Aletho News


Energy poverty is not an option for India’s 360 million poor

By Vijay Jayaraj | American Thinker | September 22, 2021

The global call to impose climate shutdowns akin to the COVID-19 lockdowns fails to recognize that there are millions of poor people for whom there is no room to compromise on energy liberty.

Political organizations like the World Economic Forum see the pandemic-driven economic pause as an opportunity to impose energy restrictions to address climate change. Many organizations now want to “save the planet” by implementing policies that will help them reduce greenhouse gas emissions, or at least make them appear sensitive to the issue. However, the poor in the developing world cannot forgo access to fossil-driven economic development just because of the climate delusions of politicians in luxurious European offices.

Speaking for my own country, India, the 360 million people living in poverty should have more of an option than continued deprivation. Presenting as morally superior their choosing to sacrifice the use of fossil fuels for the sake of a faux battle against climate change is itself immoral.

I know a family’s sole breadwinner whose only livelihood is stitching clothes in a poor neighborhood of Indias most populated city. For her, the electrical sewing machine — recently bought with help — is an absolute essential. Any intermittency in power supply is likely to make her lose out on precious money.

File photo.

For this woman, who is already below the poverty line, the real possibility of not being able to buy basic groceries is a much larger problem than a few degrees’ change in global temperature. In fact, the United Nations has forecasted that even a large rise in global average temperature during the next 80 years will result in a loss of less than five percent in global GDP (gross domestic product).

So why would this impoverished woman give up her access to cheap and reliable coal-powered electricity just because of a theoretical loss of GDP postulated as a worst-case scenario by the year 2100? How dare anybody — least of all affluent jet-setters — ask her to?

While governments in the U.S., Canada, and Europe offered cash payment during the economic lockdown, the poor in developing parts of the world suffered without any help.

Yes, many small businesses in the West suffered during the COVID-19 lockdown. But the situation in developing countries was worse. A majority of the poor in these countries work in a sector of the economy that requires no documentation or proof of identification, making it difficult to get aid to them.

We are talking about numbers larger than the entire U.S. population who do not have a home or a vehicle or people to help them.  Studies have shown that India lost years of progress against poverty during the four-month initial COVID-19 lockdown in 2020. For this reason, the countrys federal government refused to impose a nationwide lockdown during the second wave. Economic restrictions were mostly imposed by state governments.

The proposed climate lockdowns would be not at all different from the brutal COVID-19 lockdowns. They would deny the poorest hope of climbing the socio-economic ladder.

Even worse are stealthy energy restrictions that international political bodies have been imposing on developing economies. Climate alarmists have made a consistent effort to disrupt the fossil-fuel sector during the past two decades.

Oil, coal, and natural gas are requisites for the sustenance of the poor. Without them, there is no cooking fuel for billions of people in the Third World. Even a slight interruption of the coal supply will result in blackouts for more than a billion people on an everyday basis.

It makes absolutely no sense for governments to switch to intermittent renewables like wind and solar in the name of climate change. Firstly, there is no backup solution (other than fossil) that can substitute for intermittent sources in real time during peak hours. Secondly, even advanced economies like the U.K. are unable to cope with the power demand when their renewables fail. Why would developing countries fare any better? Thirdly, wind and solar are proven contributors to a rise in electricity prices globally.

Oh, yes — we should mention that there is no climate emergency. The world has been warmer for most of the last 10,000 years, and predictions of a warming catastrophe are based on consistently wrong computer models.

The clarion call from the world’s poor is not a climate SOS! Rather, they desperately need economic growth that can be fostered only through extensive use of fossil fuels.

Vijay Jayaraj is a research associate for the CO2 Coalition, Arlington, Va., and holds a masters degree in environmental sciences from the University of East Anglia, England.  He resides in Bengaluru, India.

Photo credit: Jorge RoyanCC BY-SA 3.0 license.

If you would like to comment on this or any other American Thinker article or post, we invite you to visit the American Thinker Forum at MeWe.

September 22, 2021 Posted by | Civil Liberties, Economics, Science and Pseudo-Science, Timeless or most popular | | Leave a comment

The Vaccine Roll-Out Was Based on Safetyism, Not Science

By Noah Carl • The Daily Sceptic • September 21, 2021

In a poll of experts taken by Nature earlier this year, only 6% said it was “unlikely” or “very unlikely” that SARS-CoV-2 will become endemic. By contrast, 89% said this was “likely” or “very likely”.

As Professor Francois Balloux has observed, “Eventually, Covid will become endemic everywhere in the world… claims about indefinite elimination are just empty slogans.”

This means the virus will continue to circulate for the foreseeable future, and most of us will catch it several times during our lives. In fact, it may become one that we first encounter in childhood, leading to immunity that lasts years or decades.

Covid, in other words, is here to stay. And unless more powerful vaccines are developed in the future, permanently suppressing transmission via vaccination is unlikely to work, let alone pass a cost-benefit test.

As the Great Barrington Declaration authors have argued, vaccines are best seen as a means of achieving focused protection against Covid. By vaccinating the elderly and clinically vulnerable, we have turned what – for many of those people – could have been a life-threatening illness, into something much less harmful.

However, since the start of the vaccine rollout, numerous people – including some world leaders – have taken a rather different view of the vaccines. For these individuals, the vaccines are a way of ‘crushing the curve’, and thereby ensuring that nobody ever has to get Covid.

But this view is based more on safetyism than on science. And ironically, it’s causing real harm. How so?

First, safetyism has led to the belief that everyone needs to get vaccinated, regardless of age. This is why the Government is proceeding with vaccination of 12-15 year olds, against the better judgement of its own expert panel. Yet as I and others have argued, a far better course of action would be donating those vaccines to poor countries.

Second, safetyism has led to the belief that everyone needs to get vaccinated, even if they’ve already been infected. Yet evidence suggests that people with natural immunity have better protection against infection than recipients of the Pfizer vaccine.

As Professor Marty Makary notes in a recent article for the Washington Post: “If we had asked Americans who were already protected by natural immunity to step aside in the vaccine line, tens of thousands of lives could have been saved.”

Third, safetyism has led to the belief that we need to roll out booster shots because vaccine-induced immunity wanes rapidly. So far, however, this is only true of immunity against infection; immunity against severe disease appears to hold up well.

In a recent Lancet article, Philip Krause and colleagues argue there is not yet any need for boosters, which could cause adverse reactions if administered too soon or too frequently. They point out that vaccines “will save the most lives if made available to people who are at appreciable risk of serious disease and have not yet received any vaccine”.

Fourth, safetyism has led to the belief that people should be strong-armed into getting vaccinated by means of passports and mandates, rather than persuaded. Although coercive measures may increase vaccine uptake, they risk undermining trust in government and the healthcare system.

What’s more, vaccine passports could have unintended consequences. If vulnerable people are led to believe – wrongly – that the vaccines have strong efficacy against infection, they might take more risks than they otherwise would.

A vaccine roll-out based on science – not safetyism – would have recognised that not everyone needs to be vaccinated. It would have assigned leftover vaccines to people that actually need them. And it would have eschewed coercive measures, in favour of transparency about the risks and benefits.

September 21, 2021 Posted by | Science and Pseudo-Science, Timeless or most popular | , | 1 Comment

How Did the Perpetrators Do 9/11?

All it takes is a government conspiracy


The twentieth anniversary of 9/11 has motivated some critics of the standard narrative to explore alternative explanations for what took place on that fatal day. To be sure, there has been considerable focus through the years on exactly what happened, analyzing the technical aspects of what made the twin towers and nearby Building 7, which is where the CIA Station was located, fall while also speculating over what actually occurred at the Pentagon and at Shanksville Pennsylvania.

The narrative under attack basically derives from the 585 page 9/11 Commission Report and from both media coverage and government press releases near the time of the event and ever since. The basic government approved narrative goes like this: Nineteen Arab hijackers, mostly Saudi nationals, acting under orders of Osama bin Laden, head of the terrorist group al-Qaeda, used box cutters and other implements to seize control of four commercial airliners. Two of them were flown into the twin towers of New York City’s World Trade Center, which collapsed from the damage, a third plane struck the Pentagon and a fourth plane crashed in Pennsylvania when passengers attempted to regain control from the hijackers. There was some debris from planes at the sites, but the bodies of passengers, crew and hijackers were largely consumed beyond recognition by the flames and intense heat. DNA samples collected at the various sites have, since that time, reportedly identified some of the dead. Building 7, which was not struck by a plane, caught fire from the falling debris from the nearby World Trade Center towers and the flames spread to such an extent that it had to be demolished to prevent endangering other adjacent buildings.

In support of the alternative theory that the buildings were brought down by controlled demolition type explosions is the lack of any serious forensic analysis of the fragments of masonry and steel. The debris was picked up hurriedly and dumped at sea and abroad where it could not be subjected to chemical examination. That fact alone smacks of conspiracy.

Nearly 3,000 US citizens and residents died in the multiple attacks, remembrance of which became the driving force behind a Global War On Terror (GWOT) launched by the George W. Bush Administration. Recently released FBI documents have added somewhat to the standard 9/11 tale, conceding that the Saudi government and some wealthy individuals, possibly including the royal family, helped the hijackers both directly and indirectly, but there is no evidence to suggest that there was any direct involvement by Riyadh in the conspiracy, if that is what it was. Bear in mind that “no evidence” does not mean “not guilty” and there are still a number of Saudi related documents that are classified.

The first question that should be asked relating to “whodunit?” is “Who benefits?” The Saudis would have had no motive to carry out the attack in any event as the Kingdom was very much dependent on American support to survive in its current autocratic form. Unless al-Qaeda had some desire to harm or even bring down the Saudi state, for which there is some evidence, the benefit to the group and its leadership is difficult to discern unless 9/11 is regarded as little more than a gratuitous act of violence or punishment of Washington for its misdeeds in the Middle East. Bin Laden was reportedly in a Pakistani Army hospital in Rawalpindi having dialysis on the day before the attacks and may still have been under medical care, so the timing is curious if he was indeed one of the masterminds. Also, in his first recorded comment on 9/11, bin Laden’s immediate response was that he didn’t have anything to do with it.

That leaves two prime beneficiaries of 9/11, the state of Israel and a possible secret cabal in the US government made up mostly of neoconservatives that may have been tied to the Israelis and which wanted to use the American military might to remake the Middle East. Israeli Prime Minister Benjamin Netanyahu openly admitted that Israel had much to gain from the US joining his country’s war against Muslim terrorism, saying that “It’s very good. Well, not very good, but it will generate immediate sympathy [and] strengthen the bond between our two peoples, because we’ve experienced terror over so many decades, but the United States has now experienced a massive hemorrhaging of terror.” And, of course, in Netanyahu’s view, the attack was conveniently attributable to Israel’s enemies.

There is plenty of evidence that supports possible Israeli or neocon involvement so the next question becomes “What did they do and how did they do it?” In a recent groundbreaking article former CIA Senior Analysts and Presidential Briefer Ray McGovern explains how there was plenty of warning in US government intelligence and security circles of what was coming, but somehow people at the top seemed to block any action that might have mitigated or even prevented the attack. Even high-level dire warnings from friendly intelligence services in France, Germany, Britain, Italy and Arab countries were ignored. The persistence in avoiding any follow-up or preventive measures is far beyond the point where it could have been a coincidence and one notes the presence of Vice President Dick Cheney in the chain of command at the top of the bureaucracy who was known to have favored an interventionist defense policy and may have contrived to bring it about. Cheney, of course, had close ties to the neocons in the Pentagon and on the National Security Council Staff.

Ray notes that none of the identified Administration officials who were guilty of malfeasance over 9/11 were disciplined or fired. On the contrary, many were promoted with Under Secretary of Defense Paul Wolfowitz as a prime example of someone who wound up as head of the World Bank. The failure to punish is a sure sign of a cover-up. I would add to that the fact that Israel was not even investigated during the preparation of the 9/11 Report in spite of the fact that it had a massive spy operation targeting Arabs underway in the US. Also, known Israeli intelligence agents “working” for a bogus New Jersey trucking company that may have been involved in deliveries of explosives and detonators to the WTC buildings on weekends and late at night were seen dancing and celebrating as the buildings burned behind them.

As for the WTC buildings themselves, they had conveniently been privatized by the owner, the Port Authority of New York and New Jersey, which may have provided after hours and weekend access to them. The decision to privatize was reportedly due to recommendations made by commissions headed by billionaire Ronald Lauder, who was also President of the World Jewish Congress. This resulted in Larry Silverstein obtaining a 99-year lease on the Twin Towers in July 2001. Silverstein, several of his children and some of his senior managers were supposed to be in the buildings on the morning of 9/11, but for various reasons did not show up. Silverstein later benefited to the tune of $4.55 billion from an insurance policy on the buildings, though he had sought $7.1 billion, claiming that the policy covered “per incident” and there had been two plane strikes.

The case for Israeli active intervention on a political level is also extremely strong, outlined in the 1982 Yinon Plan and in the “A Clean Break: A New Strategy for Securing the Realm”, which was prepared by a group of American neocons in 1992 for Israeli Prime Minister Benjamin Netanyahu. Neocons in their foundational document the Project for a New American Century (PNAC) expressed the desire that the United States should experience a “some catastrophic and catalyzing event – like a new Pearl Harbor” that would motivate the country to attain “full spectrum global dominance” by means of military force. And to implement their schemes, Israeli diplomats, the Israel Lobbyists, and neoconservative largely political appointees were never in short supply on Capitol Hill. Many of the American Jews involved in the neocon network wound up in the Pentagon working for Paul Wolfowitz or Doug Feith’s Office of Special Plans. Others worked for Cheney or were on the National Security Council, all well placed to influence a crime and cover-up on a massive scale.

The final question “How did they do it?” results in a speculative response, but I would argue that if the Arab hijackers really existed, both Israel, which clearly would have known about what was coming, and the cabal in Washington, just “let it happen,” making it a version of a false flag attack. If they had prior knowledge that the presumed Saudi hijackers, most of whom they likely knew by name, would be taking over the airliners and crashing them into high value targets to include the WTC and government buildings in Washington, it served their purpose to not interfere and let them do it. And Israel had plenty of “friends” in the media and government to execute the cover-up. America would be at war forever in the Middle East and Benjamin Netanyahu would be smiling as his country’s enemies would be held to blame and punished severely.

My speculation might not be accurate in every detail, but I would bet it is a lot closer to reality than what has been peddled in the United States over the past twenty years.

Philip M. Giraldi, Ph.D., is Executive Director of the Council for the National Interest, a 501(c)3 tax deductible educational foundation (Federal ID Number #52-1739023) that seeks a more interests-based U.S. foreign policy in the Middle East. Website is address is P.O. Box 2157, Purcellville VA 20134 and its email is

September 21, 2021 Posted by | Deception, False Flag Terrorism, Timeless or most popular, Wars for Israel | , , | 3 Comments

Reuters and BBC Caught Taking Money for Propaganda Campaign

This article was previously published March 10, 2021, and has been updated with new information.

By Dr. Joseph Mercola | September 20, 2021

Operation Mockingbird,1,2 publicly revealed during a 1975 Congressional hearing, was a clandestine CIA media infiltration campaign launched in 1948 under the Office of Special Projects.3

The CIA reportedly spent $1 billion a year (about one-third of its entire budget4) on under-the-table bribes to hundreds of American journalists who in return published fake stories at the CIA’s request. CIA-recruited journalists worked in most major news organizations, including CBS News, Time, Life, Newsweek and The New York Times, just to name a few.5 Later on, the campaign expanded to include foreign media as well.6 As reported by the Free Press :7

“In 1976, Senator Frank Church’s investigation into the CIA exposed their corruption of the media. The Church Committee reported: ‘The CIA currently maintains a network of several hundred foreign individuals around the world who provide intelligence for the CIA and at times attempt to influence opinion through the use of covert propaganda.

These individuals provide the CIA with direct access to a large number of newspapers and periodicals, scores of press services and news agencies, radio and television stations, commercial book publishers, and other foreign media outlets’ …

The tactic was straightforward. False news reports or propaganda would be provided by CIA writers to knowing and unknowing reporters who would simply repeat the falsehoods over and over again.”

Reuters and BBC News Were Paid for Propaganda Campaign

While Operation Mockingbird may sound like ancient history, there’s plenty of evidence to suggest it’s still in full swing. During the Cold War, CIA propaganda disparaged communist ideologies. Today, it promotes radical socialist ideas that support a technocratic economic system instead.

While the propaganda messages change with the times, the basic modus operandi of their dissemination remains the same. If anything, the system has only gotten more efficient and effective, as the number of major media outlets has shrunk over these past decades, and a vast majority of journalists and news anchors simply parrot what’s reported by the three global news agencies.

The CIA also isn’t the only intelligence agency using the media for its own propaganda purposes. Leaked documents8 reveal Reuters and BBC News have been involved in a covert program by the British Foreign and Commonwealth Office (FCO) to weaken Russia’s influence on its neighbors. In his extensive February 20, 2021, GrayZone article, Max Blumenthal writes:9

“Working through a shadowy department within the UK FCO known as the Counter Disinformation & Media Development (CDMD), the media organizations operated alongside a collection of intelligence contractors in a secret entity known simply as ‘the Consortium.’

Through training programs of Russian journalists overseen by Reuters, the British Foreign Office sought to produce an ‘attitudinal change in the participants,’ promoting a ‘positive impact’ on their ‘perception of the UK’ …

In effect, the British government was seeking to infiltrate Russian media and propagate its own narrative through an influence network of Russian journalists trained in the UK …

‘These revelations show that when MPs were railing about Russia, British agents were using the BBC and Reuters to deploy precisely the same tactics that politicians and media commentators were accusing Russia of using,’ Chris Williamson, a former UK Labour MP who attempted to apply public scrutiny to the CDMD’s covert activities and was stonewalled on national security grounds, told The Grayzone.

‘The BBC and Reuters portray themselves as an unimpeachable, impartial, and authoritative source of world news,’ Williamson continued, ‘but both are now hugely compromised by these disclosures. Double standards like this just bring establishment politicians and corporate media hacks into further disrepute.'”

Reuters, BBC Hired to Promote Pro-NATO Narratives

The leaked documents show both Reuters and the BBC received “multimillion-dollar contracts to advance the British state’s interventionist aims.” The FCO funded:

  • The cultivation of Russian journalists
  • The establishment of “influence networks” in and around Russia
  • The promotion of pro-NATO narratives in Russian-speaking regions

In its proposals, Reuters stated it has 15,000 journalists and staff within its global network, including 400 journalists within Russia. Reuters and BBC carried out their covert influencing mission in partnership with other high-profile media companies, including Bellingcat, Meduza and Mediazona.

Overseeing the operation was the Zinc Network, an intelligence contractor, which was also responsible for the establishment of a network of Russian and Central Asian YouTubers who were not registered as external sources. The Zinc Network also claimed to have the ability to “activate a range of content; to support anti-government protests inside Russia.”

This isn’t the first time Reuters and the BBC have been implicated in a Mockingbird-type media influencing operation. Documents declassified in January 2020 showed the British government funded Reuters “throughout the 1960s and 1970s to assist an anti-Soviet propaganda organization run by the MI6 intelligence agency,” Blumenthal writes.10 The BBC, meanwhile, was used as “a pass-through to conceal payments” to Reuters.

180-Degrees From the Truth

It’s no small irony that most of the organizations claiming to promote truth and counter disinformation are in fact doing the exact opposite. The Counter Disinformation & Media Development (CDMD) group sounds very much like the Centre for Countering Digital Hate (CCDH).

The CCDH is an opaquely funded group run by Imran Ahmed, who is also a member of the Steering Committee on the Countering Extremism Pilot Task Force under the British government’s Commission for Countering Extremism.

Ahmed has gone on record saying he considers anti-vaxxers “an extremist group that pose a national security risk,”11 and admits tracking and spying on 425 vaccine-related Facebook, Instagram, YouTube and Twitter accounts.12

In addition to stating that medical and scientific professionals must “convince the public that COVID is dangerous and give them confidence that a vaccine is safe and effective,”13 the CCDH is also calling for deplatforming anyone who questions vaccines,14 and to “hold platforms accountable” through fines, criminal sanctions and other measures that can impact the platform’s bottom line.

So, just as the CDMD is actually not countering disinformation but, rather, creating it, the CCDH is not in the business of countering digital hate; it’s actively creating and promoting online hate by baselessly labeling millions of law-abiding parents — whose only crime is to be concerned about their children’s health — as extremist threats and enemies of the state.

Media Have Become Integral Part of Intelligence Spy Network

Other media reports15,16,17 have also highlighted the role of intelligence agencies in the global effort to eliminate “anti-vaccine propaganda” from public discussion, and the fact that they’re using sophisticated cyberwarfare tools to do so. For example, independent investigative journalist Whitney Webb writes:18

“British and American state intelligence agencies are ‘weaponizing truth’ to quash vaccine hesitancy as both nations prepare for mass inoculations, in a recently announced ‘cyber war’ to be commanded by AI-powered arbiters of truth against information sources that challenge official narratives …

The UK’s GCHQ [Government Communications Headquarters19] ‘has begun an offensive cyber-operation to disrupt anti-vaccine propaganda being spread by hostile states’ and ‘is using a toolkit developed to tackle disinformation and recruitment material peddled by Islamic State’ to do so.20

In addition, the UK government has ordered the British military’s 77th Brigade, which specializes in ‘information warfare,’ to launch an online campaign to counter ‘deceptive narratives’ about COVID-19 vaccine candidates.

The newly announced GCHQ ‘cyber war’ will not only take down ‘anti-vaccine propaganda’ but will also seek to ‘disrupt the operations of the cyberactors responsible for it, including encrypting their data so they cannot access it and blocking their communications with each other.’

The effort will also involve GCHQ reaching out to other countries in the ‘Five Eyes’ alliance (U.S., Australia, New Zealand and Canada) to alert their partner agencies in those countries to target such ‘propaganda’ sites hosted within their borders.”

Intelligence-Led Information Warfare Against the Public

Clues that U.S. intelligence agencies — not just the CIA but also the FBI — support this cyberwar against the public can also be found in a white paper21 published in the InfraGard Journal in June 2019. InfraGard, a nonprofit national security group, collaborates with the FBI22 on educational and information-sharing initiatives “that help mitigate threats” to national security.23

The InfraGard paper24 claims the American anti-vaccine movement is being orchestrated by Russian government-aligned organizations seeking to “sow discontent and distrust in topics and initiatives that serve U.S. interests,”25 and that “The biggest threat in controlling an outbreak comes from those who categorically reject vaccination.”26

Other evidence includes the fact that the U.S. Air Force and U.S. Special Operations Command have awarded a multimillion-dollar contract to the U.S.-based “machine intelligence” company Primer, to develop “the first-ever machine learning platform to automatically identify and assess suspected disinformation.”27

According to Webb, “Primer’s ultimate goal is to use their AI to entirely automate the shaping of public perceptions and become the arbiter of ‘truth,’ as defined by the state.”28

The self-appointed arbiter of truth NewsGuard — which rates websites on criteria of “credibility” and “transparency” — is also partnered with both the U.S. State Department and the U.S. Department of Defense,29 which strongly suggests government support (if not direct involvement) of censorship.

NewsGuard is also funded by the PR firm Publicis, which also appears to have an important role in this information war.

Most Mainstream Media Are Now Propagandists

Were it not for the mainstream media pumping out misleading if not flat-out false information on a daily basis for months on end, the COVID-19 pandemic would have been a mere blip on the public’s radar. None of the draconian, freedom-robbing measures would have been remotely possible.

Considering the consistency of the narratives across the world this past year, it’s inconceivable that there isn’t some central “agency” of sorts directing it all. And, if so, there clearly must be a reason behind it. One does not fear-monger for no reason whatsoever. It has a purpose.

Historically, fear has been used by every would-be authoritarian and totalitarian regime you can think of, so there’s every reason to suspect the same applies now. The main difference is that today’s totalitarian ruler is more or less wholly unknown.

Who is it that wants to rule the world’s population through fear? Who is trying to take control over the whole globe? Who is guiding and instructing virtually all government leaders? Intelligence agencies and their media partners undoubtedly play key roles, but they’re unlikely to be the true core of the power structure behind it all.

No, the real power and leadership resides with the technocratic elite, the members of which have quietly and diligently worked to forward the agenda of a New World Order (NWO) for decades. What was once known as the NWO is now referred to as the Great Reset and the Fourth Industrial Revolution, with a public focus on a “green” carbon-based economy to “build back better” by reinventing capitalism, as defined by the World Economic Forum.30

The not-so-public focus is technological surveillance and control over every facet of everyone’s life, from health and civic involvement to labor, education and economy. Unfortunately, members of the technocracy no longer carry member cards or pay membership dues, which obscures their affiliation, but certain organizations are so intimately involved in furthering the Great Reset agenda that you can safely assume a majority of their members play some role in this scheme.

The Council on Foreign Relations

Aside from intelligence agencies, another key player behind the Great Reset is the Council on Foreign Relations (CFR). As explained by Swiss Policy Research, “Executives and top journalists of almost all major U.S. media outlets have long been members of the influential Council on Foreign Relations.”31

Not to be confused with the U.S. Senate Committee on Foreign Relations or the European Council on Foreign Relations, CFR is a nonprofit think tank, the 5,000-plus members of which also include past and present presidents, politicians, secretaries of state, CIA directors, bankers, lawyers, academic professors and corporate leaders, just to name a few.32

CFR also operates the David Rockefeller Studies Program, which in turn advises the White House on foreign policy matters. Overall, the CFR wields incredible power and influence over the U.S. White House and its policies. As reported by Swiss Policy Research:33

“In his famous article about ‘The American Establishment,’ political columnist Richard H. Rovere noted: ‘The directors of the CFR make up a sort of Presidium for that part of the Establishment that guides our destiny as a nation …

[I]t rarely fails to get one of its members, or at least one of its allies, into the White House. In fact, it generally is able to see to it that both nominees are men acceptable to it.’ It was not until the 2016 election that the Council couldn’t, apparently, prevail.”

The Synchronization of Fake News

CFR has two international affiliates: the Bilderberg Group and the Trilateral Commission, both of which were established by CFR leaders “to foster elite cooperation at the global level.”

Well-known names in the Trilateral group’s U.S. branch include David Rockefeller, Henry Kissinger, Michael Bloomberg and Google heavyweights Eric Schmidt and Susan Molinari, vice president for public policy at Google. Many of its board members are also members of the Aspen Institute, which grooms and mentors executives from around the world about the subtleties of globalization.

As you can see in the graphic below, major media are well represented in all three groups. As mentioned, CFR members also include current and former CIA directors. In his book, “American War Machine,”34,35 Peter Dale Scott also documents the ties between CFR, the CIA, the national security apparatus and the banking industry. Taken together, these ties explain how a false narrative (whatever it might be) can be so widely coordinated and synchronized.

Richard Stengel — Technocracy Poster Boy

Knowing what you now know about the CFR, comments by Richard Stengel, the top state media appointee for President Biden’s transition team, will probably make a lot more sense.

During a 2018 CFR forum on fake news, Stengel — a CFR member and Atlantic Council fellow, former State Department official for the Obama administration, former managing editor for Time magazine, strategic adviser to Snap Inc., which runs Snapchat and Bitmoji and a political analyst on MSNBC — insisted governments must use propaganda on their citizens.36

He repeated this sentiment in November 2020, after being appointed to President Biden’s transition team, saying he’s “not against propaganda. Every country does it, and they have to do it to their own population. And I don’t necessarily think it’s that awful.”37 As reported by The GrayZone :38

“A committed crusader in what he openly describes as a global ‘information war,’ Stengel has proudly proclaimed his dedication to the careful management of the public’s access to information.”

Stengel has even proposed abolishing — “rethinking” — the First Amendment, which guarantees the freedom of speech and press, “for practical reasons in society.”39

Stengel’s presence in the Biden administration may be an augury of things to come, considering he created a nonclassified government entity during his Obama years, specifically to combat Russian disinformation.40 This entity, the Global Engagement Center, now facilitates the U.S. government’s efforts to spread its own propaganda around the world.

Stengel, with his close ties to several key centers of technocratic power — the U.S. government, the CFR, the Atlantic Council, mainstream media and Big Tech — is a veritable poster boy for modern technocracy, which makes his shameless promotion of censorship and propaganda more than a little understandable.

Pre-Mockingbird Media Manipulation

While Operation Mockingbird has earned a place in history as a point at which the free press was compromised, in reality, the infiltration of the press occurred long before the 1950s.

In his February 9, 1917, Congressional remarks, Congressman Oscar Callaway, D-Texas, explained the origin and execution of the plan to control and manipulate public opinion and mindset through media, which had taken shape just two years earlier:41

“In March, 1915, the J.P. Morgan interests, the steel, shipbuilding, and powder interest, and their subsidiary organizations, got together 12 men high up in the newspaper world and employed them to select the most influential newspapers in the United States and sufficient number of them to control generally the policy of the daily press.

They found it was only necessary to purchase the control of 25 of the greatest papers. An agreement was reached; the policy of the papers was bought, to be paid for by the month; an editor was furnished for each paper to properly supervise and edit information regarding the questions of preparedness, militarism, financial policies, and other things of national and international nature considered vital to the interests of the purchasers.”

Operation Mockingbird was essentially the CIA’s effort to consolidate, while simultaneously expanding, this secret hold over the media some three decades later. It’s a sobering thought to realize that virtually no one alive today has ever been informed by a truly free and independent press.

While the situation has surely deteriorated in more recent years, the covert use of mainstream media to manipulate and misdirect the public to protect the interests of the elite few has been par for the course for over 100 years.

The Propaganda Multipliers

When it comes to the actual dissemination of fake news and propaganda, news agencies play a central role, and there’s only three of them: The Associated Press (AP), Reuters and Agence France-Presse (AFP). As explained in the Swiss Policy Research post, “The Propaganda Multiplier”:42

“The key role played by these agencies means Western media often report on the same topics, even using the same wording. In addition, governments, military and intelligence services use these global news agencies as multipliers to spread their messages around the world.

A study of the Syria war coverage by nine leading European newspapers clearly illustrates these issues: 78% of all articles were based in whole or in part on agency reports … 0% on investigative research. Moreover, 82% of all opinion pieces and interviews were in favor of a U.S. and NATO intervention, while propaganda was attributed exclusively to the opposite side.”

In short, until or unless at least one of these news agencies sends out a notice, national and local media are unlikely to report on certain events. Even photos and videos are often sourced directly from these global news agencies. This way, people hear, see and read the exact same message everywhere.

“This dependency on the global agencies creates a striking similarity in international reporting: from Vienna to Washington, our media often report the same topics, using many of the same phrases — a phenomenon that would otherwise rather be associated with ‘controlled media’ in authoritarian states,” Swiss Policy Research writes.43

Even media outlets that have foreign correspondents on their payroll do not expect those correspondents to conduct independent investigations. They too simply report whatever the Big Three news agencies want covered, and from the angle they want it covered. What you end up with is a sort of echo-chamber where only one view is presented. As one might expect, this setup makes for a perfect propaganda machine.

As noted by Swiss Policy Research, “Due to the rather low journalistic performance of the mainstream media and their high dependence on a few news agencies, it is easy for interested parties to spread propaganda and disinformation in a supposedly respectable format to a worldwide audience.” Intelligence agencies and defense ministries are well aware of this and use it with regularity, as surely does the CFR and the rest of the technocratic apparatus.

In short, the current censoring and labeling of anything that threatens the technocratic agenda and the profiteering of its members as “misinformation” and “disinformation” is a top-down scheme. It’s not random, by any means, and it’s not driven by the opinions of private companies themselves. Social media companies, for example, are mere tools for the technocratic deep state, which operates worldwide.

The question then becomes, if propaganda is that deeply entrenched in our media structure, how do we know what is true and what is not? There’s no easy answer to this question, but the solution involves first becoming aware of the fact that media lies, and that there is a reason for why the media narrative is what it is. One way to evaluate the news is to ask yourself, “Why might they want me to think of this in this particular way?” Eventually, patterns begin to form.

Ultimately, to find the truth, you must be willing to look for it, and to look in places outside the mainstream media consortium. You have to ask questions and reason your way through the information you find. If something doesn’t make sense yet you’re told to accept it without question, it’s probably propaganda.

Any number of COVID-19 restrictions, for example, have been illogical in the extreme, which tells us they’re not about protecting people from infection. It’s about something else, and that something else has often been the purposeful destruction of small businesses to facilitate wealth transfer from the middle- and lower class to the top echelon. Ultimately, that is the plan, and to stop it, we have to stop believing the propaganda. It’s just that simple. And that challenging.

Sources and References

September 20, 2021 Posted by | Deception, Fake News, Mainstream Media, Warmongering, Timeless or most popular | , , , | Leave a comment

‘Israel and the Zionist enterprise were born in sin’, says heir to an iconic Zionist family

Yaakov Sharett [Youtube]

Yaakov Sharett
MEMO | September 20, 2021

In a remarkable political conversion, Yaakov Sharett, the heir to an iconic Zionist family and son of Israel’s second Prime Minister, Moshe Sharett, has turned his back on the founding ideology of the occupation state.

“The State of Israel and the Zionist enterprise were born in sin,” said Sharett in an interview with Haaretz. The 95-year-old spoke at length about his journey from a faithful servant of Zionism in the state of Israel to one of its harshest critics.

Sharett was born in 1927 and is said to belong to a well-connected family from the cream of the Yishuv, the Jewish community in Palestine. His father was Israel’s first foreign minister and one of the country’s leaders who signed the Declaration of Independence in 1948. Sharett also dutifully served Israel as a member of the Shin Bet, the country’s security agency, and helped Soviet Jews flee to Israel.

Ending his days in Tel Aviv as an anti-Zionist, Sharett predicts dark days for the country he spent nearly his entire life serving. “This original sin pursues and will pursue us and hang over us,” said Sharett referring to the ethnic cleansing of Palestine prior to Israel’s creation in 1948. More than half of the indigenous community were expelled in an attempt to artificially construct a Jewish majority.

Sharett recollected the history of Zionism and its rise within Jewish communities. He argued that the moment Zionism called for the Jews to immigrate to Israel, in order to establish an ethno-nationalist state, a conflict was created. “I see in this whole transformation of the majority [Arab] to a minority and the minority [Jewish] into a majority as immoral,” explained Sharett.

“Have you seen anywhere in the world where the majority would agree to give in to a foreign invader, who says, ‘our forefathers were here,’ and demands to enter the land and take control?” Sharett rhetorically asked. “The conflict was inherent and Zionism denied this, ignored it… as the proportion of Jews to Arabs changed in favor of the Jews, the Arabs realized that they were losing the majority. Who would agree to such a thing?”

Lamenting his continued presence in Israel he said that he sees himself as a “a collaborator” against his will.

I’m a forced collaborator with a criminal country. I’m here, I have nowhere to go. Because of my age, I can’t go anywhere. And that bothers me. Every day. This recognition won’t leave me. The recognition that in the end, Israel is a country occupying and abusing another people.

Sharett also railed against Israel’s turn towards religious fundamentalism and ultra-nationalism. “When I see the prime minister with a kipah on his head, I don’t feel good,” he added. “This is not the Israel I want to see. How did it happen that this new place, that was to have brought innovations, became the blackest place, controlled by the nationalist ultra-Orthodox? How is it that here of all places, there’s reactionism and zealotry, messianism, the desire to expand and control another people?”

September 20, 2021 Posted by | Ethnic Cleansing, Racism, Zionism, Illegal Occupation, Timeless or most popular, War Crimes | , , | 1 Comment

Pediatricians Remove Info on Mask Risks, Dangers for Kids

By Dr. Joseph Mercola | September 20, 2021

Throughout 2020 and 2021, ever since the declared COVID-19 pandemic, government officials consistently have been inconsistent in their assessments and recommendations for public health. In August 2021, the American Academy of Pediatrics (AAP) joined the ranks when they endorsed the CDC’s recommendation for masking.1

Since they did not want to be seen holding inconsistent positions, they removed years of information from their website that explained the importance of facial cues to early brain and child development. The removal of the content culminated August 12, 2021, with the fourth in a series of tweets, in which they said:2

“Babies and young children study faces, so you may worry that having masked caregivers would harm children’s language development. There are no studies to support this concern. Young children will use other clues like gestures and tone of voice.”

At the end of the tweet, they provided a link to an article on HealthyChildren.org3 that suggested “… when one sense is taken away, the others may be heightened.” The series of tweets was aimed at masking in general, stating:4

  • Masks work to reduce the spread of COVID-19 among children
  • Masks are a vital part of keeping kids safe at school this fall
  • Masks do not compromise children’s breathing
  • Being around adults wearing masks doesn’t delay babies’ speech or language development

Experts argue over the efficacy and necessity of masking a population that has minimal risk from the virus. You need look no further than the CDC’s website,5 which shows that children ages birth to 17 had a death rate of 0.08% in 2021 and 0.05% in 2020. Yet, it was the final statement — that masking doesn’t affect children’s development — that unleashed a reaction on Twitter from parents, speech therapists and physicians who heartedly disagreed.

American Academy of Pediatrics Caught in a Quandary

To support the unsubstantiated long-term use of masks, the AAP turned their back on years of research and their own information on the importance of facial cues with infants to protect and promote brain growth and development.

To make this work, the organization has taken down significant sections from their website about early childhood development. Reuters6 asked why the content was removed the weekend after the tweets were published. They were told the content was in the process of being migrated to a different platform.

A spokesperson told Reuters, “The AAP can confirm that our web content migration has nothing to do with AAP’s mask guidance.”7 They assured Reuters the content would be republished, but were unsure about the timeline; they expect it to be complete by the end of the year.

In other words, this well-funded and organized group is coincidentally “migrating” one key section of web content that curiously contradicts their new mask guidance, and planned this so it would take months to complete.

According to Reuters,8 any links to this content that come up in the search engine are now redirected to the AAP’s homepage. However, not all the content has been deleted since other organizations use the AAP documents to educate their clients.

For example, the “Building ‘Piece’ of Mind” pdf that was pulled as a resource on the AAP website9 is available on the Ohio Bold Beginning! site and branded with the Ohio chapter of the AAP.10 You can also download the full document from an Internet archive.11

The now “migrated” document encourages parents to pay attention to their emotional responses to their children, since “Feelings are a language that your infant understands early in life.”12 Yet, without facial cues, it’s challenging for adults, much less children, to read and understand emotional reactions. In the migrated document, the AAP says:

“As your baby grows, social smiles lead to conversations. For example: When you smile, your infant will smile back … This ‘dance’ between you and your baby is fun for both of you. It is a great way to encourage your baby’s new skills as they appear. For this important dance to work, calmly and consistently meet your baby’s needs … and smile!”

But how is that supposed to work if your baby is staring at you and other adults who have two-thirds of their faces covered with masks? How do babies know you’re smiling if your entire face is covered up? In response to the AAP, Dr. James Todaro, who runs the website MedicineUncensored, tweeted:13

“AAP in 2018: ‘How Do Infants Learn? Infants love to look at you and hear your voice. In fact, faces, with all their expressions, usually are more interesting than toys. Spend time talking, singing, and laughing. Play games of touching, stroking, and peek-a-boo.’

AAP in 2021: ‘Babies and young children study faces, so you may worry that having masked caregivers would harm children’s language development. There are no studies to support this concern. Young children will use other clues like gestures and tone of voice.’”

Did Pfizer’s Funding of the AAP Influence Their Mask Policy?

Shortly after the AAP took down their facial cue documents and posted their new masking recommendations for children, a retired chief of police questioned the AAP’s motives — and in a telling opinion piece for Law Enforcement Today,14 he revealed that Pfizer is one of the AAP’s largest funders.

Twitter users15 noticed it too, with several asking what would Pfizer’s funding have to do with the AAP’s mask recommendations. Finally, one person figured it out, saying, “perhaps the plan is to get parents so fed up with their children having to wear them they break down and get them the vax.”

In fact, the AAP itself linked vaccination to mandatory mask-wearing quite clearly when they talked with NBC news,16 which reported: “The AAP said universal masking is necessary because much of the student population is not vaccinated, and it’s hard for schools to determine who is as new variants emerge that might spread more easily among children.”

When you consider that another COVID vaccine maker, Johnson & Johnson, is also a funder for the AAP — and that Dr. Anthony Fauci made the news September 9, 2021,17 saying that vaccines for children as young as 6 months may be ready as soon as November 2021 — the idea that the AAP would consider setting the stage for parents to come begging for a vaccine doesn’t sound so off the wall.

Not Just Children Are Affected

An AAP staffer was quoted in Live From Studio 6B,18 saying, “AAP recommends masks in schools and public settings to protect children. These documents are more about interactions between infants and their parents or primary caregiver, much of which will be in a home setting where masks are usually not needed.”

However, masking facial cues affects infants and young children in day care situations and when they are out of their home. This impacts “social referencing,” which the AAP finds important to child development and refers to the ability to read the face of a stranger.19

Research20 shows mothers have unique central nervous system responses when they first see the face of their newborn. This demonstrates the significance of facial cues in building mother-infant bonding. Yet, as comments on a Twitter thread point out, infants and children are not the only ones suffering from a lack of facial cues. Twitter user MDaly is a mother and teacher, who commented:21

“I teach English to students who are not native English speakers. Wearing a mask absolutely affected their language development last year. I had to ask students to repeatedly speak up and repeat themselves which negatively affects their self-esteem as well.”

A letter to the editor in The BMJ 22 expounds on the challenges faced by adults who are hearing impaired with mandatory masking. Health care has always been challenging for those with hearing impairment, especially in emergency departments where the noise level is high. Alexandra Dumitru is hearing impaired and commented:23

“Zero common sense. It’s tragic what our health institutions have become. First the CDC, now this — even adults benefit from seeing a full face. As someone hearing impaired masks have been a nightmare for me. Kids copy adults; they need to see mouths move.”

Data Are Sparse for a Very Good Reason

The AAP stated that there were no studies to support the concern that baby’s and young children’s development would be impeded by the constant use of masks in the adults who care for them. Yet, as one person on Twitter said, “If you don’t study something, you can say there are no studies.”24

However, the data are sparse and there are no studies analyzing the effect of masking on young children because before 2020 it would never have passed an ethical review board. Imagine gathering a cohort of 40 infants. Nearly from the time of birth 20 parents would wear masks anytime they had interactions with their children. The other 20 would serve as a control group, being raised in a way formerly advised by the AAP.

After five years of what could only be called abusive behavior, psychiatrists and behavior psychologists would test these children to find their brain development, language development and ability to recognize facial cues are stunted. And yet, the AAP would like us to believe that won’t happen — without testing infant development in an environment known to be detrimental, we cannot extrapolate the information and understand it would be detrimental.

In 1990, the world discovered a carefully guarded secret of the Romanian Communist Party’s leader, Nicolae Ceauşescu.25 After his execution the new government brought in Western psychologists and child specialists to help deal with the 170,000 children who were abandoned in orphanages where they received no interaction with adults.

Charles A. Nelson III, a professor of pediatrics and neuroscience at Harvard Medical School and Boston Children’s Hospital, recounts his introduction to the environment these children lived in. He recalled:26

“I walked into an institution in Bucharest one afternoon, and there was a small child standing there sobbing. He was heartbroken and had wet his pants. I asked, ‘What’s going on with that child?’ A worker said, ‘Well, his mother abandoned him this morning and he’s been like that all day.’ That was it. No one comforted the little boy or picked him up. That was my introduction.”

The children in the orphanages of Romania not only didn’t have “face time” with their caregivers, but also didn’t have any comfort or interaction. It’s not hard to imagine how an infant, who relies on cues from other people to learn and grow, could be stunted by having little exposure to facial expressions.

The Still Face Experiment

The horrific environment these children and young adults lived in was the largest human experiment in which children did not receive interaction from other humans. Until, that is, 2020 and 2021, when many infants and children are being raised in an environment where they are unable to read facial cues. In this short video, you’ll see what happens during the “still face” experiment when the infant does not get a response from the mother.

The still face experiment demonstrated how infants are vulnerable to the emotional or nonemotional reactions of people. In the COVID-19 pandemic, infants and children are lacking visual facial cues, but the expectation is they continue to receive emotional interaction at the same level they did before the mask mandates.

Research has demonstrated that when parents struggle to be emotionally present with their children, the children grow up having more trouble with trust and regulating their own emotions.27 However, there has been no data before 2020 to determine if masking facial cues would cause children to grow up with the same issues.

Are Facial Cues Recognizable Through Masks?

Research produced after 2020 has demonstrated that children and adults struggle to recognize emotion in people who are masked. How this will affect overall child development and whether the children can “catch up” if mask mandates are ever removed, is yet to be determined.

For example, in one study28 published by the University of Wisconsin-Madison in December 2020, researchers engaged children ages 7 to 13 and showed them photos of people exhibiting six different emotions. Without the masks, the children identified the emotions correctly 66% of the time.29

However, when masks were in place, this dropped to between 18% and 28% for sadness, fear and anger. A second study30 in children ages 3 to 5 years demonstrated that the younger children had even more difficulty.

The data were in line with past literature that confirmed that a face mask affected understanding emotions. They found the toddlers’ performance was more influenced by a mask than older children and adults.31

Similar studies have also been performed with adults. One study32 published in September 2020 with 41 healthy adults aged 18 to 87 years presented the participants with photos of six different expressions.

When the photos were not wearing masks, the overall performance for identifying emotions was 89.5%. This dropped significantly when masks were in place. A second study33 published in Scientific Reports in 2021, analyzed the effects of masking to measure emotion recognition and trust attribution in 122 adult men and women.

The researchers found that standard masks interfered with both measures and made it more difficult to identify an individual they had already encountered when the mask was removed.

Data produced since 2020 have shown that masks do an excellent job of masking a person’s ability to read emotions, but likely do not have the same efficacy in slowing the spread of a virus. The question we therefore must ask is, what will be the long-term effect on the emotional and mental health of society as the generation of children raised without full exposure to facial cues become doctors, lawyers, businesspeople and politicians?

Sources and References

September 20, 2021 Posted by | Corruption, Deception, Science and Pseudo-Science, Timeless or most popular | , , , , | Leave a comment

APOE-4: The Clue to Why Low Fat Diet and Statins may Cause Alzheimer’s

By Dr. Stephanie Seneff | December 15, 2009


Alzheimer’s is a devastating disease whose incidence is clearly on the rise in America. Fortunately, a significant number of research dollars are currently being spent to try to understand what causes Alzheimer’s. ApoE-4, a particular allele of the apolipoprotein apoE, is a known risk factor. Since apoE plays a critical role in the transport of cholesterol and fats to the brain, it can be hypothesized that insufficient fat and cholesterol in the brain play a critical role in the disease process. In a remarkable recent study, it was found that Alzheimer’s patients have only 1/6 of the concentration of free fatty acids in the cerebrospinal fluid compared to individuals without Alzheimer’s. In parallel, it is becoming very clear that cholesterol is pervasive in the brain, and that it plays a critical role both in nerve transport in the synapse and in maintaining the health of the myelin sheath coating nerve fibers. An extremely high-fat (ketogenic) diet has been found to improve cognitive ability in Alzheimer’s patients. These and other observations described below lead me to conclude that both a low-fat diet and statin drug treatment increase susceptibility to Alzheimer’s.

1. Introduction

Alzheimer’s is a devastating disease that takes away the mind bit by bit over a period of decades. It begins as odd memory gaps but then steadily erodes your life to the point where around-the-clock care is the only option. With severe Alzheimer’s, you can easily wander off and get lost, and may not even recognize your own daughter. Alzheimer’s was a little known disease before 1960, but today it threatens to completely derail the health system in the United States.

Currently, over 5 million people in America have Alzheimer’s. On average, a person over 65 with Alzheimer’s costs three times as much for health care as one without Alzheimer’s. More alarmingly, the incidence of Alzheimer’s is on the rise. Dr. Murray Waldman has studied epidemiological data comparing Alzheimer’s with femur fractures, looking back over the last fifty years [52]. Alarmingly, he has found that, while the incidence of femur fractures (another condition which typically increases with age) has gone up only at a linear rate, the increase in the incidence of Alzheimer’s has gone up exponentially, between 1960 and 2010 Alzheimer’s Epidemic [15]. Just between 2000 and 2006, US Alzheimer’s deaths rose by 47%, while, by comparison, deaths from heart disease, breast cancer, prostate cancer, and stroke combined decreased by 11%. This increase goes far beyond people living longer: for people 85 and older, the percentage who died from Alzheimer’s rose by 30% between 2000 and 2005 [2]. Finally, it’s likely these are under-estimates, as many people suffering with Alzheimer’s ultimately die of something else. You likely have a close friend or relative who is suffering from Alzheimer’s.

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. I have argued elsewhere that low-fat diet may be a major factor in the alarming increase in autism and adhd in children. I have also argued that the obesity epidemic and the associated metabolic syndrome can be traced to excessive low-fat diet. Statins are likely contributing to an increase in many serious health issues besides Alzheimer’s, such as sepsis, heart failure, fetal damage, and cancer, as I have argued here. I believe the trends will only get worse in the future, unless we substantially alter our current view of “healthy living.”

The ideas developed in this essay are the result of extensive on-line research I conducted to try to understand the process by which Alzheimer’s develops. Fortunately, a great deal of research money is currently being spent on Alzheimer’s, but a clearly articulated cause is still elusive. However, many exciting leads are fresh off the press, and the puzzle pieces are beginning to assemble themselves into a coherent story. Researchers are only recently discovering that both fat and cholesterol are severly deficient in the Alzheimer’s brain. It turns out that fat and cholesterol are both vital nutrients in the brain. The brain contains only 2% of the body’s mass, but 25% of the total cholesterol. 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. There are currently five known distinct variants of apoE (properly termed “alleles”), with the ones labelled “2”, “3” and “4” being the most prevalent. ApoE-2 has been shown to afford some protection against Alzheimer’s; apoE-3 is the most common “default” allele, and apoE-4, present in 13-15% of the population, is the allele that is associated with increased risk to Alzheimer’s. 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. Nonetheless, understanding apoE’s many roles in the body was a key step leading to my proposed low fat/statin theory.

2. Background: Brain Biology 101

Although I have tried to write this essay in a way that is accessible to the non-expert, it will still be helpful to first familiarize you with basic knowledge of the structure of the brain and the roles played by different cell types within the brain.

At the simplest level, the brain can be characterized as consisting of two major components: the gray matter and the white matter. The gray matter comprises the bodies of the neurons, including the cell nucleus, and the white matter contains the myriad of “wires” that connect each neuron to every other neuron it communicates with. The wires are known as “axons” and they can be quite long, connecting, for example, neurons in the frontal cortex (above the eyes) with other neurons deep in the interior of the brain concerned with memory and movement. The axons will figure prominently in the discussions below, because they are coated with a fatty substance called the myelin sheath, and this insulating layer is known to be defective in Alzheimer’s. Neurons pick up signals transmitted through the axons at junctures known as synapses. Here the message needs to be transmitted from one neuron to another one, and various neurotransmitters such as dopamine and GABA exert excitatory or inhibitory influences on signal strength. In adidtion to a single axon, neurons typically have several much shorter nerve fibers called dendrites, whose job is to receive incoming signals from diverse sources. At a given point in time, signals received from multiple sources are integrated in the cell body and a decision is made as to whether the accumulated signal strength is above threshold, in which case the neuron responds by firing a sequence of electrical pulses, which are then transmitted through the axon to a possibly distant destination.

In addition to the neurons, the brain also contains a large number of “helper” cells called glial cells, which are concerned with the care and feeding of neurons. Three principle types of glial cells will play a role in our later discussion: the microglia, the astrocytes, and the oligodendrocytes. Microglia are the equivalent of white blood cells in the rest of the body. They are concerned with fighting off infective agents such as bacteria and viruses, and they also monitor neuron health, making life-and-death decisions: programming a particular neuron for apoptosis (intentional self-destruction) if it appears to be malfunctioning beyond hope of recovery, or is infected with an organism that is too dangerous to let flourish.

The astrocytes figure very prominently in our story below. They nestle up against the neurons and are responsible for assuring an adequate supply of nutrients. Studies on neuron cultures from rodent central nervous systems have shown that neurons depend upon astrocytes for their supply of cholesterol [40]. Neurons critically need cholesterol, both in the synapse [50] and in the myelin sheath [45], in order to successfully transmit their signals, and also as a first line of defense against invasive microbes. Cholesterol is so important to the brain that astrocytes are able to synthesize it from basic ingredients, a skill not found in most cell types. They also supply the neurons with fatty acids, and they are able to take in short chain fatty acids and combine them to form the longer-chain types of fatty acids that are especially prominent in the brain [7][24][36], and then deliver them to neighboring neurons and to the cerebrospinal fluid.

The third type of glial cell is the oligodendrocyte. These cells specialize in making sure the myelin sheath is healthy. Oligodentrocytes synthesize a special sulfur-containing fatty acid, known as sulfatide, from other fatty acids supplied to them by the cerebrospinal fluid [9]. Sulfatide has been shown to be essential for the maintenance of the myelin sheath. Children born with a defect in the ability to metabolize sulfatide suffer from progressive demyelination, and rapid loss of motor and cognitive functions, resulting in an early death before the age of 5 [29]. Depletion in sulfatide is a well-known characterization of Alzheimer’s, even in early stages before it has been manifested as cognitive decline [18]. And ApoE has been shown to play a crucial role in the maintenance of sulfatide [19]. Throughout a person’s life, the myelin sheath has to be constantly maintained and repaired. This is something that researchers are only beginning to appreciate, but two related properties of Alzheimer’s are poor quality myelin sheath alongside a drastically reduced concentration of fatty acids and cholesterol in the cerebrospinal fluid [38].

3. Cholesterol and Lipid Management

In addition to some knowledge about the brain, you will also need to know something about the processes that deliver fats and cholesterol to all the tissues of the body, with a special focus on the brain. Most cell types can use either fats or glucose (a simple sugar derived from carbohydrates) as a fuel source to satisfy their energy needs. However, the brain is the one huge exception to this rule. All cells in the brain, both the neurons and the glial cells, are unable to utilize fats for fuel. This is likely because fats are too precious to the brain. The myelin sheath requires a constant supply of high quality fat to insulate and protect the enclosed axons. Since the brain needs its fats to survive long-term, it is paramount to protect them from oxidation (by exposure to oxygen) and from attack by invasive microbes.

Fats come in all kinds of shapes and sizes. One dimension is the degree of saturation, which concerns how many double bonds they possess, with saturated fats possessing none, monounsaturated fats having only one, and polyunsaturated fats having two or more. Oxygen breaks the double bond and leaves the fat oxidized, which is problematic for the brain. Polyunsaturated fats are thus the most vulnerable to oxygen exposure, because of multiple double bonds.

Fats are digested in the intestine and released into the blood stream in the form of a relatively large ball with a protective protein coat, called a chylomicron. The chylomicron can directly provide fuel to many cell types, but it may also be sent to the liver where the contained fats are sorted out and redistributed into much smaller particles, which also contain substantial amounts of cholesterol. These particles are called “lipoproteins,” (henceforth, LPP’s) because they contain protein in the spherical shell and lipids (fats) in the interior. If you’ve had your cholesterol measured, you’ve probably heard of LDL (low density LPP) and HDL (high density LPP). If you think these are two different kinds of cholesterol, you would be mistaken. They are just two different kinds of containers for cholesterol and fats that serve different roles in the body. There are actually several other LPP’s, for example, VLDL (very-low) and IDL (intermediate), as shown in the accompanying diagram. VLDL,IDL,LDL,HDLIn this essay I will refer to these collectively as the XDL’s. As if this weren’t confusing enough, there is also another unique XDL that is found only in the cerebrospinal fluid, that supplies the nutritional needs of the brain and nervous system. This one doesn’t seem to have a name yet, but I will call it “B-HDL,” because it is like HDL in terms of its size, and “B” is for “brain [13]”

An important point about all the XDL’s is that they contain distinctly different compositions, and each is targeted (programmed) for specific tissues. A set of proteins called “apolipoproteins” or, equivalently, “apoproteins” (“apo’s” for short) figure strongly in controlling whoChylomicron Structuregets what. As you can see from the schematic of the chylomicron shown at the right, it contains a rainbow of different apo’s for every conceivable application. But the XDL’s are far more specific, with HDL containing “A,” LDL containing “B,” VLDL containing “B” and “C,” and IDL containing only “E.” The apo’s have special binding properties that allow the lipid contents to be transported across cell membranes so that the cell can gain access to the fats and choleseterol contained inside.

The only apo that is of concern to us in the context of this essay is apoE. ApoE is very important to our story because of its known link with Alzheimer’s disease. ApoE is a protein, i.e., sequence of amino acids, and its specific composition is dictated by a corresponding DNA sequence on a protein-coding gene. Certain alterations in the DNA code lead to defects in the ability of the transcribed protein to perform its biological roles. ApoE-4, the allele associated with increased risk to Alzheimer’s, is presumably unable to perform its tasks as efficiently as the other alleles. By understanding what apoE does, we can better infer how the consequences of doing it poorly might impact the brain, and then observe experimentally whether the features of the Alzheimer’s brain are consistent with the roles played by apoE.

A strong clue about apoE’s roles can be deduced from where it is found. As I mentioned above, it is the only apo in both B-HDL in the cerebrospinal fluid and IDL in the blood serum. Only selected cell types can synthesize it, the two most significant of which for our purposes are the liver and the astrocytes in the brain. Thus the astrocytes provide the linkage between the blood and the cerebrospinal fluid. They can usher lipids and cholesterol across the blood-brain barrier, via the special key which is apoE.

It turns out that, although apoE is not found in LDL, it does bind to LDL, and this means that astrocytes can unlock the key to LDL in the same way that they can gain access to IDL, and hence the cholesterol and fatty acid contents of LDL are accessible to astrocytes as well, as long as apoE is functioning properly. The astrocytes reshape and repackage the lipids and release them into the cerebospinal fluid, both as B-HDL and simply as free fatty acids, available for uptake by all parts of the brain and nervous system [13].

One of the critical reshaping steps is to convert the fats into types that are more attractive to the brain. To understand this process you need to know about another dimension of fats besides their degree of saturation, which is their total length. Fats have a chain of linked carbon atoms as their spine, and the total number of carbons in a particular fat characterizes it as short, medium length, or long. The brain works best when the constituent fats are long, and, indeed, the astrocytes are able to take in short chain fats and reorganize them to make longer chain fats [24].

A final dimension of fats that plays a role is where the first double bond is located in a polyunsaturated fat, which distinguishes omega-3 from omega-6 fats (position 3; position 6). Omega-3 fats are very common in the brain. Certain ones of the omega-3 and omega-6 fats are essential fatty acids, in that the human body is unable to synthesize them, and therefore depends upon their supply from the diet. This is why it is claimed that fish “makes you smart”: because cold water fish is the best source of essential omega-3 fats.

Now I want to return to the subject of the XDL’s. It is a dangerous journey from the liver to the brain, as both oxygen and microbes are found in abundance in the blood stream. The XDL’s protective shell contains both LPP’s andunesterified cholesterol, as well as the signature apo that controls which cells can receive the contents, as shown in the accompanying schematic. lipoprotein schematicThe internal contents are esterified cholesterol and fatty acids, along with certain antioxidants that are conveniently being transported to the cells packaged in the same cargo ship. Esterification is a technique to render the fats and cholesterol inert, which helps protect them from oxidation [51]. Having the antioxidants (such as vitamin E and Coenzyme Q10) along for the ride is also convenient, as they too protect against oxidation. The cholesterol contained in the shell, however, is intentionally not esterified, which means that it is active. One of its roles there is to guard against invasive bacteria and viruses [55]. Cholesterol is the first line of defense against these microbes, as it will alert the white blood cells to attack whenever it encounters dangerous pathogens. It has also been proposed that the cholesterol in the XDL’s shell itself acts as an antioxidant [48].

HDL’s are mostly depleted of the lipid and cholesterol content, and they are tasked with returning the empty shell back to the liver. Once there, cholesterol will be recommissioned to enter the digestive system as part of the bile, which is produced by the gall bladder to help digest ingested fats. But the body is very careful to conserve cholesterol, so that 90% of it will be recycled from the gut back into the blood stream, contained in the chylomicron that began our story about fats.

In summary, the management of the distribution of fats and cholesterol to the cells of the body is a complex process, carefully orchestrated to assure that they will have a safe journey to their destination. Dangers lurk in the blood stream, mostly in the form of oxygen and invasive microbes. The body considers cholesterol to be precious cargo, and it is very careful to conserve it, by recycling it from the gut back to the liver, to be appropriately distributed among the XDL’s that will deliver both cholesterol and fats to the tissues that depend upon them, most especially the brain and nervous system.

4. 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 fetal 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 necesssary, 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 [3].

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 (Cholesterol Doesn’t Cause Alzheimer’s) 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 [54], and has been shown to be associated with better memory function [53] and reduced dementia [35]. The converse is also true: a correlation between falling cholesterol levels and Alzheimer’s [39]. As will be discussed further later, people with Alzheimer’s also have reduced levels of B-HDL, as well as sharply reduced levels of fatty acids, in the cerbrospinal fluid, i.e, impoverished supply of cholesterol and fats to the myelin sheath [38]. As we saw earlier, fatty acid supply is essential as building blocks for the sulfatide that is synthesized by oligodendrocytes to keep the myelin sheath healthy [29].

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 [46]. 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 [31], 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, reference [19] in [46] (which is reference [44] here) was very weak. The abstract for that article is repeated in full here in the Appendix. But 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.

An intuitive explanation for why high cholesterol at an early age might be correlated with Alzheimer’s risk has to do with apoE-4. People with that allele are known to have high cholesterol early in life [39], and I believe this is a protective strategy on the part of the body. The apoE-4 allele is likely defective in the task of importing cholesterol into the astrocytes, and therefore an increase in the bioavailability of cholesterol in blood serum would help to offset this deficit. Taking a statin would be the last thing a person in that situation would want to do.

5. Do Statins Cause 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 [50] and in terms of encouraging the growth of neurons through healthy development of the myelin sheath [45]. Nonetheless, the statin industry proudly boasts that statins are effective at interfering with cholesterol production in the brain [31][47] 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, and one of the authors of [50] referenced earlier. 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.”

A recent review of two large population-based double-blind placebo-controlled studies of statin medications in individuals at risk for dementia and Alzheimer disease showed that statins are not protective against Alzheimer’s [34]. The lead author of the study, Bernadette McGuinness, was quoted by a reporter from Science Daily as saying, “From these trials, which contained very large numbers and were the gold standard — it appears that statins given in late life to individuals at risk of vascular disease do not prevent against dementia.” A researcher at UCLA, Beatrice Golomb, when asked to comment on the results, was even more negative, saying, “Regarding statins as preventive medicines, there are a number of individual cases in case reports and case series where cognition is clearly and reproducibly adversely affected by statins.” In the interview, Golomb remarked that various randomized trials have shown that statins were either adverse or neutral towards cognition, but none have shown a favorable response.

A common side effect of statins is memory dysfunction. Dr. Duane Graveline, fondly known as “spacedoc” because he served as a doctor to the astronauts, has been a strong advocate against statins and is collecting evidence of statin side effects directly from statin users around the world. He was led to this assault on statins as a consequence of his own personal experience of transient global amnesia, a frightening episode of total memory loss which he is convinced was caused by the statin drugs he was taking at the time. He has now completed three books describing a diverse collection of damning side effects of statins, the most famous of which is Lipitor: Thief of Memory [17].

A second way (besides their direct impact on cholesterol) in which statins likely impact Alzheimer’s is in their indirect negative effect on the supply of fatty acids and antioxidants to the brain. It is a given that statins drastically reduce the level of LDL in the blood serum. This is their claim to fame. It is interesting, however, that they succeed in reducing not just the amount of cholesterol contained in the LDL particles, but rather the actual number of LDL particles altogether. This means that, in addition to depleting cholesterol, they reduce the available supply to the brain of both fatty acids and antixodiants, which are also carried in the LDL particles. As we’ve seen, all three of these substances are essential to proper brain functioning.

I conjecture that the reasons for this indirect effect are two-fold: (1) there is inadequate cholesterol in the bile to metabolize dietary fats, and (2) the rate-limiting effect on the production of LDL is the ability to provide adequate cholesterol in the shell to assure survival of the contents during transport in the blood stream; i.e., to protect the contents from oxidation and marauding bacteria and viruses. People who take the highest 80 mg/dl dosage of statins often end up with LDL levels as low as 40mg/dl, well below even the lowest numbers observed naturally. I shudder to think of the probable long-term consequences of such severe depletion in fats, cholesterol, and antioxidants.

A third way in which statins may promote Alzheimer’s is by crippling the ability for cells to synthesize coenzyme Q10. Coenzyme Q10 has the misfortune of sharing the same metabolic pathway as cholesterol. Statins interfere with a crucial intermediate step on the pathway to the synthesis of both cholesterol and coenzyme Q10. Coenzyme Q10 is also known as “ubiquinone” because it seems to show up everywhere in cell metabolism. It is found both in the mitochondria and in the lysosomes, and its critical role in both places is as an antioxidant. The inert esters of both cholesterol and fatty acids are hydrolyzed and activated in the lysosomes [8], and then released into the cytoplasm. Coenzyme Q10 consumes excess oxygen to keep it from doing oxidative damage [30], while also generating energy in the form of ATP (adenosine triphosphate, the universal energy currency in biology).

The final way in which statins should increase Alzheimer’s risk is through their indirect effect on vitamin D. CholesterolVitamin D is synthesized from cholesterol in the skin, upon exposure to UV rays from the sun. In fact, the chemical formula of vitamin D is almost indistinguishable from that of cholesterol, as shown in the two attached figures (cholesterol on the left, vitamin D on the right). If LDL levels are Vitamin D3kept artificially low, then the body will be unable to resupply adequate amounts of cholesterol to replenish the stores in the skin once they have been depleted. This would lead to vitamin D deficiency, which is a widespread problem in America.

It is well known that vitamin D fights infection. To quote from [25], “Patients with severe infections as in sepsis have a high prevalence of vitamin D deficiency and high mortality rates.” As will be elaborated on later, a large number of infective agents have been shown to be present in abnormally high amounts in the brains of Alzheimers patients [27][26].

Dr. Grant has recently argued [16] that there are many lines of evidence pointing to the idea that dementia is associated with vitamin D deficiency. An indirect argument is that vitamin D deficiency is associated with many conditions that in turn carry increased risk for dementia, such as diabetes, depression, osteoporosis, and cardiovascular disease. Vitamin D receptors are widespread in the brain, and it is likely that they play a role there in fighting off infection. Vitamin D surely plays other vital roles in the brain as well, as powerfully suggested by this quote taken from the abstract of [32]: “We conclude there is ample biological evidence to suggest an important role for vitamin D in brain development and function.”

6. Astrocytes, Glucose Metabolism, and Oxygen

Alzheimer’s is clearly correlated with a deficiency in the supply of fat and cholesterol to the brain. IDL, when functioning properly, is actually incredibly efficient in cholesterol and fat throughput from the blood across cell membranes, compared to LDL [8]. It gives up its contents much more readily than the other apo’s. And it achieves this as a direct consequence of apoE. IDL (as well as LDL) in the blood delivers fats and cholesterol to the astrocytes in the brain, and the astrocytes can thus use this external source instead of having to produce these nutrients themselves. I suspect, in fact, that astrocytes only produce a private supply when the external supply is insufficient, and they do so reluctantly.

Why would it be disadvantageous for an astrocyte to synthesize its own fats and cholesterol? In my opinion, the answer has to do with oxygen. An astrocyte needs a significant energy source to synthesize fats and cholesterol, and this energy is usually supplied by glucose from the blood stream. Furthermore, the end-product of glucose metabolism is acetyl-Coenzyme A, the precursor to both fatty acids and cholesterol. Glucose can be consumed very efficiently in the mitochondria, internal structures within the cell cytoplasm, via aerobic processes that require oxygen. The glucose is broken down to produce acetyl-Coenzyme A as an end-product, as well as ATP, the source of energy in all cells.

However, oxygen is toxic to lipids (fats), because it oxidizes them and makes them rancid. Lipids are fragile if not encased in a protective shell like IDL, HDL, or LDL. Once they are rancid they are susceptible to infection by invasive agents like bacteria and viruses. So an astrocyte trying to synthesize a lipid has to be very careful to keep oxygen out, yet oxygen is needed for efficient metabolism of glucose, which will provide both the fuel (ATP) and the raw materials (acetyl-Coenzyme A) for fat and cholesterol synthesis.

What to do? Well, it turns out that there is an alternative, although much less efficient, solution: to metabolize glucose anaerobically directly in the cytoplasm. This process does not depend on oxygen (a great advantage) but it also yields substantially less ATP (only 6 ATP as contrasted with 30 if glucose is metabolized aerobically in the mitochondria). The end product of this anaerobic step is a substance called pyruvate, which could be further broken down to yield a lot more energy, but this process is not accessible to all cells, and it turns out that the astrocytes need help for this to happen, which is where amyloid-beta comes in.

7. The Crucial Role of Amyloid-Beta

Amyloid-beta (also known as “abeta”) is the substance that forms the famous plaque that accumulates in the brains of Alzheimer’s patients. It has been believed by many (but not all) in the research community that amyloid-beta is the principal cause of Alzheimer’s, and as a consequence, researchers are actively seeking drugs that might destroy it. However, amyloid-beta has the unique capability of stimulating the production of an enzyme, lactate dehydrogenase, which promotes the breakdown of pyruvate (the product of anaerobic glucose metabolism) into lactate, through an anaerobic fermentation process, with the further production of a substantial amount of ATP.

The lactate, in turn, can be utilized itself as an energy source by some cells, and it has been established that neurons are on the short list of cell types that can metabolize lactate. So I conjecture that the lactate is transported from the astrocyte to a neighboring neuron to enhance its energy supply, thus reducing its dependence on glucose. It is also known that apoE can signal the production of amyloid-beta, but only under certain poorly understood environmental conditions. I suggest those environmental triggers have to do with the internal manufacture of fats and cholesterol as opposed to the extraction of these nutrients from the blood supply. I.e., amyloid-beta is produced as a consequence of environmental oxidative stress due to an inadequate supply of fats and cholesterol from the blood.

In addition to being utilized as an energy source by being broken down to lactate, pyruvate can also be used as a basic building block for synthesizing fatty acids. So anaerobic glucose metabolism, which yields pyruvate, is a win-win-win situation: (1) it significantly reduces the risk of exposure of fatty acids to oxygen, (2) it provides a source of fuel for neighboring neurons in the form of lactate, and (3) it provides a basic building block for fatty acid synthesis. But it depends upon amyloid-beta to work.

Thus, in my view (and in the view of others [28] [20] Amyloid-Beta and Alzheimer’s), amyloid-beta is not a cause of Alzheimer’s, but rather a protective device against it. The abstract of reference [28] arguing this point of view is reproduced in full in the Appendix. Several variants of a genetic defect associated with amyloid precursor protein (APP), the protein from which amyloid-beta is derived, have now been identified. A defect in this protein, which is associated with an increased risk of early onset Alzheimer’s, would likely lead to a reduced ability to synthesize amyloid-beta, which would then leave the brain with a big problem, since both the fuel and the basic building blocks for fatty acid synthesis would be in short supply, while oxygen trekking through the cell to the mitochondria would be exposing whatever fats were being synthesized to oxidation. The cell would likely be unable to keep up with need, and this would lead to a reduction in the number of fatty acids in the Alzheimer’s cerebrospinal fluid, a well-established characteristic of Alzheimer’s [38].

8. Cholesterol’s Role 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 [50]. 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 fiber, a part of the white matter. The myelin sheath which coats the nerve fiber 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. Cholesterol is crucial for the myelin as well as for the synapse, as demonstrated dramatically through experiments conducted on genetically defective mice by Gesine Saher et al. [45]. These mutant mice lacked the ability to synthesize cholesterol in myelin-forming oligodendrocytes. They had severly disturbed myelin in their brains, and exhibited ataxia (uncoordinated muscle movements) and tremor. In the abstract, the authors wrote unequivocally, “This shows that cholesterol is an indispensable component of myelin membranes.”

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 [38]. 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!

People with the apoE-4 allele tend to have high serum cholesterol. The question of whether this high cholesterol level might be an attempt on the part of the body to adjust for a poor rate of cholesterol uptake in the brain was addressed by a team of researchers in 1998 [39]. They studied 444 men between 70 and 89 years old at the time, for whom there existed extensive records of cholesterol levels dating back to several decades ago. Most significantly, cholesterol levels fell for the men who developed Alzheimer’s prior to their showing Alzheimer’s symptoms. The authors suggested that their high cholesterol might have been a protective mechanism against Alzheimer’s.

One might wonder why their cholesterol levels fell. There was no mention of statin drugs in the article, but statins would certainly be an effective way to reduce cholesterol levels. The statin industry would like people to believe that high cholesterol is a risk factor for Alzheimer’s, and they are quite thrilled that high cholesterol early in life is correlated with Alzheimer’s much later. But these results suggest quite the opposite: that blood cholesterol levels are kept high intentionally by the body regulatory mechanisms in an attempt to compensate for the defect. A high concentration will lead to an increase in the rate of delivery to the brain, where it is critically needed to keep the myelin sheath healthy and to promote neuron signaling in the synapses.

Using MRI technology, researchers at UCLA were able to measure the degree of breakdown of myelin in specific regions of the brain [6]. They conducted their studies on over 100 people between 55 and 75 years old, for whom they also determined the associated apoE allele (2, 3, or 4). They found a consistent trend in that apoE-2 had the least amount of degradation, and apoE-4 had the most, in the frontal lobe region of the brain. All of the people in the study were thus far healthy with respect to Alzheimer’s. These results show that premature breakdown of myelin sheath (likely due to an insufficient supply of fats and cholesterol to repair it) is associated with apoE-4.

To summarize, I hypothesize that, for the apoE-4 Alzheimer’s patients, defective apoE has led to an impaired ability to transport fats and cholesterol from the blood stream, via the astrocytes, into the cerebrospinal fluid. The associated high blood serum cholesterol is an attempt to partially correct for this defect. For the rest of the Alzheimer’s patients (the ones without the apoE-4 allele but who also have severely depleted fatty acids in their cerebrospinal fluid), we have to look for another reason why their fatty acid supply chain might be broken.

9. Infections and Inflammation

To summarize what I have said so far, Alzheimer’s appears to be a consequence of an inability of neurons to function properly, due to a deficiency in fats and cholesterol. A compounding problem is that the fats over time will become rancid if they cannot be adequately replenished. Rancid fats are vulnerable to attack by microorganisms such as bacteria and viruses. Amyloid-beta is part of the solution because it allows the astrocytes to be much more effective in utilizing glucose anaerobically, which protects the internally synthesized fats and cholesterol from toxic oxygen exposure, while at the same time providing the energy needed both by the astrocyte for the synthesis process and by neighboring neurons to fuel their signal firings.

Besides the astrocytes, the microglia in the brain are also implicated in Alzheimer’s. Microglia promote neuron growth when all is well, but trigger neuron programmed cell death in the presence of toxic substances secreted by bacteria such as polysaccharides [56]. Microglia will defensively secrete cytokines (communication signals that promote an immune response) when exposed to infective agents, and these in turn will lead to inflammation, another well-known feature associated with Alzheimer’s [1]. The microglia are able to control whether neurons should live or die, and they surely base this decision on factors related to how well the neuron functions and whether it is infected. Once enough neurons have been programmed for cell death, the disease will manifest itself as cognitive decline.

10. Evidence that Infection is Associated with Alzheimer’s

There is substantial evidence that Alzheimer’s is related to an increased likelihood of infective agents appearing in the brain. Some researchers believe that infective agents are the principle cause of Alzheimer’s. There are a number of bacteria that reside in the human digestive system and can co-exist with our own cells without any harm. However, H. pylori, one that is quite common, has been recently shown to be responsible for stomach ulcers. It has been suspected that H. Pylori might be implicated in Alzheimer’s, and, indeed, a recent study showed that Alzheimer’s patients had a significantly higher concentration of an antibody against H. Pylori in both their cerebrospinal fluid and their blood than non-Alzheimer’s controls [26]. H. pylori was detected in 88% of the Alzheimer’s patients but only 47% of the controls. In an effort to treat the Alzheimer’s patients, the researchers administered a potent combination of antibiotics, and assessed the degree of mental decline over the next two years [27]. For 85% of the patients, the infection was successfully routed, and for those patients, cognitive improvement was also detected after two years had elapsed. So this was a nice example of the possibility of treating Alzheimer’s through antibiotics.

C. pneumoniae is a very common bacterium, estimated to infect 40-70% of adults. But there’s a big difference between a bacterium being in the blood stream and making its way into the inner sanctum of the brain. A study of post-mortem samples from various regions of the brains of Alzheimer’s patients and non-Alzheimer’s controls revealed a remarkably different statistic: 17 out of 19 Alzheimer’s brains tested positive for the bacterium, whereas only 1 out of 19 brains from the control group tested positive [5].

Many other infective agents, both viruses and bacteria, have been found to be associated with Alzheimer’s, including herpes simplex virus, picornavirus, Borna disease virus, and spirochete [23]. One proposal was that a particularbacteriophage — a virus that infects the bacterium C. pneumoniae — might be responsible for Alzheimer’s [14]. The authors argued that the phages might make their way into the mitochondria of the host cell and subsequently initiate Alzheimer’s.

11. Ketogenic Diet as Treatment for Alzheimer’s

One of the promising new treatment paradigms for Alzheimer’s is to have the patient switch to an extremely high fat, low carb diet, a so-called “ketogenic” diet. The name comes from the fact that the metabolism of dietary fats produces “ketone bodies” as a by-product, which are a very useful resource for metabolism in the brain. It is becoming increasingly clear that defective glucose metabolism in the brain (so-called “type-3 diabetes”) is an early characteristic of Alzheimer’s. Ketone bodies, whether they enter the astrocyte directly or are produced in the astrocyte itself by breaking down fats, can be delivered to adjacent neurons, as shown in the accompanying figure.Ketone BodiesThese neurons can utilize the ketone bodies both as an energy source (replacing and therefore relieving glucose) and as a precursor to GABA, a critical neurotransmitter that is widespread in the brain.

Evidence that a ketogenic diet might help Alzheimer’s was first found through research conducted on mice who had been bred to be prone to Alzheimer’s disease [21]. Researchers found that the mice’s cognition improved when they were treated with a high-fat low-carb diet, and also that the amount of amyloid-beta in their brain was reduced. The latter effect would be anticipated based on the premise that amyloid-beta promotes full utilization of glucose anaerobically, as I discussed previously. By having ketone bodies as an additional source of fuel, the dependence on glucose is reduced. But another effect that may be more important than this is the availability of high-quality fats to improve the condition of the myelin sheath.

This idea is supported by other experiments done on human Alzheimer’s patients [11] [42]. A placebo-controlled 2004 study [42] of the effect of dietary fat enrichment on Alzheimer’s is especially informative, because it uncovered a significant difference in effectiveness for the fat-enrichment for subjects who did not have the apoE-4 allele as compared with those who did. The experimental test group were given a supplemental drink containing emulsified medium chain triglycerides, found in high concentration in coconut oil. The subjects without the apoE-4 allele showed a significant improvement in score on a standard test for Alzheimer’s, whereas those with the apoE-4 allele did not. This is a strong indicator that the benefit may have to do with an increase in uptake by the astrocyte of these high-quality fats, something that the subjects with the apoE-4 allele are unable to accomplish due to the defective IDL and LDL transport mechanisms.

12. NADH Treatment: the Crucial Role of Antioxidants

One of the very few promising treatments for Alzheimer’s is the coenzyme, NADH (nicotinamide adenine dinucleotide) [12]. In a placebo-controlled study, Alzheimer’s subjects given NADH for six months exhibited significantly better performances on verbal fluency, visual constructional ability and abstract verbal reasoning than the control subjects given a placebo.Pyruvate Metabolism

Why would NADH be effective? In the process of converting pyruvate to lactate, lactate dehydrogenase consumes oxygen by oxidizing NADH to NAD+, as illustrated in the accompanying figure. So, if the bioavailability of NADH is increased, it stands to reason that the astrocyte would have an enhanced ability to convert pyruvate to lactate, the critical step in the anaerobic metabolic pathway that is enhanced by amyloid-beta. The process, by absorbing the toxic oxygen, would reduce the damage to the lipids due to oxygen exposure, and would also provide lactate as a source of energy for the neurons.

13. Excessive Oxygen Exposure and Cognitive Decline

It has been observed that some elderly people suffer temporary and sometimes permanent cognitive decline following a lengthy operation. Researchers at the University of South Florida and Vanderbilt University suspected that this might be due to excessive exposure to oxygen [4]. Typically, during an operation, people are often administered high doses of oxygen, even as much as 100% oxygen. The researchers conducted an experiment on young adult mice, which had been engineered to be predisposed towards Alzheimer’s but had not yet suffered cognitive decline. They did however already have amyloid-beta deposits in their brains. The re-engineered mice, as well as a control group that did not have the Alzheimer’s susceptibility gene, were exposed to 100-percent oxygen for a period of three hours, three times over the course of several months, simulating repeated operations. They found that the Alzheimer’s pre-disposed mice suffered significant cognitive decline following the oxygen exposure, by contrast with the control mice.

This is a strong indication that the excessive oxygen exposure during operations is causing oxidative damage in the Alzheimer’s brain. Given the arguments I have presented above, this result makes good sense. The brain, by converting to anaerobic metabolism for generating energy (with help from amyloid-beta) is trying its best to avoid exposing the fatty acids and cholesterol to oxidative damage. But an extremely high concentration of oxygen in the blood makes it very difficult to protect the fats and cholesterol during transport through the blood, and also probably causes an unavoidable increase in oxygen uptake and therefore exposure within the brain itself.

14. Fats are a Healthy Choice!

You would practically have to be as isolated as an Australian Aborigine not to have absorbed the message that dietary fats, particularly saturated fats, are unhealthy. I am extremely confident that this message is false, but it is nearly impossible to turn the opinion tide due to its pervasive presence. Most people don’t question why fats are bad; they assume that researchers must have done their homework, and they trust the result.

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 [41]. 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 [42]. And high-fat dairy (also highly saturated) has been shown to be beneficial both to fertility among women [10] and, remarkably, to heart disease [37][22].

Despite the widespread belief that fats (particularly saturated fats) are unhealthy, an article that appeared in the American Journal of Clinical Nutrition in 2004 [37] claims that, for a group of post-menopausal women, a high-fat, high-saturated-fat diet affords better protection from coronary artery disease than a low-fat (25% of calories from fats) diet. The subjects in the study were obese women with coronary artery disease. Most of them had high blood pressure, and many had diabetes. They fit the profile for metabolic syndrome that I have previously argued is a direct consequence of a prolonged low-fat high-carb diet. I am gratified to see that my hypothesis that an increase in fat intake would decrease their risk of heart disease has been verified by a carefully controlled study.

Another investigation where fats were shown to afford protection against heart disease has just been completed. It involved a long-term study of a large number of Swedish men [22]. The authors looked at low- vs high-fat dairy, as well as consumption of fruits and vegetables, meats, grains, etc. The only statistically significant result that afforded protection from heart disease was a combination of high-fat dairy and lots of fruits and vegetables. Fruits and vegetables with low-fat dairy afforded no protection.

I suspect one of the critical nutrients the fruits and vegetables provide is antioxidants that help prolong the life of the fats. Other excellent sources of antioxidants include richly colored fruits like berries and tomatoes, coffee, green tea, and dark chocolate, and several spices, most especially cinnamon and turmeric (a major ingredient of curry). These should be consumed in abundance along with fats for optimal results.

Polyunsaturated fats such as corn oil and canola oil are unhealthy for the brain precisely because they are unsaturated. There are two major problems: (1) they have a low melting point, which means that, if they are used for frying they will be converted to trans fats, which are extremely unhealthy, and (2) they are much more susceptible to becoming rancid (oxidized) at room temperature than saturated fats, i.e., they have a shorter shelf life.

Researchers in Germany recently conducted an ingenious experiment designed to determine how the degree of freshness of polyunsaturated fats affects the metabolism of those fats in female lactating rats [43]. They divided female rats into two groups, and the only difference between the test group and the controls was that the test group was given fats that had been left in a relatively warm place for 25 days, which caused considerable oxidative damage, whereas the controls were fed fresh fats instead. The rats’ unusual diet was begun on the day that they gave birth to a litter. The researchers examined the mammary glands and the milk produced by the two groups for apparent differences. They found that the test group’s milk was markedly reduced in the amount of fat it contained, and their mammary glands correspondingly took up less fat from the blood supply. One might surmise that the rats’ metabolic mechanisms were able to detect oxidative damage to the fats, and therefore rejected them, prefering to do without rather than to risk the consequences of feeding their pups oxidized fats. Consequently, the pups of the test group gained significantly less weight than the control group’s pups.

Boxed items like cookies and crackers that contain processed polyunsaturated fats are doctored with antioxidants and even antibiotics to protect them from spoiling. Once they’re consumed, however, they still have to be protected from going rancid. Biochemical laws work the same way whether inside or outside the body. There are plenty of bacteria throughout the body that would be eager to take up house-keeping in rancid fats. The body has devised all kinds of strategies for protecting fats from oxidation (becoming rancid) and from attack by bacteria. But its task is rendered much easier for saturated rather than unsaturated fats, and for fresh rather than stale fats.

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 overabundance 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.

15. Summary and 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. It is an indication of how much progress has been made in recent years to note that 42% of the references in this essay were published in 2008 or 2009. A popular new theory is that Alzheimer’s may grow out of an impaired ability to metabolize glucose in the brain. The term “type-3 diabetes” has been coined to describe this defect, which often appears long before any symptoms of Alzheimer’s [49]. A shift from aerobic towards anaerobic glucose metabolism in the brain seems to be a harbinger of Alzheimer’s later in life, but I argue that the reason for this shift is both to provide a basic ingredient (pyruvate) from which to synthesize fatty acids, while simultaneously protecting them from potentially damaging oxidation. 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 [38] 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. In fact, most damningly, the statin usage evidence that would answer the question was “unavailable” to the researchers who conducted the seminal study.

Beatrice Golomb is an M.D. Ph.D. who heads up the UCSD Statin Study group, a research team who are actively investigating the risk-benefit balance of statin drugs. She is increasingly becoming convinced that statin drugs should not be recommended for the elderly: that in their case the risks clearly outweigh the benefits. She makes a strong case for this position in an on-line article available here [15]. The section on Alzheimer’s is particularly compelling, and it points out the pitfalls in relying on previous studies done by the statin industry, where often those who have memory problems as side-effects of the statin drugs are excluded from the study, so that the results end up inappropriately biased in favor of statins. In summary, she wrote: “It must be emphasized that the randomized trial evidence has, to date, uniformly failed to show cognitive benefits by statins and has supported no effect or frank and significant harm to cognitive function.”

In addition to refusing to take statin therapy, another way in which an individual can improve their odds against Alzheimer’s is to consume plenty of dietary fats. It seems odd to suddenly switch from a “healthy” low-fat diet to an extremely high fat ketogenic diet, once a diagnosis of Alzheimer’s is made. A ketogenic diet consists, ideally, of 88% fat, 10% protein, and 2% carbohydrate [11]. That is to say, it is absurdly high in fat content. It seems much more reasonable to aim for something like 50% fat, 30% protein, and 20% carbohydrate, so as to pro-actively defend against Alzheimer’s.

I highly recommend a recent book written by the pediatric brain surgeon, Larry McCleary, M.D., called The Brain Trust Program [33]. This book gives a wealth of fascinating information about the brain, as well as specific recommendations for ways to improve cognitive function and avert later Alzheimer’s. Most significantly, he recommends a diet that is high in cholesterol and animal fats, including an abundance of fish, seafood, meat, and eggs. He also recommends coconuts, almonds, avocados and cheese, all foods that contain a significant amount of fat, while encouraging the avoidance of “empty carbs.” His knowledge on this subject grew out of his interest in helping his young patients heal more rapidly after brain trauma.

Our nation is currently bracing itself for an onslaught of Alzheimer’s, at a time when baby boomers are approaching retirement, and our health care system is already in a crisis of escalating costs and shrinking funds. We can not afford the high cost of caring for the swelling population of Alzheimer’s patients that our current practices of low-fat diet and ever expanding statin usage are promoting.

Appendix In this appendix, I include the full abstract of two papers that are relevant to the theory presented here. The first is the abstract of reference [19] in [46], which is reference [44] here [see the section on statin drugs above for context]:

Abstract, “Epidemiological and clinical trials evidence about a preventive role for statins in Alzheimer’s disease:”

“This paper reviews epidemiological and clinical trials data about whether statin use reduces the risk of Alzheimer’s disease (AD). The available information has come in three waves. The initial, mostly cross-sectional observational reports suggested that statins might prevent dementia. Next, two large clinical trials with cognitive add-on studies showed no benefit and neither did the third wave, again with observational studies. The latter were mostly longitudinal, and were critical of the first studies for not adequately addressing confounding by indication (i.e. that patients with dementia would be denied statins). Most recently, new data from the Canadian Study of Health and Aging have produced a mixed result. While methodological considerations are clearly important in understanding why the reports are so variable, there might also be merit in differentiating between statins, based on their presumed – and variable – mechanisms of action in dementia prevention, before concluding that the initial reports are entirely artefactual. Still, the first reports appear to have overestimated the extent of protection, so that unless there are important effects achievable with specific statins, a more than a modest role for statins in preventing AD seems unlikely.” The second abstract is taken from reference [28], on the “alternative hypothesis” that amyloid-beta is protective rather than detrimental to Alzheimer’s, i.e., that it is a “protective response to neuronal insult:”

Abstract, “Amyloid-beta in Alzheimer disease: the null versus the alternate hypotheses:”

“For nearly 20 years, the primary focus for researchers studying Alzheimer disease has been centered on amyloid-beta, such that the amyloid cascade hypothesis has become the “null hypothesis.” Indeed, amyloid-beta is, by the current definition of the disease, an obligate player in pathophysiology, is toxic to neurons in vitro, and, perhaps most compelling, is increased by all of the human genetic influences on the disease. Therefore, targeting amyloid-beta is the focus of considerable basic and therapeutic interest. However, an increasingly vocal group of investigators are arriving at an “alternate hypothesis” stating that amyloid-beta, while certainly involved in the disease, is not an initiating event but rather is secondary to other pathogenic events. Furthermore and perhaps most contrary to current thinking, the alternate hypothesis proposes that the role of amyloid-beta is not as a harbinger of death but rather a protective response to neuronal insult. To determine which hypothesis relates best to Alzheimer disease requires a broader view of disease pathogenesis and is discussed herein.”



[1] H. Akiyama, S. Barger, S. Barnum, B. Bradt, J.Bauer, G.M. Cole, N.R. Cooper, P. Eikelenboom, M. Emmerling, B.L. Fiebich, C.E. Finch, S. Frautschy, W.S. Griffin, H. Hampel, M. Hull, G. Landreth, L. Lue, R. Mrak, I.R. Mackenzie, P.L. McGeer, M.K. O’Banion, J. Pachter, G. Pasinetti, C. Plata-Salaman, J. Rogers, R.Rydel, Y. Shen, W. Streit, R. Strohmeyer, I. Tooyoma, F.L. Van Muiswinkel, R. Veerhuis, D. Walker, S. Webster, B. Wegrzyniak, G. Wenk, and T. Wyss-Coray, “Inflammation and Alzheimer’s disease.” Neurobiol Aging (2000) May-Jun;21(3):383-421,
[2] Alzheimer’s Association, “Alzheimer’s Disease Facts and Figures,” Alzheimer’s and Dementia (2009) Vol. 5, Issue 3.
[3] K.J. Anstey, D.M. Lipnicki and L.F. Low, “Cholesterol as a risk factor for dementia and cognitive decline: a systematic review of prospective studies with meta-analysis.” Am J Geriatr Psychiatry (2008) May, Vol. 16, No. 5, pp. 343-54.
[4] G. Arendash, A. Cox, T. Mori, J. Cracchiolo, K. Hensley, J. Roberts 2nd, “Oxygen treatment triggers cognitive impairment in Alzheimer’s transgenic mice,” Neuroreport. (2009) Jun 18.
[5] B.J. Balin, C.S. Little, C.J. Hammond, D.M. Appelt, J.A. Whittum-Hudson, H.C. Gerard, A.P. Hudson, “Chlamydophila pneumoniae and the etiology of late-onset Alzheimer’s disease.” J. Alz. Dis. (2008) Vol. 13, pp. 371-380.
[6] G. Bartzokis, MD; P.H. Lu, Psy, D.H. Geschwind, MD, N.Edwards, MA, J. Mintz, PhD, and J.L. Cummings, MD, “Apolipoprotein E Genotype and Age-Related Myelin Breakdown in Healthy Individuals: Implications for Cognitive Decline and Dementia,” Arch Gen Psychiatry (2006) Vol. 63, pp. 63-72.
[7] N. Bernoud, L. Fenart, C. Bénistant, J. F. Pageaux, M. P. Dehouck, P. Molière, M. Lagarde, R. Cecchelli,d, and J. Lecerf, “Astrocytes are mainly responsible for the polyunsaturated fatty acid enrichment in blood-brain barrier endothelial cells in vitro” Journal of Lipid Research (1998) Sept., Vol. 39, pp. 1816-1824.
[8] M. S. Brown and J. L. Goldstein, “A Receptor-Mediated Pathway for Cholesterol Homeostasis,” Nobel Lecture, December 9, 1985.
[9] N. Cartier, C. Sevin, A. Benraiss, P. DeDeyn, D. Bonnin, M-T Vanier, M. Philippe, V. Gieselmann and P. Aubourg, “AAV5-Mediated Delivery of Human Aryl Sulfatase A (hARSA) Prevents Sufatide Storage and Neuropathological Phenotype in Metachromatic Leukodystrophy (MLD) Mice,” Molecular Therapy (2005) 11, S166-S167; doi: 10.1016/j.ymthe.2005.06.431
[10] J. Chavarro, W.C. Willett, and P.J. Skerrett, The Fertility Diet, (2008) McGraw Hill.
[11] L.C. Costantini, L.J. Barr, J.L. Vogel and S.T. Henderson, “Hypometabolism as a therapeutic target in Alzheimer’s disease” BMC Neurosci (2008) Vol. 9, Suppl. 2, S16. doi: 10.1186/1471-2202-9-S2-S16.
[12] V. Demarin, S.S. Podobnik, D. Storga-Tomic and G. Kay, “Treatment of Alzheimer’s disease with stabilized oral nicotinamide adenine dinucleotide: A randomized, double-blind study” Drugs Exp Clin Res. (2004) Vol. 30, No. 1, pp. 27-33.
[13] R.B. DeMattos, R.P. Brendza, J.E. Heuser, M.Kierson, J.R. Cirrito, J. Fryer, P.M. Sullivan, A.M. Fagan, X. Han and D.M. Holtzman, “Purification and characterization of astrocyte-secreted apolipoprotein E and J-containing lipoproteins from wild-type and human apoE transgenic mice,” Neurochem Int. (2001) Nov-Dec;39(5-6):415-25. doi:10.1016/S0197-0186(01)00049-3.
[14] M. Dezfulian, M.A. ShokrgozarA, S. Sardari, K. Parivar and G. Javadi, “Can phages cause Alzheimer’s disease?” Med Hypotheses (2008) Nov;71(5):651-6.
[15] B.A. Golomb, M.D., Ph.D., “Statin Adverse Effects: Implications for the Elderly,” Geriatric Times (2004) May/June, Vol. V, Issue 3
[16] W.R. Grant, Ph.D., “Does Vitamin D Reduce the Risk of Dementia?” Journal of Alzheimer’s Disease (2009) May, Vol. 17, No. 1., pp. 151-9.
[17] Dr. Duane Graveline, Lipitor: Thief of Memory, Statin Drugs and the Misguided War on Cholesterol, (2004)
[18] X. Han, “Potential mechanisms contributing to sulfatide depletion at the earliest clinically recognizable stage of Alzheimer’s disease: a tale of shotgun lipidomics,” J Neurochem (2007) November, Vol. 103, Suppl. 1. pp. 171-179. doi: 10.1111/j.1471-4159.2007.04708.x.
[19] X. Han, H. Cheng, J.D. Fryer, A.M. Fagan and D.M. Holtzman, “Novel Role for Apolipoprotein E in the Central Nervous System: Modulation of Sulfatide Content” Journal of Biological Chemistry, March 7, 2003, Vol. 278, pp. 8043-8051, DOI 10.1074/jbc.M212340200.
[20] K. Heininger, “A unifying hypothesis of Alzheimer’s disease. IV. Causation and sequence of events,” Rev Neurosci. (2000) Vol. 11, Spec No, pp.213-328.
[21] S.T. Henderson, “Ketone Bodies as a Therapeutic for Alzheimer’s Disease,” NeuroTherapeutics,, (2008) Jul;5(3):470-80, doi:10.1016/j.nurt.2008.05.004
[22] S. Holmberg, A. Thelin and E.-L. StiernstrNvm, “Food Choices and Coronary Heart Disease: A Population Based Cohort Study of Rural Swedish Men with 12 Years of Follow-up,” Int. J. Environ. Res. Public Health (2009) Vol. 6, pp. 2626-2638;
[23] K. Honjo, R. van Reekum, and N.P. Verhoeff, “Alzheimer’s disease and infection: do infectious agents contribute to progression of Alzheimer’s disease?” Alzheimers Dement. (2009) Jul;5(4):348-60.
[24] S.M. Innis and R.A. Dyer, “Brain astrocyte synthesis of docosahexaenoic acid from n-3 fatty acids is limited at the elongation of docosapentaenoic acid,” (2002) Sept. Journal of Lipid Research, Vol. 43, pp. 1529-1536.
[25] L. Jeng, A.V. Yamshchikov, S.E. Judd, H.M. Blumberg, G.S. Martin, T.R. Ziegler and V. Tangpricha, “Alterations in Vitamin D Status and Anti-microbial Peptide Levels in Patients in the Intensive Care Unit with Sepsis,” Journal of translational Medicine,” (2009) Vol. 7, No. 28.
[26] J. Kountouras, M. Boziki, E. Gavalas, C. Zavos, G. Deretzi, N. Grigoriadis, M. Tsolaki, D. Chatzopoulos, P. Katsinelos, D. Tzilves, A. Zabouri, I. Michailidou, “Increased cerebrospinal fluid Helicobacter pylori antibody in Alzheimer’s disease,” Int J Neurosci. (2009) 119(6):765-77.
[27] J. Kountouras, M. Boziki, E. Gavalas, C. Zavos, N. Grigoriadis, G. Deretzi, D. Tzilves, P. Katsinelos, M. Tsolaki, D. Chatzopoulos, and I. Venizelos, “Eradication of Helicobacter pylori may be beneficial in the management of Alzheimer’s disease,” J Neurol. (2009) May;256(5):758-67. Epub 2009 Feb 25.
[28] H.G. Lee, X. Zhu, R.J. Castellani, A. Nunomura, G. Perry, and M.A. Smith, “Amyloid-beta in Alzheimer disease: the null versus the alternate hypotheses,” J Pharmacol Exp Ther. (2007) June, Vol. 321 No. 3, pp. 823-9. doi:10.3390/ijerph6102626.
[29] J. Marcus, S. Honigbaum, S. Shroff, K. Honke, J. Rosenbluth and J.L. Dupree, “Sulfatide is essential for the maintenance of CNS myelin and axon structure,” Glia (2006), Vol. 53, pp. 372-381.
[30] R.T. Matthews, L. Yang, S. Browne, M. Baik and M.F. Beal, “Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects,” Proc Natl Acad Sci U S A. (1998) Jul 21, Vol. 95, No. 15, pp.8892-7.
[31] D. Lutjohann and K. von Bergmann, “24S-hydroxycholesterol: a marker of brain cholesterol metabolism”Pharmacopsychiatry (2003) January 10, Vol. 36 Suppl 2, pp. S102-6, DOI: 10.1055/s-2003-43053.
[32] J. C. McCann and B.N. Ames, “Is there convincing biological or behavioral evidence linking vitamin D deficiency to brain dysfunction?”, (2008) FASEB J. Vol. 22, pp. 982-1001. doi: 10.1096/fj.07-9326rev.
[33] Larry McCleary, M.D., The Brain Trust Program (2007) September, The Penguin Group, New York, New York.
[34] B. McGuinness et al., “Statins for the prevention of dementia,” Cochrane Database of Systematic Reviews,(2009) No. 2.
[35] M.M. Mielke, P.P. Zandi, M. Sjogren, et al. “High total cholesterol levels in late life associated with a reduced risk of dementia,” Neurology (2005) Vol. 64, pp. 1689-1695.
[36] S.A. Moore, “Polyunsaturated Fatty Acid Synthesis and Release by Brain-Derived Cells in Vitro,” Journal of Molecular Neuroscience (2001), Vol. 16, pp. 195ff.
[37] D. Mozaffarian, E.B. Rimm, D.M. Herrington, “Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women,” Am J Clin Nutr (2004) Vol. 80, pp. 1175-84.
[38] M. Mulder, R. Ravid, D.F. Swaab, E.R. de Kloet, E.D. Haasdijk, J. Julk, J.J. van der Boom and L.M. Havekes, “Reduced levels of cholesterol, phospholipids, and fatty acids in cerebrospinal fluid of Alzheimer disease patients are not related to apolipoprotein E4,” Alzheimer Dis Assoc Disord. (1998) Sep, Vol. 12, No. 3, pp. 198-203.
[39] I.L. Notkola, R. Sulkava, J. Pekkanen, T. Erkinjuntti, C. Ehnholm, P. Kivinen, J. Tuomilehto, and A. Nissinen, “Serum total cholesterol, apolipoprotein E epsilon 4 allele, and Alzheimer’s disease,” Neuroepidemiology (1998) Vol. 17, No. 1, pp. 14-20.
[40] F.W. Pfrieger, “Outsourcing in the brain: Do neurons depend on cholesterol delivery by astrocytes?”, BioEssays(2003) Vol. 25 Issue 1, pp.72-78.
[41] A. Phivilay, C. Julien, C. Tremblay, L. Berthiaume, P. Julien, Y. Giguère and F. Calon, “High dietary consumption of trans fatty acids decreases brain docosahexaenoic acid but does not alter amyloid-beta and tau pathologies in the 3xTg-AD model of Alzheimer’s disease.” Neuroscience (2009) Mar 3, Vol. 159, No. 1, pp. 296-307. Epub 2008 Dec 14.
[42] M.A. Reger, S. T. Henderson, C. Hale, B. Cholerton, L.D. Baker, G.S. Watson, K. Hyde, D. Chapman and S. Craft, “Effects of Beta-hydroxybutyrate on cognition in memory-impaired adults,” Neurobiology of Aging (2004) Vol. 25, No. 3, March, pp. 311-314,
[43] R. Ringseis, C. Dathe, A. Muschick, C. Brandsch and K. Eder, “Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions Oxidized Fat Reduces Milk Triacylglycerol Concentrations by Inhibiting Gene Expression of Lipoprotein Lipase and Fatty Acid Transporters in the Mammary Gland of Rats,” American Society for Nutrition J. Nutr. (2007) Sept., Vol. 137, pp. 2056-2061.
[44] K. Rockwood, “Epidemiological and clinical trials evidence about a preventive role for statins in Alzheimer’s disease.” Acta Neurol Scand Suppl. (2006) Vol. 185, pp. 71-7.
[45] G. Saher, B. Brugger, C. Lappe-Siefke, W. Mobius, R. Tozawa, M.C. Wehr, F. Wieland, S. Ishibashi, and K.A. Nave, “High cholesterol level is essential for myelin membrane growth.” Nat Neurosci (2005) Apr, Vol. 8, No. 4, pp. 468-75. Epub 2005 Mar 27.
[46] A. Solomon, M. Kivipelto, B. Wolozin, J. Zhou, and R.A. Whitmer, “Midlife Serum Cholesterol and Increased Risk of Alzheimer’s and Vascular Dementia Three Decades Later,” Dementia and Geriatric Cognitive Disorders (2009) Vol. 28, pp. 75-80, DOI: 10:1159/000231980.
[47] M. Simons, MD, P. Keller, PhD, J. Dichgans, MD and J.B. Schulz, MD, “Cholesterol and Alzheimer’s disease: Is there a link?” Neurology (2001) Vol. 57, pp. 1089-1093.
[48] L.L. Smith, “Another cholesterol hypothesis: cholesterol as antioxidant,” Free Radic Biol Med. (1991) Vol. 11, No. 1, pp. 47-61.
[49] E. Steen, B.M. Terry, E.J. Rivera, J.L. Cannon, T.R. Neely, R. Tavares, X.J. Xu, J.R. Wands, and S.M. de la Monte “Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer’s disease – is this type 3 diabetes?” Journal of Alzheiner’s Disease (2005) Vol. 7, Number 1, pp. 63-80.
[50] J. Tong, P.P. Borbat, J.H. Freed and Y-K Shin, “A scissors mechanism for stimulation of SNARE-mediated lipid mixing by cholesterol,” PNAS (2009) March 31 Vol. 106, No. 13, pp. 5141-5146.
[51] M-C Vohl, T. A.-M. Neville, R. Kumarathasan, S. Braschi, and D.L. Sparks, “A Novel Lecithin-Cholesterol Acyltransferase Antioxidant Activity Prevents the Formation of Oxidized Lipids during Lipoprotein Oxidation,”Biochemistry (1999) Vol. 38 No. 19, pp. 5976-5981. DOI: 10.1021/bi982258w.
[52] M. Waldman, MD,, 9th International Conference on Alzheimer’s and Parkinson’s Diseases (2009) Abstract 90, Presented March 12-13.
[53] R. West, M.A., M. Schnaider Beeri, Ph.D., J. Schmeidler, Ph.D., C. M. Hannigan, B.S., G. Angelo, M.S., H.T. Grossman, M.D., C. Rosendorff, M.D., Ph.D., and J.M. Silverman, Ph.D., “Better memory functioning associated with higher total and LDL cholesterol levels in very elderly subjects without the APOE4 allele,” Am J Geriatr Psychiatry(2008) September; Vol. 16, No. 9, pp. 781-785. doi: 10.1097/JGP.0b013e3181812790.
[54] A.W.E. Weverling-Rijnsburger, G.J. Blauw, A.M. Lagaay, D.L. Knook, A.E. Meinders, and R.G.J. Westendorp, “Total cholesterol and risk of mortality in the oldest old,” The Lancet, (1997) Vol. 350, No. 9085, pp. 1119-1123,
[55] R.F. Wilson, J.F. Barletta and J.G. Tyburski, “Hypocholesterolemia in Sepsis and Critically Ill or Injured Patients”Critical Care (2003), Vol. 7, pp. 413-414.
[56] S.-C. Zhang and S. Fedoroff, “Neuron-microglia Interactions in Vitro,” Acta Neuropathol (1996) Vol. 91, pp. 385-395.

September 20, 2021 Posted by | Book Review, Science and Pseudo-Science, Timeless or most popular | , , , | Leave a comment

The Simpsons predicted the pandemic, Apocalypse Meow

Club Z Pão

Original image shows the words “Apocalypse Meow” and was present in episode 6 of the 22nd season of the series, entitled “The Fool Monty”, in which a conglomerate of TV channels come together to spread a new deadly virus that would infect the population through cats

September 20, 2021 Posted by | Timeless or most popular, Video | | 3 Comments

Elderly Australian woman knocked down & Pepper-Sprayed by police during protest against lockdowns

RT | September 19, 2021

An elderly woman believed to be in her 70s was attacked by Melbourne police and pepper-sprayed while she was on the ground during a protest against Covid-19 lockdowns on Saturday.

As she held an Australian flag and stood on the road facing toward a group of approaching police, one officer shoved the woman, sending her tumbling to the ground. Another officer then pepper-sprayed the woman as she laid motionless and unable to protect herself.

Seconds after the attack – with the offending officers having already moved on – another group of police officers came to the woman’s aid and attempted to help her up.

Videos of the attack from multiple angles went viral on social media this weekend, with many Australians accusing the Melbourne officers of police brutality.

Australian MP Craig Kelly called the attack “despicable,” “disgusting,” and “ILLEGAL,” and tweeted, “This is not my Australia… We cannot accept Police in Australia pushing to the ground an unarmed 70 yr old woman (or anyone) who presents no threat & then have 2 officers pepper spray the unarmed, defenceless person in the face while on the ground.”

Former New South Wales Senator David Leyonhjelm also condemned the attack, calling the officers “gutless,” while journalist Ky Chow wrote, “I’ve watched several videos of this, and it’s hard to see how the Vic cops defend this.”

Several other incidents of violence between police and protesters broke out during the protest in Melbourne on Saturday and 235 people were reportedly arrested.

Melbourne police were also caught on camera pepper-spraying dozens of other Australians who were involved with the “unauthorized protest.”

Both Melbourne and Sydney have experienced repeated protests over the past few months in response to Covid-19 lockdown restrictions in the two cities. In August, a man from the state of Victoria was sentenced to a maximum of eight months in prison for helping to organize a protest in Sydney, New South Wales.

September 19, 2021 Posted by | Civil Liberties, Subjugation - Torture, Timeless or most popular, Video | , , | 3 Comments

‘Are you undercover?’ Riot cops at Justice for J6 rally detain masked man with a GUN… and a badge

RT | September 19, 2021

Among just four people detained during the remarkably nonviolent Justice for J6 rally in Washington, DC, was an armed man who flashed a badge, raising speculations that he was an ‘undercover fed’ accidentally outed by colleagues.

Despite weeks of constant media reports fueling fears of imminent violence, the Saturday protest proceeded peacefully. It attracted only a few hundred activists – and several times as many police and other law enforcement agents. Authorities reported only a handful of minor disturbances, and a total of four arrests, one of which was particularly curious.

In a video captured by independent journalist Ford Fischer, around half a dozen officers in full riot gear surround a man suspected of carrying a concealed handgun.

“Are you undercover?”, police are heard asking the suspect, as they check his pockets only to find what appears to be a badge. “I’m just here,” he responds when asked again whether he was “undercover” or a “part of the event.”

The man was then escorted away, without being handcuffed or disarmed at the scene, Fischer noted, triggering many speculations about whether he was an undercover fed, an off-duty cop, or if the badge was even real at all.

While the Capitol Police acknowledged the incident in a tweet, they never mentioned the badge.

“The man did have a gun,” police said. “At this time, it is not clear why the man was at the demonstration. Officers charged him with 40 U.S. Code § 5104 – Unlawful activities.”

September 18, 2021 Posted by | Deception, False Flag Terrorism, Timeless or most popular, Video | | Leave a comment