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The Cause of Alzheimer's - Glycotoxins (AGE)

alzheimers glycotoxins age vegan vegetarian raw food coconut oil type 3 diabetes

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#1 playground

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Posted 21 June 2015 - 12:47 PM


Background

Recently, I have been exploring the issue of amyloid plagues in Alzheimer's disease (AD),
considering which plant based polyphenols might prevent amyloid formation and/or
might have some activity in dis-aggregating them.  So EGCG from green tea, Rosmarinic
Acid from various herbs (esp. spearmint and lemon balm), turmeric ... etc.

And all the while i keep thinking, this is treating the symptoms,
not treating the cause.  Amyloid is probably not the cause, because the
research has been focused on combating Amyloid for decades and even the
medications which have been shown to have anti-amyloid activity dont
even slow down the progression of AD (eg Donepezil).
 
So what's the cause?

The problem is that i strongly suspect that Big Pharma doesn't want a cure.   
Because if someone shouts 'Eureka!' and solves the enigma.
Then the pharmaceutic profits 'money-go-round' ends.  
Eternally recurring revenues from ineffective medications will halt.
If there is a powerful industry that would lose millions from a societal
change, then that change is unlikely to happen.

It's instructive to remember the story of what happened when two Australian
doctors stood up and shouted 'Eureka' over stomach ulcers.
The medical/pharmaceutic establishment were blaming stress and anxiety,
lack of sleep, fatigue, too much alcohol and cigarette smoking etc.
Hundreds of research papers, conferences, literature reviews all
converged on the industry agreed consensus.
It was all nonsense, nothing to do with any of those factors.
Ulcers are caused by a bacteria called 'Helicobacter pylori'.

Big Pharma was making millions in profits every year from a range of
medicines which were completely ineffective.  Of-course, each pharma
company had evidence supporting the efficacy of their respective drugs.
Of-course, the evidence was bullshit. The evidence was marketing lies.

The doctors' names were: Barry Marshall and Robin Warren.
Between them, they figured out that Helicobacter Pylori was the cause
of stomach ulcers ... and could be cured with simple antibiotics.
They wrote papers and sent them to journals.  
They wrote to Pharma companies and medical bodies to announced their findings.  
They were stone walled and ignored.  Seriously.

The establishment did not want a solution to this problem.
One of the two Ozzie doctors resorted to contaminating
himself with the bacteria, by drinking a culture of it,
demonstrating that he then developed the classic stomach ulcer
symptomology, and the cured himself with a simple antibiotic.
(Quite a heroic move, i gather stomach ulcers are extremely painful)
They did all this on video which was released in a documentary.
This antibiotic 'cure' is widespread today only because these doctors
went to extraordinary lengths to inform the world after being
consistently ignored.  Inevitably, big pharma lost millions
from ineffective ulcer medications that no longer had a market.

Here's an article about this story:
http://discovermagaz...medical-mystery

There is a documentary floating around on the internet about
this case.... i couldn't find it on youtube, but it's there somewhere.

The moral of the story is.  Don't trust Big Pharma.
Remember that Big Pharma is making millions from the status quo.
Rely on your own intelligence.

With that in mind.

What's the cause of Alzheimer's Disease ?
After doing some research, here are my conclusions:


1. AD is not a predominantly genetic condition.
2. The cause of AD is diet...  specifically a toxin, virus or
    bacteria spread by food ingestion.
3. AD has a common cause with (type 2) diabetes.   

Given the above conclusions, the following must be true:

Since the cause of AD is diet:

4. If the cause of AD is a toxin, you can halt the progression of AD
    by limiting, or eliminating, exposure to the toxin .... and/or...
    with well established detox practices (glutathione, vitamin C, coffee enemas etc)
   
5. If the cause of AD is a bacteria or virus, you can halt the progression
    of the disease by boosting the immune system ...and/or... with a vaccine.

6. You can inhibit AD progression with lifestyle changes that inhibit (type 2) diabetes.
   
   
I will now briefly justify my conclusions:

1. AD is not a predominantly genetic condition because:

1(a)  It doesn't recur generation after generation in families.
        The parents of most current suffers didn't have the condition.
1(b)  AD was a rare condition before 1960.
1©  The rate of AD has exploded since 1960.  AD is currently
         the 6th leading cause of death (in the USA).. it was 12th in 1980.
1(d)  This explosive growth in AD is not compatible with a 'genetic' cause.
         An explosive growth in a condition usually mean a virial/bacterial
         outbreak or exposure to some environmental/dietary toxin.
1(e)  AD rates vary internationally.  India, Indonesia, Thailand & sub-saharan Africa
        have the lowest rates of AD (According to the Alzheimer's website).
        North America and Europe have the highest rates.  Indian and african
        people living in North America & Europe have similar rates to caucasians.
        On that basis, it must be environmental not genetic.
      
2.  The cause of AD is diet, because:

2(a)  Those populations eating a western diet have the highest rates of AD.
2(b)  Those populations eating the least processed diet have the lowest rates
         of AD (sub-sarahan Africa, India, Indonesia, Thailand)
2©  Within the western economies, meat eaters have 3 times the incidence
         of AD than vegetarians....    

3.  AD has a common cause with (type 2) diabetes .. because:

3(a)  The explosion in AD rates has been accompanied by an explosion in type 2
         diabettes rates... over the same period.
         eg: China in 2000 at 2.5% diabetes, in 2010 it had 9.8% diabetes
         (Chinese rice consumpton dropped 30%, pork consumption rose 40%)
         source: http://nutritionfact...at-about-china/
3(b)  AD symptoms are relieved by, and even reversed by, regular consumption of
        coconut oil.  This effect is mediated by medium chain triglcerides which is
        used as an alternative form of energy by neural cells.  This has lead to
        a new understanding of glucose metabolism in the brain.  AD is now referred
        to by some as Type 3 diabetes.
       
                     
3©  The incidence of diabetes is 2.5 times higher in meat eaters vs vegetarians.
        This is similar to the 3 times greater incidence of AD in meat eaters.
4(d)  High blood sugar is an early warning marker for AD.
4(e)  People with pre-diabetes or Type 2 diabetes are more likely to get AD.
         source: https://www.alz.org/...re_diabetes.pdf
      
A quick review:

=> AD is caused by something in the diet.
=> AD is associated with eating meat.
=> AD is associated with diabetes.
=> The cause of AD also causes diabetes and occurs with greatest frequency in
     animal products, this is either a toxin, a bacteria or a virus.      
   => If the cause is a toxin, you can address it by reducing exposure to the toxin
        and by standard detox procedures.
   => If the cause is a virus or bacteria you can address it with immune system
        boosting agents or vaccines.
      
So my prediction is, that you would reduce your AD risk to just (approx) 33%
by adopting a vegetarian (preferably a vegan) based diet and taking 30-40 minutes
of aerobic exercise 3 times a week.  This is a common recommendation for
reducing the risk of Type 2 diabetes in pre-diabetic patients.

Another recommendation for actually _reversing_ type 2 diabetes is a
raw food diet... so, nothing cooked.  I don't know the incidence rate
for raw-food eaters and diabetes.  I suspect it is lower than for vegans.
(but this is speculation on my part). So by extension, perhaps a raw food
diet would further cut a person's AD risk.
   
------------------

A big question is:  Is the cause of AD a toxin, or a bacteria/virus ?

I don't know.  
I'm not sure... but glycotoxins could be a causal agent.

First, i'll introduce this topic by offering you some evidence from
china.  Above i referred to  China's soaring diabetes rate:

In 2000 China had a type 2 diabetes rate of 2.5%
10 years later, in 2010, dietary habits had changed significantly and
so had the diabetes rate.  They _reduced_ rice consumption by 30%.
They _increased_ pork consumption by 40%.  Their diabetes rate had risen
to 9.8%.  How strange !  There is a theory that refined carbs cause
diabetes.  Yet the Chinese are eating _less_ white rice and yet they
are getting _more_ diabetes.


Glycotoxins are also referred to as 'Advanced Glycation End-Products' (AGE)
Here's what the wikipedia page says about glycotoxins:

    AGEs are formed both outside and inside the body. Specifically, they stem
    from glycation reaction, which refers to the addition of a carbohydrate to a
    protein without the involvement of an enzyme. Glucose can bind with proteins
    in a process called glycation, making cells stiffer, less pliable and more
    subject to damage and premature aging.

    Outside the body, AGEs can be formed by heating (for example, cooking).[2][3]

    
So you mix carbohydrate with protein in a process called 'glycation'.
And you can form glycation products with cooking.

If you compare the insulin spikes produced by eating:
1.  rice
2.  meat
3.  rice + meat

The shortest spike is for meat (as expected)
The largest spike is _not_ rice, it's actually rice + meat.
And the insulin spike increases with the more meat you add.
There is something about protein + carbohydrate that causes a much bigger
spike in insulin that you might imagine.

Presumably this is the reason for the Chinese soaring diabetes level, they've
basically increased meat consumption by 40%.  And they eat most meals with rice.
source: http://nutritionfact...at-about-china/


Interestingly, this same pattern of increased meat consumption has also occured
in the west.  And this has occurred at the same time when diabetes and AD rates
have risen dramatically.

Here's another quote from  the wikipedia  page:
https://en.wikipedia...ion_end-product

    In human nutrition and biology, advanced glycation end products,
    known as AGEs, are substances that can be a factor in the development or worsening
    of many degenerative diseases, such as diabetes, atherosclerosis, chronic renal
    failure, and Alzheimer's disease.[1]

    These harmful compounds can affect nearly every type of cell and molecule in the
    body and are thought to be one factor in aging and in some age-related chronic
    diseases. They are also believed to play a causative role in the blood-vessel
    complications of diabetes mellitus. AGEs are seen as speeding up oxidative damage
    to cells and in altering their normal behavior.


The greatest sources of glycotoxins are cooked meats, particularly meats that are
often smothered with a sweet tasting flavouring, like BBQ chicken wings, honey
glazed pork, beef, etc.  
For more on glycotoxins, see here:  
http://nutritionfact...a-sugary-grave/


Carbohydrates + protein + heat = glycotoxins
                               = increased diabetes risk
                               = increased AD risk
                               
This suggests that we should separate carbs from meats.
We might have chicken and veggies  or.
we might have veggies and rice ..
but not chicken and rice.


The very lowest levels of glycotoxins are rendered by eating a raw food vegan diet
(ie. no meat, no fish, no egg, no milk, no cheese and ... no cooking)


And there is a specific theory relating glycotoxins and amyloid plaques.
The scenario is that glycotoxins reduces SIRT1.  
Reduced SIRT1 is associated with increases in amyloid plaques.
For more on glycotoxin, SIRT1 and amyloid, see here:  
http://nutritionfact...ent-alzheimers/


In summary:
=> AD is caused by diet, it's associated with meat eating and diabetes.
=> AD is increasingly being referred to as Type 3 diabettes
=> AD can be treated with lifestyle changes that work for Type 2 diabetes.
=> The glycotoxin perspective suggests we switch to a raw food vegan diet
   to reduce future, or current, Alzheimer's risk.

 

I hope some of you find the stuff i've written above useful and/or interesting.

Writing this post helped me to clarify my thoughts...

 

Playground

 

 


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#2 resveratrol_guy

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Posted 21 June 2015 - 02:44 PM

I think the meat correlation, while accurate, is mostly a proxy for increased wealth and urbanization. It happened in the West in the 19th century, and is happening now in Asia.

The explosion of pork consumption in China has emerged as a result of industrialization which has largely obviated manual farming practices. That means, instead of getting a good workout in the field and plenty of vitamin D from the sun, many Chinese are now working in factories or behind desks. All of them, but for a few wealthy and well educated, are now ingesting heavy metals and volatile organic compounds at the very fringes of survivability. Birth defects, cardiovascular disease, cancer, and dementia are exploding. Such is the steep price for a myopic focus on wealth creation at the expense of all else.

There is perhaps a connection between red meat and cardiovascular disease, via L-carnitine. (We used to think it was the cholesterol and saturated fat. Oops!) L-carnitine evidently increases atherosclerosis, which would catalyze the deterioration of the BBB, eventually leading to amyloid deposition, and ultimately Alzheimer's. (This is ironic because acetyl L-carnitine is rumored to have nootropic capabilities; perhaps the long term effect is delerious, however.) But the oldest person to ever live, Jean Calment, was an avid chicken consumer. Granted, there is no evidence that she was an overeater. But I think "meat" is too wide a net, and in any case should not include high-cholesterol seafood, which appears to have protected the arctic Inuit people from dementia until their introduction to the Western diet.

That said, I think it's overwhelmingly pollution and an increasingly Western diet, which is causing the explosion of health problems in China and other developing nations. We know that heavy metals nucleate amyloid (and presumably phosphotau) aggregates (for example); this explains the moderate success of chelation therapies for the disease. And carbon monoxide from traffic congestion creates dead spots in the brain. Additionally, the connection between air pollution and insulin resistance is well established. Finally, the oils used to prepare modern Chinese foods -- chiefly easily oxidized seed oils rich in omega-6 -- are a cardiovascular nightmare, even though they may lower LDL.

 

For its part, I agree that APOE4 is merely a genetic accelerator. But even in this case, Alzheimer's does not typically arise until middle age, so there must still be an environmental trigger. If we remove the triggers early in life, it may be possible to push the disease back into obscurity. The challenge, of course, is that Western food is addictive through pathways involving dopamine and probably unhealthy modifications to gut flora. Try telling your kid that even though burgers, fries, and pancakes taste good, they should be avoided because they'll cause health problems much later in life.

 


Edited by resveratrol_guy, 21 June 2015 - 02:47 PM.

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#3 playground

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Posted 22 June 2015 - 02:35 AM

Here's more evidence of the association between food and AD.

 

Intro:

In the west, we expect a 10 to 20 year difference in the diagnoses of

Type 2 Diabetes (T2D) and Alzheimer's disease (AD).  

People start being diagnosed with T2D in their 40's and 50's.

People start being diagnosed with AD in their 60s and 70's.

 

I suspect the damage starts at the same time, for T2D & AD, but

the results of the damage for AD doesn't become 'diagnosable' until

many years have passed.

 

Statistics:

Type 2 Diabetes in China:

In 2000  T2D rate = 2.4%

In 2010  T2D rate = 9.8%

(note: 4 fold increase over 10 years)

 

AD in China:

1990  3.7 million suffers

2010  9.2 million suffers

(note: nearly a 3 fold increase over 20 years)

 

source:  http://www.thelancet...(13)60770-9.pdf

Quote:

They estimated the number of people with dementia to
be 3·68 million (95% CI 2·22–5·14) in 1990, compared
with 9·19 million (5·92–12·48) in 2010.....

 

The Punchline:

If these two medical conditions had a common cause, you'd expect them to rise and fall together,

(albeit with a 10 to 20 year latency between peaks and troughs).

 

If they were unrelated, they wouldn't rise and fall together.

They'd move independently.

 

The Prediction:

If the common cause hypothesis is correct, we might expect to see a large spike

in the incidence of AD in the  period 2020 to 2030.

This is the 10 to 20 year period after 2010, when we've already witnessed a peak

in the T2D rate.

 

If the common cause hypothesis is incorrect,  the rate of AD growth will

remain on it's current trajectory, or wander around up and down etc.

 

Playground

 

 


Edited by playground, 22 June 2015 - 03:23 AM.

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#4 playground

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Posted 22 June 2015 - 04:02 AM

preamble:

My conclusions are:

1.  AD is caused by diet.

2.  AD has a common cause with type 2 diabetes.

 

 

The Article:

Interesting article here from 'Asian Scientist' magazine:

http://www.asianscie...tern-diet-2013/

 

 

7 fold increase in AD in japan between 1985 and 2008:

 

 The prevalence of AD for those aged 65+ years in Japan rose from 1% in 1985 to 7% in 2008 while

 the prevalence of another major type of dementia, vascular dementia, remained nearly constant at

 4-5% during the same period.

 

Similar pattern of reduced rice consumption and increased meat and animal products consumption:

 

They found significant dietary changes in Japan between 1961 and 1985 that included large increases

in alcohol, animal fat, meat, and animal product consumption. In particular, meat and animal product

consumption rose by 7 and 4 fold, respectively, while rice consumption was cut almost in half.

 

And here's mention of that 10 to 20 year 'lag' time frame:

 

The researchers found that these dietary changes were significantly correlated with the increase

in AD prevalence, with a lag of between 15 to 20 years. This suggests that the nutrition transition in

Japan, i.e., switching from the traditional Japanese diet (where energy is derived mainly from rice)

towards the Western diet (where a high percentage of energy is derived from meat and animal products)

may have caused the rapid rise in AD prevalence in Japan.

 

 

The Advice:

The glycotoxin theory would say that the reason why meat consumption is a particular factor here

is that cooking carbohydrate and meat together creates glycotoxins. 

These glycotoxins suppress SRT1 activity, SRT1 activity protects our brains.  

 

When SRT1 activity is suppressed we get the formation of amyloid plaques (a symptom) and

disruptions to glucose metabolism in the brain (the cause).

 

Assuming the glycotoxin theory is correct, the following advice could be given:

 

If you want to continue to eat meat:

(a) don't eat meat with carbohydrates (eat meat with salad or non-carb veggies)

(b) don't fry or roast meat .... boil it or steam it.

 

If you want to absolutely minimise your AD (and diabetes) risk:

(a) go vegan (no animal products, no milk, eggs, cheese, fish or meat)

(b) go raw (don't cook)

 

For more on glycotoxins see this short video:

http://nutritionfact...eo/glycotoxins/

 

Playground

 


Edited by playground, 22 June 2015 - 04:21 AM.

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#5 Ark

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Posted 22 June 2015 - 04:34 AM

Could multiple causes all equally attributed to Alzheimer's?
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#6 playground

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Posted 22 June 2015 - 05:04 AM

source:  http://www.wjgnet.co...f/v6/i5/744.pdf

 

title:  Emerging links between type 2 diabetes and Alzheimer's disease.

 

Notice this laundry list of commonalities between AD and T2D.

And notice  that you get amyloid deposits in the pancreas as well  as

in the brain.  Both centers of insulin production witness the same 

amyloid symptoms.

...
Common pathogenic factors in both conditions span a
broad sweep including chronic hyperglycemia
per se, hyperinsulinemia, insulin resistance, acute hypoglycemic
episodes
, especially in the elderly, microvascular disease,
fibrillar deposits (in brain in Alzheimer’s disease and in
pancreas in type 2 diabetes
), altered insulin processing,
inflammation, obesity, dyslipidemia, altered levels of
insulin like growth factor and occurrence of variant forms
of the protein butyrylcholinesterase.

 

And notice this... intranasal insulin has a beneficial effect on AD:

 

Of interest not only do lifestyle measures have a protective
effect against the development of cognitive impairment due to Alzheimer’s
disease, but so do some of the pharmacological agents
used in the treatment of diabetes such as insulin
(especially when delivered intranasally)
, metformin,
peroxisome proliferator-activated receptors γ agonists,
glucagon-like peptide-1 receptor agonists and dipeptidyl
peptidase-4 inhibitors.

 

 

The case for a common cause between diabetes and AD strengthens

every time I read a paper about it.

 

I suspect that probably, the Big Pharma knew all about this AD and T2D link. 

But kept schtum to keep 'money-go-round' going.

 

The good thing is... the  empowering thing is...  is that it is NOT true

that AD is progressive, incurable and untreatable.

 

AD is treatable and reversible via just the same means that type 2

diabetes is treatable and reversible: Diet and Exercise.

 

The flip side of this, however, is that for suffers of type 2 diabetes,

their condition is much worse they they previously realised.  This isn't

simply an inconvenient dietary problem, it's brain wasting dementia problem.

 

playground


Edited by playground, 22 June 2015 - 05:15 AM.

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#7 playground

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Posted 22 June 2015 - 05:30 AM

Somehow, i trust Chinese research much more than i trust western

research.  The latter have too much Pinocchio history.

 

 

source:  http://www.google.co...2,d.bGg&cad=rja

 

 

title: Commonality Between Diabetes and Alzheimer’s Disease
and A New Strategy for the Therapy

 

abstract: 

A surprising common pathological processes is found between Alzheimer’s disease (AD) and type
2 diabetes mellitus (T2DM) [1] . AD and T2DM share some common pathological processes: Amyloid
β (Aβ), τ hyperphosphoralation, insulin abnormality. Disturbance in insulin signalling is not only
involved in blood glucose level but also in numerous degenerative processes. Glucagon-like peptide
1 (GLP-1) has attracted substantial attention for its advantage in treating T2DM.
GLP-1 can reduce
Aβ levels in brain. All these encourage us in a medical hypothesis: that is, that GLP-1 is a promising
agent in the therapy of AD.

 

This is new research, 2015, from china.

Medication that works for T2D, works for AD.

 

I confidently expect that Western Pharma companies will panic at the prospect of losing millions in revenue

from AD medications.  They will figure out a path that minimises their loses by publishing lies in scientific

journals: To contradict arguments about a common cause for AD and T2D.  False data will be published.

Misleading and fallacious arguments will be presented in review papers.  It's all nonsense.

 

Playground. 

 


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#8 playground

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Posted 22 June 2015 - 05:42 AM

Could multiple causes all equally attributed to Alzheimer's?

 

Hi Ark,

I'm sure multiple factors could have a causal influence:

heavy metal burden,  pesticides in food,  eating 20 jam donuts....etc.

 

but whether they were 'equally' important... is hard to say.

 

What scenario were you considering ?

 

Playground



#9 Ark

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Posted 22 June 2015 - 06:06 AM

Some sort of enzyme dysfunction yet to be discovered, something that can set off a chain reaction that causes multiple system failures and those failures the order is influenced by genes>environment>age to determine what symptoms are caused on different pathways making multiple treatment options necessary.
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#10 playground

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Posted 22 June 2015 - 07:29 AM

Some sort of enzyme dysfunction yet to be discovered, something that can set off a chain reaction that causes multiple system failures and those failures the order is influenced by genes>environment>age to determine what symptoms are caused on different pathways making multiple treatment options necessary.

 

You mean, the kind of multiple-action disruption that might be caused by eating toxins ?

Where the toxins go everywhere in your body and cause disruption of multiple kinds 

in multiple places in the body ?

 

What kinds of things do you normally eat Ark ?

eg, what did you have to eat for breakfast and lunch?

(i'm just curious)

 

Playground



#11 Ark

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Posted 22 June 2015 - 12:34 PM


Some sort of enzyme dysfunction yet to be discovered, something that can set off a chain reaction that causes multiple system failures and those failures the order is influenced by genes>environment>age to determine what symptoms are caused on different pathways making multiple treatment options necessary.


You mean, the kind of multiple-action disruption that might be caused by eating toxins ?
Where the toxins go everywhere in your body and cause disruption of multiple kinds
in multiple places in the body ?

What kinds of things do you normally eat Ark ?
eg, what did you have to eat for breakfast and lunch?
(i'm just curious)

Playground

I am fasting at the moment so just water.


Also I was referring to Brain Enzymes, rather than stomach enzymes.

#12 resveratrol_guy

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Posted 22 June 2015 - 03:38 PM

I think the evidence for a connection between T2D and AD is frankly overwhelming. It's clear at this point that the modern urban lifestyle is to blame, namely the consumption of industrialized food, ubiquitous air pollution in developing nations, and lack of exercise and sun exposure.

Playground, you've raised an interesting point about consuming carbs and meat together. It's unsurprising that this would be unhealthy, because if you think about it, historically, we hunted or gathered one thing at a time. Wolly mammoths did not come with potatoes! So it makes intuitive sense that this combination could throw insulin into overdrive.

That said, the connection between cholesterol and AD is complicated. (See this essay by Stephanie Seneff of MIT, addressing the reason that APOE4 and statin drugs (which lower cholestrol) both accelerate AD.) On the one hand, consuming industrial food will raise one's small kernel LDL, resulting in vascular damage and eventually AD. But OTOH eggs and seafood provide protection against AD, due to the provision of choline and (safer) large kernel LDL required for myelin and lipid bilayer maintenance.

 

I think the fact that intrnasal insulin ameliorates AD is only more evidence of the fact that most cases are primarily type 3 diabetes (T3D). However, some forms AD may occur for other reasons (e.g. neuronal death due to excessive toxin exposure), in the absence of sugar metabolism problems. (We really shouldn't call it "AD" at all. It's several different diseases which sometimes overlap, but it's too late to change that now.) Also, intranasal insulin merely exacerbates insulin resistence in the long term, so I don't regard it as a viable therapy. Coconut oil is much safer and at least as effective.

 

Unfortunately, by the time T3D becomes evident, the disease is much more than a mitochondrial problem with glucose metabolism. For one thing, at that point, there is a preponderance of amyloid in most cases. So we have to deal with both. I do realize, BTW, that amyloid removal has failed to reverse disease, and has been identified as a useful antimicrobial peptide, perhaps trigged by a viral infection of the brain. But that doesn't mean that amyloid is beneficial. It might just be a necessary evil, shielding the brain from a viral onslaught, at the expense of memory performance. So removing it successfully and safely may require simultaneously supporting microglial function. Our best answer to that is probably GMCSF, but it's expensive and impractical. (Lauric acid from unrefined coconut oil may help, on account of its antiviral properties, but I don't know if it crosses the BBB.) It's also been observed that some individuals exhibiting high amyloid load nevertheless function quite competently, but this could be the result of better education, more social activity, better mitochondrial health, etc., as opposed to the hypothesis that amyloid is innocuous or unrelated to AD.

 

I think it's unclear whether AGEs or industrial seed oils (e.g. corn, canola) are ultimately more harmful. Both of these products exist in industrialized grilled-meat-with-oil-and-carbs meals, for example, fried chicken with mashed potatoes and gravy in the West, or fried rice in the East. And let's not forget that the Japanese and Chinese, like Westerners before them, have been eating vastly more refined carbs (crackers, fries, etc.) in the past few decades, which are frequently seasoned with MSG (or "yeast extract" or some such misleading euphemism.)

 

EDIT: You can't make this stuff up (see video below)!

 

 


Edited by resveratrol_guy, 22 June 2015 - 03:53 PM.

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#13 Nuke

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Posted 23 June 2015 - 01:48 PM

Something I wonder about, Metformin is a AGE blocker. On the long term it seems to increase the risk of AD, not decrease it. http://www.ncbi.nlm....pubmed/22458300. I find it strange, any thoughts on it?



#14 Dolph

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Posted 23 June 2015 - 02:11 PM

Well... You show me your paper, I show you mine. Believe what you want...  ;)

http://www.medscape....warticle/807886


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#15 playground

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Posted 23 June 2015 - 04:10 PM

Well... You show me your paper, I show you mine. Believe what you want...  ;)

http://www.medscape....warticle/807886

 

Hallo Dolph

 

I presume you have an account on medscape.

I don't, so  when i click your link, it invites me to login.

So, consequently, i can't read the paper you've linked to.

 

Can you put it somewhere more public ?

Danke.

 

Playground.
 



#16 Dolph

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Posted 23 June 2015 - 04:12 PM

Metformin Cuts Dementia Risk in Type 2 Diabetes

Megan Brooks

July 16, 2013

BOSTON, Massachusetts — Type 2 diabetes doubles the risk for dementia, and a large new observational study suggests that treatment with metformin may significantly lower that risk. In contrast, other diabetes treatments, including insulin, were associated with increased dementia risk.

"These results provide preliminary evidence that the benefits of insulin sensitizers may extend beyond glycemic control to neurocognitive health," said Rachel Whitmer, PhD, senior scientist at the Kaiser Permanente Northern California Division of Research, Oakland.

The results build on a "nice line of evidence" from animal models and cell culture studies showing that metformin might be neuroprotective by promoting neurogenesis and ameliorating neuronal insulin resistance.

Dr. Whitmer presented her group's findings here at the Alzheimer's Association International Conference (AAIC) 2013.

New Users

For this report, researchers studied a cohort of 14,891 patients with type 2 diabetes age 55 years and older who began diabetes therapy between October 1999 and November 2001. In this "new user" cohort, only patients who started a single drug (metformin, sulfonylureas [SU], thiazolidinediones [TZDs], or insulin) were included.

During 5 years of follow-up, dementia was diagnosed in 1487 (9.9%) patients.

Compared with patients starting SU, those starting metformin had about a 20% reduced risk for dementia (hazard ratio  , 0.79; 95% confidence interval [CI], 0.65 - 0.95), Dr. Whitmer reported.

Compared with patients starting TZD, those starting metformin had a 23% lower risk for dementia during follow-up (HR, 0.77; 95% CI, 0.66 - 0.90).

In contrast, starting SU (compared with metformin) was associated with a 24% increased risk for dementia (HR, 1.24, 95% CI, 1.1 - 1.4); TZD, an 18% increased risk (HR, 1.18; 95% CI, 1.1 - 1.4); and insulin, a 28% increased risk (HR, 1.28; 95% CI, 1.1 - 1.6).

The results were the same after the researchers took into account diabetes duration, age, and glycemic control and when they considered dementia subtypes. The findings provide "preliminary evidence that metformin may have benefits on brain health," Dr. Whitmer said.

Diabetes and Dementia

David S. Knopman, MD, from the Mayo Clinic, Rochester, Minnesota, who moderated a press briefing on this topic, noted that the relationship between diabetes and the development of dementia has generated "great interest" in the scientific community.

 

This type of epidemiologic study, he noted, is intended to "generate hypotheses that can be tested in proper therapeutic trials." The findings from Dr. Whitmer's group suggest a rationale for doing such a trial. Indeed, trials are underway to evaluate metformin as a potential therapeutic agent for mild cognitive impairment and dementia.

The study was funded by Kaiser Community Benefits and the National Institute of Diabetes and Digestive and Kidney Diseases. The authors have disclosed no relevant financial relationships.

Alzheimer's Association International Conference (AAIC) 2013. Oral Presentation: O1-05-05. Presented July 15, 2013.

 


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#17 playground

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Posted 23 June 2015 - 04:45 PM

In most of the posts above,  i've asserted that T2D and AD share a 'common cause'.

And on that basis, AD can addressed with lifestyle and dietary tactics that address T2D.

 

The more i read about the commonalities between T2D and AD the more i'm inclined

to the view that they are actually the same disease.... this is because there is far

too much commonality for them to be distinct diseases.  

 

We have insulin centers in the pancreas and in the brain.

When someone begins to have glucose regulation problems usually both centers show symptoms. 

Diabetics typically have memory and other cognitive impairments.

Someone with AD will have 'diabetic' issues with glucose tolerance and insulin resistance.

Amyloid plaques appear in the pancreas as well as in the brain.

In reality there isn't a distinction between 'Alzheimer's neuropathy' and 'diabetic neuropathy'.. it's the same neuropathy.

 

I incline to the view that AD typically appears as advanced, or late stage, T2D.

 

The 'official' line on AD is that it is progressive, irreversible and there's no effective treatment.

It's absolutely not true.

 

The fuckers are still chanting this mantra of 'progressive, irreversible and no effective treatment'

even though it's been years since regular coconut oil has been documented to halt the progression

of AD and effect a partial recovery in AD suffers.

 

There's no way to quantify all the pain, stress and abject fear that the 'official' line has inflicted

on ordinary people... how it must have stripped them of hope.

 

Amyloid plaques my arse. 

What a red herring that's been.... just another excuse to develop more drugs and cash in on suffering.

Pharma companies don't want to solve this problem.... there's profit in human misery.

 

People should be told that T2D will descend into AD if not properly

vanquished with diet and lifestyle changes.

People should be told that they can screen for "pre-AD" by testing for insulin and glucose levels.

 

Someone should start a campaign.

 

Playground.

 

 

 

 

If you have T2D or pre diabetes, you're on the road to AD.

 

 


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#18 Dolph

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Posted 23 June 2015 - 04:47 PM

The fuckers are still chanting this mantra of 'progressive, irreversible and no effective treatment'

even though it's been years since regular coconut oil has been documented to halt the progression

of AD and effect a partial recovery in AD suffers.

 

Please... Don't make a fool of yourself...


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#19 playground

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Posted 23 June 2015 - 05:02 PM

.....


Edited by playground, 23 June 2015 - 05:04 PM.


#20 playground

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Posted 23 June 2015 - 05:17 PM

Posted Today, 06:47 PM

playground, on 23 Jun 2015 - 6:45 PM, said:snapback.png

The fuckers are still chanting this mantra of 'progressive, irreversible and no effective treatment'

even though it's been years since regular coconut oil has been documented to halt the progression

of AD and effect a partial recovery in AD suffers.

 

Please... Don't make a fool of yourself...

 

-----------

 

I absolutely stand by those statements.

And ... i'm up for making a fool of you Dolph.

 

Your rude statement above means, either

 

1) you disagree that the official line on AD is 'progressive, irreversible and no effective treatment'

 => The wikipedia page on AD has this line:

"No treatments stop or reverse its progression, though some may temporarily improve symptoms."

Also the alzheimer's website essentially repeats this view that AD is progressive, irreversible and

that there are no effective treatments.

 

2) You are completely ignorant of the coconut oil results ?

I am absolutely making the assertions that:

 => regular coconut oil halts the progression of AD.

 => a partial recovery in cognitive functioning is achieved with coconut oil.

     (as measured by improved scores on standard dementia assessment scores)

 

Dolph are you just an idiot troll,  or... do you wish to contradict any of these points ?

 

Playground.


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#21 Dolph

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Posted 23 June 2015 - 05:29 PM

 

Posted Today, 06:47 PM

playground, on 23 Jun 2015 - 6:45 PM, said:snapback.png

The fuckers are still chanting this mantra of 'progressive, irreversible and no effective treatment'

even though it's been years since regular coconut oil has been documented to halt the progression

of AD and effect a partial recovery in AD suffers.

 

 

2) You are completely ignorant of the coconut oil results ?

I am absolutely making the assertions that:

 => regular coconut oil halts the progression of AD.

 => a partial recovery in cognitive functioning is achieved with coconut oil.

     (as measured by improved scores on standard dementia assessment scores)

 

Dolph are you just an idiot troll,  or... do you wish to contradict any of these points ?

 

Playground.

 

 

There is NO evidence for those claims whatsoever, only the desperate claims of one single delusional woman who fed her husband shitloads of coconut oil, believing he did not as bad as he might have without it.  

 

If you take THIS serious I'm very sorry for you. You're lost in confusion and will believe literally everything. 


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#22 playground

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Posted 23 June 2015 - 05:39 PM

 

 

Posted Today, 06:47 PM

playground, on 23 Jun 2015 - 6:45 PM, said:snapback.png

The fuckers are still chanting this mantra of 'progressive, irreversible and no effective treatment'

even though it's been years since regular coconut oil has been documented to halt the progression

of AD and effect a partial recovery in AD suffers.

 

 

2) You are completely ignorant of the coconut oil results ?

I am absolutely making the assertions that:

 => regular coconut oil halts the progression of AD.

 => a partial recovery in cognitive functioning is achieved with coconut oil.

     (as measured by improved scores on standard dementia assessment scores)

 

Dolph are you just an idiot troll,  or... do you wish to contradict any of these points ?

 

Playground.

 

 

There is NO evidence for those claims whatsoever, only the desperate claims of one single delusional woman who fed her husband shitloads of coconut oil, believing he did not as bad as he might have without it.  

 

If you take THIS serious I'm very sorry for you. You're lost in confusion and will believe literally everything. 

 

 

grow up Dolph.
 


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#23 Dolph

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Posted 23 June 2015 - 05:42 PM

That's plain crazy. You claim something that is COMPLETELY NUTS without any plausibility let alone evidence beyond anecdotal "testimonies" coming from... let's say very "weird" people, and get the nerve to tell ME to grow up? May be you should go and see a doctor, it might not be too late yet. But cocnut oil won't save you from whatever your problem is, that I can tell you for sure...


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#24 playground

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Posted 23 June 2015 - 05:51 PM

That's plain crazy. You claim something that is COMPLETELY NUTS without any plausibility let alone evidence beyond anecdotal "testimonies" coming from... let's say very "weird" people, and get the nerve to tell ME to grow up? May be you should go and see a doctor, it might not be too late yet. But cocnut oil won't save you from whatever your problem is, that I can tell you for sure...

 

:)
 


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#25 alc

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Posted 23 June 2015 - 06:20 PM

You might want to look at Dr. Michael Fossel work/approach:

 

 

http://www.michaelfo...om/blog/?cat=21

 

 

http://www.michaelfossel.com/blog/

 

 



#26 playground

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Posted 23 June 2015 - 06:33 PM

You might want to look at Dr. Michael Fossel work/approach:

 

 

http://www.michaelfo...om/blog/?cat=21

 

 

http://www.michaelfossel.com/blog/

 

Hi alc,

 

Fossel is saying that AD is epigenetic.

 

There was a 7 fold increase in Japanese AD cases from 1985 to 2008.

There was a 3 fold increase in Chinese AD cases from 2000 to 2010.

In 1980 AD was the 12th leading cause of death in the USA,  in 2014 it was 6th.

 

Those are staggering increases in prevalence. 

Not the kind of increases you'd expect of epigenetic effects.

 

playground.


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#27 Dolph

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Posted 23 June 2015 - 06:51 PM

Couldn't have to do anything with increases in life expectancy. No, impossible... m(


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#28 alc

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Posted 23 June 2015 - 07:11 PM

Hi alc,

 

Fossel is saying that AD is epigenetic.

 

There was a 7 fold increase in Japanese AD cases from 1985 to 2008.

There was a 3 fold increase in Chinese AD cases from 2000 to 2010.

In 1980 AD was the 12th leading cause of death in the USA,  in 2014 it was 6th.

 

Those are staggering increases in prevalence. 

Not the kind of increases you'd expect of epigenetic effects.

 

playground.

 

 

I think you have a good point - I already clicked on "good point" on your post.

Also I would say, let's ask Dr. Michael Fossel. He has a vast knowledge and he might provide a valid answer to your point.
 


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#29 alc

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Posted 23 June 2015 - 09:08 PM

Did you look into Alkahest's approach? with heterochronic parabiosis-like (plasma from youg people) approach?

 

http://www.bizjourna...wyss-coray.html

 

 

http://www.bizjourna...ope-plasma.html

 

 

 

 

 


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#30 resveratrol_guy

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Posted 24 June 2015 - 02:56 AM

Alkahest is taking the too little, too late approach. A few blood transfusions will never make much difference in AD. Even the mice (who always seem to recover from AD the way we recover from a hangover) needed constant ciruculatory connection between heterochronic peers to create a clinically significant health improvement. That said, I do think the human trials are worth doing, mainly because they stand to illuminate some of the growth factors which have therapeutic effect, e.g. GDF11 or VEGF. Hopefully, there will be enough improvement in the older peers, however short lived, to provide statistical backbone to such analysis.

As to coconut oil and AD, there seems to be plenty of evidence that it addresses the mitochondrial pathology aspect quite well, in particular, by making up the energy deficit due to inefficient OXPHOS (around 15%, if I recall). In other words, mitochrondria in an AD brain are only modestly less efficient at extracting energy from glucose than in a healthy one. But the difference is enough that noncritical functions such as autophagy of waste products (especially junk phosphotau which is too big to be excreted across the bilayer) do not occur properly, leading to intraneuronal accumulation, and eventually, neurofibrillary tangles where a healthy neuron once existed. By ameliorating this small deficit, these "cleanup" functions can be brought back online, not to mention simply allowing improved interneuronal communication. That secondary and more immediate benefit has been explored in depth by both healthy and diseased individuals on a ketogenic diet.

I've actually been thinking of this very question for a while now: If we remain in ketosis starting at a healthy adult age, then it might be very hard to develop T2D or T3D within a reasonable human life expectancy. In other words, we would have to die of something other than mitochondrial senesence. Can one develop AD without that? Well, it's surely possible to mimic AD symptoms if one has sufficiently many infarcts, or sufficiently high plaque load due to heavy metal nucleation of aggregates, or simply enough brain atrophy due to hypoxia or VOC exposure (e.g. glue sniffing). But is that really the same disease? I think not. What we call AD is really the superposition of (1) vascular infarcts, (2) brain plaque, (3) brain atrophy, and (4) mitochondrial senesence. Curing #4 alone is unlikely to cure the disease, but it might prevent it in the first place if the other 3 could be held in check long enough. And it's doubly important because shutting down mitochondrial senesence (notably, cristae disintegration) favors OXPHOS over glycolysis, which in turn impedes cancer.

In other words, if you exclude carbohydrates except to the extent necessary to power the liver (which cannot feed on ketones, apparently), could you still end up with prodementia and procancer energy deficits? Probably, but perhaps not before you died of old age or a bus accident. Ketones rock!

Full disclosure: I'm biased because I'm in ketosis. But it's certainly possible to obtain similar benefits by cutting calories while still consuming a relatively large portion of them from carbs.
 


Edited by resveratrol_guy, 24 June 2015 - 02:57 AM.

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