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  #46   ^
Old Fri, Jan-04-19, 07:51
Ms Arielle's Avatar
Ms Arielle Ms Arielle is offline
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Posts: 19,176
 
Plan: atkins, carnivore 2023
Stats: 200/211/163 Female 5'8"
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Progress: -30%
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Quote:
Originally Posted by Meme#1
Exactly! That's only what's obvious and visible. Like you said, who knows what other damage it's causing with blood vessels.
It's like we're all human guinea pigs, disposable. There is probably a reserve they keep to payoff claims. We're just a cost of doing business these days.
Just unbelievable!


While listening to NPR radio yesterday, a guest discussed the differences in allowable drugs and chemical between the US and the EU. OVerall, US is more lenient.
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  #47   ^
Old Wed, Apr-03-19, 09:02
JEY100's Avatar
JEY100 JEY100 is online now
Posts: 13,368
 
Plan: P:E/DDF
Stats: 225/150/169 Female 5' 9"
BF:45%/28%/25%
Progress: 134%
Location: NC
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Related to the Broken Brain 2 seminar, Dr Hyman podcast today is with Dr. Perlmutter. Early on, he mentions that November study that not only do the Alzheimers drugs not work, but can make it worse. https://drhyman.com/podcast/

How to Prevent Alzheimers with your Fork. He is quite vocal that Alzheimer's is largely a preventable disease. Mark Hyman still interrupts too much for me, but Dr. Perlmutter can talk a lot over him.
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  #48   ^
Old Wed, Apr-03-19, 13:01
Ms Arielle's Avatar
Ms Arielle Ms Arielle is offline
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Posts: 19,176
 
Plan: atkins, carnivore 2023
Stats: 200/211/163 Female 5'8"
BF:
Progress: -30%
Location: Massachusetts
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Over and over many of the chronic diseases come back to diet.
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  #49   ^
Old Thu, Apr-04-19, 08:48
GRB5111's Avatar
GRB5111 GRB5111 is offline
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Posts: 4,036
 
Plan: Very LC, Higher Protein
Stats: 227/186/185 Male 6' 0"
BF:
Progress: 98%
Location: Herndon, VA
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Quote:
Originally Posted by JEY100
Related to the Broken Brain 2 seminar, Dr Hyman podcast today is with Dr. Perlmutter. Early on, he mentions that November study that not only do the Alzheimers drugs not work, but can make it worse. https://drhyman.com/podcast/

How to Prevent Alzheimers with your Fork. He is quite vocal that Alzheimer's is largely a preventable disease. Mark Hyman still interrupts too much for me, but Dr. Perlmutter can talk a lot over him.

Thanks, Janet. Excellent session; although, they need to apply virtual duct tape to Mark's mouth and teach him to listen to his guests and allow them to expound.
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  #50   ^
Old Wed, Aug-21-19, 07:55
teaser's Avatar
teaser teaser is offline
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Posts: 15,075
 
Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
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Location: Ontario
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https://www.sciencedaily.com/releas...90812144930.htm

Quote:
An alternate theory for what causes Alzheimer's disease

Alzheimer's disease, the most common cause of dementia among the elderly, is characterized by plaques and tangles in the brain, with most efforts at finding a cure focused on these abnormal structures. But a University of California, Riverside, research team has identified alternate chemistry that could account for the various pathologies associated with the disease.

Plaques and tangles have so far been the focus of attention in this progressive disease that currently afflicts more than 5.5 million people in the United States. Plaques, deposits of a protein fragment called beta-amyloid, look like clumps in the spaces between neurons. Tangles, twisted fibers of tau, another protein, look like bundles of fibers that build up inside cells.

"The dominant theory based on beta-amyloid buildup has been around for decades, and dozens of clinical trials based on that theory have been attempted, but all have failed," said Ryan R. Julian, a professor of chemistry who led the research team. "In addition to plaques, lysosomal storage is observed in brains of people who have Alzheimer's disease. Neurons -- fragile cells that do not undergo cell division -- are susceptible to lysosomal problems, specifically, lysosomal storage, which we report is a likely cause of Alzheimer's disease."

Study results appear in ACS Central Science, a journal of the American Chemical Society.

An organelle within the cell, the lysosome serves as the cell's trashcan. Old proteins and lipids get sent to the lysosome to be broken down to their building blocks, which are then shipped back out to the cell to be built into new proteins and lipids. To maintain functionality, the synthesis of proteins is balanced by the degradation of proteins.

The lysosome, however, has a weakness: If what enters does not get broken down into little pieces, then those pieces also can't leave the lysosome. The cell decides the lysosome is not working and "stores" it, meaning the cell pushes the lysosome to the side and proceeds to make a new one. If the new lysosome also fails, the process is repeated, resulting in lysosome storage.

"The brains of people who have lysosomal storage disorder, another well-studied disease, and the brains of people who have Alzheimer's disease are similar in terms of lysosomal storage," Julian said. "But lysosomal storage disorder symptoms show up within a few weeks after birth and are often fatal within a couple of years. Alzheimer's disease occurs much later in life. The time frames are, therefore, very different."

Julian's collaborative team of researchers in the Department of Chemistry and the Division of Biomedical Sciences at UC Riverside posits that long-lived proteins can undergo spontaneous modifications that can make them undigestible by the lysosomes.

"Long-lived proteins become more problematic as we age and could account for the lysosomal storage seen in Alzheimer's, an age-related disease," Julian said. "If we are correct, it would open up new avenues for treatment and prevention of this disease."

He explained that the changes occur in the fundamental structure of the amino acids that make up the proteins and is the equivalent of flipping the handedness of the amino acids, with amino acids spontaneously acquiring the mirror images of their original structures.

"Enzymes that ordinarily break down the protein are then not able to do so because they are unable to latch onto the protein," Julian added. "It's like trying to fit a left-handed glove on your right hand. We show in our paper that this structural modification can happen in beta-amyloid and tau, proteins relevant to Alzheimer's disease. These proteins undergo this chemistry that is almost invisible, which may explain why researchers have not paid attention to it."

Julian explained these spontaneous changes in protein structure are a function of time, taking place if the protein hangs around for too long.

"It's been long known that these modifications happen in long-lived proteins, but no one has ever looked at whether these modifications could prevent the lysosomes from being able to break down the proteins," he said. "One way to prevent this would be to recycle the proteins so that they are not sitting around long enough to go through these chemical modifications. Currently, no drugs are available to stimulate this recycling -- a process called autophagy -- for Alzheimer's disease treatment."

The research was done in the lab on living cells provided by Byron D. Ford, a professor of biomedical sciences in the School of Medicine. The findings could have implications for other age-related diseases such as macular degeneration and cardiac diseases linked to lysosomal pathology.

Julian and Ford were joined in the research by Tyler R. Lambeth (co-first author), Dylan L. Riggs (co-first author), Lance E. Talbert, Jin Tang, Emily Coburn, Amrik S. Kang, Jessica Noll, and Catherine Augello.

Next, the team will examine the extent of the protein modifications in human brains as a function of age. The researchers will study brains of people with Alzheimer's disease as well as of people not afflicted by it.


Quote:
Currently, no drugs are available to stimulate this recycling -- a process called autophagy -- for Alzheimer's disease treatment."




Hurmm...

Interesting about amino acids "flipping" in long-lived proteins, first time I've come across that.
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  #51   ^
Old Wed, Aug-21-19, 10:38
GRB5111's Avatar
GRB5111 GRB5111 is offline
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Posts: 4,036
 
Plan: Very LC, Higher Protein
Stats: 227/186/185 Male 6' 0"
BF:
Progress: 98%
Location: Herndon, VA
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It is interesting research. I like the knee-jerk reaction that a drug is needed to stimulate autophagy to achieve recycling. Typical. Perhaps more research might confirm that we can address stimulating autophagy naturally, but scientists are inclined to report a solution that is also profitable. How else will they get their research funded?
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  #52   ^
Old Wed, Aug-21-19, 12:07
s93uv3h's Avatar
s93uv3h s93uv3h is offline
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Posts: 1,662
 
Plan: Atkins & IF / TRE
Stats: 000/000/000 Male 5' 10"
BF:
Progress: 97%
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sleep. diet. (bicycle helmet).

take care of your brain!
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  #53   ^
Old Wed, Aug-21-19, 12:16
Ms Arielle's Avatar
Ms Arielle Ms Arielle is offline
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Posts: 19,176
 
Plan: atkins, carnivore 2023
Stats: 200/211/163 Female 5'8"
BF:
Progress: -30%
Location: Massachusetts
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Quote:
Originally Posted by GRB5111
It is interesting research. I like the knee-jerk reaction that a drug is needed to stimulate autophagy to achieve recycling. Typical. Perhaps more research might confirm that we can address stimulating autophagy naturally, but scientists are inclined to report a solution that is also profitable. How else will they get their research funded?


Which is why we needed the NIH funded. My understanding is that only taxpayer money paid for that research.
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  #54   ^
Old Wed, Aug-21-19, 12:19
Ms Arielle's Avatar
Ms Arielle Ms Arielle is offline
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Posts: 19,176
 
Plan: atkins, carnivore 2023
Stats: 200/211/163 Female 5'8"
BF:
Progress: -30%
Location: Massachusetts
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Talked to a friend with MS last night, while its not Alzheimers, it seems to have similarities; he has decided to stop his $2k treatments despite how well this makes him feel. Gave him Dr Terry Wahl's information and told him her story of recovery. He is excited to have a look at it.
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  #55   ^
Old Wed, Aug-21-19, 12:25
JEY100's Avatar
JEY100 JEY100 is online now
Posts: 13,368
 
Plan: P:E/DDF
Stats: 225/150/169 Female 5' 9"
BF:45%/28%/25%
Progress: 134%
Location: NC
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New MS study results out a few days ago. A Phase 1 trial, using Wahl's Paleo plus. https://multiplesclerosisnewstoday....eo-diet-and-ms/
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  #56   ^
Old Wed, Aug-21-19, 14:51
WereBear's Avatar
WereBear WereBear is online now
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Posts: 14,602
 
Plan: EpiPaleo/Primal/LowOx
Stats: 220/125/150 Female 67
BF:
Progress: 136%
Location: USA
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Quote:
Originally Posted by Ms Arielle
Talked to a friend with MS last night, while its not Alzheimers, it seems to have similarities; he has decided to stop his $2k treatments despite how well this makes him feel. Gave him Dr Terry Wahl's information and told him her story of recovery. He is excited to have a look at it.


After reading Dr. Wahl's book I went on a hunt about auto-immune treatments. Once you've worn out the cortisol and the body no longer responds, now they bring out the big guns which are really a devil's bargain.

They often bring about considerable resolution of symptoms, but at the expense of suppressing the immune system. From what I read, which is just a sampling of what came up with my key words, a LOT of people get ten years of pretty smooth sailing and then some combination of exposure and vulnerability brings a health catastrophe.

This all evolved from the science of organ transplantation. In which case it is usually life or death... and thus, an easier choice.

If, as I now believe, we are better off treating these kinds of issues with diet and lifestyle changes, there is a lot of needless suffering going on that people can't really choose.

Last edited by WereBear : Wed, Aug-21-19 at 14:58.
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  #57   ^
Old Tue, Jan-14-20, 05:26
JEY100's Avatar
JEY100 JEY100 is online now
Posts: 13,368
 
Plan: P:E/DDF
Stats: 225/150/169 Female 5' 9"
BF:45%/28%/25%
Progress: 134%
Location: NC
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New article in JAMA.

In Alzheimer Research, Glucose Metabolism Moves to Center Stage


https://jamanetwork.com/journals/ja...Jwjt1L-mNXmZKS8


After the amyloid hypothesis, diabetes drugs, and insulin devices, come up empty...they try a ketogenic lifestyle!

Quote:
With a dearth of treatment options, Craft and others are also turning to lifestyle interventions that may have beneficial metabolic effects in both the body and brain. Craft recently published results of a pilot crossover trial comparing a modified version of the ketogenic diet incorporating Mediterranean diet elements with a low-fat diet among patients with memory complaints or mild cognitive impairment.

Six weeks after completing the modified ketogenic diet, patients had improved Alzheimer disease biomarkers in their cerebrospinal fluid. “With the ketogenic diet, we are moving the β-amyloid in a healthier direction,” Craft said. Patients also had better blood flow to the hippocampus and improved body-wide insulin sensitivity. A larger trial of the modified ketogenic diet is now under way.
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  #58   ^
Old Tue, Jan-14-20, 06:52
WereBear's Avatar
WereBear WereBear is online now
Senior Member
Posts: 14,602
 
Plan: EpiPaleo/Primal/LowOx
Stats: 220/125/150 Female 67
BF:
Progress: 136%
Location: USA
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Quote:
Originally Posted by JEY100
New article in JAMA.

In Alzheimer Research, Glucose Metabolism Moves to Center Stage


https://jamanetwork.com/journals/ja...Jwjt1L-mNXmZKS8


After the amyloid hypothesis, diabetes drugs, and insulin devices, come up empty...they try a ketogenic lifestyle!


It would be funny if it weren’t so sad.

If that doctor who used coconut oil on her early onset Alzheimer’s husband had those improvements on a drug, we’d be living in wall to wall advertisements for it. It would be $5,000 a month and rich people would be popping them like peanuts.

I’m a fan of Pete Egoscue, whose system of exercises have helped so many. It springs from the same, simple, principles as keto: give the body what it needs, and it can heal itself.
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  #59   ^
Old Tue, Jan-14-20, 07:01
WereBear's Avatar
WereBear WereBear is online now
Senior Member
Posts: 14,602
 
Plan: EpiPaleo/Primal/LowOx
Stats: 220/125/150 Female 67
BF:
Progress: 136%
Location: USA
Default

Quote:
Originally Posted by Ms Arielle
Talked to a friend with MS last night, while its not Alzheimers, it seems to have similarities; he has decided to stop his $2k treatments despite how well this makes him feel. Gave him Dr Terry Wahl's information and told him her story of recovery. He is excited to have a look at it.


Dr Terry Wahls and Dr Sarah Myhill, along with some other sources, are increasingly convinced that all autoimmune is the same disease; and mitochondrial dysfunction is the cause.

Tell me a Non-infectious, Non-acute illness that doesn’t have its roots in mitochrondria, then high insulin, then inflammation, and then the body’s attempts to protect itself from it. This chain of events was crucial in me putting my edge-of-lupus situation, a year ago, into remission.

My experiments over the holidays caused a flare. So I know where the problem lies.
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  #60   ^
Old Thu, Nov-19-20, 09:44
teaser's Avatar
teaser teaser is offline
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Posts: 15,075
 
Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
BF:
Progress: 104%
Location: Ontario
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https://www.sciencedaily.com/releas...01116112846.htm

Quote:
Overly reactive star-shaped cells explain the unpredictability of Alzheimer's disease


Though Alzheimer's disease (AD) is a common and fatal neurodegenerative brain disorder, most of AD treatments seem to not be making much headway to unravel the mystery of its cause. Many AD drugs have targeted the elimination of beta-amyloid (A?) or amyloid plaques, which block cell-to-cell signaling at synapses. But some AD patients continue to show neurodegeneration and cognitive decline even after the removal of the amyloid plaques. Conversely, many people indicate no signs of neurodegeneration and cognitive impairment even in very high level of A?. Also, it has never been precisely clear as to why the star-shaped non-neuronal cells, called astrocytes, change in their shapes and functions from the early onset of AD, and continue such reactive state throughout the AD progression.

Researchers at the Center for Cognition and Sociality, within the Institute for Basic Science (IBS) and Korea Institute of Science and Technology (KIST) have demonstrated that the severity of 'reactive astrocytes' is a key indicator for the onset of AD, raising profound implications of the current theory of AD mechanism. In its toxin-receptor-based animal model, the research team fine-tuned astrocytic reactivity in vivo. They found that the mild reactive astrocytes can naturally reverse its reactivity, whereas severe reactive astrocytes can cause irreversible neurodegeneration, brain atrophy and cognitive deficits, all within 30 days. Notably, this severe-reactive-astrocyte-induced neurodegeneration was successfully replicated in virus-injected APP/PS1 mice, which have been widely known to lack neurodegeneration. These results indicate that severe reactive astrocytes are sufficient for neurodegeneration.

"This finding suggests experiences such as traumatic brain injury, viral infection, and post-traumatic stress disorder might be needed to transform a healthy brain to be vulnerable to Alzheimer's disease via excessive oxidative stress," says Director C. Justin LEE (at IBS), the study's corresponding author. "The excessive oxidative stress disables the body's ability to counteract the harmful effects of overproduced oxygen-containing molecules, subsequently transforming mild reactive astrocytes into neurotoxic severe reactive astrocytes," explains Dr. Lee. The team revealed that toxin-responsive astrocytes activate a cellular restoration mechanism (or autophagy-mediated degradation pathway) and increase hydrogen peroxide (H2O2) by triggering monoamine oxidase B (MAO-B). MAO-B plays an important role in the reduction of dopamine that hinders the signal transmission to produce smooth, purposeful movement.

Such mechanistic system results in morphological hypertrophy of astrocytic processes followed by a cascade of neurodegenerative events: turning-on of the nitric oxide synthesizing enzyme iNOS, nitrosative stress, microglial activation and tauopathy. The research team verified that all of these events of the AD pathology were halted by a recently developed reversible MAO-B inhibitor, KDS2010 or a potent H2O2 scavenger, AAD-2004. This reinforces that severe reactive astrocytes are the cause of neurodegeneration, not the result of it as previously assumed, notes Director Lee. Finally, these molecular features of the severe reactive astrocytes are commonly shared in various animal models of AD and in the brain of human AD patients.

This study offers plausible explanations for why AD has been so unpredictable: neurodegeneration cannot be reversed once severe reactive astrocytes are on; and mild reactive astrocytes can be recovered unless being stretched by other pathological burdens. "Notably, this study suggests that an important step to establishing a new treatment strategy for Alzheimer's disease should be by targeting reactive astrocytes that appear to be overly activated in the early stages," says Dr. RYU Hoon (at KIST), another corresponding author of the study. This should be accompanied by the development of the diagnostic tools for reactive astrocytes and early Alzheimer's disease, adds Dr. Ryu.

Dr. CHUN Heejung (at IBS), the first author of the study says, "The reactive astrocytes are a general phenomenon occurring in various brain diseases such as Parkinson's disease and brain tumors, as well as Alzheimer's disease. Building upon this study, we have plans to expand our mechanistic insights of the reactivity-dependent neuronal death into other brain diseases for which treatment has not yet been developed."



https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2792615/


Garlic?

Quote:
Evidences for the involvement of monoaminergic and GABAergic systems in antidepressant-like activity of garlic extract in mice


This study used garlic extract in mice. Not added to food, looks like either injected or force-fed orally. Separation from food is important because that might change food intake or pattern of intake. They don't give a fresh garlic dose that I can see, to see if realistic amounts could be taken as food. Anyways, decrease of MAO-B is included in the data.

On the depression front--the garlic extract dose-dependently decreased immobility in a forced swim test. Happier mice try for a longer time to find a way out when placed in water over their head, depressed mice give up sooner.
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