Scientists call it the “killer lipid” because it seeps into the brain, forming amyloid plaques that lead to Alzheimer’s… But there is a natural way to stop it from ever happening to you…
Use the Kraepelin Method to destroy the killer lipid and prevent Alzheimer’s
I discovered a way to burn up the killer lipid safely in the body, and convert it into usable energy.
It’s called the Kraepelin Method, and it’s completely natural.
The Kraepelin Method destroys the killer lipid before it slips into the bloodstream and travels to the brain.
So you can prevent Alzheimer’s from ever happening to you – and enjoy other health benefits such as better blood sugar, higher testosterone, and less belly fat.
This is the true cause of Alzheimer’s – and here’s how to stop it
There are a few things strongly linked to Alzheimer’s.
This is partially because the Alzheimer’s diagnosis has become just another word for dementia…
And since there are a great many things that negatively affect memory – or cause dementia – there are just as many associated with Alzheimer’s.
The Alzheimer’s diagnosis is most often made based on behavior alone, with little or no actual biochemical data.
So the “Alzheimer’s diagnosis” can be given on account of a few discrete and quite different biochemical problems.
But things such as aluminum, the omega-3 to omega-6 ratio, and even persorbed dry starch particles have all been proven to negatively affect memory – all in different ways.
So we already know a few things to avoid.
Aluminum causes the “classic” Alzheimer’s symptom, or the neurofibrillary tangle.
This is an inclusion body that has never been found without aluminum present.
And that’s because aluminum has a very high affinity for phosphorylated proteins such as tau, which has even been proven to crosslink in vitro.
And the epidemiological correlations between dementia and aluminum are so strong, the chemical data so conclusive, that only the disingenuous will argue that it doesn’t play a role.
The dietary omega-3 to omega-6 fatty acid ratio determines, for the most part, the brain DHA/arachidonic ratio.
These important lipids can only be created by specific fatty acids, and the omega-3 fatty acids are in no way interchangeable with omega-6 fatty acids.
The brain highly prefers DHA in its cell membranes, and its glucose permeability really depends on this.
This fatty acid determines the brain’s metabolic rate by affecting glucose flux.
Too many omega-6 fatty acids can actually interfere with the enzymes needed to make DHA – blocking its synthesis.
The omega-6 product arachidonic acid can even displace it.
So it’s very important to avoid omega-6 fatty acids for yet another reason besides general inflammation.
So besides the risk factor that can bind to the nerves (aluminum) and those needed for the cell membrane (DHA), there is yet one more separate risk factor that plays a role:
After examining brain lipids using the most accurate technique available, these researchers noticed two brain changes between people with Alzheimer’s and control cases.
The lipids known as sulfatides were increased in the Alzheimer’s patients.
And just as importantly: its degradation product, ceramides, were proportionally depleted.
(Ceramides are sulfatides without the sulfate group.)
And these were the only two significant differences found.
“The results demonstrate that…sulfatides were depleted up to 93% in gray matter and up to 58% in white matter from all examined brain regions from AD subjects with very mild dementia – whereas all other major classes of lipid in these subjects were not altered in comparison to those from age-matched subjects with no dementia…”
This is a powerful finding, and even more so because nothing else was found to be abnormal – on the molecular level.
And to find out if there was an enzyme deficiency responsible for this, they even checked the brain’s ability to properly use sulfate groups.
But there was no absolutely no change in enzyme activity between the groups of subjects, implying that sulfate alone was missing.
This would be such a simple fix that it almost sounds too easy.
If this was the only study showing this, I’d probably either just disregard it or overlook it.
But this is not the only study.
The strength of association is very strong and highly plausible, considering all the evidence.
These researchers noted a reduced ability to detoxify acetaminophen (Tylenol) in their Alzheimer’s patients.
And to find out why, they tested their sulfate levels.
This is because Tylenol is sulfated by the body for excretion:
And they also tested for cysteine.
This is because most of the body’s sulfate is derived from this amino acid.
The result was a greatly unbalanced sulfate to cysteine ratio:
And they found no significant change in total blood cysteine.
This means the only real difference was the total sulfate concentration.
It was substantially lower in people with three separate classes of dementia – not just Alzheimer’s.
“Parkinson’s patients have significantly lower plasma sulphate levels than controls.”
And this could be a cheap and easy fix!
Sulfate is commonly available as Epsom salt (biologically available magnesium sulfate – MgSO₄).
Like in the other study, this study did not note any differences in enzyme activity.
So here are two very strong indications that a lack of sulfate could very well contribute to dementia.
Personally, I would take extra sulfate based on these two studies alone.
But there is more. There is very much more…
Besides the classic inclusion bodies found in Alzheimer’s disease – the neurofibrillary tangles caused by aluminum – this condition has one more defining histological feature.
The beta-amyloid protein is often found “misfolded” or aggregated into unusual thread-like structures.
As far back as 1988, scientists showed that this was identical to a previously characterized protein, a sulfated glycoprotein.
These are proteins with sulfated polysaccharides attached:
So to be normal, beta-amyloid actually needs sulfate groups.
And this is another defining feature of Alzheimer’s.
So could the lack of sulfate groups observed by Dr. Heafield and again by Dr. Han be what’s causing it to “misfold”?
“Heparan sulfate proteoglycans (HSPGs) are the major class of proteoglycans in the nervous system (8).”
This is not even speculation, as it has been proven many times.
It has been shown by many others that the degree of sulfation determines how it aggregates:
The beta-amyloid protein is normally made by cells and secreted into the extracellular space – the area found in between cells.
It is normally invisible by light microscopy, being interspersed everywhere.
This protein is only found aggregated in dementia.
And a group of chemists synthesized polysaccharides having varying degrees of sulfation, mixed them in with the beta-amyloid protein, and visualized the result using a very powerful microscope.
Aggregation was determined by the number of sulfate groups.
So could the “misfolded” beta-amyloid protein really just be a symptom of having low sulfate groups?
The sulfate groups are necessary in both the intracellular space and in myelin – as sulfatides…
I think it’s highly probable.
A lack of sulfate groups appears to be the common denominator of Alzheimer’s and beta-amyloid issues.
“Glycopolymers with sulfated saccharide inhibited the amyloid fibril formation of all kinds of amyloid beta peptides. As glycopolymers without sulfated saccharide didn’t show an inhibitory effect at all, the sulfated group was indispensable.”
And sulfates can even do this in vivo:
In a study using few groups of rats, Robert Kisilevsky induced amyloid tangles in them by forcefully injecting them with an amyloid enhancing factor.
And he also gave all groups besides the control group either sulfates or sulfonates in their drinking water.
He found that simple sulfates alone were able to prevent amyloid deposits from forming, and could even reverse them.
“These observations are consistent with our findings that small-molecule anionic sulfonates and sulfates markedly reduce…amyloid deposition in vivo…”
This is in total accordance with all the other findings.
I think it seems pretty clear that these are the four primary factors that cause dementia:
- Omega-6 fatty acids
- Persorbed starch particles
- Lack of sulfate groups
But (and this is good) coffee has been shown to help keep the brain active and is almost always found inversely correlated with dementia.
Many studies also show nicotine to be protective, most likely by increasing acetylcholine receptors in the brain.
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- Han, X. "Substantial sulfatide deficiency and ceramide elevation in very early Alzheimer's disease: potential role in disease pathogenesis." Journal of neurochemistry (2002)
- Heafield, M. "Plasma cysteine and sulphate levels in patients with motor neurone, Parkinson's and Alzheimer's disease." Neuroscience letters (1990)
- Schubert, D. "Amyloid beta protein precursor is possibly a heparan sulfate proteoglycan core protein." Science (1988)
- Miura, Y. "Inhibition of alzheimer amyloid aggregation with sulfated glycopolymers." Biomacromolecules (2007)
- Kisilevsky, R. "Arresting amyloidosis in vivo using small-molecule anionic sulphonates or sulphates: implications for Alzheimer's disease." Nature medicine (1995)
- BASICS OF ALZHEIMER’S DISEASE AND DEMENTIA
- Alzheimer Disease and other Dementias