I did my own searching and found Trehalose as a promising therapeutic candidate for the treatment of Parkinson's disease - 2019 ncbi.nlm.nih.gov/pmc/articl...
Neuroprotective Effects of Trehalose and Sodium Butyrate on Preformed Fibrillar Form of α-Synuclein-Induced Rat Model of Parkinson’s Disease - 2021 pubs.acs.org/doi/10.1021/ac...
I did find this article "Natural Compounds and Autophagy: Allies Against Neurodegeneration" frontiersin.org/articles/10... from 2020 that says you can't take Trehalose orally, but that confuses me because sunvox linked to ncbi.nlm.nih.gov/pmc/articl... seems to indicate taking 100 grams a day does make it into your blood.
There is also this article from 2017 Autophagy induction by trehalose: Molecular mechanisms and therapeutic impacts researchgate.net/publicatio... if you scroll down past the abstract it shows a bunch of citations with cool factoids.
Looks like I will be adding to my smoothie.
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Yikes! I thought I'd found the magic bullet Well, at least if you get C.diff you are in line for poop pills.
WHEN TO AVOID TREHALOSE
For most people most of the time, there’s no need to avoid foods containing trehalose. Under normal circumstances, helpful bacteria in your gut outcompete C. diff, preventing illness.
But a great danger exists when you have a serious infection treated with “broad-spectrum” antibiotics, especially the kind that is serious enough to land you in the hospital. Those antibiotics wipe out helpful gut bacteria. Take action: Read ingredients lists on all packaged foods you eat, and avoid any that include trehalose while you are taking such antibiotics and for several weeks afterward. And avoid trehalose if you have or have recently recovered from a C. diff infection.
It seems like it may pose a hazard whenever gut dysbiosis is present because that is when it could potentially have a better chance to feed pathogenic bacteria associated with C-Diff. I think it is these super C. Diff. infections where FMT can shine and do its thing to try and regain control and shift the microbiota back toward health promoting bacteria. FMT seems to be a last resort measure in such cases where everything else has failed to stop C- Diff.
A year ago, when I was new to all this, a reputable func med doc recommended 1 teaspoon a day of Trehalose. PB and I recently had a post / message stream about this. His research states that that is a pointless volume. I understand that for the purpose of autophagy / protein removal it is. So then why did the func med recommend 1 teaspoon? I fail to see the point. I don’t want to pay for another session especially if it was bad advice.
Because bears like blueberries if you eat blueberries does not mean a bear is going to attack you. The only way one is going to get C. Diff is by going to a nursing home and hanging out with old folks that have it. Eating trehalose will do nothing to reduce or increase your chances of contracting C. Diff. You're a smart guy Art; not sure why you would go down the scare tactic route for something that is used in food manufacturing and has a loooong history of safety in humans AND MIGHT just MIGHT help people with Parkinsons or other neurological disorders when there is virtually NOTHING the medical community has to offer that can slow progression of such diseases. Even IF you want to believe that somehow there is a risk associated with trehalose I argue it is FAR outweighed by the potential benefit.
Well, if you eat that blueberry in front of a bear, you may have a problem! 😋
Not trying to scare anyone, just trying to show some of what has been seen as regards Trehalose. It seems that everything used for PD has some risk and this includes prescription meds such as C/L and popular supplements such as HDT. Even exercise has some risk involved such as falling while walking or losing your balance on a treadmill and falling off. Just swallowing a pill confers the risk of choking in a person who has swallowing issues as is sometimes seen in PwP. I think it is useful to know what the risks might be, before starting something. If the risk seems low enough then it may be worth testing, but if the perceived risk is too high for the individual, then maybe not.
I absolutely agree that the medical community has nothing to slow the disease process and if that is what you seek, then you will have to look elsewhere, such as this forum as one example.
I hope you share some of your newer findings, Joe!
And then there is this: Neuroprotective Effects of Trehalose and Sodium Butyrate on Preformed Fibrillar Form of α-Synuclein-Induced Rat Model of Parkinson’s Disease - 2021 pubs.acs.org/doi/10.1021/ac...
α-syn was used to induce PD in wistar rats, which were thereafter subjected to treatment with trehalose (tre, 4g/kg, orally), a potent autophagy inducer and sodium butyrate (SB, 300 mg/kg, orally), a pan histone deacetylase inhibitor alone as well as in combination.
Using the park_bear adjustment factor for metabolic rate (divide dose by 12 to adjust from mouse to human, and by 8 for rats) for a 70 kg person (me) that would be taking trehalose (4x70/8) 35 grams (that is less than 2 tablespoons full I think) and sodium butyrate (300x70/8) 2625 mg. That's only twice the recommended dose on the first sodium butyrate capsules I found and a quick search easily found a study where they were giving people 4 grams of sodium butyrate a day ncbi.nlm.nih.gov/pmc/articl...
I don't know if I am going to be able to resist this.
I doubt it. My little toy poodle has very dry eyes condition and was prescribed cyclosporine. I was concerned about systemic absorption and his vet/ophthalmologist was negative. I believe the same applies to humans.
A recent study has demonstrated that trehalose decreased the A53T α‐synuclein expression level in transduced PC12 cells at low concentration (lower than 1 mM). In contrast, at a high concentration (higher than 1 mM), trehalose induced the expression of A53T α‐synuclein and attenuated cell viability through stabilization of A53T α‐synuclein oligomers (Zhao et al., 2017; Table 1). Likewise, a high concentration of trehalose induced cytotoxic effects, an effect also observed in previous studies (Lan et al., 2012; Table 1). Along these same lines, trehalose did not efficiently induce autophagy in the brain of mice after long‐term treatment (3 or 12 weeks; Tanji et al., 2015; Table 2). Short‐term treatment with trehalose ameliorates dopamine‐related pathology in the mouse tauopathy model by induction of mitophagy and improvement in the redox status. However, long‐term treatment leads to energy deficits due to the uncontrolled activation of the autophagic pathway. The detrimental long‐term effect of trehalose is more noticeable in cerebral regions associated with higher metabolic activity and oxidative stress like the striatum, which has a high content of dopamine (Table 2; Rodríguez‐Navarro et al., 2010). As shown by Zhao et al. (2017), a high trehalose concentration in PC12 cells affected mitochondrial morphology and reduced the mitochondrial membrane potential (Table 1). Therefore, it appears that the lowest effective dose and duration of maximum neuroprotective effect need to be defined to avoid the adverse effects of a high dosage.
The study's conclusion supports the use of trehalose, and the toxic levels from the Zhao studies were achieved in petri dishes using amounts that would be almost impossible to reach in human cells without direct injection. In fact, there is scant evidence that trehalose can cross the Blood-Brain Barrier. Studies show that less than 2% of what one ingests orally crosses the gut undigested so imagine the amount that ultimately gets to the brain. It will be tiny if at all. That is why I am a strong proponent of attacking neurological disorders thru multiple paths including exercise, diet, AND numerous supplements that have some proof of potential efficacy including but not limited to: Trehalose or Mannitol, Niagen, Theracurmin HP, Ubiquinol, Creatine and several others. You can find my full list here: longecity.org/forum/topic/1...
My final comment is to say that I have been eating 40-50g per day of Trehalose for 5 years (along with numerous other supplements) and have a disease with underlying pathology similar to Parkinsons, but I have experienced no change in symptoms and continue to live a normal life at 55. I also have a full blood panel done every 6 months and show nothing abnormal; in fact my blood panel is rock star material medically speaking.
I believe the same or similar applies to all autophagy inducing treatments are actions. They should not be used indefinitely but in a hit and run manner.
Do others here prefer a particular dose of trehalose? I just took 25 grams as my initial experiment with it.
I just bought two tubs of trehalose, but now I see "added sugars 9%" on the back of the jar. I suppose this is to make it taste better. I wish it wasn't there, but perhaps that is unavoidable in other brands too.
I saw another article which talked about injecting trehalose to maximize chances of it ever crossing the blood-brain barrier. The article speculated that this was the problem with trehalose for PD - how to get it across the BBB to disaggregate a-syn.
Joe, your stable conditions are great to hear about. Do you attribute that to everything in your exercise and supplements list, or do you believe that trehalose was particularly instrumental in maintaining statis. Thanks!
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Well, at least if you get C.diff you are in line for poop pills.
Parkinson's Disease: emerging treatment target, the NLRP inflammasome. 
