Gear_Addict
New Member
I will like to know this too.
MESO-Rx
Anabolic Steroids
Alzheimer’s
- Thread starter Michael Scally MD
- Start date
I will like to know this too.
Investigate it and let us know.
My personal opinion is that diet and lifestyly may have some effect on the prosess but that it predominantly geneticially determined. Researchers are focusing in on specific genes that appear to control the brains glucose metabolism and probably other mechanisms as well.
My personal opinion is that diet and lifestyly may have some effect on the prosess but that it predominantly geneticially determined. Researchers are focusing in on specific genes that appear to control the brains glucose metabolism and probably other mechanisms as well.
cvictorg
New Member
coconut oil and Alzheimer's
http://www.tampabay.com/news/aging/article879333.ece
Ketone Esters Treat Alzheimer's 10 Times Better Than Coconut Oil | Dementia & Alzheimer's Weekly
Coconut oil's benefits in treating Alzheimer's-dementia can be potentially concentrated in ketone esters. This approach is gaining a growing pool of advocates. Implied support is in from researchers at the U.S. government's NIH (National Institutes of Health) and Harvard / Columbia.
The NIH's Dr. Richard Veech advocates production of a ketone ester similar to Axona. Dr. Theodore VanItallie of Harvard and Columbia has gone on the record to state,
"My view of the ketone ester story is that - if the results in human subjects bear out the findings in laboratory animals - they could well be the major advance in nutrition in the 21st century."
http://www.tampabay.com/news/aging/article879333.ece
Ketone Esters Treat Alzheimer's 10 Times Better Than Coconut Oil | Dementia & Alzheimer's Weekly
Coconut oil's benefits in treating Alzheimer's-dementia can be potentially concentrated in ketone esters. This approach is gaining a growing pool of advocates. Implied support is in from researchers at the U.S. government's NIH (National Institutes of Health) and Harvard / Columbia.
The NIH's Dr. Richard Veech advocates production of a ketone ester similar to Axona. Dr. Theodore VanItallie of Harvard and Columbia has gone on the record to state,
"My view of the ketone ester story is that - if the results in human subjects bear out the findings in laboratory animals - they could well be the major advance in nutrition in the 21st century."
cvictorg
New Member
Not on alzheimer's but an interesting study anyway
http://www.ajcn.org/content/34/8/1552.full.pdf
Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau Island studies
http://www.ajcn.org/content/34/8/1552.full.pdf
Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau Island studies
cvictorg
New Member
Hypometabolism as a therapeutic target in Alzheimer's disease
BMC Neuroscience | Full text | Hypometabolism as a therapeutic target in Alzheimer's disease
Ketone bodies provide an alternate energy source for hypometabolic neurons, and may offer a novel treatment for AD as well as other neurodegenerative disorders that are characterized by neuronal hypometabolism. The results from studies with AC-1202 indicate that patients exhibit cognitive improvements in response to elevation of ketone levels, and support data linking AD to glucose/insulin metabolism.
BMC Neuroscience | Full text | Hypometabolism as a therapeutic target in Alzheimer's disease
Ketone bodies provide an alternate energy source for hypometabolic neurons, and may offer a novel treatment for AD as well as other neurodegenerative disorders that are characterized by neuronal hypometabolism. The results from studies with AC-1202 indicate that patients exhibit cognitive improvements in response to elevation of ketone levels, and support data linking AD to glucose/insulin metabolism.
cvictorg
New Member
Ketone Bodies as a Therapeutic for Alzheimer’s Disease
http://multivu.prnewswire.com/broadcast/36441/36441-Henderson2008Neurotherapeutics.pdf
http://multivu.prnewswire.com/broadcast/36441/36441-Henderson2008Neurotherapeutics.pdf
Is Hope Near?
By the third quarter, scientists may have a better idea of whether two drugs can help any of the world's 26 million Alzheimer's victims.
http://online.barrons.com/article/SB50001424052748703754104577237652227653404.html?
FEBRUARY 25, 2012
By ANDREW BARY
Big pharmaceutical companies have struggled for years to develop a drug that will halt the progression of Alzheimer's disease, a terrible neurological ailment that begins with memory loss and steadily robs patients of brain function, leading to dementia and death. Success would have an enormous societal impact and help to contain the cost of an ever-increasing population of Alzheimer's patients, which number an estimated five million in the U.S. -- and 26 million worldwide.
It would also have an enormous impact on the health of the pharmaceutical industry, which has struggled to replace revenue lost from patent expirations on some of its biggest drugs and fallen from investor favor. Two compounds, now in late-stage clinical trials, have the potential to do just that. Some think a successful treatment or treatments for Alzheimer's could generate $10 billion to $20 billion in annual revenue.
Results from these pivotal trials on solanezumab, developed by Eli Lilly (ticker: LLY), and bapineuzumab, developed by Pfizer (PFE), Elan (ELN) and Johnson & Johnson (JNJ) -- are expected in the third quarter of this year. If either drug works and clears the Food and Drug Administration, it could be on the market as early as next year. "If these Alzheimer's drugs hit it big, they could become the next Lipitor,"observes Tim Anderson, who covers the pharmaceutical industry for Bernstein Research. But the odds of success aren't high. Anderson pegs the chance of success for the Lilly drug at no more than 20%, calling solanezumab a "lottery ticket" with a huge potential payoff. Bapineuzumab has a better shot, though most analysts view its odds at less than 50%.
LILLY AND ELAN SHARES offer the biggest payoffs if the drugs work, followed by Pfizer and J&J. Bapineuzumab is 50%-owned by Pfizer, 25% by Elan and 25% by J&J.
Another promising drug is Baxter International's (BAX) Gammagard, which showed encouraging results in a Phase II trial and is in two separate Phase III trials, the first of which is due for completion next year. And there are many other drugs in Phase II trials. But bapineuzumab and solanezumab are the farthest along in the process.
The key determinant of the stock-market impact is the drug's potential sales, relative to the owner's stock-market value and yearly revenue. Lilly is leveraged to solanezumab because its market value -- $45 billion -- is the smallest among the Big Pharma outfits, and it owns 100% of its anti-Alzheimer's product.
Analysts estimate that Lilly and Elan may have 10% downside if the drugs fail and upside of 50% or more if they score. Success for bapineuzumab could prompt an attempt by J&J to buy out Elan's 25% stake in the drug, or purchase the entire company.
Catherine Arnold, the drug analyst at Credit Suisse, thinks Pfizer offers a good play on bapineuzumab because the stock currently reflects little chance of success. Lilly and Elan now discount some hope for their drugs. Pfizer, at $21, trades for a modest 9 times projected 2012 profits, carries a 4% dividend yield and has a number of promising drugs in late-stage clinical trials. Arnold has an Outperform rating on Pfizer, with a 12-month price target of $24, noting that, if successful, bapineuzumab could add a few dollars to that target.
Lilly doesn't have a lot going for it now besides solanezumab. Its shares, around $39, trade for 12 times projected 2012 profits, a premium to the group, despite a weaker profit outlook than many of its peers, thanks to patent expirations. Few Wall Street analysts have Buy recommendations on Lilly; Bernstein's Anderson rates the stock Market Perform. Success with solanezumab could quickly change the Street's view on the stock, which is supported by a 5% dividend yield that management has vowed to maintain.
Shares of Lilly and Elan could rise in the coming months as investors bet on favorable trial results. And just what those results will be is still anyone's guess. "A consensus view on the phase III results…has not been reached, by either the clinical community or investor base, implying high likelihood of material stock moves upon data release," wrote Arnold in a recent client note.
Both bapineuzumab and solanezumab are aimed at people with mild to moderate Alzheimer's, a group that accounts for the majority of those suffering from the disease. It's considered much tougher to treat patients in the ailment's late stage.
Bapineuzumab probably has a greater chance of success in its Phase III trial -- the final stage of testing before a drug is submitted for approval to the FDA -- because it had a more robust earlier-stage, Phase II trial. That study showed that the compound helped certain Alzheimer's patients, although the overall results were deemed disappointing when they were released in 2008 because not all patients showed improvement. In addition, there was no evidence of any link between higher doses and better results.Barron's published a favorable cover story on the drug's prospects four years ago ("Breakthrough?" Apr. 7, 2008).
It's important to note that neither drug is likely to be capable of curing or reversing the course of the disease. The producers are hoping that the treatments simply will slow the progression of Alzheimer's. That would mark progress, however, because Alzheimer's research is littered with drug failures. Existing treatments, including Aricept and Namenda, address some symptoms of the disease, but don't arrest its progression.
"What solanezumab is really intended to do is slow the rate of decline," said Eric Siemers, the senior medical director of the Alzheimer's disease team at Lilly, on a Bernstein-sponsored conference call with investors in December.
Still, an FDA-approved product that could slow the course of the disease could generate billions of dollars in annual revenues, given the desperation among Alzheimer's sufferers and their families. Most patients are older than 65. The total number of sufferers worldwide could hit 100 million by 2050. The current cost for treating Alzheimer's patients worldwide is estimated at $150 billion per year.
INVESTORS ARE CAUTIOUS on the two drugs because the disease, despite its global toll, still isn't well understood by scientists, complicating the formulation of any treatment.
Among the unknowns are what causes Alzheimer's and what prompts its spread in the brain, killing nerve cells. "It's very different than diabetes and hypertension," Arnold says. "There is a lot of debate among the clinical experts on how the disease evolves and produces the symptoms that it does. When you talk to opinion leaders and scholars, you may get five different hypotheses."
Drug companies usually want a Phase III trial to have a 50%-plus chance of success because a large clinical trial can cost several hundred million dollars. But because of the potentially enormous payoff, the industry is willing to take more chances on drugs for difficult and widespread diseases like Alzheimer's than it normally would.
Bapineuzumab and solanezumab both seek to clear the brain of a plaque caused by a protein called beta-amyloid, which accumulates in Alzheimer's patients. What isn't clear is whether clearing that plaque will have any meaningful benefit.
The drugs work in different ways. Bapineuzumab crosses the so-called blood/brain barrier and seeks to clear brain cells of amyloid plaque. Solanezumab binds with a precursor of the plaque in the blood, with the aim of prompting the body to pull amyloid plaque from the brain.
The optimism about bapineuzumab stems from Phase II trial results that showed the drug slowed the mental decline in patients who lacked a genetic marker that appears to speed the progression of Alzheimer's. People without the marker make up about 40% of sufferers.
The Pfizer group's Phase III clinical trial will study 4,100 people, so that the researchers can evaluate bapineuzumab's effects on a substantial number of patients with and without the genetic marker. Arnold sees a 55% chance that the drug will show "modest benefits" in patients without the marker and she sees only a 10% chance of any success with the "tougher-to-treat" carriers.
The Lilly Phase II trial of solanezumab involved about 50 people and didn't show a lot, other than the presence of certain "biomarkers" that suggested some success, including the presence of the destructive amyloid protein in spinal fluid, an indication that it had been cleared from the brain. Lilly didn't test cognitive function, preferring to conduct a small Phase II test and then jump to a large Phase III with 2,000 patients to gauge solanezumab's effectiveness.
Wall Street and drug companies figure the pricing of Alzheimer's drugs, which are delivered intravenously, will hinge on their clinical impact. The better they work, the more they will cost. Bernstein's Anderson has estimated that the cost could range from $5,000 to $20,000 annually per patient. Multiply that by several million patients and the yearly sales figures run into the billions.
Arnold has various 2020 sales scenarios for the two drugs. Her range is $2.3 billion to $21.6 billion for bapineuzumab, and $517 million to $17.5 billion for solanezumab, depending on how well they work and how large a patient population they can address. The very wide range reflects the uncertainty about the products. She's more upbeat about bapineuzumab.
ONE OF THE CHALLENGES to formulating a drug is that neurodegenerative diseases generally are hard to treat. For all the attention to Alzheimer's, it still isn't easy to identify sufferers early because there can be other reasons for initial symptoms like memory loss. There's concern that once people are diagnosed with Alzheimer's, the disease may be beyond effective treatment. Arnold says some studies suggest that newly diagnosed patients may already have lost more than half their neurons -- the cells that transmit information within the brain via electrical and chemical signaling.
"There's concern that amyloid-lowering agents are effective only if given very early or even before symptoms appear," says Dr. Samuel Gandy, director of the Alzheimer's research center at Mount Sinai hospital in New York. To have an effective treatment, patients may have to be identified in their 50s or early 60s via screening. He adds that another possible contributor to Alzheimer's, a protein called tau, has been tough to tackle.
To approve bapineuzumab or solanezumab, the FDA probably wants to see cognitive improvement in patients, or at least a lessoning in the decline of mental functions. The agency also will determine whether the drugs clear plaque from the brain and slow the shrinkage of the brain that afflicts Alzheimer's sufferers.
Alzheimer's patients often are evaluated based on two clinical tests, one for cognition, and one for day-to-day tasks. Alzheimer's sufferers lose, on average, about four points per year on the cognition test (the scale goes up to 70).
It's a measure of the difficulty of treating the disease that Lilly scientists said they would be happy if their drug could reduce the deterioration by a third, to four points from six, over the 18-month course of the Phase III clinical trial. One issue is whether the tests can be done uniformly and precisely, thus capturing relatively small differences in mental function. Lilly is optimistic. "The number that we think is clinically significant is about one-third, and that's what we're statistically powered to detect in our phase III studies," said Lilly's Siemers at the Bernstein forum.
Given the limited understanding of Alzheimer's, the optimistic scenario for bapineuzumab and solanezumab is that they can slow its fatal progression, not cure patients. But even that would be good news for the millions of victims of the disease, not to mention the shareholders of the companies behind the medications.
By the third quarter, scientists may have a better idea of whether two drugs can help any of the world's 26 million Alzheimer's victims.
http://online.barrons.com/article/SB50001424052748703754104577237652227653404.html?
FEBRUARY 25, 2012
By ANDREW BARY
Big pharmaceutical companies have struggled for years to develop a drug that will halt the progression of Alzheimer's disease, a terrible neurological ailment that begins with memory loss and steadily robs patients of brain function, leading to dementia and death. Success would have an enormous societal impact and help to contain the cost of an ever-increasing population of Alzheimer's patients, which number an estimated five million in the U.S. -- and 26 million worldwide.
It would also have an enormous impact on the health of the pharmaceutical industry, which has struggled to replace revenue lost from patent expirations on some of its biggest drugs and fallen from investor favor. Two compounds, now in late-stage clinical trials, have the potential to do just that. Some think a successful treatment or treatments for Alzheimer's could generate $10 billion to $20 billion in annual revenue.
Results from these pivotal trials on solanezumab, developed by Eli Lilly (ticker: LLY), and bapineuzumab, developed by Pfizer (PFE), Elan (ELN) and Johnson & Johnson (JNJ) -- are expected in the third quarter of this year. If either drug works and clears the Food and Drug Administration, it could be on the market as early as next year. "If these Alzheimer's drugs hit it big, they could become the next Lipitor,"observes Tim Anderson, who covers the pharmaceutical industry for Bernstein Research. But the odds of success aren't high. Anderson pegs the chance of success for the Lilly drug at no more than 20%, calling solanezumab a "lottery ticket" with a huge potential payoff. Bapineuzumab has a better shot, though most analysts view its odds at less than 50%.
LILLY AND ELAN SHARES offer the biggest payoffs if the drugs work, followed by Pfizer and J&J. Bapineuzumab is 50%-owned by Pfizer, 25% by Elan and 25% by J&J.
Another promising drug is Baxter International's (BAX) Gammagard, which showed encouraging results in a Phase II trial and is in two separate Phase III trials, the first of which is due for completion next year. And there are many other drugs in Phase II trials. But bapineuzumab and solanezumab are the farthest along in the process.
The key determinant of the stock-market impact is the drug's potential sales, relative to the owner's stock-market value and yearly revenue. Lilly is leveraged to solanezumab because its market value -- $45 billion -- is the smallest among the Big Pharma outfits, and it owns 100% of its anti-Alzheimer's product.
Analysts estimate that Lilly and Elan may have 10% downside if the drugs fail and upside of 50% or more if they score. Success for bapineuzumab could prompt an attempt by J&J to buy out Elan's 25% stake in the drug, or purchase the entire company.
Catherine Arnold, the drug analyst at Credit Suisse, thinks Pfizer offers a good play on bapineuzumab because the stock currently reflects little chance of success. Lilly and Elan now discount some hope for their drugs. Pfizer, at $21, trades for a modest 9 times projected 2012 profits, carries a 4% dividend yield and has a number of promising drugs in late-stage clinical trials. Arnold has an Outperform rating on Pfizer, with a 12-month price target of $24, noting that, if successful, bapineuzumab could add a few dollars to that target.
Lilly doesn't have a lot going for it now besides solanezumab. Its shares, around $39, trade for 12 times projected 2012 profits, a premium to the group, despite a weaker profit outlook than many of its peers, thanks to patent expirations. Few Wall Street analysts have Buy recommendations on Lilly; Bernstein's Anderson rates the stock Market Perform. Success with solanezumab could quickly change the Street's view on the stock, which is supported by a 5% dividend yield that management has vowed to maintain.
Shares of Lilly and Elan could rise in the coming months as investors bet on favorable trial results. And just what those results will be is still anyone's guess. "A consensus view on the phase III results…has not been reached, by either the clinical community or investor base, implying high likelihood of material stock moves upon data release," wrote Arnold in a recent client note.
Both bapineuzumab and solanezumab are aimed at people with mild to moderate Alzheimer's, a group that accounts for the majority of those suffering from the disease. It's considered much tougher to treat patients in the ailment's late stage.
Bapineuzumab probably has a greater chance of success in its Phase III trial -- the final stage of testing before a drug is submitted for approval to the FDA -- because it had a more robust earlier-stage, Phase II trial. That study showed that the compound helped certain Alzheimer's patients, although the overall results were deemed disappointing when they were released in 2008 because not all patients showed improvement. In addition, there was no evidence of any link between higher doses and better results.Barron's published a favorable cover story on the drug's prospects four years ago ("Breakthrough?" Apr. 7, 2008).
It's important to note that neither drug is likely to be capable of curing or reversing the course of the disease. The producers are hoping that the treatments simply will slow the progression of Alzheimer's. That would mark progress, however, because Alzheimer's research is littered with drug failures. Existing treatments, including Aricept and Namenda, address some symptoms of the disease, but don't arrest its progression.
"What solanezumab is really intended to do is slow the rate of decline," said Eric Siemers, the senior medical director of the Alzheimer's disease team at Lilly, on a Bernstein-sponsored conference call with investors in December.
Still, an FDA-approved product that could slow the course of the disease could generate billions of dollars in annual revenues, given the desperation among Alzheimer's sufferers and their families. Most patients are older than 65. The total number of sufferers worldwide could hit 100 million by 2050. The current cost for treating Alzheimer's patients worldwide is estimated at $150 billion per year.
INVESTORS ARE CAUTIOUS on the two drugs because the disease, despite its global toll, still isn't well understood by scientists, complicating the formulation of any treatment.
Among the unknowns are what causes Alzheimer's and what prompts its spread in the brain, killing nerve cells. "It's very different than diabetes and hypertension," Arnold says. "There is a lot of debate among the clinical experts on how the disease evolves and produces the symptoms that it does. When you talk to opinion leaders and scholars, you may get five different hypotheses."
Drug companies usually want a Phase III trial to have a 50%-plus chance of success because a large clinical trial can cost several hundred million dollars. But because of the potentially enormous payoff, the industry is willing to take more chances on drugs for difficult and widespread diseases like Alzheimer's than it normally would.
Bapineuzumab and solanezumab both seek to clear the brain of a plaque caused by a protein called beta-amyloid, which accumulates in Alzheimer's patients. What isn't clear is whether clearing that plaque will have any meaningful benefit.
The drugs work in different ways. Bapineuzumab crosses the so-called blood/brain barrier and seeks to clear brain cells of amyloid plaque. Solanezumab binds with a precursor of the plaque in the blood, with the aim of prompting the body to pull amyloid plaque from the brain.
The optimism about bapineuzumab stems from Phase II trial results that showed the drug slowed the mental decline in patients who lacked a genetic marker that appears to speed the progression of Alzheimer's. People without the marker make up about 40% of sufferers.
The Pfizer group's Phase III clinical trial will study 4,100 people, so that the researchers can evaluate bapineuzumab's effects on a substantial number of patients with and without the genetic marker. Arnold sees a 55% chance that the drug will show "modest benefits" in patients without the marker and she sees only a 10% chance of any success with the "tougher-to-treat" carriers.
The Lilly Phase II trial of solanezumab involved about 50 people and didn't show a lot, other than the presence of certain "biomarkers" that suggested some success, including the presence of the destructive amyloid protein in spinal fluid, an indication that it had been cleared from the brain. Lilly didn't test cognitive function, preferring to conduct a small Phase II test and then jump to a large Phase III with 2,000 patients to gauge solanezumab's effectiveness.
Wall Street and drug companies figure the pricing of Alzheimer's drugs, which are delivered intravenously, will hinge on their clinical impact. The better they work, the more they will cost. Bernstein's Anderson has estimated that the cost could range from $5,000 to $20,000 annually per patient. Multiply that by several million patients and the yearly sales figures run into the billions.
Arnold has various 2020 sales scenarios for the two drugs. Her range is $2.3 billion to $21.6 billion for bapineuzumab, and $517 million to $17.5 billion for solanezumab, depending on how well they work and how large a patient population they can address. The very wide range reflects the uncertainty about the products. She's more upbeat about bapineuzumab.
ONE OF THE CHALLENGES to formulating a drug is that neurodegenerative diseases generally are hard to treat. For all the attention to Alzheimer's, it still isn't easy to identify sufferers early because there can be other reasons for initial symptoms like memory loss. There's concern that once people are diagnosed with Alzheimer's, the disease may be beyond effective treatment. Arnold says some studies suggest that newly diagnosed patients may already have lost more than half their neurons -- the cells that transmit information within the brain via electrical and chemical signaling.
"There's concern that amyloid-lowering agents are effective only if given very early or even before symptoms appear," says Dr. Samuel Gandy, director of the Alzheimer's research center at Mount Sinai hospital in New York. To have an effective treatment, patients may have to be identified in their 50s or early 60s via screening. He adds that another possible contributor to Alzheimer's, a protein called tau, has been tough to tackle.
To approve bapineuzumab or solanezumab, the FDA probably wants to see cognitive improvement in patients, or at least a lessoning in the decline of mental functions. The agency also will determine whether the drugs clear plaque from the brain and slow the shrinkage of the brain that afflicts Alzheimer's sufferers.
Alzheimer's patients often are evaluated based on two clinical tests, one for cognition, and one for day-to-day tasks. Alzheimer's sufferers lose, on average, about four points per year on the cognition test (the scale goes up to 70).
It's a measure of the difficulty of treating the disease that Lilly scientists said they would be happy if their drug could reduce the deterioration by a third, to four points from six, over the 18-month course of the Phase III clinical trial. One issue is whether the tests can be done uniformly and precisely, thus capturing relatively small differences in mental function. Lilly is optimistic. "The number that we think is clinically significant is about one-third, and that's what we're statistically powered to detect in our phase III studies," said Lilly's Siemers at the Bernstein forum.
Given the limited understanding of Alzheimer's, the optimistic scenario for bapineuzumab and solanezumab is that they can slow its fatal progression, not cure patients. But even that would be good news for the millions of victims of the disease, not to mention the shareholders of the companies behind the medications.
Mike, if you really make some money consider my Marcellus gas well property. 47 prime acres a mile above a trillion cubic feet of methane. Info upon request-serious inquiries only please.
Back on topic: Is there enough evidence to put the MCI/Alz people on a keto diet?
The principle does make sense. Maybe a trial run would be a good.
Back on topic: Is there enough evidence to put the MCI/Alz people on a keto diet?
The principle does make sense. Maybe a trial run would be a good.
I quoted an article a while back where this was done for Parkinson's - with REVERSAL of symptoms! - and the patients still freakin complained about the lack of carbs in the diet!! You get some of your cognitive capacity back but all you can think of to do is complain that you cant eat carrots anymore?!
Yes, its worth a try.
Neuroprotective and disease-modifying effects of the ketogenic diet
Pearson - Science News
The Ketogenic Diet's Side-Effects | Dementia & Alzheimer's Weekly
Sodium (salt food heavily) and magnesium and potassium supplementation are a must.
Youve done it again.
Lots of MCT C8 C10, coconut/olive oil. Mainstay carbare lotsa fresh veggies, oat bran, hummus, barley. Gotta get that local grass fed farm connection going.
I'm still looking into this but the idea is that carb-intake derived reactive oxygen species are what screw up membranes in the mitochondria and the absence of carbs and replacement with fats helps to actually clean up the mess.
One thing I see that encourages me is that researchers are looking to mimic that benefit with designer drugs because they still think SFAs are evil and pharmaceutical companies cant patent a high fat diet.
One thing I see that encourages me is that researchers are looking to mimic that benefit with designer drugs because they still think SFAs are evil and pharmaceutical companies cant patent a high fat diet.
cvictorg
New Member
Caloric restriction and intermittent fasting: Two potential diets for successful brain aging
Perfect Health Diet ? Is Alzheimer’s Caused By a Bacterial Infection of the Brain?
Perfect Health Diet ? Eleven Steps for Overcoming Alzheimer’s and Other Chronic Infectious Diseases
Intermittent fasting for health and longevity?/? Getting Stronger
Alternate-day fasting and chronic disease prevention: a review of human and animal trials
Fasting can help protect against brain diseases, scientists say | Science | The Observer
http://people.csail.mit.edu/seneff/EJIM_PUBLISHED.pdf
Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet
Neuroprotective and disease-modifying effects of the ketogenic diet
http://donmatesz.blogspot.com/2011/03/alzheimers-disease-studies-suggest-that.html
Neuroprotective signaling and the aging brain: tak... [Brain Res. 2000] - PubMed - NCBI
Perfect Health Diet ? Is Alzheimer’s Caused By a Bacterial Infection of the Brain?
Perfect Health Diet ? Eleven Steps for Overcoming Alzheimer’s and Other Chronic Infectious Diseases
Intermittent fasting for health and longevity?/? Getting Stronger
Alternate-day fasting and chronic disease prevention: a review of human and animal trials
Fasting can help protect against brain diseases, scientists say | Science | The Observer
http://people.csail.mit.edu/seneff/EJIM_PUBLISHED.pdf
Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet
Neuroprotective and disease-modifying effects of the ketogenic diet
http://donmatesz.blogspot.com/2011/03/alzheimers-disease-studies-suggest-that.html
Neuroprotective signaling and the aging brain: tak... [Brain Res. 2000] - PubMed - NCBI
Last edited:
What's good for the kidneys...is good for the heart...is good for the brain...
http://video.pbs.org/video/2146699556
New drugs? Nah.
“Let food be thy medicine and medicine be thy food”
? Hippocrates
http://video.pbs.org/video/2146699556
New drugs? Nah.
“Let food be thy medicine and medicine be thy food”
? Hippocrates
Tarawneh R, Lee JM, Ladenson JH, Morris JC, Holtzman DM. CSF VILIP-1 predicts rates of cognitive decline in early Alzheimer disease. Neurology 201278(10):709-19. CSF VILIP-1 predicts rates of cognitive decline in early Alzheimer disease
Objective: Measures of neuronal damage/dysfunction are likely good surrogates for disease progression in Alzheimer disease (AD). CSF markers of neuronal injury may offer utility in predicting disease progression and guiding prognostic and outcome assessments in therapeutic trials. Visinin-like protein-1 (VILIP-1) has demonstrated potential utility as a marker of neuronal injury. We here investigate the utility of VILIP-1 and VILIP-1/A?42 in predicting rates of cognitive decline in early AD.
Methods: Individuals with a clinical diagnosis of very mild or mild AD (n = 60) and baseline CSF measures of VILIP-1, tau, p-tau181, and A?42 were followed longitudinally for an average of 2.6 years. Annual assessments included the Clinical Dementia Rating (CDR), CDR–sum of boxes (CDR-SB), and global composite scores. Mixed linear models assessed the ability of CSF biomarker measures to predict rates of cognitive decline over time.
Results: Baseline CSF VILIP-1 and VILIP-1/A?42 levels predicted rates of future decline in CDR-SB and global composite scores over the follow-up period. Individuals with CSF VILIP-1 ?560 pg/mL (corresponding to the upper tercile) progressed much more rapidly in CDR-SB (1.61 boxes/year; p = 0.0077) and global scores (?0.53 points/year; p = 0.0002) than individuals with lower values (0.85 boxes/year and ?0.15 points/year, respectively) over the follow-up period. CSF tau, p-tau181, tau/A?42, and p-tau181/A?42 also predicted more rapid cognitive decline in CDR-SB and global scores over time.
Conclusion: These findings suggest that CSF VILIP-1 and VILIP-1/A?42 predict rates of global cognitive decline similarly to tau and tau/A?42, and may be useful CSF surrogates for neurodegeneration in early AD.
Objective: Measures of neuronal damage/dysfunction are likely good surrogates for disease progression in Alzheimer disease (AD). CSF markers of neuronal injury may offer utility in predicting disease progression and guiding prognostic and outcome assessments in therapeutic trials. Visinin-like protein-1 (VILIP-1) has demonstrated potential utility as a marker of neuronal injury. We here investigate the utility of VILIP-1 and VILIP-1/A?42 in predicting rates of cognitive decline in early AD.
Methods: Individuals with a clinical diagnosis of very mild or mild AD (n = 60) and baseline CSF measures of VILIP-1, tau, p-tau181, and A?42 were followed longitudinally for an average of 2.6 years. Annual assessments included the Clinical Dementia Rating (CDR), CDR–sum of boxes (CDR-SB), and global composite scores. Mixed linear models assessed the ability of CSF biomarker measures to predict rates of cognitive decline over time.
Results: Baseline CSF VILIP-1 and VILIP-1/A?42 levels predicted rates of future decline in CDR-SB and global composite scores over the follow-up period. Individuals with CSF VILIP-1 ?560 pg/mL (corresponding to the upper tercile) progressed much more rapidly in CDR-SB (1.61 boxes/year; p = 0.0077) and global scores (?0.53 points/year; p = 0.0002) than individuals with lower values (0.85 boxes/year and ?0.15 points/year, respectively) over the follow-up period. CSF tau, p-tau181, tau/A?42, and p-tau181/A?42 also predicted more rapid cognitive decline in CDR-SB and global scores over time.
Conclusion: These findings suggest that CSF VILIP-1 and VILIP-1/A?42 predict rates of global cognitive decline similarly to tau and tau/A?42, and may be useful CSF surrogates for neurodegeneration in early AD.
Like the quote !
Got a months supply of MCT, or more, from Swanson.
Looks like Olive, Coconut, and MCT is the main course for a while.
Havent really tracked the olive oil consumption but estimate at least a pint/w for the two of us- heavier toward me. Coconut is catching up fast but sittin on a gallon of MCT, who knows what will happen.
Fresh vegs- lots of em
Oat bran with olive and coconut- tastes like nuts
Someone likes carots and corn chips, not to mention bread.
Wonder if this is not the body crying out that the brain needs food. If it understood the biochemistry a little more fully if might not cry for glucose but call out for fats. But you know how addictions go.
The brain is picky about fuel sources. It wont run on FFAs. Only glucose or ketones. After keto-adaptation, the brain's glucose requirements fall with ketones making up any deficit. You dont need dietary carbohydrate to feed the brain; the liver will happily make glucose from protein and ketones from fat. Try keeping total daily carb intake in the 50 to 75 gm range for a while. If you decide to go lower than that (flat-out ketosis with no more than 20 to 50 gm carbs/day) remember the warning about fluid and mineral intake.
The accumulation of non-functional proteins ('junk' proteins) play a role in the aging process.
Detection of Inactive Enzyme Molecules in Ageing Organisms -- Gershon and Gershon 2002 (37): 16 -- <i>Science</i>'s SAGE KE
Ketosis CLEANS this junk away because when the body thinks it's starving - which a HFLC diet mimics - the body scavenges for all the protein it can find.
Ketone Bodies Stimulate Chaperone-mediated Autophagy
HAS to be good for them mitochondria...and all the other cells for that matter...except for retinal and red blood cells that can ONLY operate on glucose...but they'll do just fine on the glucose made by the liver.
The accumulation of non-functional proteins ('junk' proteins) play a role in the aging process.
Detection of Inactive Enzyme Molecules in Ageing Organisms -- Gershon and Gershon 2002 (37): 16 -- <i>Science</i>'s SAGE KE
Ketosis CLEANS this junk away because when the body thinks it's starving - which a HFLC diet mimics - the body scavenges for all the protein it can find.
Ketone Bodies Stimulate Chaperone-mediated Autophagy
HAS to be good for them mitochondria...and all the other cells for that matter...except for retinal and red blood cells that can ONLY operate on glucose...but they'll do just fine on the glucose made by the liver.
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