Jay
#182
RapAdmin, The specific form of vitamin K used was MK-7, a form of vitamin K2. My impression of the article at Medical News Today is that the author thinks it’s all about vitamin K1, but it is not.
From the article, "The researchers administered Menaquinone-7 (MK-7), which the authors note “is a major form of vitamin K2.”
It’s interesting to note that a photo of kale was shown at the top of the article, but leafy greens do not contain vitamin K2. They contain Vitamin K1. Vitamin K2 (MK-4) is found in organ meats such as liver, pork, chicken, egg yolks and full-fat, grass fed dairy products. Vitamin K2 (MK-7) is found in fermented foods with live bacteria such as natto, sauerkraut and cheeses. Canned sauerkraut and American cheese won’t do because they don’t contain any live bacteria. That other fake cheese called Velveeta also contains no live bacteria.
2 Likes
AnUser
#185
Or you can just take some anti-inflammatory drugs that are pretty safe and good.
2 Likes
IDO1 inhibitors
IDO1 (indoleamine 2,3-dioxygenase 1) inhibitors are a class of drugs being investigated for their potential to modulate immune responses, particularly in the context of cancer and autoimmune diseases. Some of the notable IDO1 inhibitors that have been identified and studied include:
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Epacadostat (INCB024360): Developed by Incyte Corporation, epacadostat has been one of the most well-known IDO1 inhibitors, though its development has seen ups and downs, including clinical trials with mixed results.
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Indoximod: This compound is being investigated for its ability to inhibit IDO1 and has been studied in various cancer trials.
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Navoximod (GDC-0919): Developed by Genentech/Roche, navoximod is another IDO1 inhibitor that has been evaluated in clinical trials for its efficacy in cancer treatment.
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Kynic: This IDO1 inhibitor is in preclinical development and aims to address the IDO1 pathway to enhance immune responses against cancer.
These drugs target IDO1 to potentially enhance the immune system’s ability to fight tumors or manage autoimmune conditions. The effectiveness and safety of these inhibitors continue to be evaluated in clinical trials.
(ChatGPT)
5 Likes
adssx
#187
In mice!
What I find more interesting is this:
Neuroscientists believe one of the key mechanisms by which Alzheimer’s disease impairs brain function is through the disruption of glucose metabolism, which is essential for energizing a healthy brain. Essentially, a decrease in metabolism deprives the brain of vital energy, thereby hindering cognitive functions and memory.
GLP-1RAs seem to restore glycolysis, so they’re quite interesting.
6 Likes
adssx
#189
I think I posted this study before. What’s especially concerning for acarbose users is: “Metformin displayed the lowest risk of dementia across diverse antidiabetics, whereas α-glucosidase inhibitors demonstrated the highest risk.”
[EDIT: here was the previous discussion about this paper: Acarbose with food extends mice lifespan, does Acarbose "without" food also extend mice lifespan? - #47 by adssx ]
Also: it looks like they didn’t analyze GLP-1RAs.
5 Likes
adssx
#190
Just published on the same topic: Repurposing antidiabetic drugs for Alzheimer’s disease: A review of preclinical and clinical evidence and overcoming challenges
Antidiabetic drug classes, notably GLP-1 analogs and SGLT2 inhibitors, and a reduced risk of dementia in patients with diabetes mellitus. […] On the other hand, alpha-glucosidase inhibitors (AGIs) and sulfonylureas may potentially increase the risk, especially in those experiencing recurrent hypoglycemic events.
Another paper highlighting the risk of alpha-glucosidase inhibitors (aka acarbose) for Alzheimer’s disease…
2 Likes
ng0rge
#191
Are you sure that’s the right link? That appears to go to - Effect of SGLT-2 inhibitors on arrhythmia events. All about A-Fib, nothing about Alzheimer’s or dementia.
adssx
#192
Oops sorry, fixed. Thanks.
1 Like
NMN may protect against Alzheimers
Therapeutic effect of nicotinamide mononucleotide on Alzheimer’s disease through activating autophagy and anti-oxidative stress
http://www.sciencedirect.com/science/article/pii/S0753332224010837
1 Like
adssx
#194
From the great “Research Center for Modernization of Characteristic Chinese Medicine, and Key Laboratory of Ningxia Ethnomedicine Modernization” 
2 Likes
I’m just putting it out there, but, yes it is a low grade paper.
1 Like
ng0rge
#196
Are you saying that just because it’s from China? It says from Ningxia Medical University and funded by National Natural Science Foundation of China. Does that automatically mean “bad science”? Or “suspect”? Why?
3 Likes
AnUser
#197
Ultimately, the journal and the country where a paper is from doesn’t matter. I think it’s funny to remark on MDPI, the pattern publications in that journal follows. But I should start reading MDPI papers as I dislike this bias more.
Papers can be bad but not because of who published it or where, or in which journal.
adssx
#198
Most papers are incorrect or even fraudulent. The % of garbage is higher in some countries such as China, Iran, and Egypt. And then in each of these countries there are differences as well. If it’s from Peking University that’s probably okay. If it’s from an “Ethnomedicine” research group in a shitty uni in… Ningxia then it can probably go to the trash.
6 Likes
ng0rge
#199
Just a follow-up on this.
Neuroscientists believe one of the key mechanisms by which Alzheimer’s disease impairs brain function is through the disruption of glucose metabolism, which is essential for energizing a healthy brain. Essentially, a decrease in metabolism deprives the brain of vital energy, thereby hindering cognitive functions and memory.
In the brain, kynurenine regulates production of the energy molecule lactate, which nourishes the brain’s neurons and helps maintain healthy synapses. Andreasson and her fellow researchers specifically looked at the enzyme indoleamine-2,3-dioxygenase 1 — or IDO1, for short — which generates kynurenine. Their hypothesis was that increases in IDO1 and kynurenine triggered by accumulation of amyloid and tau proteins would disrupt healthy brain metabolism and lead to cognitive decline.
“The kynurenine pathway is over activated in astrocytes, a critical cell type that metabolically supports neurons. When this happens, astrocytes cannot produce enough lactate as an energy source for neurons, and this disrupts healthy brain metabolism and harms synapses” Andreasson said. Blocking production of kynurenine by blocking IDO1 restores the ability of astrocytes to nourish neurons with lactate.
The next step is to test IDO1 inhibitors in human Alzheimer’s patients to see if they show similar improvements in cognition and memory.
And here is the paper:
https://www.science.org/doi/10.1126/science.abm6131
This makes me wonder…what if you could improve this pathway/process? Improve glucose metabolism to provide more energy to a healthy brain. Would that improve cognitive functions and memory?
Another new article on the IDO1 inhibitor study from one of the authors.
https://theconversation.com/what-links-aging-and-disease-a-growing-body-of-research-says-its-a-faulty-metabolism-236047
1 Like
ng0rge
#200
My question is why do you say that? My search for “ethnomedicine” shows nothing in the study. Some studies could be good? Are you basing it just on location? Beijing vs Ningxia? Size of the University? Do you know details of the departments?
adssx
#201
“Ethnomedicine” and “Chinese medicine” are in the author affiliation. These are red flags for BS. And yes Ningxia was one of the poorest Chinese provinces. It’s now average in terms of GDP per capita, just thanks to their wine industry (which is quite funny given that Ningxia is a Muslim autonomous province). So the most cutting edge serious research will most likely not come out of Ningxia 
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