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ALS – Trying Luck With Uncle Google

This entry is part 28 of 35 in the series ALS Experimental Theory

Please don´t be concerned with the title – I´m indeed not linking the disease with the technology giant in any way. I have just done another experiment when thinking about search engine optimization.

In this post I´m just sharing my results from the game I decided to play for a while with Google and its famous search algorithm . Today everyone is familiar with Google. Not many people including me use the second I´m feeling lucky search button. It basically opens automatically a highest ranked web page related to the search text phrase entered. Now let´s try few examples which basically correspond with the conclusion of ALS Experimental Theory (i.e. the post series on ALS you are just reading now).

Example #1

In the first example I was directed to a Washington Post article​1​ whose title says The man who beat Lou Gehrig’s disease. I indeed was not aware of this case so Google helped me. On repeated attempts I was directed to different pages already – or am I so bad that I haven´t remebered exactly what I typed first? Who knows. Anyway this article describes Ted Harada case, a man who received experimental treatment consisting of injecting stem cells directly into place of injury (or inflammation?) in his spinal cord. And guess what, it worked for him. His motoric functions improved, at least it is clearly stated. Please read the article for more details. A question naturally arises – why me or anyone else is not really aware of it and ALS remains a deeply unresolved problem? Unfortunately Ted Harada then developed a brain cancer which was already fatal for him. I need to admit I was little bit emotional when I read about it – it again fully corresponds with the ALS Experimental Theory I presented on this site and this unfortunate consequence is even mentioned in my last “interview like” post. If people only hack and don´t get to the root cause the disease will find another way and everyone who lands on this website should be ideally leaving with a possibly new information – ALS is most likely caused by viral and bacterial infections. It is not surprising cancer is highly suspected to be caused by EBV as well. Perhaps I will analyze cancer much closely in future and in similar depth as I tried with ALS. Many my relatives died on cancer so it is sort of obligation for me.

Example #2

In the second example I used above search phrase and I was immediatelly directed to already familiar National Institute of Health (NIH) website but scientific article​2​ describing possible role of enteroviruses. Well it is not the herpetic virus which I mainly suspect but the human enterovirus sounded really familiar to me. I actually included short citation on HERV virus in my Stealth Enemy post too. That is a good catch! I´m very grateful I got this idea to play luck with Google. I went throught the article and I would summarize it for my readers as I doubt everyone will get to reading the scientific article, still it is pretty accessible text and every person with real interest in ALS deciphering can follow it.

  • These EV viruses are usually part of our intestinal tract and usually do not cause big harm.
  • However above is not always true as there are more virus types and some can cause very bad damage to central nervous system (CNS). For example poliovirus. I also mentioned this virus on my site before so everyone should really realize I´m not super crazy fool but strange kind of researcher who is pretty close, but OK, I´m just analyzing texts and articles and I compare it with my real life ALS experience. This poliovirus can really go wild under certain conditions and cause paralysis to the infected person.
  • Since brain and CNS is a very fortified place in terms of protection by immune system, virus won´t reach it easilly. Still in some cases the virus probably succeeds and penetrates all those lines of defense. Science is considering three main ways of brain infiltration. First is by infecting PNS and getting access to nerve system which it leverages and gets to CNS. This would be in line with typical ALS symptoms, or not? People often register some problem with limbs which is PNS (peripherial nerve system). Second possible way can be by somehow penetrating the Blood-Brain barrier, meaning the virus is spread in blood and finds a way even through such heavilly protected gate like BBB. For me the most important way of infiltrating the brain is the third one. Here it is assumed the virus can actually get to brain in Trojan horse fashion – who wouldn´t heard about the famous siege of Troja, right? Perhaps movie with Brad Pitt helped to educate people more 😉 So in this case the virus can actually hijack immune cells like macrophags, dendritic cells or lymphocytes. This would make great sense to me.
  • So what is the problem with convicting the virus from causing ALS? Again it is this problem with statistics and inability to reliably find it in tissue samples. It is really weird how these scientists work. Please note following. Three studies revealed the virus incidence is 60-88% in ALS patients which is very high number, moreover if the control set, meaning nonALS persons show 0-14% incidence of the virus. Virus was detected even in the “brain fluid” (CSF) of ALS patients. However then there are other studies which fail to find anything and guess what! The article states it is probably due to some differences in methodology, in samples taken etc. Is science really like that? Someone finds something interesting. Then someone tries with perhaps sloppy approach and does not find anything. Conclusion? Nothing is confirmed, science is in doubts and confusion as two teams did not get to same results? Holy crap, I have no words for such scientifical approaches. 😲😤🤯 But OK, it is not easy task. Anyway why would you need to find your lost car keys twice to realize you have actually found it?

I´m adding few citation below. As a reader you can just ask yourself, if you ever heard about viral theory in case of ALS.

Although EVs are regarded as highly lytic viruses and EV-related diseases are commonly resulted from acute infection, EVs, such as poliovirus (Julien et al., 1999), EV-A71 (Han et al., 2010), and coxsackievirus (Feuer et al., 2009), can persist in various tissues, including the CNS. Glial cells and neuronal progenitor cells were reported to be the sites of CVB3 persistence (Feuer et al., 2009; Zhang et al., 2013). Multiple viral and host factors, including viral receptors, viral mutations, viral evasion of host immune response, and host translation machinery, participate in establishing a persistent EV infection (Rhoades et al., 2011; Huang and Shih, 2015). Latent EVs might be reactivated years later, either spontaneously or in response to exogenous stimulations, such as local trauma (Andréoletti et al., 2000; Feuer et al., 2002). EV persistence in cardiomyocytes and pancreatic cells has been associated with chronic clinical conditions, such as dilated cardiomyopathy and type 1 diabetes, mainly through continuous inflammatory responses (Chapman and Kim, 2008; Oikarinen et al., 2012). However, the long-term impacts of EV infection within the CNS are largely unclear. Clinically, it is observed that polio survivors decades after the recovery from the acute paralytic poliomyelitis can develop post-poliomyelitis syndrome, a neurological disorder characterized by new and progressive muscular weakness, accompanied by the detection of defective viral particles in the cerebrospinal fluid of some patients (Dalakas, 1995), indicating a possible long-lasting effect of latent poliovirus infection. In addition, a murine model has shown that a neonatal CVB3 infection can have a chronic impact on neurogenesis and CNS development, further supporting a potential link between early subclinical infections and late neurological sequelae (Ruller et al., 2012)​2​.

A potential role of EVs in ALS has been proposed for decades due to their ability to target motor neurons and the development of the ALS-like post-poliomyelitis-syndrome (Ravits, 2005). Multiple clinical studies have been conducted to detect EVs in ALS patient tissues; however, the available data are controversial and inconclusive. Using RT-PCR, three studies reported a 60%–88% incidence of EV genome detection in spinal cord/brain of ALS patients, compared to 0%–14% in controls (Woodall et al., 1994; Berger et al., 2000; Giraud et al., 2001). Additionally, RT-PCR analysis of cerebrospinal fluid showed EV detection in 14.5% of 242 ALS patients and 7.6% of 354 controls (Vandenberghe et al., 2010). However, three additional studies failed to detect EV RNA in spinal cord/brain of either ALS patients or controls (Swanson et al., 1995; Walker et al., 2001; Nix et al., 2004). The discrepancies between these studies are likely due to methodological differences, such as the use of fresh vs. archived (or frozen vs. fixed) tissues, and differences in PCR primers/amplification methods, which can all affect the integrity of viral RNA and the sensitivity/specificity of viral genome detection. Moreover, the stage of the disease when samples are collected may also be critical for viral detection, as viruses may be detectable or active only in certain phases of the disease or in only a subset of patients​2​.

This is a clear and scientifical evidence the role of viruses plays some role. The problem is the mechanics is unknown and cure is not available. However I repeat again – trust your immune system and give it a maximal support. Healthy immune system can resolve any problem, it can fight any bacteria, it can fight any virus, but only when it is in great shape. On contrary humans are unable to cure majority of viral infections and as we already know they apply pretty silly methods in research.

Example #3

Another example is similar to the previous one but now I´m trying luck with bacterial infections. Note I highly suspect ALS patients are under combined attack of more pathogens – viral as well as bacterial. So where did I land? It is again nice result. I´m directed to following article​3​ which I also haven´t read before, good shot, thanks Uncle Google. Wow, I need to cite the whole article abstract as it really is important and 100% in line with ALS Experimental Theory.

Despite great efforts in the investigation, the exact etiology of amyotrophic lateral sclerosis (ALS) is a matter of intensive research. We recently advanced the idea that ALS might be caused by fungal infection. Indeed, fungal yeast and hyphal structures can be directly visualized in neural tissue of ALS patients, and a number of fungal species have been identified in the central nervous system (CNS). In the present work, we tested the possibility that bacterial infections can accompany these mycoses. Our findings establish the presence of bacterial DNA in different regions of the CNS from all ALS patients examined. Specifically, we used PCR and next generation sequencing (NGS) to precisely determine the bacterial species present in ALS tissue. Consistent with these findings, immunohistochemistry analysis of CNS sections using specific anti-bacterial antibodies identified prokaryotic cells in neural tissue. Finally, we assayed for the repeat expansion of the hexanucleotide repeat GGGGCC in C9orf72, which is considered the most common genetic cause of ALS in patients, using DNA extracted from ALS CNS tissue. We failed to find this repeated sequence in any of the eleven patients analyzed. Our results indicate that bacterial DNA and prokaryotic cells are present in CNS tissue, leading to the concept that both fungal and bacterial infections coexist in patients with ALS. These observations lay the groundwork for the use of appropriate therapies to eradicate the polymicrobial infections in ALS​3​.

How it is possible the article does not mention Borrelia spirochetes? I would expected them there, is that another forgotten link? In ALS Experimental Theory these bacteria play critical role but I would not deny any other or fungi per se. For me all are just pathogens and they all are found and confirmed in ALS patients.

Example #4

Now a final example – of course I could not finish the post without trying luck with heavy metals. Their effect is really highly suspected to contribute to the disease development and I also mentioned it on this website. In this case Uncle Google sent me right to the following article​4​. Let´s also start with the full abstract.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder that affects central and peripheral motor neuron cells. Its etiology is unknown, although a relationship between genetic background and environmental factors may play a major role in triggering the neurodegeneration. In this review, we analyze the role of environmental factors in ALS: heavy metals, electromagnetic fields and electric shocks, pesticides, β-N-methylamino-L-alanine, physical activity and the controversial role of sports. The literature on the single issues is analyzed in an attempt to clarify, as clearly as possible, whether each risk factor significantly contributes to the disease pathogenesis. After summarizing conflicting observations and data, the authors provide a final synthetic statement​4​.

I would recommend reading the article, at least the conclusion sections of each factor. It is surprising for me that metals were not found to be so important – can we trust it? However in terms of pesticides science agrees without any hesitation. A clear connection with my article and Gulf War is established.

Interest in pesticides grew following the observation of an increased incidence of ALS among Gulf War veterans, albeit in the absence of sufficient epidemiological evidence on this population. Furthermore, pesticides seem to be implicated in the pathogenesis of other neurodegenerative disorders, particularly PD. Indeed, a higher incidence of neurodegenerative disorders, such as PD and ALS, among subjects from rural areas is documented in the literature (Sutedja et al., 2009).​4​

Strong evidence indicates that pesticides play a role in ALS. This, in addition to the involvement of pesticides in other neurodegenerative diseases such as Parkinson’s disease, leads to the conclusion that they are a reliable risk factor for neurodegeneration.​4​

The article also mentions the higher risk of ALS in sports. The study in italian soccer is quite known and it is not clear what caused the relatively high disease incidence among italian soccer players. The use of drugs is suspected though. In the experimental theory drugs are known triggers as described here.

Another interesting fact is the high ALS ocurrence in the pacific – Guam island and Kii Peninsula in Japan. On Guam a cycad seeds which people started to eat is mentioned as a possible factor. In the Japan location it was suspected drink watter low on calcium and magnesium could contribute to the higher incidence of ALS. I also know the importance of magnesium. It is on the list. I would ask – what about radiation? Perhaps the nuclear fallout together with the before mentioned deficite played role. Radiation and toxicity in general is considered a risk factor. Please note it is all about adding factors together – it is clear one such thing like one source of toxicity is not confirmed as a cause of such complex disease like ALS. Note the toxicity, liver factor and possible consequences on complement system which can appear problematic in case of fighting infections.

The deficit of magnesium contributes to cramps, muscle twitching. Magnesium also plays important role in endocrinal system and nerve system. Information for any ALS patients.

Although many toxins have been found in cycad tissues used for human consumption, none have emerged as the clear culprit of neurodegeneration​5​.

The Koza, Kozagawa and Kushimoto (K.) area in the Kii Peninsula of Japan was reported to have a higher incidence of ALS in the 1950s than other areas of the world (1–5). Epidemio-logic research showed that drinking water sourced from Kozagawa River in the K. area contained severely low levels of Ca and Mg, and Ca/Mg deficiency was speculated to have a role in the development of ALS in these areas (5,6)​6​.

Summary

  • I did not plan to write this post, it was rather instant idea.
  • However today I also tested Google search and SEO for my site and did some basic tests involving “Anthony William”. During this work I found some articles heavilly criticizing him and again accusing him from pseudoscientifical approach. It already was not surprising for me the critics itself used very non-scientific approach. A real example of hypocracy! That was sort of red flag for me and I started thinking about writing a post on this. However then I got back to work with Google.
  • Now I have just realized I actually provided a great support to people like Anthony William Coviello. Now I´m ignoring some of the business aspects of his work but all I can write here is that the scientifical sources I hit during Google plays are in non-trivial correlation with what Mr. William states as well. Viruses, bacteria, fungi, metals, pesticids, various deficiencies – this all you can find in his work so why the conflict? I´m leaving it for readers to think about it. Never underestimate natural and non-harmful detoxication, it is a great relief to immune system and as I wrote everyone wants immunity in top shape, a ruthless and fast killer of all bad pathogens so chronic inflammation is not allowed to develop. Doctors don´t like when people heal by themselves but if all they can provide is death sentencing diagnosis what are they expecting?
  • I may still write the supportive post but this should already help as well.
Is there still someone who thinks ALS patients are not under attack of multiple infectional agents? Please show me someone or direct him to this website! There is plenty of referenced scientifical material to read.

References

  1. 1.
    Thiessen MA. The man who beat Lou Gehrig’s disease. WashingtonPost. Published 2017. Accessed February 2021. https://www.washingtonpost.com/opinions/the-man-who-beat-lou-gehrigs-disease/2017/01/03/5cf898e4-d1b4-11e6-945a-76f69a399dd5_story.html
  2. 2.
    Xue Y, Feuer R, Cashman N, Luo H. Enteroviral Infection: The Forgotten Link to Amyotrophic Lateral Sclerosis? Front Mol Neurosci. 2018;11:63. doi:10.3389/fnmol.2018.00063
  3. 3.
    Alonso R, Pisa D, Carrasco L. Searching for Bacteria in Neural Tissue From Amyotrophic Lateral Sclerosis. Front Neurosci. 2019;13:171. doi:10.3389/fnins.2019.00171
  4. 4.
    Bozzoni V, Pansarasa O, Diamanti L, Nosari G, Cereda C, Ceroni M. Amyotrophic lateral sclerosis and environmental factors. Funct Neurol. 2016;31(1):7-19. doi:10.11138/fneur/2016.31.1.007
  5. 5.
    Forest R. Cause of WWII-era ALS Cluster on Guam May Be Younger Cycad Seeds. ALSNewsToday. Published 2020. Accessed February 2021. https://alsnewstoday.com/news-posts/2020/09/08/young-cycad-seeds-may-be-source-of-als-cluster-on-guam-in-world-war-two-study-says/
  6. 6.
    Kihira T, Yoshida S, Kondo T, et al. An increase in ALS incidence on the Kii Peninsula, 1960-2009: a possible link to change in drinking water source. Amyotroph Lateral Scler. 2012;13(4):347-350. doi:10.3109/17482968.2012.674140
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Trace #7 – Fuzzy Disease Scope

This aspect of ALS disease is very important and it could actually indicate also other primary trigger than infection. Anyway we know ALS patients definitely are not pathogens free - it is rather the opposite. The insidious character of the hard to recognize silent progression presents a big trap which is kind of "supported" even by the medical system.

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