mice had a 23% reduction of phosphofructokinase, and 89% reduction by 105 days.  This enzyme is needed for glycolysis, which provides energy to the muscles.  Additionally, the mechanism the body is using to cope causes increased oxidative stress which is harmful.  Coconut oil has medium chain triglycerides that are also anti-bacterial making them an idea source of alternate energy that also help to fight pathogens.  Coconut oil sometimes requires time to adjust to consuming it.  Start with just a teaspoon.  If there is intestinal distress, wait until the next day to consume more, other wise have a teaspoon at each meal.  It may only take 2-3 days to work up to 3-6 tablespoons per day, and it may take up to two weeks for the body to adjust.

Coconut oil is also good to rub into skin to help with muscle cramping and spasms and the MCT are also absorbed through the skin.

Coconut oil also has stearic acid which helps with mitochondrial signaling.

Do a search on coconut oil fat bombs for ideas on how to eat coconut oil.

Rebuild cellular membranes - Phospholipids

The mitochondria in the liver of ALS patients have been found to have disrupted cell membranes and oversized mitochondria and Dr Garth Nicholson promotes lipid replacement therapy to help the mitochondria.  NTFactor is the propitiatory blend that he mentions in his talks that people can access without a prescription.

Naturals sources of phospholipids are raw organic egg yolks, organic liver and organic soy lecithin.  Kim Cherry, of ALSwinners, supplemented with 100 mg of Phosphatidylserine twice per day.  Phosphatidylserine is believe to promote rapid dead cell removal in smooth muscles.

Reduce inflammation - Balance Omega 6:3 Ratio

Processed and refined oils are inflammatory so they need to be avoided.  Processed foods tend to be inflammatory, so they need to be avoided.  Inflammation in the gut is linked to poor nutrient absorption and this is an extremely serious problem with ALS.

Eliminate all refined oils: soybean, corn, canola, sunflower, safflower and especially cottonseed oil.

Eliminating these oils goes a long way towards balancing your omega 6:3 ratio.  Mixing equal amounts of olive oil with flax seed oil keeps these oils relatively balanced.  Krill oil is a good omega 3 supplement and Odo's 3-6-9 oil is balanced with other beneficial components.

Glutamate toxicity

Glutamate is involved in the process that leads to neuron death.  The body releases glutamate as a protective mechanism to keep neurons firing, however, food additives have increase the concentration of glutamate in the blood to the range to 20-50 times of what we evolved with.  The blood brain barrier offers considerable protection in controlling all of this excess glutamate from reaching the brain, however, once the brain is diseased or injured, the blood brain barrier fails to regulate glutamate and over excitation of neurons is believed to be a mechanism in neuron death.  Glutamate and other compounds that over excite neurons to the point of death are called excitotoxins.  With ALS excitotoxins are about 100 times more damaging than when the blood brain barrier was doing its job.  Excitotoxins are found in almost all store bought dressings and salad dressing, HP sauce, barbecue sauce, etc., low fat foods, and most processed foods.  Excitotoxins need to be removed from the diet.

Anti-bacterial, anti-viral, anti-fungal foods and herbs

Ginger is has anti-bacterial, and anti-viral properties, but it is also anti-inflammatory, which is extremely good for the digestive track.  ALS patients have huge problems with inflammation in the digestive track, which is related to poor absorption of nutrients.  Have a piece of ginger the size of your thumb twice per day.  It can go into a smoothie, or it can be grated and served with half of a fresh squeezed lemon in water.

Turmeric has anti-bacterial, anti-oxidant and anti-inflammatory properties.  It can be used as seasoning for vegetables or added to salad dressing or get the actual turmeric root and add some to a smoothie, but first time users be aware that it stains.

Garlic is anti-bacterial, anti-viral, anti-inflammatory, anti-oxidant and rich in selenium, which is important for liver function.  Garlic can be crushed into homemade salad dressing, with 1 tbs cold pressed olive oil, 1 tbs cold pressed flax seed oil and apple cider vinegar.  Use herbs like parsley and rosemary to further up your food choices with healing properties.  Healing properties are lost with cooking.  It can also be mixed in hummus.

Other foods/herbs with healing properties to choose from, some which can be consumed via herbal teas:
  • onions
  • cabbage
  • rosemary
  • cilantro (extremely good for liver as well)
  • cloves
  • cinnamon
  • oregano
  • marjoram
  • sage
  • thyme
  • licorice root
  • peppermint
  • cayenne
  • astragalus
  • wild cherry bark
  • dandelion root and greens
  • mustard
  • chamomile
  • echinacca
  • green tea
  • aloe vera
Aloe vera is a large source of mannose and that help to protect you from lectins and to make mannose binding lectin, which helps innate immunity.

Usnea is a very powerful herb and is made into a tincture for use.  It has strong anti-microbe and anti-inflammatory properties.  It has precautions for the liver if taken orally.

Raw honey is anti-bacterial as well, but sugars should be avoided as much as possible.  Never heat the raw honey or the anti-bacterial properties are destroyed.  Use raw honey sparingly if sweetening is needed but try and limit to no more than a tablespoon per day.

Quinine is anti-malaria and is in tonic water.  Sevia tonic water has 27-29 mg of quinine and is sweetened with stevia.  Some people report this helps with muscle cramps.


Magnesium is involved in thousands of processes in the body and a deficiency starts to show up with muscle cramping.  The ReMag pico magnesium is absorbed the best.

Probiotics are essential at every meal.  An ALS mouse study found a leaky gut and a microbiome shift by 60 days old.   You want to constantly encourage and protect the growth of good bacteria in your gut against this harmful change.  The anti-microbe foods and herbs can also reduce the population of good microbes, so they need to be replaced and over crowd the bad microbes.  Fermented foods contain large amounts of probiotics, but you can kill off bad pathogens too fast and they release toxins as they are killed off.  Fermented foods can be added after a couple weeks of taking probiotics.  Fermented foods include things like live culture sauerkraut or kefir.

GABA has a calming effect in the brain and foods that are good precursors for GABA include cabbage, raw spinach, kale, parsley, beans, beets, carrots, brussels sprouts, and wild salmon.  Eating precursor foods ensures a continuous supply of GABA.

There are many recommendations for vitamins, D3, C, E, B complex.  There is also a very good write up on an approach to ALS on ALStdi that lists the "pile of pills."  These need to be evaluated on an individual basis.

Vitamin E is very complicated because it actually has 16 different isomers, 8 of which are biologically inactive stereoisomers, and the different parts interfere with absorption if taken at the same time.  An long time ALS survivor with expertise in molecular chemistry takes Swanson Vit E mixed tocopherols, 400 IU, once a day, and TOCO-30 Tocotrienols from Barlowe's, 500 mg, twice a day, with coconut oil and at different times because of the interference.

Eat According to the Wahls Protocol

Dr Terry Wahls was fully in a wheel chair for MS and she reversed her MS to become an active person again through the diet she developed by looking at the what the mitochondria need to work properly.  With ALS the mitochondria are very broken, so the diet has the proper nutrition to fix the mitochondria.

  1. Consume 3-6 tablespoons of coconut oil per day.  Avoid all processed oils.
  2. Remove MSG and hidden forms of MSG.
  3. Ensure adequate phospolipids in the diet and/or supplement. 
  4. Have thumb sized piece of ginger 2x per day.
  5. Have 750 mg of turmeric per day.
  6. Eat whole bulbs of garlic.
  7. Take usnea 2x per day (liver precaution)
  8. Avoid sugars and processed foods.
  9. Take 500 mg Krill oil/day or Udo's 3-6-9 oil
  10. Take 300-500 mg of Magnesium (not oxide) 2x per day, or 1 tsp 2x day of ReMag
  11. Take probiotics with every meal, rotate strains but try for lactobacillus rhamnosus inclusion
  12. GABA 250 mg 2x/day
  13. 2000 IU vitamin D3
  14. 1000 mg Vitamin C
  15. 400 IU Vitamin E mixed tocopherols 1x/day, 500 mg mixed tocotrienols 2x/day, all different times
  16. Take B vitamins
  17. Watch "Minding your Mitochondria," for an overview of how to eat.
Avoid anything and everything fortified with iron.

For the next step, in order to get doctors to assist you, you need to work on a complete medical history.

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Saturday, April 09, 2016

In ALS, is TDP-43 being produced to control herv-k?

I was just commenting on "Evidence for Fungal Infection in Cerebrospinal Fluid and Brain Tissue from Patients with Amyotrophic Lateral Sclerosis" and by the time I finished I had a question about TDP-43.

I believe that artificial deficiencies in complement control are playing a role in creating massive confusion about what is happening in ALS, and candida is a very good example.
What I have been studying in the research on ALS is from a complement perspective. Factor h is supposed to be pulling C3b off the spines of ALS patients and that isn't happening, so, what's happening to factor h? This is where I started looking. I lead me to the mass range of complement evasion strategies, and candida is huge in this department.
The other thing that I found about candida is that it is cleaved by galectin-3 without going through complement (Kohatsu et al), but it favour salmonella (Li et al) . Galectin-3 has been identified as cadidate biomarker for ALS (Zhou et al).
So, then you have studies on galectin-3 in ALS (Lerman et al), and I guess because galectin-3 appears to be increasing quite out of control, they did a gene knock out for galectin-3 and progression was faster.
I haven't found a specific reference for this, "Borrelia binds GAL-3 to induce Walerian degradation of myelin tissues, (creates artificial GAL-3 deficiency)." Dinglasan et al has many evasion strategies of borrelia but it did not specifically mention galectin-3. Binding factor H is a big problem with borrelia.
Candida has a lot of complement evasion strategies (Lou et al). It captures host complement regulators, such as Factor H, FHL-1, C4BP and plasminogen from human plasma to its surface. Creating artificial deficiencies in these complement components is a big problem in ALS. Factor H is needed to protect self cells and I believe C4 is a very critical player in ALS.
So then, cleaving candida with galectin-3 leads to potentially more salmonella problems and salmonella can also mess up complement. According to Ho et al, salmonella can also bind C4b and factor h, so more messing up these complement components. This same study mentions that E.coli can also evade complement with the same strategies. C4 is the second step to the complement cascade response.
Other pathogens can be messing up complement, Aspergillus also binds both factor H and C4b (Vogl et al), and B Steptococcus (Maruvada etal) and Streptococcus pyogenes (Haapasalo et al) both bind to factor H.
Aspergillus is probably huge in ALS. How do you get cluster data for ALS in an apartment building? (Melmed et al) My best educated guess is mold.
Back to how huge C4 is in ALS. Sekar et al have an excellent explanation and study on the different alleles of C4. Herv-k lives in C4 and is implicated in ALS (Li et al). According to Sekar et al, "First, RNA expression of C4A and C4B increased proportionally with copy number of C4A and C4B respectively (Fig. 3a, band Extended Data Fig. 4). These observations mirror earlier observations in human serum 24. Second, expression levels of C4A were two to three times greater than expression levels of C4B, even after controlling for relative copy number in each genome (Fig. 3c). Third, copy number of the C4–HERV sequence increased the ratio of C4A to C4B expression (P < 10 −7, P < 10 −2, P < 10 −3, respectively, in the three cohorts examined, by Spearman rank correlation)." So, a certain copy of C4 results in more herv-k and that copy is also associated with schizophrenia.
With messed up complement more C4 is needed to get the complement cascade going properly, but because of this mess, there is potentially way more herv-k.
Another interesting point, there is about 150 times the risk of ALS to Jewish pedigrees with schizophrenia in their family (Goodman et al).
And then it seems, TDP-43 suppresses retroviruses, for example HIV (Kuo et al). So then the question I have is about TDP-43, is it being produced to control herv-k?
It also seems that treatment with antivirals for HIV has been a beneficial treatment for HIV ALS patients (Smith et al).

Kohatsu, Luciana, et al. "Galectin-3 induces death of Candida species expressing specific β-1, 2-linked mannans." The Journal of Immunology 177.7 (2006): 4718-4726.
Li, Yubin, et al. "Galectin-3 is a negative regulator of lipopolysaccharide-mediated inflammation." The Journal of Immunology 181.4 (2008): 2781-2789.
Zhou, Jian-Ying, et al. "Galectin-3 is a candidate biomarker for amyotrophic lateral sclerosis: discovery by a proteomics approach." Journal of proteome research 9.10 (2010): 5133-5141.
Lerman, Bruce J., et al. "Deletion of galectin‐3 exacerbates microglial activation and accelerates disease progression and demise in a SOD1 G93A mouse model of amyotrophic lateral sclerosis." Brain and behavior 2.5 (2012): 563-575.
Dinglasan, Rhoel R., and Marcelo Jacobs-Lorena. "Insight into a conserved lifestyle: protein-carbohydrate adhesion strategies of vector-borne pathogens." Infection and immunity 73.12 (2005): 7797-7807.
Luo, Shanshan, et al. "Complement and innate immune evasion strategies of the human pathogenic fungus Candida albicans." Molecular immunology 56.3 (2013): 161-169.
Ho, Derek K., et al. "Functional recruitment of human complement inhibitor C4B-binding protein to outer membrane protein Rck of Salmonella." PloS one 6.11 (2011): e27546.
Vogl, G., et al. "Immune evasion by acquisition of complement inhibitors: the mould Aspergillus binds both factor H and C4b binding protein." Molecular immunology 45.5 (2008): 1485-1493.
Maruvada, Ravi, Nemani V. Prasadarao, and C. E. Rubens. "Acquisition of factor H by a novel surface protein on group B Streptococcus promotes complement degradation." The FASEB Journal 23.11 (2009): 3967-3977.
Haapasalo, Karita, et al. "Acquisition of complement factor H is important for pathogenesis of Streptococcus pyogenes infections: evidence from bacterial in vitro survival and human genetic association." The Journal of Immunology 188.1 (2012): 426-435.
Melmed, Calvin, and Charles Krieger. "A cluster of amyotrophic lateral sclerosis." Archives of neurology 39.9 (1982): 595.
Sekar, Aswin, et al. "Schizophrenia risk from complex variation of complement component 4." Nature 530.7589 (2016): 177-183.
Li, Wenxue, et al. "Human endogenous retrovirus-K contributes to motor neuron disease." Science translational medicine 7.307 (2015): 307ra153-307ra153.
Goodman, Ann B. "Elevated risks for amyotrophic lateral sclerosis and blood disorders in Ashkenazi schizophrenic pedigrees suggest new candidate genes in schizophrenia." American journal of medical genetics 54.3 (1994): 271-278.
Kuo, Pan-Hsien, et al. "Structural insights into TDP-43 in nucleic-acid binding and domain interactions." Nucleic acids research 37.6 (2009): 1799-1808.
Smith, Bryan, et al. "Activation of HERV-K and response to antiretroviral therapy in patients with HIV infection and motor neuron disease (S37. 001)." Neurology 84.14 Supplement (2015): S37-001.

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Wednesday, February 03, 2016

Factor h and ALS

Lyme has factor H evasion strategies and in innate immunity its role is to amplify the immune response.  I do not believe that lyme is the only pathogen involved in ALS, but that together a group of them with factor H evasion strategies mess up complement and factor H so it no longer does its job properly.

Lyme divides very slowly compared to other bacteria and it forms these "blebs" in response to antibiotics.  Antibiotics do not kill the blebs and there is evidence that the blebs do not come out in the presence of antibiotics.  Lyme is also extremely easy to kill when it is not in the protective bleb form.  Dr Eva Sapi is the foremost expert researcher into lyme,

Factor h is a part of complement and lyme can bind to it and hide from the body's innate immunity.  Factor h is responsible for pulling C3b off host cells and it isn't doing its job in the spines of ALS patients.

There is medical evidence that complement, or innate immunity, is involved in ALS.

  • The complement factor C5a contributes to Pathology in a Rat Model of ALS,, "With end-stage disease, SOD1G93A rats displayed marked deposition of C3/C3b, and a significant up-regulation of the C5aR in the lumbar spinal cord."
  • Complement upregulation and activation on motor neurons and neuromuscular junction in the OSD1 G93A mouse model of familial ALS,, "We determined complement expression and activation in the SOD1 G93A mouse model of familial ALS (fALS). At 126days, C3 mRNA was upregulated in spinal cord and C3 protein accumulated in astrocytes and motor neurons. C3 activation products C3b/iC3b were localized exclusively on motor neurons. At the neuromuscular junction, deposits of C3b/iC3b and C1q were detected at day 47, before the appearance of clinical symptoms, and remained detectable at symptomatic stage (126days). Our findings implicate complement in the denervation of the muscle endplate by day 47 and destruction of the neuromuscular junction and spinal neuron loss by day 126 in the SOD1 G93A mouse model of fALS."
So, the stuff killing the neurons is from complement.  And, lyme can hide from complement, and therefore innate immunity, and it binds to factor H, which is supposed to be protecting host cells.
This paper, Evidence for Fungal Infection in Cerebrospinal Fluid and Brain Tissue from Patients with ALS,, means that you can not ignore candida in ALS.  Page 552 on this paper, where they talk about the results of looking at the brains of 3 deceased ALS patients, "the most striking finding was that C. albicans appeared in all three patients."  They tested 5 ALS against 3 controls for the spine and the C. albicans antibodies were on average 12 times higher in ALS compared to the controls.  C.famata 5 times, penicillium double, enolase 1.5 times and β tubulin peptide about 4 times the antibodies over the controls.  C.glabrata, C.parapsilosis were about the same in the ALS patients and the controls.
Unfortunately, Candida can also hide from factor H, Immune evasion of the human pathogenic yeast Candida albicansPra1 is a Factor H, FHL-1 and plasminogen binding surface protein,

You also have to ask the question, it the C3b landing on the spine because the candida is there?  I have not seen a study look for lyme on patient's spine, but could that also be a reason for the C3b to be on patient's spine?

The lyme binds factor H via OspE proteins, Outer surface protein E antibody response and its effect on complement factor H bind to OspE in Lyme borreliosis,
I don't have a reference for this as it was a question I asked an ALS research, but gene expression for factor H is up in the ALS mouse model after the onset of symptoms, but it is unknown whether it is actually being produced, or what is happening to it.  I don't think the mouse model has lyme, but it could have other pathogens with factor H evasion strategies messing it up.
When I learned the stuff clogging up the spines of ALS patients was coming from complement and the role of factor H, I started trying to find pathogens with factor H evasion strategies as it just seemed to me that since there is something wrong happening in innate immunity with ALS, it would be a good idea to look at these other pathogens and be on guard for them, and it also seemed this could be a reason for differences in ALS.
Pathogens with factor H evasion strategies:
  • SteptococcusAcquisition of factor H by a novel surface protein on group B Streptococcus promotes complement degradation,
  • Salmonella with E.ColiHuman Complement Factor H Binds to Outer Membrane Protein Rck of Salmonella, (I know of a PALS whose ALS onset was after a food poisoning and he passed away 9 months later.)
  • AspergillusImmune evasion by acquisition of complement inhibitors: the mould Aspergillus binds both factor H and C4b binding protein,
  • B. duttonii, B. recurrentisRelapsing fever spirochetes Borrelia recurrentis and B. duttonii acquire complement regulators C4b-binding protein and factor H,
  • Haemophilus influenzae, Identification of a Haemophilus influenzae factor H-Binding lipoprotein involved in serum resistance.,
  • Neisseria meningitidis, The Factor H Binding Protein of Neisseria meningitidis Interacts with Xenosiderophores in Vitro,
  • Streptococcus pyogenes, Acquisition of complement factor H is important for pathogenesis of Streptococcus pyogenes infections: evidence from bacterial in vitro survival and human genetic association,
This is what I've found.  From what I've seen in the ALS community, Lyme, mold and candida keep coming up.

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