Niacinamide May Improve Symptoms Of ALS

haidut

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Just over a week ago I posted a thread on ALS being linked to increased fatty acid oxidation (FAO) and as such a decreased glucose availability/oxidation.

ALS Tied To Increased Fat Oxidation (FAO), Increasing Glucose May Treat It

Now, the study below further corroborates this FAO-disease association by demonstrating a causative link between a change in the microbiome and the development/progression of ALS. The change in microbiome was such that there was a decrease in the amount of bacteria producing niacinamide/nicotinamide and as a result the animals with the changed microbiome developed vitamin B3 deficiency. When those animals were given a supplementation of niacinamide the symptoms of ALS improved. However, the beneficial effects were weaker compared to restoring the levels of the beneficial bacteria, which suggests that lack of vitamin B3 is not the only factor in ALS pathology. My suspicion is that the B3-producing bacteria is a non-endotoxin species and as such increasing its levels decreases levels of the Gram-negative, endotoxin-producing Parabacteroides distasonis whose levels were found to be higher in patients with ALS. The study also examined stool and CSF from humans with ALS and confirmed that the human patients also had lower levels of the niacinamide-producing bacteria in the colon, as well as lower levels of vitamin B3 in their CSF.

Potential roles of gut microbiome and metabolites in modulating ALS in mice
Commensal Bacterium Reduces ALS Symptoms in Mice

"...In a mouse model of amyotrophic lateral sclerosis, animals that had ample levels the bacterium Akkermansia muciniphila in their gut microbiomes fared better than those carrying almost no members of the species, which produces vitamin B3, according to a study published this week (July 22) in Nature. Moreover, restoring A. muciniphila in mice that had low levels slowed the progression of their disease. “When we gave it to ALS-prone mice it very significantly improved ALS severity in these mice,” coauthor Eran Elinav, a microbiome researcher at the Weizmann Institute of Science in Israel and of the German Cancer Research Center in Heidelberg, tells The Guardian. On the other hand, two other members of the microbiome—Ruminococcus torques and Parabacteroides distasonis—were more common in mice with severe disease.

"...The researchers suspect that A. muciniphila’s production of B3 may have something to do with its apparently therapeutic effects. Treating mice with a form of vitamin B3 called nicotinamide improved some of their symptoms. However, this did not increase the mice’s lifespan as boosting levels of the bacteria had, suggesting there’s more to the bacterium’s effect than just B3. “Usually you don’t expect one miracle metabolite can rescue the mice completely,” Jun Sun, a medical microbiologist at the University of Illinois at Chicago who was not involved in the study, tells Science News. The researchers gathered some preliminary data that suggest A. muciniphila abundance may relate to ALS in humans as well. Examining the microbiomes of 37 ALS patients and 29 healthy family members, Elinav and colleagues found lower levels of the bacterium in the stool of the ALS patients and lower levels of nicotinamide in their blood and cerebrospinal fluid. In addition, the levels of nicotinamide in the blood correlated with the severity of the patient’s disease: patients with lower levels tended to have worse symptoms."
 

Bart1

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So this contradicts that all bacteria are bad and we should work on having an sterile gut? So you once said probiotics are dangerous, probably so are antibiotics?
 

yerrag

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Just over a week ago I posted a thread on ALS being linked to increased fatty acid oxidation (FAO) and as such a decreased glucose availability/oxidation.

ALS Tied To Increased Fat Oxidation (FAO), Increasing Glucose May Treat It

Now, the study below further corroborates this FAO-disease association by demonstrating a causative link between a change in the microbiome and the development/progression of ALS. The change in microbiome was such that there was a decrease in the amount of bacteria producing niacinamide/nicotinamide and as a result the animals with the changed microbiome developed vitamin B3 deficiency. When those animals were given a supplementation of niacinamide the symptoms of ALS improved. However, the beneficial effects were weaker compared to restoring the levels of the beneficial bacteria, which suggests that lack of vitamin B3 is not the only factor in ALS pathology. My suspicion is that the B3-producing bacteria is a non-endotoxin species and as such increasing its levels decreases levels of the Gram-negative, endotoxin-producing Parabacteroides distasonis whose levels were found to be higher in patients with ALS. The study also examined stool and CSF from humans with ALS and confirmed that the human patients also had lower levels of the niacinamide-producing bacteria in the colon, as well as lower levels of vitamin B3 in their CSF.

Potential roles of gut microbiome and metabolites in modulating ALS in mice
Commensal Bacterium Reduces ALS Symptoms in Mice

"...In a mouse model of amyotrophic lateral sclerosis, animals that had ample levels the bacterium Akkermansia muciniphila in their gut microbiomes fared better than those carrying almost no members of the species, which produces vitamin B3, according to a study published this week (July 22) in Nature. Moreover, restoring A. muciniphila in mice that had low levels slowed the progression of their disease. “When we gave it to ALS-prone mice it very significantly improved ALS severity in these mice,” coauthor Eran Elinav, a microbiome researcher at the Weizmann Institute of Science in Israel and of the German Cancer Research Center in Heidelberg, tells The Guardian. On the other hand, two other members of the microbiome—Ruminococcus torques and Parabacteroides distasonis—were more common in mice with severe disease.

"...The researchers suspect that A. muciniphila’s production of B3 may have something to do with its apparently therapeutic effects. Treating mice with a form of vitamin B3 called nicotinamide improved some of their symptoms. However, this did not increase the mice’s lifespan as boosting levels of the bacteria had, suggesting there’s more to the bacterium’s effect than just B3. “Usually you don’t expect one miracle metabolite can rescue the mice completely,” Jun Sun, a medical microbiologist at the University of Illinois at Chicago who was not involved in the study, tells Science News. The researchers gathered some preliminary data that suggest A. muciniphila abundance may relate to ALS in humans as well. Examining the microbiomes of 37 ALS patients and 29 healthy family members, Elinav and colleagues found lower levels of the bacterium in the stool of the ALS patients and lower levels of nicotinamide in their blood and cerebrospinal fluid. In addition, the levels of nicotinamide in the blood correlated with the severity of the patient’s disease: patients with lower levels tended to have worse symptoms."
Thanks haidut.

I have symptoms of ALS from taking orally cinnamon bark oil in a sugar cube instead of diluted in a carrier oil and placed inside a capsule and taking it orally. I believe that the strong antibiotic in cinnamon bark oil must have destroyed a large amount of a. municiphila bacteria and this may be causing my ALS symptoms as well as other neuromuscular weakness, as well as a reduction in my sense of balance.

Even before reading this thread, I had been suspecting that the cinnamaldehyde (and possibly the lower amount of eugenol), the two main components of cinnamon bark oil, may be responsible for wiping out some beneficial flora that is involved in maintaining the autonomic system involved in how the throat muscles manage the interplay between breathing and eating through the narrow passage that is the trachea. After all, it is well known that antibiotics of the fluoquinolone class (such as Ciprofloxacin and Levaquin/Levofloxacie) can cause ALS.

While talk of microbiome is mostly centered on the gut, I think in my case the microbiome involved is above the gut, specifically above the throat up to the brain. As when I took the cinamon bark oil wrongly, my gut has largely been unaffected while my lungs and my throat and my neural functions have. My lungs are almost recovered from the bronchial irritation and inflammation, and breathing is back to near normal, with just a few minor lingering issues such as residual phlegm. My early difficulties in swallowing and in talking have also improved, but to a lesser extent. And I have vertigo issues that border on Meniere's. While these issues are not as bad as those of elderly people, whom I have seen taking care of my mom and dad before, they speak to neurological issues that began only when I took the cinnamon bark oil.

Currently, I am taking more B3 along with B1 and B6. being that they seem to more identified with involvement in neuromuscular functions. I am also using red light therapy at the hands of a medical professional (using a red laser device) intended to boost cytochrome oxidase for improvement mitochondrial oxidation, but I now am considering the intake of a. municiphila supplements.

A search of the bacteria leads me to a probiotic product by Pendulum in Amazon:

Amazon product ASIN B0B3GF96C3View: https://www.amazon.com/Pendulum-Akkermansia-Probiotic-Supplement-Increases/dp/B0B3GF96C3


While this product is directed at the gut, I am hoping the gut would just be the gateway for the bacteria to transpose into circulation and onto my neural system, where it would effect the restoration of the autonomic ability of my throat muscles, as the bacteria regain its population size and its production of niacinamide.

I'll place an order for 1 bottle for a month's supply.

I may already be well before the order arrives, on account of my current treatment. But if not, and if the probiotic brings about an improvement, then I would be able to confirm that the a. municiphila bacteria is necessary for treating ALS, and perhaps people who suffer ALS (from Cypro) can find in restoring the bacteria in their microbiome a viable approach.

But if this doesn't work, I can still continue finding a solution by adding progesterone/pregnenolone/DHEA based on this post of yours: Copper May Treat Als
 

T-3

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Following and hoping your symptoms @yerrag continue to improve.

Have you noticed any improvements from B1, B3, B6?
From copper?
From pregnanolone /progesterone?

I'd be keen to know what ratios of the Bs and dosing of copper/preg/prog your reading and self-experimentation suggest.
 

yerrag

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Following and hoping your symptoms @yerrag continue to improve.

Have you noticed any improvements from B1, B3, B6?
From copper?
From pregnanolone /progesterone?

I'd be keen to know what ratios of the Bs and dosing of copper/preg/prog your reading and self-experimentation suggest.
With regard to copper, all I can do is to try to incorporate copper-rich food in my diet in a way that it's the equivalent of daily or every other dosing of low dose copper. Picking up on Ray's idea of eating shrimps (given that copper to shrimp is like iron to us in blood and magnesium and calcium in green leaves) I have been eating a native delicacy made of tiny crustaceans that are like shrimps to accompany my intake of well-cooked green leaves (convolvus, locally known as kangkong in the Phils.). I've been doing this for some time now, at least for a year and though I have made no tests yet for improvements in my serum ceruloplasmin, I hope this would build up my copper stores without it being excessive that it turns into overload. It's my approach to knowing that copper deficiency is not easy to overcome by supplementation, as getting too little is just as likely as getting too much when doing it blindly, which appears to be the conundrum supplementing with copper involves.

Assuming that my copper levels are sufficient, that at least takes care of a needed substrate for cytochrome oxidase, and it would be easier to use red light therapy to improve mitochondrial production of energy - to improve metabolism and to support healing from ALS.

So I would, apart from the occasional red laser therapy I get from a holistic doctor, need to get my red light device set up so I can get my daily dose, which until lately I have been putting off dor lack of urgency. Dealing with my ALS symptoms has shifted the level of urgency for me.
____

I began my daily dose of 500/500/120mg of B1/B2/B6 divided into two doses for am/pm, I'll be monitoring and hopefully I can see results ad time goes on.

It's likely I will have an ample time of 3 weeks to see if this has a beneficial and lasting effect, before my order of Pendulum's Akkemansia prebiotic arrives. I will then add supplementation of this prebiotic to see if this stacks up better than just going alone on the B vitamin supplementation.
 

T-3

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Thanks for those details, Yerrag.

I just wanted to double-check the dosing of "B2" you mentioned: "500/500/120mg of B1/B2/B6 divided into two doses for am/pm". No B3?

I think I tend to feel noticeable improvements of various kinds on that type of pharmacological dose of B6 (50mg and up) but have never tried a dose as high as 120mg daily for any period of time. I cycle B6 at 50mg-75mg per day for one or two days in a row, cycling with 5-day breaks in between, due to negative side-effects like (temporary) neuropathy-like symptoms I've read about but never experienced myself. I never experienced any negative sides from B6 as p5p as far as I can tell. I sometimes use B6 as pyridoxine HCL because it's cheaper and much easier to get where I live, but I sometimes have vague negative side-effects from the cheap one.

I've tried numerous high-dose B1 experiments up to1.5g or 2g daily. But I've never tried carefully matching B1:B2 ratio at 1:1. After I hear back from you confirming that it's B1:B2 rather than B1:B3 in equal doses, I'd like to try a similar experiment.

Regarding copper: this seems to be one of the most "subtle" nutrient metals for me (i.e., it's proved difficult for me to reliably self-assess what its effects on my metabolic health really are). After reading numerous threads here about things that can easily go wrong over-dosing supplemental (i.e. non-food) copper sources, I stopped taking any supplements with copper in it years ago. I recently got interested in trying to understand copper-rich foods' effects on myself. I've only used clean-sourced dark chocolate. Maybe I'll try using crustaceans like you're doing.

Question about how you monitor copper levels, given the particulars of your own situation (chronic high blood pressure, infection from periodontal disease that may have spread elsewhere, careful monitoring of CO2 levels and acid-base balance, etc.)....can you reliably tell whether you're too low or too high on copper? Which symptoms/biomarkers are reliable in your view? I've never felt any confidence in my own attempts at self-monitoring. I'll request lab tests soon.

I wish I had access to the crustaceans you mentioned with greens--sounds like a treat! If one were to visit the Phils, could this be found in a restaurant?: "native delicacy made of tiny crustaceans that are like shrimps to accompany my intake of well-cooked green leaves (convolvus, locally known as kangkong)" ...me plotting a future 'culinary copper-repletion tour'.
 

yerrag

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I just wanted to double-check the dosing of "B2" you mentioned: "500/500/120mg of B1/B2/B6 divided into two doses for am/pm". No B3?
Sorry, typo. Should be 500/10/500/120 of B1/B2/B3/B6. Good catch.

I think I tend to feel noticeable improvements of various kinds on that type of pharmacological dose of B6 (50mg and up) but have never tried a dose as high as 120mg daily for any period of time. I cycle B6 at 50mg-75mg per day for one or two days in a row, cycling with 5-day breaks in between, due to negative side-effects like (temporary) neuropathy-like symptoms I've read about but never experienced myself. I never experienced any negative sides from B6 as p5p as far as I can tell. I sometimes use B6 as pyridoxine HCL because it's cheaper and much easier to get where I live, but I sometimes have vague negative side-effects from the cheap one.

I used to take 2 x 60 mg P5P but now I only have pyrodixine hcl available but I haven't felt anything negative taking pyrodixine at that dosage. But that's just me. I hardly feel anything taking any of the b vitamins negative or positive, in a direct way.

Question about how you monitor copper levels, given the particulars of your own situation (chronic high blood pressure, infection from periodontal disease that may have spread elsewhere, careful monitoring of CO2 levels and acid-base balance, etc.)....can you reliably tell whether you're too low or too high on copper? Which symptoms/biomarkers are reliable in your view? I've never felt any confidence in my own attempts at self-monitoring. I'll request lab tests soon.
Except for a blood test for ceruloplasmin two years ago, I haven't really monitored my copper levels. The cerulosplasmin test turned out well, as it was within range, but is on the low side. But my CBC tests come out with me not being anemic in any way, so there wasn't much urgency in improving my copper levels, given that it impacts red blood cell production.

But with my current need to improve my metabolism and my need to improve cytochrome oxidase to maximize mitochondrial energy production with red light therapy, I would need to reassess my copper status with a ceruloplasmin. That would also serve to validate if my approach of taking 'bagoong,' the sauce I use to accompany my intake of well-cooked convolvus (made of tiny crustaceans) is really improving my copper status.

I wish I had access to the crustaceans you mentioned with greens--sounds like a treat! If one were to visit the Phils, could this be found in a restaurant?: "native delicacy made of tiny crustaceans that are like shrimps to accompany my intake of well-cooked green leaves (convolvus, locally known as kangkong)" ...me plotting a future 'culinary copper-repletion tour

You can easily find bagoong at a Filipino or Asian grocery store or supermarket. It is a common ingredient especially in Southeast Asian foods but called by other names, but the bagoong is usually sold in a small sauce bottle already sauteed and ready to serve, where you mix it to taste with the well-cooked convolvus. If you add minced or chopped tomatoes and onions, it makes it more interesting.
 

yerrag

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@T-3

I began to use T-3 (Tyronene) and Pregnenolone (together with DHEA in haidut's Pansterone) yesterday. Very conservatively.

This is already after starting and continuing a protocol based on the B -vitamins I mentioned, plus red light therapy, and EMF therapy. As well as essential oil therapy directed at removing phlegm to improve the intake of oxygen in the lungs. Last week, I began to take the Akkemansia Muciniphila probiotics, in the hope that it will cure my ALS condition.

I call one condition (the other one being bronchitis - phlegm blocking oxygen intake causing low spO2) ALS because I still am not swallowing very well, as after eating I would often find that some of what I ate would be stuck in my throat, and only when it is coughed out later would I know it is stuck. I suspect the autonomic muscles in my throat are still in recovery, and this would also cause phlegm to be stuck there when it should be coming out, and this is the cause of why I would occasionally get into fits of hiccups. Because this is all neuromuscular, I also associate it with weakness in my left leg, where I would find the motor nerves not really following my mind in going over an obstruction as I walk, and I find myself often bumping into them. I would also have episodes of being groggy, and I would put them all under ALS, if not Parkinson's, just for convenience sake.

I took the T-3 and pregnenolone because I hoped it would improve metabolism, which is the same reason I took the B-vitamins (especially niacinamide) and the probiotic with Akkermansia bacteria (which the OP reports on). Improving metabolism would address both the inability of the lungs to expel mucus as well as enable the motor function of neck muscles involving in chewing, swallowing, and breathing.

However, things did not turn out as planned, not in the straight line I was hoping it would.

Surprisingly, I woke up feeling spaced out. I tested my ECG QTc, my proxy for thyroid health, and found it went higher, to mean I got more hypothyroid, contrary to my expectation. My blood pressure went down but I see this as a result of my metabolism going down. My heart rate went up towards 100+, meaning my heart is being strained and needed more pumping action to get the work done.

Checking my spO2, I find that the highest I could muster was 94. And my spO2 chart confirmed that the values are dipping into the 85 level. These were values at rest, so it points to values not influenced by stress such as exercise.

This leads me to conclude that in using thyroid and pregnenolone to pump up my metabolism, i was straining my lung's ability to provide oxygen, and this was causing the opposite effect in a blowback of sorts. it was leading me to actually lowering my metabolism as an oxygen deficit results from the increased oxygen demand from artificially supplementing with thyroid and pregnenolone, while my lungs are still in a state of reduced oxygen absorption due to it still suffering from bronchitis.

I'll still have to find my way around as I figure out how to get out of this hole.
 
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Jam

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@T-3

I began to use T-3 (Tyronene) and Pregnenolone (together with DHEA in haidut's Pansterone) yesterday. Very conservatively.

This is already after starting and continuing a protocol based on the B -vitamins I mentioned, plus red light therapy, and EMF therapy. As well as essential oil therapy directed at removing phlegm to improve the intake of oxygen in the lungs. Last week, I began to take the Akkemansia Muciniphila probiotics, in the hope that it will cure my ALS condition.

I call one condition (the other one being bronchitis - phlegm blocking oxygen intake causing low spO2) ALS because I still am now swallowing very well, as after eating I would often find that what some of what I ate would be stuck in my throat, and only when it is coughed out later would I know it is stuck. I suspect the autonomic muscle in my throat are still in recovery, and this would also cause phlegm to be stuck there when it should be coming out, and this is the cause of why I would occasionally get into fits of hiccups. Because this is all neuromuscular, I also associate it with weakness in my left leg, which where I would find the motor nerves not realy following my mind in going over an obstruction as I walk, and I find myself often bumping into them. I would also have episodes of being groggy, and I would put them all under ALS, if not Parkinson's, just for conveience sake.

I took the T-3 and pregnenolone because I hoped it would improve metabolism, which is the same reason I took the B-vitamins (especially niacinamide) and the probiotic with Akkermansia bacteria (which the OP reports on). Improving metabolism would address both the inability of the lungs to expel mucus as well as enable the motor function of neck muscles involving in chewing, swallowing, and breathing.

However, things did not turn out as planned, not in the straight line I was hoping it would do.

Surprisingly, I woke up feeling spaced out. I tested my ECG QTc, my proxy for thyroid health, and found it went higher, to mean I got more hypothyroid, contrary to my expectation. My blood pressure went down but I see this as a result of my metabolism going down. My heart rate went up towards 100+, meaning my heart is being strained and needed more pumping action to get the work done.

Checking my spO2, I find that the highest I could muster was 94. And my spO2 chart confirmed that the values are dipping into the 85 level. These were values at rest, so it points to values not influenced by stress such as exercise.

This leads me to conclude that in using thyroid and pregnenolone to pump up my metabolism, i was straining my lung's ability to provide oxygen, and this was causing the opposite effect in a blowback of sorts. it was leading me to actually lowering my metabolism as an oxygen deficit results from the increased oxygen demand from artificially supplementing with thyroid and pregnenolone, while my lungs are still in a state of reduced oxygen absorption due to it still suffering from bronchitis.

I'll still have to find my way around as I figure out how to get out of this hole.
I would be very careful with hormones. Here is an interesting article from @haidut :


I made a few posts in the past about ALS characterized by adrenal hyperactivity and suppressed gonadal function, as well as mitochondrial dysfunction and copper deficiency. Also, non-familial ALS is known to occurs 4-5 times more often in active/retired elite athletes. All of these findings strongly suggest ALS is linked to stress and dysregulated metabolism. The study below explains that the metabolic dysregulation of ALS is tied to increased fatty acid oxidation (FAO) and increased glycolysis due to glucose wastage as a result. The increased requirements of glucose and its increased wastage due to upregulated glycolysis are apparently a major reason for the progressive character of this condition. As such, providing extra (5-10 higher than normal dietary levels) dietary glucose enabled the affected neurons to survive much longer and be much more resilient to degeneration. So, according to the studies below, the metabolic phenotype of ALS is not much different from cancer and diabetes (type I). As such, just like them, ALS is also a wasting disease. If providing extra dietary glucose and/or restoring glucose metabolism with chemicals like DCA is therapeutic to ALS, might the same approach work in cancer and diabetes I?? My guess is YES.
Now, the study only looked at supplying extra glucose to the malfunctioning neurons. It did not look at why patients with ALS waste away so rapidly. The culprit, hinted at by the increased FAO, is increased lipolysis. It is that same uncontrolled lipolysis that is responsible for the wasting seen in diabetes I and (partially) cancer as well. So, considering the benefits of niacinamide and aspirin in restraining excessive glycolysis, I’d venture a guess that adding either one of those nutrients to the extra dietary glucose regimen would be dramatically more effective.

Peat spoke in one interview about a friend of his who was diagnosed with ALS about 20 years ago and is not only still alive but highly active and gainfully employed. His secret? Apparently, 3-5 tablets of aspirin daily when the disease was first starting and then decreasing this to 1 tablet daily about 6 months later and continuing on 1 tablet daily to this day. (emphasis mine)

The late Stephen Hawking was diagnosed with ALS in the 1960s and survived for decades, albeit with severe motor deficits. Later on in his life doctors started questioning if his condition was ALS because, you know, nobody can survive with ALS for so long. I wonder if Mr. Hawking’s self-professed habit of taking an aspirin tablet twice a week had something to do with it…

Metabolic Dysregulation in Amyotrophic Lateral Sclerosis: Challenges and Opportunities - PubMed
“…These models provide the tools for genetic and dietary interventions that can distinguish between cause and consequence. For example, although the primary cause remains unknown, in ALS muscles, there seems to be a reduction in glycolysis that is compensated by utilization of alternate fuels such as fatty acids (Figure 1). In contrast, in motor neurons, the impairment in mitochondrial function may lead to compensatory mechanisms that counterbalance the defects in oxidative phosphorylation such as increased glycolysis as reported in cultured cells, or altered interactions with lactate producing glial cells.
Another study using asymptomatic SOD1G86R mice indicated decreased glucose handling in glycolytic muscles of the diseased animals [43]. This is due to concerted effects caused by downregulation of the key glycolytic enzyme phosphofructokinase 1 (PFK 1), and upregulation of pyruvate dehydrogenase kinase 4 (PDK4), an enzyme that inhibits pyruvate dehydrogenase complex through phosphorylation, thus blocking conversion of pyruvate into acetyl-coA. As a consequence, the lipid pathway was stimulated in these animals as early as during the pre-symptomatic stage, and remained active till end stage of the disease, thus switching the fuel preference towards fatty acids by suppressing glucose utilization. Consistent with this, treatment with DCA, a specific inhibitor of PDK, restored normal mRNA expression of Pdk and Pfk1 mRNAs, and resulted in decreased expression of denervation and atrophy markers. This was further translated at the functional level by restoration of muscle strength, larger muscle fibers and overall weight gain in DCA-treated animals compared to non-treated SOD1G86R mice. Thus altogether, this and previous reports show that as the glycolytic muscles progressively lose their ability to utilize glucose, they switch to lipids as an alternate energy source, and that, this metabolic switch happens largely in the early pre-symptomatic stage.
Glycolysis upregulation is neuroprotective as a compensatory mechanism in ALS
People with ALS May Benefit From More Glucose
“…Increased glucose, transformed into energy, could give people with amyotrophic lateral sclerosis, or ALS, improved mobility and a longer life, according to new findings by a University of Arizona-led research team.”
People with ALS use more energy while resting than those without the disease, while simultaneously they often struggle to effectively make use of glucose, the precise ingredient a body needs to make more energy. Experts have not known exactly what happens in a patient’s cells to cause this dysfunction or how to alleviate it. “This project was a way to parse out those details,” said Manzo, who described the results, published online in eLife, as “truly shocking.”
“…The study revealed that when ALS-affected neurons are given more glucose, they turn that power source into energy. With that energy, they’re able to survive longer and function better. Increasing glucose delivery to the cells, then, may be one way to meet the abnormally high energy demands of ALS patients. “These neurons were finding some relief by breaking down glucose and getting more cellular energy,” Manzo said.”
“The fact that we uncovered a compensatory mechanism surprised me,” Zarnescu said. “These desperate, degenerating neurons showed incredible resilience. It is an example of how amazing cells are at dealing with stress.” The novelty of the findings partially lies in the fact that metabolism in ALS patients has remained poorly understood, Zarnescu said.”
“…Their findings were consistent with a pilot clinical trial, which found a high carbohydrate diet was one possible intervention for ALS patients with gross metabolic dysfunction. “Our data essentially provide an explanation for why that approach might work,” Zarnescu said. “My goal is to convince clinicians to perform a larger clinical trial to test this idea.”


Personally, I would try a combination of red light around the back of the neck/spine, methylene blue (10mg 3x daily), SSKI (150mg 3x daily, fundamental in any dis-eased state), NAC + lysine + taurine (high dose short-term only for the mucus and toxins), and aspirin, with a high-carb diet (preferably from fruit and honey).
 
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yerrag

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I would be very careful with hormones. Here is an interesting article from @haidut :





Personally, I would try a combination of red light, methylene blue (10mg 3x daily), SSKI (150mg 3x daily, fundamental in any dis-eased state), NAC + lysine + taurine (high dose short-term only for the mucus and toxins), and aspirin, with a high-carb diet (preferably from fruit and honey).
Caution is warranted. That's why I took very conservative doses of Tyronene and StressNon. Yet it made me take a step back in my recovery.

Still, it has nothing to do with FAO in my case. Had to do with oxygen insufficiency from also suffering from bronchitis. Seems like there is more work to be done with my bronchitis before I attempt to rev up my metabolism with hormones (to help cure my ALS condition).
 

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