Alzheimer’s is a devastating disease that currently affects almost 500,000 people in the UK and this number is expected to drastically rise in the future with dietary and lifestyle choices being one of the main catalyst for this rise. Alzheimer’s was a little known disease before 1960, but today it threatens to completely derail the health system not only in the UK – but Worldwide.
Our article this week is provided by Stephanie Seneff – A senior Research Scientist at the Massachusetts Institute of Technology (MIT) Computer Science and Artificial Intelligence Laboratory.
Stephanie looks at the important role that cholesterol plays in the correct functioning of the brain and the mechanism behind how Statins may in fact increase the risk of Alzheimer’s developing.
Something in our current lifestyle is increasing the likelihood that we will succumb to Alzheimer’s. My belief is that two major contributors are our current obsession with low-fat diet, combined with the ever expanding use of statin drugs.
Researchers are only recently discovering that both fat and cholesterol are severely deficient in the Alzheimer’s brain. Cholesterol is essential both in transmitting nerve signals and in fighting off infections. A crucial piece of the puzzle is a genetic marker that predisposes people to Alzheimer’s, termed “apoE-4.” ApoE plays a central role in the transport of fats and cholesterol.
A person with apoE-4 allele inherited from both their mother and their father has up to a twenty-fold increased likelihood of developing Alzheimer’s disease. However, only about 5% of the people with Alzheimer’s actually have the apoE-4 allele, so clearly there is something else going on for the rest of them.
Cholesterol in the Brain
The brain comprises only 2% of the body’s total weight, yet it contains nearly 25% of the total cholesterol in the body. It has been determined that the limiting factor allowing the growth of synapses is the availability of cholesterol, supplied by the astrocytes.
Cholesterol plays an incredibly important role in the synapse, by shaping the two cell membranes into a snug fit so that the signal can easily jump across the synapse. So inadequate cholesterol in the synapse will weaken the signal at the outset, and inadequate fat coating the myelin sheath will further weaken it and slow it down during transport. A neuron that can’t send its messages is a useless neuron, and it only makes sense to prune it away and scavenge its contents.
The neurons that are damaged in Alzheimer’s are located in specific regions of the brain associated with memory and high level planning. These neurons need to transmit signals long distances between the frontal and prefrontal cortex and the hippocampus, housed in the midbrain.
The transport of these signals depends on a strong and tight connection in the synapse, where the signal is transferred from one neuron to another, and a secure transmission across the long nerve fibre, a part of the white matter. The myelin sheath which coats the nerve fibre consists mainly of fatty acids, along with a substantial concentration of cholesterol. If it is not well insulated, the signal transmission rate will slow down and the signal strength will be severely reduced.
In a post-mortem study comparing Alzheimer’s patients with a control group without Alzheimer’s, it was found that the Alzheimer’s patients had significantly reduced amounts of cholesterol, phospholipids (e.g, B-HDL), and free fatty acids in the cerebrospinal fluid than did the controls.
This was true irrespective of whether the Alzheimer’s patients were typed as apoE-4. In other words, reductions in these critical nutrients in the spinal fluid are associated with Alzheimer’s regardless of whether the reduction is due to defective apoE.
The reductions in fatty acids were alarming: 4.5 micromol/L in the Alzheimer’s patients, compared with 28.0 micromol/L in the control group. This is a reduction by more than a factor of 6 in the amount of fatty acid available to repair the myelin sheath!
The Relationship between Cholesterol and Alzheimer’s
Through retrospective studies, the statin industry has been very successful at the game of pretending that benefits derived from high cholesterol are actually due to statins, as I have described at length in an essay on the relationship between statins and foetal damage, sepsis, cancer, and heart failure.
In the case of Alzheimer’s, they are playing this game in reverse: they are blaming cholesterol for a very serious problem that I believe is actually caused by statins.
The statin industry has looked long and hard for evidence that high cholesterol might be a risk factor for Alzheimer’s. They examined cholesterol levels for men and women of all ages between 50 and 100, looking back 30 or more years if necessary, to see if there was ever a correlation between high cholesterol and Alzheimer’s. They found only one statistically significant relationship: men who had had high cholesterol in their 50’s had an increased susceptibility to Alzheimer’s much later in life.
The statin industry has jumped on this opportunity to imply that high cholesterol might cause Alzheimer’s, and, indeed, they have been very fortunate in that reporters have taken the bait and are promoting the idea that, if high cholesterol many years ago is linked to Alzheimer’s, then statins might protect from Alzheimer’s.
Fortunately, there exist lengthy web pages that have documented the long list of reasons why this idea is absurd.
Men who have high cholesterol in their 50’s are the poster child for statin treatment: all of the studies that have shown a benefit for statins in terms of reducing the number of minor heart attacks involved men in their 50’s.
High cholesterol is positively correlated with longevity in people over 85 years old, and has been shown to be associated with better memory function and reduced dementia. The converse is also true: a correlation between falling cholesterol levels and Alzheimer’s.
The obvious study that needs to be done is to ‘bin’ the men who had high cholesterol in their 50’s into three groups: those who never took statins, those who took smaller doses for shorter times, and those who took larger doses for longer times.
Such a study would not be hard to do; in fact, I suspect something like it has already been done. But you’ll never hear about it because the statin industry has buried the results.
In a very long term retrospective cohort study of members of the Permanente Medical Care Program in northern California, researchers looked at cholesterol data that were obtained between 1964 and 1973.
They studied nearly ten thousand people who had remained members of that health plan in 1994, upon the release of computerized outpatient diagnoses of dementia (both Alzheimer’s and vascular dementia). The subjects were between 40 and 45 years old when the cholesterol data were collected.
The researchers found a barely statistically significant result that people who were diagnosed with Alzheimer’s had higher cholesterol in their 50’s than the control group. The mean value for the Alzheimer’s patients was 228.5, as against 224.1 for the controls.
The question that everybody ought to be asking is: for the Alzheimer’s group, how did the people who later took statins stack up against the people who didn’t? In extreme understatement, the authors offhandedly remark in the middle of a paragraph: “Information on lipid-lowering treatments, which have been suggested to decrease dementia risk, was not available for this study.”
You can be sure that, if there was any inkling that the statins might have helped, these researchers would have been allowed access to those data.
The article they refer to for support was very weak. The concluding sentence sums it up well: “A more than a modest role for statins in preventing AD [Alzheimer’s Disease] seems unlikely.”
This is the best they can come up with to defend the position that statins might protect from Alzheimer’s.
Statins and Alzheimer’s
There is a clear reason why statins would promote Alzheimer’s. They cripple the liver’s ability to synthesize cholesterol, and as a consequence the level of LDL in the blood plummets.
Cholesterol plays a crucial role in the brain, both in terms of enabling signal transport across the synapse and in terms of encouraging the growth of neurons through healthy development of the myelin sheath.
Nonetheless, the statin industry proudly boasts that statins are effective at interfering with cholesterol production in the brain as well as in the liver.
Yeon-Kyun Shin is an expert on the physical mechanism of cholesterol in the synapse to promote transmission of neural messages. In an interview by a Science Daily reporter, Shin said:
“If you deprive cholesterol from the brain, then you directly affect the machinery that triggers the release of neurotransmitters. Neurotransmitters affect the data-processing and memory functions. In other words — how smart you are and how well you remember things.”
Fats – A Healthy Choice!
To say that the current situation with regard to dietary fats is confusing would be an understatement. We are repeatedly told to keep our total fat intake down to, ideally, 20% of our total calories. This is difficult to achieve, and I believe it is misguided advice.
In direct contradiction to this “low-fat” goal, we are encouraged to consume as much as possible of the “good” kinds of fats. Fortunately, the message is finally becoming widely embraced that omega-3 fats are healthy and that trans fats are extremely unhealthy.
DHA (docosahexaenoic acid) is an omega-3 fat that is found in large quantities in the healthy brain. In the diet, it is available mainly from cold water fish, but eggs and dairy are also good sources. Trans fats are generated by a high-heat process that hydrolyzes polyunsaturated fats into a more stable configuration, which increases their shelf life but makes them so unnatural they almost can no longer be called a food. Trans fats are extremely damaging both to heart and brain health. A high consumption of trans fats has recently been shown to increase the risk of Alzheimer’s. Trans fats are especially prevalent in highly processed foods — particularly when fats are converted to a powdered form.
We are told to avoid saturated fats, mainly because they have appeared, from empirical evidence, to be more likely to raise LDL levels than unsaturated fats. Yet these fats are less susceptible to oxidation, and this may be why they show up in LDL — because they are of higher quality and therefore should preferentially be delivered to the tissues for functional roles rather than as fuel (i.e., free fatty acids). Coconut oil, a saturated fat, has been shown to benefit Alzheimer’s patients.
If we stop trying to get by on as few fats as possible in the diet, then we don’t have to become so preoccupied with getting the “right” kinds of fats. If the body is supplied with an over abundance of fats, it can pick and choose to find the perfect fat to match each particular need; excess or defective fats can just be used as fuel, where it’s not very important which fat it is, as long as it can be broken down to release energy.
Conclusion
This is an exciting time for Alzheimer’s research, as new and surprising discoveries are coming out at a rapid pace, and evidence is mounting to support the notion that Alzheimer’s is a nutritional deficiency disease.
The ApoE-4 allele, which is associated with increased risk to Alzheimer’s, clearly implicates defects in fat and cholesterol transport, and the remarkable 6-fold reduction in the amount of fatty acids present in the cerebrospinal fluid of Alzheimer’s patients speaks loudly the message that fat insufficiency is a key part of the picture.
The observation that the myelin is degraded in the frontal lobes of the brains of people possessing the apoE-4 allele further substantiates the theory that the myelin repair mechanism is defective.
Cholesterol obviously plays a vital role in brain function. A whopping 25% of the total cholesterol in the body is found in the brain, and it is present in abundance both in the synapses and in the myelin sheath. The cholesterol in both of these places has been shown to play an absolutely essential role in signal transport and in growth and repair.
Given the strong positive role played by cholesterol, it can only be assumed that statin drugs would increase the risk of developing Alzheimer’s.
However, the statin industry has been remarkably successful thus far in hiding this painful fact. They have managed to make much of the observation that high cholesterol much earlier in life is associated with an increased risk to Alzheimer’s thirty years later. Yet they offer not a single study, not even a retrospective study, to substantiate any claim that actively reducing cholesterol through statin therapy would improve the situation for these people.
To read the full article please follow this link.
Stephanie Seneff is a Senior Research Scientist at the MIT Computer Science and Artificial Intelligence Laboratory. She received the B.S. degree in Biophysics in 1968, the M.S. and E.E. degrees in Electrical Engineering in 1980, and the PhD degree in Electrical Engineering and Computer Science in 1985, all from MIT.
In recent years, Dr. Seneff has focused her research interests back towards biology. She is concentrating mainly on the relationship between nutrition and health. Since 2011, she has written over a dozen papers (7 as first author) in various medical and health-related journals on topics such as modern day diseases (e.g., Alzheimer, autism, cardiovascular diseases), analysis and search of databases of drug side effects using NLP techniques, and the impact of nutritional deficiencies and environmental toxins on human health.
Read more about Stephanie here.
With many thanks to Stephanie for this insightful article on a topic that is relevant to many men and women around the world. If you have any questions regarding the topics that have been raised, or any other health matters please do contact me (Amanda) by phone or email at any time.
amanda@cytoplan.co.uk, 01684 310099
Amanda Williams and the Cytoplan Editorial Team: Joseph Forsyth & Simon Holdcroft
Last updated on 20th August 2015 by cytoffice
This is a timeley and very useful article. Alongside poor nutrition, iatrogenec (doctor caused) factors play an increasingly worrying part in chronic ilness and dementia in particular. Statins are amongst my greatest concerns but I appreciate it is not always easy to suggest to people that they should stop them. People are often under the impression that taking their statin is all that stands between them and a gauranteed heart attack -health care providers often give the same impression too.
The reality is this –
1. Statins are proven to have NO mortality benefit in primary prevention – they may change what is written as the cause on your death certificate (slight reduction in heart attacks) but not the date written on your death certificate.
2. Statins have never been shown to have any mortality benefit women even if they have heart disease- the drug companies claim this is because not so many women have been studied but they have looked at tens of thousands so this is a doubtful excuse.
3. In men who have had a heart attack between the ages of 45 and 70 then studies show statins do reduce mortality ….
BUT here’s the rub –
– they will have no impact on 97% of the men taking them – ie you will live or die regardless of whether taking the statin.
– for the 3% that they improve mortality in it is worth remembering they don’t make you immortal – they can only delay death !
And that delay on average is SIX months
Now its not for any of us to state whether someone should or should not take a statin BUT it is imperative on us to clearly indicate the reality of their “benefit” and allow people to make genuinely informed decisions.
Very interesting and thought-provoking article. My sister recently had a mini-stroke and although her cholesterol was the high end of normal, she was prescribed statins for life. Is there any evidence of statins reducing the risk of strokes? Obviously she is shaken by her TIA and although very averse to taking the statins, feels she must do as the doctor orders.
Atherogenic Dyslipidemia is arguably the commonest lipid abnormality due commonly to excess processed CHO consumption. The growth graph for AD since early 1900’s shadows CVD mortality. Patients with Atherogenic Dyslipidemia most commonly have CVD and it seems most likely they will have AD.