The benefits of Fucoidan and neurodegeneration !
Mitochondrial health babyyyy !
I hope everyone reading this had a good weekend. I am mostly avoiding sending e-mails on the weekend or sending them late into Sunday, so people enjoy life without any sort of anxiety or “bad feels” you might get from some of my e-mails.
In a different style of posts (which means I am not analyzing pathologies and molecular pathways), I will write some posts in tone with my pinned one, on reasons to use X.
This was prompted by a post I shared on Twitter, about this paper Sulfated polysaccharides effectively inhibit SARS-CoV-2 in vitro. I have recommended Fucoidan before, given its mitochondrial health aspects.
In there I wrote, that while not strictly necessary, it is an amazing tool. Now I will share some more information and explain why and how. Any person suffering from Long Covid, especially with some level of autoimmunity involved should look into it, and since I wrote quite a few pieces lately on the neuroinflammatory aspects of Long Covid and the viral infection itself, this will be the main focus.
My thread in question, is very superficial though.
Since certain “experts” are pushing certain topics, not out of intellectual honesty, but curiosity, here.
Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder. As the aging population is increasing, AD is becoming one of the leading causes of disability and death among the elderly. However, currently there is no cure for this disease. Fucoidan is a complex sulfated polysaccharide mainly found in brown seaweed. Recent studies have shown that fucoidan is neuroprotective and may have potential to be used for treating and/or preventing neurodegenerative diseases such as AD. In this study, we investigated the effects and possible mechanisms of fucoidan on Abeta induced toxicity in a transgenic Caenorhabditis elegans (C. elegans) AD model. The results showed that the supplementation of fucoidan alleviated the paralyzed phenotype induced by Abeta. The number of Abeta deposits in the AD animals was reduced by fucoidan treatment. Further analysis of the levels of Abeta showed that fucoidan significantly decreased the accumulation of Abeta in transgenic AD C. elegans. It was found that fucoidan treatment elevated the activity of proteosomes; therefore, fucoidan might decrease Abeta accumulation by promoting proteolysis. In addition, fucoidan treatment reduced the production of reactive oxygen species (ROS) stimulated by Abeta induction. These results suggested that fucoidan might exert its protective effects against Abeta-induced toxicity in transgenic AD C. elegans by reducing the accumulation of toxic Abeta and decreasing Abeta-induced production of ROS, thus ameliorating the progression of the AD phenotype.
Protective Effects of the Alga Fucoidan Against Amyloid-β-Induced Neurotoxicity in SH-SY5Y Cells
Dementia is expected to affect an increasing number of patients with global aging populations. About 70% of all dementia is related to Alzheimer's disease (AD). Overaccumulation of amyloid-β protein (Aβ) in the brain forms senile plaques, one of the main features of neurodegeneration in AD. However, there are few drugs available to specifically inhibit senile plaque formation. Fucoidan, a sulfated polysaccharide derived from brown algae, has various bioactivities, such as anti-tumoral and anti-obesity effects. This study aimed to clarify the mechanism underlying the protective effect of fucoidan against Aβ-induced neurotoxicity in human neuroblastoma SH-SY5Y cells. Cell viability and Aβ-induced cytotoxicity were measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, calcein AM, and ethidium homodimer-1. Aβ-induced oxidative stress was evaluated through reactive oxygen species (ROS), cell membrane phospholipid peroxidation, mitochondrial ROS, and Mn-SOD, a mitochondrial radical scavenger. In addition, mitochondrial membrane permeability transition, and ATP concentration were evaluated. Fucoidan significantly improved Aβ-reduced cell viability. With respect to oxidative stress, Aβ exposure increased ROS, lipid peroxidation, and mitochondrial ROS, while fucoidan significantly suppressed these changes. Fucoidan also suppressed the decline in mitochondrial permeability transition and ATP caused by Aβ. Therefore, through its numerous antioxidant activities, fucoidan might have a neuroprotective role in preventing Aβ-induced neurotoxicity.
One thing all different types of neurodegeneration have in common is particular mechanisms in which they set off the primary driver of diseases (bad proteins that build up and instigate low-grade inflammation and low-grade immune responses in your brain, leading to the progression of the disease).
They all share a similar aggravating aspect. ROS (Reactive Oxygen Species. Unstable molecules that react with oxygen inside cells, my preferred crude way to refer to these is “cellular rust”, slowly “eating” away the structure of DNA, proteins, and lipids, producing “bad chemicals” inside you.
What these all share in common, almost all of these degenerative diseases, and even some autoimmune is “simple. Mitochondrial Dysfunction. Without a proper “bioenergetic” machine functioning at optimal levels, repairing damage, cell production, even homeostasis (the state of equilibrium your body wants to be most of the time) become a hurdle, then a problem.
In my first SARS-CoV-2 and the brain, I covered the MPP+, which is a chemical used to simulate neurotoxicity in neurodegenerative diseases, because it is pretty similar to what happens inside a brain with this class of disease.
In the case of neurological class of diseases, it is quite literally a self-feeding loop.
And one of the main drivers of these said “disease progressors” is simple, direct, and easy to understand.
Sugar. Hyperglycemia. A dysfunctional state where your body doesn’t respond properly to insulin. A lot of doctors argue any Alzheimer Class disease (there are 24 of them, Dementia and Alzheimer's are but 2) should be classified as Diabetes Type 3.
Well, do you remember the second Covid and the Brain post ? Where the exact receptor the Spike Protein is using to activate the brain immune system and set off neuroinflammation was *check notes Toll-Like Receptor 4, TLR-4.
Another aspect is the immune regulation by bringing T-Regs into balance, this is a rather complex subject, but I referred to it in my Reverse AIDS series, it is one of the drivers of autoimmunity and many of the issues you see around, the nosedive these immune cells suffer in quite a few number of people.
Here is a spoiler alert. A lot of amyloid/protein diseases, especially in relation to the brain, use very specific cytokines and “factors” for the disease to progress. If you go into case studies and reports from people who died from these diseases at atypical timelines (too quick mostly), they all have something in common.
They often have a decent amount of IL-6, but 90% of the cases I found last year when I was researching these heavily was Tumor Necrosis Factor Alpha. Fucoidan is used as a therapy to achieve control of it, in certain countries/hospitals.
Fucoidan can get pricey, the Grade A ones can be up to 70 to 100 dollars. The best one used to treat even autoimmune diseases is 300+. Not everybody needs it, it is just a nice tool to have in your arsenal IF you need it.
But if you have Long Covid with some degree of severity and other things didn’t work for you, Fucoidan will most likely be the one that actually does it. I would HIGHLY advise you to try the “brain stack” in the first piece linked inside the “Things Hidden Series” before directly jumping into Fucoidan and spending a lot of money.
Another one you should try before, especially if your problems are of too much inflammation is Beta HydroxyButyrate. “Can I consume Fucoidan without selling my kidney ?”
Yes, just buy brown or red seaweeds cheaper around your area, with a lower carbohydrate diet, and that will definitely do the trick. I would know because one of my friends with 10.000+ of critical care for Covid patients did the same, never got Covid after the first time, and decided to do a trial of a few among his doctor friends to see how did it go.
This piece is to mitigate any anxiety some might have, to give hope to people who almost nothing worked, and to already give you a partial explanation of the amyloid question.
Wish you all a great week ahead !!!!
In case you are wondering, here it is my "brain stack", to be precise at the end of the article -> https://hiddencomplexity.substack.com/p/things-hidden-since-the-foundation?utm_source=substack&utm_campaign=post_embed&utm_medium=web&s=w
If you have brain fog, difficult with memory retention, degrees of dementia because of advanced age or something else, I strongly advise you to try it. It changed the life of many people (mine included but I am obviously biased), and the fathers of some followers on Twitter with early dementia.
Don't ask me what this does to the brain to have such a effect, we would need research on it, and there will never be research with something that effective and cheap.
I've given it some thought. Hate to say this, but I think I'm growing fond of my brain fog. It seems to be providing a degree of resilience to societal collapse. It seems as long as I can't focus for more than a minute or 2, I can't worry for longer than a minute or 2 . Before the fog descends again. 🤷