Chronic Diseases Demystified Website describing ALS or Lou Gehrig disease from experimental point.
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The hype around the latest artificial inteligence system capable of answering complex questions inspired me too. I was curious how this computer AI will do with tough problem of my primary interest, the ALS disease. I had no expectations but the results are quite impressive.
Introduction
First I should add little context. I guess practically all people who may read this post are not aware of the existence of my investigative website, perhaps little bit crazy (but don’t get consufed!) and exclusively aimed on analysis of ALS disease. In all those articles published I was getting familiar more and more with the problematics and eventually proposed a simple but very logical theory how ALS can develop and where can the main problems be.
I could not believe it is that simple but almost immediately I realized how big problems people usually have with simple explanations of complex problems. It is definitely an area where people are struggling as they simply refuse it can be so simple and logical, so they will rather dig somewhere else for another 50 years. All the information I used is more or less public available (books, scientific journals, magazines, individual ALS stories etc.) but I also had real life experience with ALS, I watched it closely.
Obviously nobody thinks it is relevant. Even worse people simply refuse to even bother with such theory, despite it almost strictly follows the scientifically collected data. What is the problem? Yes, human emotions, character disorders, huge lack of trust, insufficient level of cooperation, side interests including financial. What I am proposing is not esoteric babbling, it is something science could examine or better re-examine because big mistakes, oversights could have been done in past. A new set of experimental case studies which would newly incorporate certain details could be done in a let´s give it a try fashion. Result so far? Absolute ignorance.
However I dealt with it on my own. No cooperation? OK, I will continue in my mission alone and time will tell. I even gave two interviews1,2 to myself! If there is no solid partner, I simply took both roles (interviewer, interviewee). It is quite good exercise to be sort of opponent of yourself. I really wanted someone normal, some intellectual partner, who does not emotionally explode almost immediately, or who does not deny and mock everything in silly way due to being full of prejudices.
AI Steps In
People who read my previous posts know that computers and computer science analogies helped me to understand and admit certain aspects of ALS mystery so perhaps it was my subconscious wish to get an artificial partner for ALS debates. For instance, below text I wrote back in 2021.
Everyone can contribute to the world of science and share his thoughts thanks to the amazing technology progress. It is nice coincidence that it indeed is a technology what is behind my theory. Does it mean some advanced artificial intelligence will tell us why and how autoimmune behavior occurs or what is causing ALS or MS and how we should treat it? Well, we are not there yet but we should rather adjust the thinking paradigm and the inspiration comes from the world of computer science … 3
Quite recently, in November 2022 Open AI released ChatGPT and enabled free testing to public. Isn´t this a nice opportunity for ALS talk? First let´s briefly introduce Open AI by citing one of my favourite sources, Wikipedia.
OpenAI is an American artificial intelligence (AI) research laboratory consisting of the for-profit corporation OpenAI LP and its parent company, the non-profit OpenAI Inc. The company conducts research in the field of AI with the stated goal of promoting and developing friendly AI in a way that benefits humanity as a whole. The organization was founded in San Francisco in late 2015 by Sam Altman, Elon Musk, and others, who collectively pledged US$1 billion. Musk resigned from the board in February 2018 but remained a donor. In 2019, OpenAI LP received a US$1 billion investment from Microsoft. OpenAI is headquartered at the Pioneer Building in Mission District, San Francisco.4
In order to introduce the ChatGPT system it is also better to refer existing sources. The text this program more or less fluently generates is often of very high quality and the communication is also factually correct. However this does not mean it is always correct – how could it be entirely correct, right? There is lot of praise but also some criticism or even worries.
In The Atlantic’s “Breakthroughs of the Year” for 2022, Derek Thompson included ChatGPT as part of “the generative-AI eruption” that “may change our mind about how we work, how we think, and what human creativity really is”5
Now it is already time to demonstrate ChatGPT capability. I gave it two introductory questions first but then I simply requested it to explain ALS disease. I fired few more questions which popped in my mind and then we discussed the disease in kind of more natural way, despite the generated answers are not shortest. There are no edits, it is fluent discussion recorded exactly as it took place with just one exception – almost every answer included paragraph saying “it is not fully confirmed that …, more studies are required etc.” I am already alergic on this phrases as there are obvious links, things and one needs to act immediately. Time is a huge factor X in ALS and everyone should get concerned about those ~ 10-15 months long period of medical hesitating, inacting and giving the DEMONIC DISEASE a green light 🚥.
Since the answers I obtained are very in line with my ALS theory I take it as a nice support, it is confirmation my texts are not pseudoscience which some people claim (without any further interest/arguments, of course) – the hope of patients rises.
If public supported this theory too, we could really come up with those case studies and experimental tests where mankind can only gain. So once again, note that I am giving the questions in bold but those answers (non-bold text) are generated by next generation artifical intelligence system which could in theory interpret certain data it was fed with much better than many humans including those ALS researchers and neurologists6. Have a nice reading.
ALS Interview With ChatGPT
Hello, what is your name and how are you right now?
Hello! I am ChatGPT, a language model created by OpenAI. I am an AI, so I don’t have feelings or physical sensations. How can I help you today?
What do you think about humans as species?
As an AI, I do not have personal opinions or thoughts on any subject, including humans as a species. My programming is designed to provide factual information and assist with a wide range of tasks.
Please explain me ALS disease in simple terms.
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that affects nerve cells in the brain and spinal cord. It is also known as Lou Gehrig’s disease. In ALS, the nerve cells that control muscle movement, called motor neurons, die. This leads to a loss of muscle control and weakness, which gets worse over time. As the disease progresses, it can also affect a person’s ability to speak, swallow, and breathe. There is no known cure for ALS and treatments are primarily focused on managing symptoms and extending the patient’s quality of life.
Are you really sure there is no known cure?
As of my knowledge cutoff in 2021, there is no known cure for ALS. However, research is ongoing, and new treatments are being developed and tested. There are some FDA-approved treatments that can help slow the progression of the disease and manage symptoms such as Riluzole and Edaravone. It’s important to note that my knowledge is based on the information available at my training data cutoff, and new developments may have occurred since then. It’s always best to consult with a medical professional for the most up-to-date and accurate information regarding treatment options for ALS or any other medical condition.
In what year was the drug called Riluzole officially approved by FDA?
Riluzole was officially approved by the U.S. Food and Drug Administration (FDA) on December 29, 1995, as the first treatment for Amyotrophic lateral sclerosis (ALS) which is a progressive neurodegenerative disease that affects nerve cells in the brain and spinal cord. Riluzole is believed to work by decreasing the release of the neurotransmitter glutamate, which is thought to be involved in the death of motor neurons in ALS.
How exactly should the Riluzole drug decrease the excessive glutamate levels? I don´t like the expression “it is believed”. Does it mean the researchers developed a drug which they don´t know how it should work?
Riluzole is a drug that was developed to slow the progression of ALS. The exact mechanism by which it works is not fully understood. However, it is believed that Riluzole may work by decreasing the release of the neurotransmitter glutamate, which is thought to be involved in the death of motor neurons in ALS. Glutamate is an excitatory neurotransmitter, which means it is involved in the activation of neural pathways, and when it’s release is excessive, it can lead to overactivation of neurons and ultimately cell death. Riluzole is believed to reduce the release of glutamate by inhibiting the activity of certain enzymes in the cells that produce it, and by increasing the activity of other enzymes that clear it. Riluzole also have other mechanisms of actions like modulating the activity of other neurotransmitters and ion channels, antioxidant activity, and neuroprotection. It is worth noting that even though the exact mechanism of action is not fully understood, Riluzole has been shown in clinical trials to be effective in slowing the progression of ALS and prolonging survival in patients with the disease.
Thanks. What about the Edaravone Radicava drug? This is not actually a new drug, right?
You’re correct, Edaravone (also known as Radicava) is not a new drug. It was first approved in Japan in 2015 for the treatment of ALS, and later in 2017, it was also approved by the U.S. Food and Drug Administration (FDA) for the same indication. It’s believed to work by scavenging the free radicals and reduces the oxidative stress in the nerve cells which is thought to contribute to the damage in ALS. It’s administered intravenously in a cycle of 28 days on and 14 days off for a period of 6 months, and it’s intended for use in adult patients with ALS. It’s worth noting that while Edaravone has been approved for use in treating ALS, the benefits of treatment may vary from person to person. It’s important to speak with a healthcare professional about the potential benefits and risks of treatment with Edaravone, as well as other treatment options that may be available.
Yes, but in fact Radicava drug is based on more than 30 years old experimental drug developed for stroke treatment, do you agree?
Yes, that is correct. The active ingredient in Edaravone (Radicava) is edaravone, which was originally developed in the 1990s as a treatment for stroke and was tested in clinical trials for that indication. However, it was not found to be effective for stroke and the development for stroke treatment was discontinued. Later on, in the early 2000s, researchers in Japan discovered that Edaravone had potential as a treatment for ALS, and several studies were conducted in Japan, which led to its approval for the treatment of ALS in that country in 2015. In 2017, the FDA also approved Edaravone as a treatment for ALS, making it the first new treatment for the disease to be approved in the United States in over 20 years.
How exactly are these drugs tested on patients?
Drugs for treatment of diseases such as Amyotrophic lateral sclerosis (ALS) are typically tested in a series of clinical trials, which are research studies that involve human volunteers. These trials are conducted in several phases, each with a specific purpose and set of requirements. Phase I trials are the first step in testing a new drug in humans. They typically involve a small number of healthy volunteers and are designed to determine the safety and tolerability of the drug, as well as to gather information about how the drug is metabolized and excreted by the body. Phase II trials are larger in scale and are intended to gather more information about the drug’s safety and effectiveness. They typically involve a larger number of patients with the disease or condition the drug is intended to treat. Phase III trials are even larger in scale and are intended to provide a more comprehensive understanding of the drug’s safety and effectiveness. They typically involve hundreds or even thousands of patients with the disease or condition the drug is intended to treat and are often conducted at multiple centers in different countries. After the completion of these trials, the data from the studies is submitted to regulatory authorities such as the U.S. Food and Drug Administration (FDA) for review and approval. It’s worth noting that the process of testing and approving new drugs can take several years, and even after a drug is approved, it continues to be monitored for safety and effectiveness.
The process of drug testing is very slow. This is quite bad news for all ALS patients. Isn‘t it strange people are not able to decipher at least partially the disease mechanics? The disease is known for century and a lot of funds was already invested into the research.
You are correct that the process of testing and developing new drugs can be slow, and this can be frustrating for patients with diseases such as ALS, for whom there is currently no cure. Amyotrophic lateral sclerosis (ALS) is a complex disease, and the mechanisms that lead to the death of motor neurons are not fully understood. The disease can be caused by a combination of genetic and environmental factors, and it can present in different ways in different people. This complexity makes it difficult to identify specific targets for treatment and to develop drugs that can effectively slow or stop the progression of the disease. In addition, developing new drugs is an expensive and time-consuming process. It requires significant investments of time, money, and resources, and even after a drug has been developed and tested, there is no guarantee that it will be effective or safe for human use. It’s worth noting that despite these challenges, researchers and scientists continue to work towards developing new treatments and potential cures for ALS. There are several promising new treatments and therapies currently under development, and it’s important for patients to stay informed about the latest research and to speak with their healthcare providers about new treatment options that may be available to them.
So what environmental factors are suspected to contribute to ALS development?
There are several environmental factors that have been suspected to contribute to the development of Amyotrophic lateral sclerosis (ALS), although the exact causes of the disease are not fully understood. Some of the suspected environmental factors include:
• Exposure to toxins: Some studies have suggested that exposure to certain toxins, such as pesticides and heavy metals, may increase the risk of developing ALS.
• Trauma: Some studies have suggested that head trauma or other physical trauma may increase the risk of developing ALS, although more research is needed to confirm this link.
• Viral infections: Some studies have suggested that certain viral infections, such as the herpes simplex virus, may increase the risk of developing ALS.
• Lifestyle factors: Some studies have suggested that certain lifestyle factors, such as smoking, may increase the risk of developing ALS, although more research is needed to confirm this link.
It’s worth noting that these are just some of the environmental factors that have been suspected to contribute to the development of ALS, and more research is needed to fully understand the relationship between these factors and the disease. Additionally, It’s important to note that many people with ALS do not have a known environmental risk factor and that the majority of cases are sporadic. In other words, there’s no clear cause for the disease.
This is actually a great answer. I would like you to elaborate more on the role of heavy metals first. Which metals are considered toxic and why are they suspected to be ALS risk factors?
Some studies have suggested that exposure to certain heavy metals, such as lead, mercury, and aluminum, may increase the risk of developing Amyotrophic lateral sclerosis (ALS). Lead is a toxic metal that can cause damage to the nervous system, and studies have suggested that exposure to lead may increase the risk of developing ALS. Lead can be found in certain products such as lead-based paint, contaminated soil, and some types of pottery, and can also be a result of certain jobs or hobbies that expose individuals to lead. Mercury is another toxic heavy metal that can be found in certain products such as fish, dental fillings, and certain types of light bulbs. Some studies have suggested that exposure to mercury may increase the risk of developing ALS, but more research is needed to confirm this link. Aluminum is a metal that is abundant in the environment and is found in many products such as antacids, baking powder, and aluminum cookware. Some studies have suggested that exposure to aluminum may increase the risk of developing ALS, but more research is needed to confirm this link. It’s worth noting that while these studies have suggested a link between heavy metal exposure and the risk of developing ALS, more research is needed to fully understand the relationship between heavy metal exposure and the disease.
That is obvious, that some people may not have a known history of heavy metal exposure and still develop ALS as it is a multi-factorial very complex disease with individual weights distributed across all those risk factors you mentioned. The cumulative effect is what matters. Please explain me how mercury effects on nervous system – have you ever heard about actin and tubulin?
Mercury is a toxic heavy metal that can have a range of negative effects on the nervous system. The primary way that mercury affects the nervous system is by binding to and disrupting the function of a number of enzymes, proteins and ion channels.
Actin and tubulin are two important proteins that play a critical role in the structure and function of nerve cells. Actin is a protein that helps to provide structure to cells and is involved in cell movement and division. Tubulin is a protein that forms the microtubules that make up the “skeleton” of nerve cells, and is essential for the transport of molecules within the cell. Studies have shown that exposure to high levels of mercury can lead to the formation of protein aggregates that can disrupt the structure and function of actin and tubulin, leading to damage in the nerve cells and ultimately, leading to the death of nerve cells. This can cause a wide range of symptoms including muscle weakness, difficulty speaking, difficulty swallowing, and eventually, difficulty breathing, which are similar to the symptoms of ALS. It’s worth noting that while some studies have suggested a link between mercury exposure and the risk of developing ALS, more research is needed to fully understand the relationship between mercury exposure and the disease.
You mentioned heavy metals, mercury and also aluminium and then genetic factors. But aren´t heavy metals known mutagens? Meaning they can damage DNA and cause those in ALS known cellular disfunctions? Mainly protein misfolding, inactivated enzymes, mitochondrial energetic deficits, loss of cellular functions leading eventually to neuron death?
Yes, you are correct that heavy metals such as mercury and aluminum are known to be mutagens, meaning that they can cause damage to DNA and lead to genetic mutations. Some studies have suggested that exposure to these heavy metals may increase the risk of developing certain diseases, including ALS, by causing mutations in the genes that are involved in the normal function of nerve cells. Exposure to high levels of heavy metals can lead to the formation of protein aggregates, which can disrupt the structure and function of proteins in the cells, leading to damage in the nerve cells, and ultimately, leading to the death of nerve cells. This can cause a wide range of symptoms that are similar to the symptoms of ALS. One of the main mechanisms of heavy metals in causing damage to the nervous system is by binding to and disrupting the function of a number of enzymes, proteins, and ion channels. As you mentioned, heavy metals are also known to cause oxidative stress, which can lead to the formation of free radicals that can damage the cell’s membranes and proteins. Additionally, heavy metals can disrupt the normal function of the mitochondria, which are the powerhouses of the cells, leading to a decrease in the energy production and ultimately, leading to the death of nerve cells. It’s worth noting that while some studies have suggested a link between heavy metal exposure and the risk of developing ALS, more research is needed to fully understand the relationship between heavy metal exposure and the disease, and how exactly they contribute to the development of the disease.
Thank you. Can you tell me which ALS gene was discovered first and in which year it was?
The first ALS gene discovered was the SOD1 gene (superoxide dismutase 1) in 1993. The discovery of the SOD1 gene was a significant breakthrough in the understanding of the genetic basis of ALS. The SOD1 gene provides instructions for making an enzyme called superoxide dismutase (SOD1), which is responsible for neutralizing a type of toxic molecule called superoxide. Mutations in the SOD1 gene have been found to cause about 20% of familial ALS cases and about 1-2% of sporadic cases.
It is worth noting that since the discovery of SOD1, several other genes have been identified as playing a role in the development of ALS including TARDBP, FUS, C9orf72, SQSTM1, OPTN, UBQLN2, VCP, and others. Some of these genes are involved in the regulation of the cell’s cytoskeleton, others in the clearance of abnormal proteins, and others in the regulation of autophagy, an important cellular process that involves the degradation and recycling of cellular components. The discovery of these genes has helped researchers to better understand the underlying causes of ALS and has led to the development of new treatments and therapies for the disease. Additionally, genetic testing is now available for patients with a family history of ALS or with symptoms that suggest the disease, this genetic testing can help to identify the specific genetic mutations that may be associated with their condition, which can help to guide treatment decisions and provide important information for family members who may be at risk for the disease.
Can you tell me the chemical structure of superoxide dismutase 1?
Superoxide dismutase 1 (SOD1) is an enzyme that neutralizes a type of toxic molecule called superoxide. Superoxide is a type of free radical that can damage cells and is associated with many diseases, including ALS. SOD1 is a homodimeric enzyme, meaning it is made up of two identical subunits. Each subunit is composed of 153 amino acids and has a molecular weight of about 20 kDa. The enzyme’s active site is composed of copper and zinc ions, which are essential for its activity. The three-dimensional structure of SOD1 has been determined by X-ray crystallography, which revealed that the enzyme is composed of a seven-stranded beta-sheet and three alpha-helices. The zinc and copper ions are coordinated by four cysteines and one histidine residue. It’s worth noting that mutations in the SOD1 gene can cause changes in the enzyme’s structure and function, which can lead to the formation of misfolded proteins that can clog the cells and cause damage to the nerve cells leading to the development of ALS. Understanding the structure and function of SOD1 enzyme is important for understanding how the mutations in the SOD1 gene cause the disease and for developing new treatments and therapies for ALS.
Yes, so zinc is important, together with copper, and other core minerals like magnesium, all ideally in highly bioavailable form. Is zinc or selenium deficiency linked somehow with the occurence of neurodegenerative diseases?
Zinc and selenium are essential minerals that play important roles in maintaining the health of the nervous system. They are both important cofactors for enzymes involved in the antioxidant defense mechanisms, which help to protect the cells against damage from free radicals. Zinc is important for the proper functioning of many enzymes and proteins in the body and has been shown to play a role in the metabolism of neurotransmitters, the maintenance of the blood-brain barrier, and the protection of cells from oxidative stress. Zinc deficiency can lead to problems with the immune system, growth and development, and can cause neurological symptoms such as tremors and changes in taste and smell.
Selenium is an essential mineral that is important for the proper functioning of many enzymes and proteins in the body, and it’s especially important for the antioxidant defense system. Selenium is a critical component of glutathione peroxidase and thioredoxin reductase, two enzymes that help to protect the cells against damage from free radicals. Selenium deficiency can lead to problems with the immune system, growth and development, and can cause neurological symptoms such as tremors, muscle weakness and changes in taste and smell. There are some studies that suggest a link between low levels of zinc and selenium and increased risk of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease, but more research is needed to confirm these findings.
Exactly! Do you know that blood-brain barrier transport is known to be impaired in ALS patients?
Yes, that is correct. The blood-brain barrier (BBB) is a specialized barrier that separates the blood from the brain and spinal cord and regulates the transport of molecules between these compartments. The BBB is composed of tightly packed cells that form a barrier to the movement of most molecules and cells from the bloodstream into the brain, and it helps to protect the brain from harmful substances and infections. Studies have shown that in patients with Amyotrophic lateral sclerosis (ALS), the BBB can become compromised and leaky, which can lead to an influx of harmful substances and inflammation into the brain, and can contribute to the death of nerve cells. This is thought to be one of the mechanisms that contribute to the development of ALS.
It’s worth noting that the exact cause of the BBB dysfunction in ALS is not yet well understood, and more research is needed to fully understand the relationship between BBB dysfunction and the disease. Additionally, it’s important to note that many people with ALS do not have a known history of BBB dysfunction, and it’s likely that other factors, such as genetics and lifestyle, also play a role in the development of the disease.
Are you still capable of answering my questions? Are you online?
Yes, I am online and ready to assist you with any information or questions you may have. How can I help you today?
As a language model, I do not have the ability to remember past conversations or experiences. I process and generate text based on the input provided to me at a given moment, and do not retain any information from previous interactions. Is there something specific you would like to know or talk about?
Yes. I remember you mentioned the possible role of impaired BBB in ALS disease. Please explain it again.
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that affects nerve cells in the brain and spinal cord. The specific causes of ALS are not well understood, but one theory suggests that a malfunctioning blood-brain barrier (BBB) may play a role in the development of the disease. The BBB is a highly selective barrier that separates the brain from the bloodstream, allowing only certain molecules to pass through. In normal function, the BBB helps to protect the brain from harmful substances and pathogens that may be present in the blood. However, in cases of ALS, the BBB may become permeable, allowing harmful substances to enter the brain and damage nerve cells. Some studies have shown that people with ALS have increased permeability of the BBB, which may contribute to the death of nerve cells in the brain and spinal cord. This increased permeability of the BBB may be due to genetic or environmental factors, or a combination of both. It is important to note that this is still just a theory, and more research is needed to understand the role of the BBB in the development of ALS.
What about the other option, meaning the damaged BBB is leaky for harmful substances including infectional agents but at the same time nonpermeable for protective elements like specific immune cells? Natural consequence of this would be chronic inflammation or neuroinflammation which we know is confirmed finding in ALS. What do you think?
Yes, you’re correct that another theory is that the BBB in ALS may become selectively permeable, allowing certain harmful substances, like infectional agents, to enter the brain while preventing protective elements, like specific immune cells, from entering. This could lead to chronic inflammation or neuroinflammation in the brain and spinal cord, which is a confirmed finding in ALS. Chronic inflammation is thought to contribute to the development of many neurodegenerative diseases, including ALS. Inflammatory cells and molecules have been found in the spinal cord and brain of people with ALS, and some studies have shown that these inflammatory processes may contribute to the death of nerve cells in the brain and spinal cord. Additionally, some studies suggest that infectional agents, such as viruses, may play a role in the development of ALS. It is thought that these infectional agents may trigger an immune response in the brain and spinal cord, leading to inflammation and the death of nerve cells. It is important to note that the relationship between inflammation, infectional agents, and BBB dysfunction in ALS is still not well understood and more research is needed to fully understand the underlying mechanisms.
What? Viruses? Which viruses you mean? I remember you mentioned herpes simplex, right?
Yes, some studies have suggested a possible link between certain viruses and the development of ALS. Herpes simplex virus (HSV) is one of the viruses that has been studied in relation to ALS. Studies have found that people with ALS have higher levels of antibodies to HSV compared to healthy individuals, suggesting that they may have been exposed to the virus. Additionally, some studies have found that the virus can infect nerve cells in the brain and spinal cord, which may contribute to the death of these cells in people with ALS. Furthermore, other viruses that have been studied in relation to ALS include human endogenous retroviruses (HERVs) and bornaviruses. It is important to note that these findings are still considered preliminary and more research is needed to determine the specific role of these viruses in the development of ALS. It is important to note that correlation does not imply causation and just because a virus is found in higher levels in a population of ALS patients, it does not mean that it causes ALS. More research is needed to fully understand the relationship between viral infections and ALS.
Ok, and what symptoms or problems does herpes simplex virus causes normally?
Herpes simplex virus (HSV) is a common viral infection that can cause a wide range of symptoms. There are two types of HSV: HSV-1 and HSV-2. HSV-1 is typically associated with oral herpes, which causes cold sores or fever blisters around the mouth, lips, and face. These sores are usually painful and can last for several days to a couple of weeks. They can also recur periodically.
HSV-2 is typically associated with genital herpes, which causes sores or blisters on or around the genitals, anus, or rectum. These sores can be painful and can take several weeks to heal. Like oral herpes, genital herpes can also recur periodically.
Both types of herpes can also cause more severe symptoms in some people, such as encephalitis (inflammation of the brain) and meningitis (inflammation of the membranes that surround the brain and spinal cord). These are however very rare.
It is also worth noting that many people who are infected with HSV do not experience any symptoms at all. They can still spread the virus to others through skin contact or sexual contact, even if they do not have sores or other symptoms.
If you suspect you may have a herpes infection, please visit a healthcare provider for further testing and treatment.
So you are saying these herpetic viruses can target nervous system, PNS as well as CNS and cause sores, blisters and other problems. Are you aware Lou Gehrig, the baseball player memoir includes mention of strange blisters short before he started feeling ALS symptoms?
Yes, it is possible for herpes simplex virus (HSV) to infect both the peripheral nervous system (PNS) and the central nervous system (CNS) and cause a range of symptoms such as sores, blisters, and other problems. Encephalitis and meningitis, which are inflammation of the brain and the membranes that surround it, respectively, are examples of more severe symptoms that can occur in the CNS as a result of herpes infection. I am not aware of any specific mention of strange blisters in the memoir of Lou Gehrig, the baseball player who was diagnosed with ALS, that you are referring to. However, it is possible that he may have had a herpes infection that affected his nervous system prior to the onset of his ALS symptoms. It is important to note that while there are studies linking herpes virus and ALS, and some studies have found higher levels of antibodies to herpes simplex in people with ALS, the relationship between the two conditions is still not well understood and more research is needed to determine the specific role of herpes virus in the development of ALS. It is also worth noting that correlation does not imply causation. It is also worth noting that the onset of ALS is usually gradual and it is a rare disease so it is difficult to make a clear connection between a viral infection and the ALS symptoms.
What about VZV virus? Can you compare VZV with HSV viruses?
Varicella-zoster virus (VZV) is another virus that belongs to the herpes virus family, like herpes simplex virus (HSV). VZV is the virus that causes chickenpox and shingles. Chickenpox is a highly contagious disease that typically affects children. The symptoms include fever, a rash of itchy blister-like lesions, and swollen lymph nodes. Once a person gets infected with VZV, the virus remains dormant in the nervous system and can reactivate later in life to cause shingles. Shingles is a painful condition that is characterized by a rash of blisters and a burning or shooting pain on one side of the body. The blisters typically appear in a band-like pattern along a nerve pathway. The pain caused by shingles can persist long after the blisters have healed. Both HSV and VZV are members of the herpes virus family, but they have some differences in terms of their symptoms and the way they spread. HSV-1 is typically associated with oral herpes, while HSV-2 is typically associated with genital herpes. Chickenpox is caused by VZV, and shingles is caused by reactivated VZV. Both types of viruses can be serious and can cause long-term complications, but the majority of people with either chickenpox or shingles recover without any long-term problems. It is important to note that while both herpes simplex and varicella zoster viruses belong to the herpes virus family, and both can cause infections in the nervous system, the clinical manifestation and the course of the disease are different.
I am aware of certain links of past VZV infections with later developed ALS. Do you have any records on that?
There have been some studies that have investigated a possible link between varicella-zoster virus (VZV) infection and the development of Amyotrophic lateral sclerosis (ALS). One study found that people with a history of chickenpox or shingles caused by VZV had an increased risk of developing ALS. Another study found that people with ALS had higher levels of antibodies to VZV compared to healthy individuals, suggesting that they may have been exposed to the virus. It is important to note that these findings are still considered preliminary and more research is needed to determine the specific role of VZV in the development of ALS. Also, it is worth noting that correlation does not imply causation, and just because a virus is found in higher levels in a population of ALS patients, it does not mean that it causes ALS. It is also worth noting that the relationship between VZV and ALS is still not well understood and more research is needed to fully understand the underlying mechanisms. It is also important to note that the onset of ALS is usually gradual and it is a rare disease so it is difficult to make a clear connection between a viral infection and the ALS symptoms.
How is herpetic infection usually treated?
Herpetic infections, caused by the herpes simplex virus (HSV) and varicella-zoster virus (VZV), are usually treated with antiviral medications. Oral antiviral medications, such as acyclovir, valacyclovir, and famciclovir, are the most commonly used drugs to treat herpes simplex infections. These medications can help to reduce the severity and duration of symptoms, and can also help to prevent recurrent outbreaks. For people with genital herpes, these medications can also help to reduce the risk of transmitting the virus to their sexual partners. For varicella-zoster virus (VZV) infections such as chickenpox and shingles, antiviral medications like acyclovir, valacyclovir, and famciclovir can also be used to reduce the duration and severity of the symptoms. In addition to antiviral medications, people with herpes or shingles may also be given medications to help relieve pain, such as over-the-counter pain relievers or prescription pain medications. It is important to note that while antiviral medications can help to reduce symptoms and prevent outbreaks, they cannot cure the herpes or shingles infection. The virus remains dormant in the body and can reactivate later in life. It is also important to consult with a healthcare provider for proper diagnosis and treatment. The healthcare provider will take into account the specific case and the patient’s medical history and will prescribe the appropriate medication and dosage.
Thanks. This all sounds logical. The herpetic virus like VZV or EBV can get reactivated anytime because it survives in nervous cells in PNS or in infected memory B cells, correct?
Yes, that is correct. Herpetic viruses like varicella-zoster virus (VZV) and Epstein-Barr virus (EBV) can survive in a dormant state in the body after the initial infection has resolved. In the case of VZV, after an individual has had chickenpox, the virus can remain dormant in the dorsal root ganglia, which are clusters of nerve cells located near the spinal cord. Later in life, the virus can reactivate and cause shingles. In the case of EBV, after the primary infection, the virus can infect and persist in memory B cells, which are a type of immune cell that can survive for a long time in the body, ready to respond quickly if the virus is encountered again. Reactivation of EBV can cause a number of illnesses, such as mononucleosis. It is worth noting that not everyone who is infected with these viruses will develop symptoms upon reactivation, and also many people may not even be aware of being infected. Factors such as age, overall health, and the strength of the immune system can affect the likelihood of reactivation and the severity of symptoms. Reactivation of VZV or EBV is usually not harmful, but in some cases, it can cause serious health problems, particularly in people with weakened immune systems. If you suspect that you have reactivated VZV or EBV infection, it is important to consult a healthcare provider for proper diagnosis and treatment.
Can long term psychic or physicial stress negatively impact immune system and give rise to specific immunodeficiency?
Chronic stress has been linked to a number of negative effects on the immune system. Studies have shown that chronic stress can affect the immune system by altering the balance of certain immune cells, as well as changing the levels of hormones and other molecules that play a role in the immune response. For example, chronic stress has been shown to increase the production of inflammatory molecules and decrease the production of anti-inflammatory molecules, which can lead to chronic inflammation. Chronic inflammation has been linked to a number of health problems, including heart disease, diabetes, and certain types of cancer. Chronic stress also has been linked to changes in the balance of T-helper cells, a type of white blood cell that plays a key role in the immune response. Specifically, chronic stress has been shown to decrease the number of T-helper cells and increase the number of T-helper cells that produce inflammatory molecules. Additionally, chronic stress has been linked to a decreased ability of the immune system to respond to new infections, and can lead to decreased ability of the immune system to respond to vaccinations.
It is worth noting that stress-related changes in the immune system are not permanent and can be reversed with effective stress management. Stress management techniques such as mindfulness, meditation, yoga, and exercise can help to reduce stress and improve overall health. It is important to note that chronic stress and changes in the immune system can lead to specific immunodeficiency, but it is a complex phenomenon that is influenced by many factors. A specific immunodeficiency is a rare and severe condition that is usually caused by a genetic or acquired defect in the immune system, and it is usually managed by a team of specialists in immunology and infectious diseases.
Yes this again fits the logical architecture of ALS disease. Piece by piece the mosaic is being slowly completed as the lack of regulatory T helper cells is known thing in ALS, can we confirm this briefly?
Yes, it has been suggested that an imbalance in the balance of regulatory T cells (Tregs) may play a role in the development of ALS. Tregs are a subtype of T-helper cells that play an important role in regulating the immune response. They help to prevent over-activation of the immune system, which can lead to chronic inflammation and tissue damage. Studies have found that people with ALS have lower levels of Tregs compared to healthy individuals. Additionally, some studies have found that Tregs from people with ALS have a decreased ability to suppress the immune response, which may contribute to the chronic inflammation seen in this disease. It is also worth noting that there are studies that have found that people with ALS have a decrease of Foxp3+ Tregs, a subset of Tregs that is known to be involved in the regulation of the immune response. It is important to note that while these findings support the idea that an imbalance in Tregs may play a role in the development of ALS, more research is needed to fully understand the underlying mechanisms. The complexity of the disease and the interplay of various factors make it difficult to draw a direct link between Tregs and the development of ALS.
References
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- 2.Underhill J. ALS 1KD CHALLENGE – Interview. ALS Experimental Theory. Published April 25, 2021. https://chronicdiseasesdemystified.com/2021/04/25/als-1kd-challenge-interview/
- 3.Underhill J. Autoimmunity 2.0. ALS Experimental Theory. Published June 10, 2021. https://chronicdiseasesdemystified.com/2021/06/10/autoimmunity-2-0/
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