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Green Tea and carrots- Reverse Alzheimers
I firmly believe that green tea is healthy. My grandmother drank plain old Lipton green tea, several cups per day, all her life. She lived to be 100.
As for the grains you mentioned, it's well known that rice contains arsenic, wheat in its present form (which is much different from wheat grown decades ago) causes a lot of digestive issues, and oats often (100% in a recent test) contain glycophosphate (Round up).
My comments above do not address dementia; they address general health. I think the best we can do to attempt to stave off Alzheimer's is live a healthy lifestyle.
My mom was born and raised in Japan, then moved to US when she married my dad some 62 years ago. However, every day she drank green tea (loose leaves) and ate Japanese rice among other Japanese cuisine, until her Alzheimer's left her unable to figure out how to use her rice cooker and make tea.
I pesonally don't take much stock in hearing "green tea and carrots can reverse Alzheimer's", to be quite honest. It's a matter of "your mileage may vary" - what works for some may not work for others and frankly I am skeptical of that actually working for others.
But, my dad is forever "falling" for these online scams (where he has to sit and listen to a 30-45 minute 'sales pitch') from these 'nutritional' sites, saying "big Pharma doesn't want you to know about xxx" and ends up paying a LOT of money for various snake oil and pills, in a desperate effort to get mom cured, because that's what these sales pitches are exactly designed to do ...
just my 2¢...
How did they know the mice had cognitive impairments (e.g. Alzheimer's) before running this study?
I have to doubt any study that says eating or drinking something will make brain cells magically regenerate. It's like saying drinking green tea will heal a broken leg or make an amputated arm grow back.
If a person has a real-life experience with something, and believes that it was helpful for themselves or a loved one, certainly they should share it.
A few years ago, a poster with connections to Japan brought to my attention (and others) a product called Feru-guard: ferulic acid in rice bran oil and Angelica archangelica for dementia. The initial studies were promising and it is now being tested in a large-scale trial through the Oregon Health and Science University.
The behavioral and psychological symptoms of dementia place a heavy burden on caregivers. Antipsychotic drugs, though used to reduce the symptoms, frequently decrease patients' activities of daily living and reduce their quality of life. Recently, it was suggested that ferulic acid is an effective treatment for behavioral and psychological symptoms. We have also reported several patients with dementia with Lewy bodies showing good responses to ferulic acid and Angelica archangelica extract (Feru-guard). The present study investigated the efficacy of Feru-guard in the treatment of behavioral and psychological symptoms in frontotemporal lobar degeneration and dementia with Lewy bodies.
We designed a prospective, open-label trial of daily Feru-guard (3.0 g/day) lasting 4 weeks in 20 patients with frontotemporal lobar degeneration or dementia with Lewy bodies. Behavioral and psychological symptoms of dementia were assessed at baseline and 4 weeks after the start of treatment, using the Neuropsychiatric Inventory. The Neuropsychiatric Inventory scores were analyzed using the Wilcoxon rank sum test.
Treatment with Feru-guard led to decreased scores on the Neuropsychiatric Inventory in 19 of 20 patients and significantly decreased the score overall. The treatment also led to significantly reduced subscale scores on the Neuropsychiatric Inventory ("delusions", "hallucinations", "agitation/aggression", "anxiety", "apathy/indifference", "irritability/lability" and "aberrant behavior"). There were no adverse effects or significant changes in physical findings or laboratory data.
Feru-guard may be effective and valuable for treating the behavioral and psychological symptoms of dementia in frontotemporal lobar degeneration and dementia with Lewy bodies.
I am all for natural, eating well and the rest of it, but from what I know about the brain, is once cells are gone, they are gone. Other parts of the brain take over is how it works if I am not mistaken. My problem with this is that people will go YES GReen Tea! Who needs medicines, research, tests, just drink tea! Its all about public perceptions, financial needs, research, being taken seriously, that ALZ is NOT just memory and there is actually a whole family of dementias that need research and if drink tea, don't stress, have a carrot smoothie are advertised as a cure, then the rest of the nightmare diseases get pushed aside and we aren't taken seriously.
Its like saying to someone with type 1 diabetes, just eat better, you don't need insulin
I don't mean to ignore the relative merits or lack thereof of dietary approaches to the prevention or treatment of Alzheimer's disease, but I wanted to focus on one potentially important finding: brain cells probably can be regenerated in the hippocampus.
It also seem possible that memories that were thought lost can potentially be retrieved.
Some mice studies (which are not always reliable) suggest that certain types of memory are recoverable: spatial recognition and object recognition, for instance. These are memories associated with the hippocampus. Other types of memory in which other parts of the brain are involved (the frontal cortex, for example) such as memory of past events or the ability to put thoughts into some kind of logical order rarely show the same kind of improvement. So may be the damage to certain parts of the brain is easier to repair than damage to other parts of the brain.
It is also possible that certain difficult behavioral aspects of dementia can also partially be reversed. None of this simple and relatively little of it has been explored (and some times too much is promised), but some claims have to be given a serious look.
"How did they know the mice had cognitive impairments (e.g. Alzheimer's) before running this study?" (Humor here).
They used a standard cheese wheel test -- cheddars - sharp, extra sharp, mild
soft- brie- imported vs domestic
canned and cubed
Mice were then scored on which they could identify. Hard to understand them since they ate non-stop. And the orange dust from the cheese puffs got all over the test cages.
Fondues were offered to older mice with dental issues.
For a second I got to laugh.
But now I have to go back to being serious. There are two parts to this disease one is increasing oxidation and nitration in the brain. The second is decreasing antioxidants in the brain. Diets high in polyphenols (found in fruits, vegetables, green tea, rice bran, spices, etc.) such as a Mediterranean diet, a diet from India, or from China and Japan increase antioxidants in the brain. They may delay the onset of Alzheimer's disease and slow its progression.
But just because you have a diet high in antioxidants does not mean it will offset forever triggers for oxidation. You can do A, B, and C (eat a healthy diet, exercise, and not smoke) and still get Alzheimer's disease because of X, Y, and Z (environmental toxins, stress, and genetics).
Here are a couple of examples. Members of families with a presenilin 1 gene mutation that leads to early onset Alzheimer's disease develop Alzheimer's disease ten years early than members of families with the exact same gene in Japan (the Spanish carried the gene to both places in the sixteenth century). The families in Colombia are exposed to some of the highest levels of mercury contamination in the world due to mining operations. The families in Japan have a diet high in rice bran and drink green tea.
Japanese American men in Hawaii have a higher incidence of dementia than those who live in Japan. The main key is likely a difference in diet.
So many factors can lead to Alzheimer's disease that you cannot expect adherence to any factor that reduces the risk for the disease or avoidance of any factor that increases the risk for the disease to help you escape the disease for certain. However, when antioxidants in the brain begin to be depleted as oxidation in the brain is increasing with age, you have to look for specific herbs, essential oils, etc. that help to put this imbalance back into some balance.
How did they know the mice had cognitive impairments (e.g. Alzheimer's) before running this study?
Made you laugh!
Loved the fondue ... good laugh. I prefer a nice sharp white cheddar but the mice in my shed seem to prefer Milky Way candy and Cheetos.
Actually, there are mice with genetic mutations that are are bred and sold for ALZ research. Their mutations are ones that cause biological changes associated with ALZ. I would assume some of the biological changes result in behavioral changes which are measurable. There are a number of these JAX mouse models used in neurobehavioral and ALZ research.
It's important to note that this study was about specific compounds found in green tea and carrots.....the mice were given these compounds, not the actual food. The compounds were probably given at higher concentration than found naturally in the foods. So whether or not this study will prove to be meaningful has yet to be seen.
Just a caution. Mice are often not-so-good as a model for humans (but they're cheap and easy to do research on). Pharma companies have spent millions and millions over the past 10 years on things that worked really well in mice, but when the human trials were done, it didn't work on humans at all. Just sayin'.
The last two comments were quite good.
The problem with mice models is that you are giving mice amyloid rather than Alzheimer's disease and the two are not the same. Some of the damage to the brain precedes amyloid and not all of the damage to the brain is caused by amyloid. This is true even in cases of early onset Alzheimer's disease where mutations lead to the overproduction of amyloid.
If amyloid were the only cause of Alzheimer's disease than removing it early on would prevent and treat Alzheimer's disease. Secondly if amyloid were the only cause of oxidative stress than almost any antioxidant (including compounds found in carrots and green tea) would prevent and treat the disease. But to create a mice model that mirrored Alzheimer's disease you would have to have a mouse exposed to high levels of air pollutants, pesticides, chain-smoking, fed a diet high in salt, sugar, and carbohydrates, given medicines that increase cognitive decline, and exposed to various viruses and bacteria. If you can reverse Alzheimer's disease in that kind of mouse you have a shot at doing it humans.
Amyloid oligomers (and I was wrong on this) were not necessarily the wrong target for treatment they were simply not the only target for treatment. The problem was not that all the clinical trials targeting them started to late in the process. The problem was that these trials did not target what caused amyloid in the first place (oxidative stress) and did not target what amyloid oligomers and all the other triggers to Alzheimer's resulted in (oxidative stress). That is why both mouse models and pharmaceutical companies targeting amyloid have led to what one journalist called the intellectual cul-de-sac of Alzheimer's disease treatment.
One of the best animals models for Alzheimer's disease is canine cognitive dysfunction. Here is one more thing we can learn from dogs.
Animal models that simulate various aspects of human brain aging are an essential step in the development of interventions to manage cognitive dysfunction in the elderly. Over the past several years we have been studying cognition and neuropathology in the aged-canine (dog). Like humans, canines naturally accumulate deposits of beta-amyloid (Abeta) in the brain with age. Further, canines and humans share the same Abeta sequence and also first show deposits of the longer Abeta1-42 species followed by the deposition of Abeta1-40. Aged canines like humans also show increased oxidative damage. As a function of age, canines show impaired learning and memory on tasks similar to those used in aged primates and humans. The extent of Abeta deposition correlates with the severity of cognitive dysfunction in canines. To test the hypothesis that a cascade of mechanisms centered on oxidative damage and Abeta results in cognitive dysfunction we have evaluated the cognitive effects of an antioxidant diet in aged canines. The diet resulted in a significant improvement in the ability of aged but not young animals to acquire progressively more difficult learning tasks (e.g. oddity discrimination learning). The canine represent a higher animal model to study the earliest declines in the cognitive continuum that includes age associated memory impairments (AAMI) and mild cognitive impairment (MCI) observed in human aging. Thus, studies in the canine model suggest that oxidative damage impairs cognitive function and that antioxidant treatment can result in significant improvements, supporting the need for further human studies.
Dogs are still not the perfect models as canine cognitive dysfunction follows along the lines of mild cognitive impairment, but you may at least improve some aspects of cognitive function and memory with the use of specific antioxidants in human beings even in the later stages of Alzheimer's disease (ability to recognize places and objects, for instance).
Welcome, freemare and thank you for your comments. Ashwagandha and Bacopa monnieri may help slow down the progression of Alzheimer's disease.
Certain genetic mutations guarantee the onset of Alzheimer's disease, but other factors such as exposure to environmental toxins or a healthy diet may either lower or raise the age of onset. My favorite example of this is that family members in Colombia with a presenilin-1 gene mutation develop Alzheimer's disease ten years earlier on average than family members with the exact same gene in Japan. The Colombian families are exposed to some of the highest mercury levels in the world due to mining operations whereas the Japanese families drink lots of green tea and eat lots of rice.
There is no way for any of us to absolutely prevent Alzheimer's disease and there is no cure for the disease, but there are likely ways to delay its onset and slow its progression (or perhaps even to largely stabilize it).
The Ferulic acid and EGCG study sees interesting. Has anyone tested this approach?
I am considering trying it. Where would one get 2 or 3 gram capsules of pure ferulic acid and EGCG.
Any ideas or thoughts.