HPV Vaccine leaves ANOTHER teenager chained to a wheelchair for LIFE. By Tracey Watson

HPV-vaccine-young-girl

HPV Vaccine leaves ANOTHER teenager chained to a wheelchair for LIFE
05/01/2019 / By Tracey Watson
https://www.newstarget.com/2019-05-01-hpv-vaccine-leaves-another-teenager-chained-to-a-wheelchair-for-life.html

The human papillomavirus, known as HPV, is an incredibly common sexually transmitted infection. Though just the name HPV strikes fear into the hearts of many, for the most part, it is totally harmless. The CDC’s website notes that, “HPV is so common that nearly all sexually active people get it at some point in their lives.” While the agency warns that HPV can cause genital warts and cervical cancer, and that the vaccine is therefore vitally important, the figures just don’t back that statement up. The CDC’s own statistics show that 79 million Americans are currently infected with HPV, yet only about 100 of these will have genital warts at any given time, and only about 11,000 women are diagnosed with cervical cancer in any given year.

While it is not my intention to diminish the suffering of those 11,000 women in any way, it does seem startling that the CDC is recommending that everybody be vaccinated against a disease that only affects around 0.014 percent of all those infected with the virus – especially when hordes of distraught families have spoken out about the devastating effect this vaccine has had on their children.

One of the affected families is the Beattie family from Wigton, England. Zara Beattie, 13, was once a sporty young girl who loved football, netball and cycling. She now virtually never leaves her bed, and is wheelchair-bound when she does leave home, after suffering a reaction to the Gardasil HPV vaccine back in 2015.

Zara’s mom, Anthea, describes her daughter as an “80-year-old in a teenager’s body.” Zara is unable to stand without feeling faint, has to be homeschooled because she’s simply too exhausted to go to school, and can barely cope with sitting up to have a meal. She also suffers from constant headaches, as well as muscle and joint pain.

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“On a bad day the poor girl can’t even stand up,” Anthea explains. “She will stay in bed all day and crawl to the toilet. She’s got a stool by the sink for when she cleans her teeth.”

What is particularly noteworthy about this story is that Anthea is a nurse who has practiced for over 30 years. This really is one of medicine’s own speaking out against a procedure she obediently subjected her daughter to because she believed in the system. The entire family will now have to live with that decision for the rest of their lives.

Zara has been diagnosed with a condition called postural orthostatic tachycardia syndrome (PoTS), but her doctors at the University of Newcastle Royal Victoria Infirmary, while staunchly insisting that the vaccine didn’t cause her illness, have been unable to come up with a viable alternative cause.

Doctors claim that around 400 lives are saved each year because of the HPV vaccines Gardasil and Cervarix. That figure looks dubious when one considers the overall HPV statistics, but even if their claim is true, it fails to take into account all the damage the vaccine also causes.

At least 44 girls have died from these vaccines, and more than 15,000 have reported adverse effects, including seizures, blood clots, lupus, brain inflammation and Guillain-Barré syndrome. (RELATED: Lead developer of HPV vaccine admits it’s a giant, deadly scam.)

In Ireland, more than 200 teenagers have reported “acute physical side-effects” after being given the HPV vaccine at their schools.

In Denmark, one of the country’s national television stations, TV2, aired a documentary entitled The Vaccinated Girls – Sick and Betrayed, which revealed that many young girls had developed severe health problems after being vaccinated against HPV.

And in Japan, dozens of teenage girls injured by the toxic HPV vaccine have filed suit against both the government and the drug companies who produce the vaccine.

How many more young girls and their families will have to suffer before these governments stop focusing on lining the pockets of Big Pharma, and start focusing on protecting the people under their care?

Sources include:

DailyMail.co.uk

NaturalNews.com

NaturalNews.com

CDC.gov

Is this depopulation bioweapon experiment?

Woman-Doctor-Sick-Whooping-Cough
“Mystery virus” spreading like wildfire across U.S. population, putting people in bed for a MONTH… is this a depopulation bioweapon experiment?

01/11/2019 / By Isabelle Z.

A cough can be rather annoying, especially when it keeps you up at night, but you can usually take comfort from knowing that it tends to run its course rather quickly and you’ll be back to normal in no time. Unfortunately, a new virus is going around that is turning what is normally a week-long nuisance into a month-long nightmare – and speculation abounds regarding its origin.

Physicians around the nation are reporting a spike in cases of people suffering from a very unusual cough. It’s caused by a virus and it’s lasting anywhere from four to six weeks – and in some cases, even longer.

One doctor, Texas Health Dallas’s Dr. Gary Gross, says he has been seeing at least a patient a day suffering from the virus, and he lamented the fact that it lasts so long without seeming to get better.

Dr. Gross told CBS DFW that the virus has no quick fix. Patients have no choice but to let it run its course, although some medications can help soothe the cough somewhat. Patients are advised to get plenty of sleep as well as lots of fluids.

Emergency medicine specialists in Cincinnati have warned the public about the virus, which they say has caused a surge in patients presenting with upper respiratory symptoms such as a cough, congestion, and shortness of breath.

Bethesda North Hospital’s Dr. Kenneth Patton describes the difficulties patients with the virus experience in breathing, saying: “They are retracting, their ribs are doing a lot of work. You can see their neck muscles, you can really see that they are having a hard time breathing.”

Patients’ biggest complaint, however, is the duration, with many people stuck in bed for weeks. Avoiding the virus is a matter of washing your hands frequently and keeping your distance from people who are sick. Once you get it, however, you’ll simply have to wait it out.
What is the source of this virus?

bill_collage

Naturally, any time a new virus like this emerges seemingly out of nowhere, it’s hard not to wonder if it could be part of a depopulation bioweapon experiment.

Plant Pathology Professor Dr. Cyril Broderick has stated his belief that the Ebola virus was manufactured and then released intentionally in Africa as a weaponized virus. Other experts agreed with his theory. Meanwhile, in the wake of the Zika outbreak, governments in Latin America urged women to avoid pregnancy because of the potential for birth defects.

The idea that depopulation efforts are underway is bolstered by the ongoing push toward reducing human populations in the name of somehow saving the planet from “global warming” and the testing of vaccines and experimental drugs in African nations. Influential names like Bill Gates have openly declared that reducing the human population could help “save” the planet, and The New York Times recently printed an editorial arguing that the end of humanity would actually be a good thing for the planet.

There’s also the fact that pharmaceutical companies have a lot to gain in the wake of such outbreaks by developing new vaccines and drugs. In fact, a team of researchers at California’s Scripps Research Institute have engineered a deadly new bird flu strain that can infect humans on the pretense of learning what such a virus could do in order to prepare for it. The mutations they’ve created allow the virus to make its way into human lung cells. What could possibly go wrong?

When you pay attention to everything that is going on in the world today, it’s not a stretch to question whether depopulation efforts are behind viruses that emerge mysteriously and suddenly affect a significant number of people.

Sources for this article include:

DFW.CBSLocal.com

KUTV.com

NaturalNews.com

Dirty electricity in the home threatens human health

Dirty electricity in the home threatens human health
https://www.naturalhealth365.com/dirty-electricity-emf-2822.html
Posted by: Lloyd Burrell in EMF Pollution, Natural Personal Care December 31, 2018 0 Comments

What if electromagnetic or EMF pollution wasn’t strictly a wireless technology problem? Well, it turns out that dirty electricity – mainly caused by the electrical wires in your home – can cause serious health issues like, migraines, poor brain function and, even, contribute to cancer cell growth.

This is clearly a much more serious health concern – almost never addressed by the mainstream media. Bottom line: wouldn’t you want to know if the electrical supply that powers your home was a major source of electrical pollution and the cause of health problems?

As a little background, the standard electrical frequency – that is in North American homes and offices – is 60 hertz. This is what’s used to operate our TVs, cookers, refrigerators, washing machines and lights.

But, increasingly so, there are a large number of other electrical frequencies that can be found on our wiring. These frequencies are known as ‘high frequency voltage transients.’ The problem is these high frequencies are believed to cause a number of serious health problems.

Hence, these high frequencies have earned the name, ‘dirty electricity’.

Where can I find dirty electricity inside the home?
A major source of dirty electricity is the electronic devices that are in our homes and in the homes of our neighbors.

Dave Stetzer, a leading expert on dirty electricity, and other scientists, have found that these high frequency voltages come from our computers, printers, copiers, TVs, game consoles, tube fluorescent lights, compact florescent light bulbs, dimmer light switches, variable speed motors, treadmills, vacuum cleaners, sewing machines, wind turbines, solar energy inverters, smart meters, and other electronic devices.

Many modern electronic devices add high frequency transients to our home electrical wiring.

Dirty electricity can also be caused by arcing on power lines during storms when lines touch trees. It can also be created from unfiltered cell phone and broadcast frequencies from nearby antennas.

The rarely spoken truth about premature aging and death
Leading epidemiologist Samuel Milham, MD, MPH – who has studied this subject in detail and even wrote a book on it – believes that these exposures coupled with the proliferation of wireless technology mean that “we may be facing a looming epidemic of morbidity and mortality”.

Dirty electricity in electrical wiring has been linked to many serious diseases and health conditions, including:

Cancer
Multiple Sclerosis
Elevated blood sugar
Obesity
Migraine headaches
Attention deficit disorders
Asthma
Chronic fatigue syndrome
Multiple chemical sensitivities
Miscarriages
Infertility
Depression and suicide
How is dirty electricity created inside the homes?
Most modern electronic devices now use Direct Current (DC) power. These devices are equipped with switch-mode power supply (SMPS) converters that convert the alternating electrical current (AC) from the wall outlets into DC current.

These SMPS converters can create dirty electricity – which are then added to our electrical wires. These converters can often be found in rectangular boxes in surge protector strips or on larger electronic devices. And, they may be built into the equipment.

Let’s talk about the worst offenders.

Compact florescent light (CFL) bulbs are believed to be among the worst contributors to dirty electricity.

They use ‘pulsed electronic technology.’

These new bulbs, unlike the old incandescent variety, switch on and off some 20,000 times per second. And, it’s this switching activity, which breaks up the normal 60-hertz sine wave of electrical power into fragments, returns the unused electrical fragments to the electrical system and thereby creates dirty electricity.

Compact florescent light bulbs add pollution to house and office wiring in the 50 to 100 KHZ range. One CFL bulb can contaminate the electrical system of an entire house when it’s in use.

The mainstream media continue to ignore the ‘biological effects’ of dirty electricity
Dr. Magda Havas, of Trent University, in Canada has been studying the biological effects of high frequency voltage transients and similar forms of electromagnetic pollution since the early 1990s. She says:

“Most of the research on the biological effects of nonionizing radiation is done at one of two frequency ranges: extremely low frequency associated with electricity (50/60 Hz) and radio frequency associated with wireless telecommunication devices (800 MHz to 2.5 GHz range).

An intermediate frequency range [high frequency voltage transients], at the low end of the RF spectrum (kHz), flows along and radiates from wires and thus has characteristics of the two major types of electromagnetic pollution mentioned above.

Scientists doing research on the biological effects of power line frequencies seldom measure this frequency range and thus ignore the effects it might have on health.”

How can electricity in a wire be a health risk?
First, there is the issue of ground current. According to Dave Stetzer ground current has become a major problem in the U.S. since 1992 when the electric utility companies started using the earth, the ground we walk on, as if it was an electric wire.

Previously utility companies used a neutral wire to return unused electricity to their substations.

Since 1992, energy companies have decided to just run wires down the side of electrical poles into the ground.

In North America ground current is now practically everywhere. These dangers are compounded by the presence of large amounts of dirty electricity – which flow through the ground and our electrical wiring.

Dirty electricity does not stay in your wiring. It manifests the skin effect.

It travels on the outer skin of the wire and can easily radiate through walls into our living spaces and our bodies.

Great tips on protecting your health
Here are some simple ways to reduce your exposure to dirty electricity:

1. Eliminate/minimize the use of these devices in your home.
2. Replace dimmer switches with on/off switches.
3. Replace CFLs with traditional light bulbs.
4. Replace smart (utility) meters with an analog meter.
5. Eliminate/minimize use of any device susceptible to be equipped with a SMPS converter.

To deal with this issue effectively you need to measure the dirty electricity levels in your home and install dirty electricity filters if the readings are above 50 GS units. GS units are measured with a Graham micro-surge meter.

For more tips on reducing your dirty electricity exposures – learn how to use a GS filter.

What is the correlation between electricity and disease?
Dr. Milham studied U.S. vital statistics and census records for 1920–1960. He found that urban death rates were much higher than rural rates for a number of diseases including cardiovascular diseases, diabetes and suicide.

He believes that many of these diseases could be prevented today if appropriate steps were taken to reduce the harmful effects of ground current, dirty electricity and radiation from cell phones, cell towers and the like.

Governmental agencies, utility companies and corporations who create electrical products continue to underestimate and often downplay the potential harm of electromagnetic fields.

Get smart before it’s too late. Act now to take steps to protect your health from dirty electricity and other EMF exposures.

About the author: Lloyd Burrell is the founder of ElectricSense.com. His website offers solutions to the growing number of people whose health is being compromised by exposure to wireless and similar technologies. Download his free EMF Health Report today!

ANTI-AGEING BREAKTHROUGH: Ageing process REVERSED in human cells for first time SCIENTISTS have successfully reversed the process of ageing in cells for the first time in a move which could help beat the likes of Alzheimer’s and dementia

ANTI-AGEING BREAKTHROUGH: Ageing process REVERSED in human cells for first time
SCIENTISTS have successfully reversed the process of ageing in cells for the first time in a move which could help beat the likes of Alzheimer’s and dementia.
By Sean Martin
PUBLISHED: 10:54, Tue, Aug 14, 2018 | UPDATED: 12:03, Tue, Aug 14, 2018
https://www.express.co.uk/news/science/1002867/science-news-Ageing-process-REVERSED-human-cells-University-of-Exeter

//players.brightcove.net/2540076170001/BkgUZbYn2M_default/index.html?videoId=5816751026001#t=46s

Scientists reveal new reverse ageing method tested on mice

Many people hope to reverse the process of ageing in a bid to remain healthier and live longer or ultimately to live forever.

And now researchers have made a breakthrough.

As the body ages, it loses its ability to control how genes are regulated and they ultimately become more damaged until we ultimately die.

A gene is activated by signals from inside or outside the cell to make a molecular message known as RNA.
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The decision on which type of ‘message’ is created by a group of around 300 proteins is known as “splicing factors”.

However, as we get older the amount of splicing factors the proteins are able to make steadily decreases.

Older cells are then ultimately less able to turn genes on and off to react to the environment which makes us more vulnerable to diseases which ultimately kill us off.

However, researchers have found a way to turn splicing factors back on.


SCIENCE BREAKTHROUGH: Ageing process REVERSED in human cells for first time (Image: GETTY)
Professor Dongsheng Cai explains his work in ageing research
//players.brightcove.net/2540076170001/SJletUlwOz_default/index.html?videoId=5522349415001#t=1s
Lorna Harries, Associate Professor in Molecular Genetics and Matt Whiteman, Professor of Experimental Therapeutics, both at University of Exeter, write for the Conversation: “In our new work, we showed that by treating old cells with a chemical that releases small amounts of hydrogen sulphide, we were able to increase levels of some splicing factors, and to rejuvenate old human cells.

“Hydrogen sulphide is a molecule that is found naturally in our bodies and has been shown to improve several features of age-related disease in animals.

“But it can be toxic in large amounts, so we needed to find a way to deliver it directly to the part of the cell where it is needed.

“By using a ‘molecular postcode’ we have been able to deliver the molecule directly to the mitochondria, the structures that produce energy in cells, where we think it acts, allowing us to use tiny doses, which are less likely to cause side effects.”

Who Ya Gonna Call Before August 16 to Complain about 4G and 5G Small Cell Towers Being Installed in Front of Homes, etc.? The Senate Commerce, Science and Transportation Committee


Who Ya Gonna Call Before August 16 to Complain about 4G and 5G Small Cell Towers Being Installed in Front of Homes, etc.? The Senate Commerce, Science and Transportation Committee (Contact Info Provided).

https://www.activistpost.com/2018/08/call-before-august-16-complain-4g-5g-towers-contact-list.html

August 8, 2018

By B.N. Frank

Big Thanks to all EMF activists for providing so much information to Activist Post so we can pass it on to readers who also want to stop the widespread “Roll Out” of risky 5G technology and other Telecom Industry, FCC, and other elected officials’ nonsense.

Since 2004, The International Association of Firefighters has opposed the use of their stations as base stations for cell towers and antennas until it can be proven that this is NOT hazardous to their health. So why would any of the rest of us be okay with allowing small cell towers to be installed in front of our homes, in public rights-of-ways, and everywhere else? This violates “The Precautionary Principle.”

In addition to contacting your local, state, and federal elected officials ASAP, a list of senate committee members and their contact information is posted at the end of this article. Please contact them before August 16.

With a little luck, we can help it out. We can make this whole damn thing work out.

Here’s the deal as relayed via excerpts from an article posted by Radio + TV Business Report:

On Aug, 16 the Federal Communications Commission (FCC) has an oversight hearing which will be conducted by Senate Commerce, Science and Transportation Committee.

According to Committee Chairman John Thune (R-S.D.)

The hearing, the Committee notes, will examine policy issues before the Commission and review the FCC’s ongoing duties and activities. This includes efforts to better utilize spectrum powering our wireless economy to expanding rural broadband access, combatting robocalls, and reviewing the media landscape.

(A little more background):

For several hours on July 25, the four voting members of the FCC answered questions and, in a handful of instances, sparred with House of Representatives members who wanted assurances that the White House would not sway the Commission on its decision to send Sinclair Broadcast Group‘s intended merger with Tribune Media to an Administrative Law Judge.

Because of this, the FCC Four went to the Senate side of Capitol Hill for an oversight hearing that was conducted by Senate Commerce, Science and Transportation Committee one day later than originally planned.

On July 30, the committee announced that it would convene its hearing on August 15 at 10:15am. However, now it’s been pushed back again and will be held on August 16 at 10am at Russell Senate Office Building, Room 253.

Witness testimony, opening statements, and a live video of the hearing will be available on http://www.commerce.senate.gov.

The following list of committee members and their contact information was provided by EMF activists. Websites are not working for some officials and this has been noted next to their names. Please contact some or all of them before August 16 and let them know how you feel about all of this:

Committee on Commerce, Science, and Transportation

https://www.commerce.senate.gov/public/index.cfm/committeemembers

Contact Information for the Committee Full Committee Office
Majority: 202-224-1251
Majority Address: 512 Dirksen Senate Building; Washington DC, 20510
Minority: 202-224-0411

MAJORITY MEMBERS:

1. CHAIRMAN: Senator John Thune, South Dakota
Washington D.C. Office
United States Senate SD-511
Washington, DC 20510
Phone: (202) 224-2321
Fax: (202) 228-5429
Toll-Free: 1-866-850-3855
EMAIL FORM: https://www.thune.senate.gov/public/index.cfm/contact

2. Senator Roger Wicker Mississippi
Washington, D.C.
555 Dirksen Senate Office Building
Washington, DC 20510
Main: (202) 224-6253
Fax: (202) 228-0378
EMAIL FORM https://www.wicker.senate.gov/public/index.cfm/contact

3. Senator Roy Blunt Missouri
Washington, D.C.
260 Russell Senate Office Building
Washington, DC 20510
Phone: (202) 224-5721
EMAIL CONTACT FORM: https://www.blunt.senate.gov/public/index.cfm/contact-roy

4. Senator Ted Cruz Texas
WASHINGTON, D.C.
(202) 224-5922
404 Russell
Washington, DC 20510
EMAIL: https://www.cruz.senate.gov/?p=form&id=16

5. Senator Deb Fischer Nebraska
Washington D.C.
454 Russell Senate Office Building
Washington, DC 20510
Phone: (202) 224-6551
Fax: (202) 228-1325
EMAIL: https://www.fischer.senate.gov/public/?p=email-deb

6. Senator Jerry Moran Kansas
Washington, D.C.
Dirksen Senate Office Building
Room 521
Washington, D.C. 20510
Phone: (202) 224-6521
Fax: (202) 228-6966
https://www.moran.senate.gov/public/index.cfm/e-mail-jerry

7. Senator Dan Sullivan Alaska
WASHINGTON, D.C.
702 Hart Senate Office Building
Washington, DC 20510
Phone: (202)-224-3004
Fax: (202)-224-6501
https://www.sullivan.senate.gov/contact/email

8. Senator Dean Heller Nevada
Washington, DC
324 Hart Senate Office Building
Washington, DC 20510
Phone: 202-224-6244
Fax: 202-228-6753
https://www.heller.senate.gov/public/index.cfm/contact-form

9. Senator Jim Inhofe Oklahoma (site down)

10. Senator Mike Lee Utah (site down)

11. Senator Ron Johnson Wisconsin
328 Hart Senate Office Building
Washington, DC 20510
Phone: (202) 224-5323
Fax: (202) 228-6965
https://www.ronjohnson.senate.gov/public/index.cfm/email-the-senator

12. Senator Shelley Moore Capito West Virginia

13. Senator Cory Gardner Colorado
Washington, D.C.
354 Russell
Senate Office Building
Washington, DC 20510
P: (202) 224-5941
F: (202) 224-6524
https://www.gardner.senate.gov/contact-cory/email-cory

14. Senator Todd Young Indiana (site down)

MINORITY MEMBERS:

1. Ranking Member Bill Nelson Florida
WASHINGTON, DC OFFICE
United States Senate
716 Senate Hart Office Building
Washington, DC 20510
Phone: 202-224-5274
Fax: 202-228-2183
https://www.billnelson.senate.gov/contact-bill

2. Senator Maria Cantwell Washington
Washington, DC
511 Hart Senate Office Building
Washington, DC 20510
Phone: (202) 224-3441
Fax: (202) 228-0514
https://www.cantwell.senate.gov/contact/email

3. Senator Amy Klobuchar Minnesota
Washington, DC
302 Hart Senate Office Building
Washington, DC 20510
phone: 202-224-3244
fax: 202-228-2186
https://www.klobuchar.senate.gov/public/index.cfm/email-amy

4. Senator Richard Blumenthal Connecticut
https://www.blumenthal.senate.gov/contact
Washington D.C.
706 Hart Senate Office Bldg.
Washington, DC, 20510
tel (202) 224-2823
fax (202) 224-9673

5. Senator Brian Schatz Hawaii
722 HART SENATE OFFICE BUILDING
WASHINGTON, DC 20510
PHONE: (202) 224-3934
FAX: (202) 228-1153
https://www.schatz.senate.gov/contact

6. Senator Ed Markey Massachusetts
Washington, D.C.
255 Dirksen Senate Office Building
Washington, D.C. 20510
202-224-2742
https://www.markey.senate.gov/contact

7. Senator Tom Udall New Mexico
Washington/Capitol Hill
531 Hart Senate Office Building
Washington DC, 20510
(202) 224-6621
https://www.tomudall.senate.gov/contact/email-tom

8. Senator Gary Peters Michigan
Hart Senate Office Building
Suite 724
Washington, DC 20510
(202) 224-6221
https://www.peters.senate.gov/contact/email-gary

9. Senator Tammy Baldwin Wisconsin (site down)

10. Senator Tammy Duckworth Illinois (site down)

11. Senator Maggie Hassan New Hampshire (site down)

12. Senator Catherine Cortez Masto Nevada (site down)

13. Senator Jon Tester Montana (site down)

There is no end to what we can do together. There is no end.

Free ebook How To Survive the Job Automation Apocalypse
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Sick pelicans showing up along Southern California coast By The Associated Press (Gasp! OMG! How shocking that any are still alive at all. Fukushima is still melting down, like Ddduuuuhhhhh!)


FILE–In this April 28, 2018, file photo, made from video provided by Pepperdine University, shows one of a pair of pelicans crashing a graduation ceremony at Pepperdine University in Malibu, Calif. The wildlife organization, International Bird RescuThe Associated Press

Sick pelicans showing up along Southern California coast
By The Associated Press
LOS ANGELES — May 10, 2018, 5:00 PM ET

FILE–In this April 28, 2018, file photo, made from video provided by Pepperdine University, shows one of a pair of pelicans crashing a graduation ceremony at Pepperdine University in Malibu, Calif. The wildlife organization, International Bird Rescue, said Thursday, May 10, 2018, that there’s been a surge in the number of sick and dying brown pelicans along the Southern California coast in the past week. (Grant Dillion/Pepperdine University via AP, file)
more +

A wildlife organization says there’s been a surge in the number of sick and dying brown pelicans along the Southern California coast in the past week.

International Bird Rescue said Thursday that more than 25 pelicans have been brought to its wildlife center in the San Pedro district of Los Angeles.

The big birds are showing signs of emaciation, hypothermia and anemia. The organization did not cite a cause.

Wildlife center manager Kylie Clatterbuck says it’s normal to receive recently fledged baby pelicans this time of year but the current wave includes many second-year birds.

The organization says there are many cases of pelicans landing on city streets, residential yards and airport runways.

A well-publicized incident occurred April 28 when two pelicans landed at Pepperdine University’s graduation ceremony in Malibu.

———

Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly. In fact, “high LDL-C may be protective is in accordance with the finding that LDL-C is lower than normal in patients with acute myocardial infarction”.


Cardiovascular medicine
Research
Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review
http://bmjopen.bmj.com/content/6/6/e010401.full?sid=cfb00014-f0a8-407d-ae71-a3278160ca49

Uffe Ravnskov1, David M Diamond2, Rokura Hama3, Tomohito Hamazaki4, Björn Hammarskjöld5, Niamh Hynes6, Malcolm Kendrick7, Peter H Langsjoen8, Aseem Malhotra9, Luca Mascitelli10, Kilmer S McCully11, Yoichi Ogushi12, Harumi Okuyama13, Paul J Rosch14, Tore Schersten15, Sherif Sultan6, Ralf Sundberg16
Author affiliations
Abstract

Objective It is well known that total cholesterol becomes less of a risk factor or not at all for all-cause and cardiovascular (CV) mortality with increasing age, but as little is known as to whether low-density lipoprotein cholesterol (LDL-C), one component of total cholesterol, is associated with mortality in the elderly, we decided to investigate this issue.

Setting, participants and outcome measures We sought PubMed for cohort studies, where LDL-C had been investigated as a risk factor for all-cause and/or CV mortality in individuals ≥60 years from the general population.

Results We identified 19 cohort studies including 30 cohorts with a total of 68 094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found.

Conclusions High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

http://dx.doi.org/10.1136/bmjopen-2015-010401
Statistics from Altmetric.com
Article has an altmetric score of 1664

Strengths and limitations of this study

This is the first systematic review of cohort studies where low-density lipoprotein cholesterol (LDL-C) has been analysed as a risk factor for all-cause and/or cardiovascular mortality in elderly people.

Lack of an association or an inverse association between LDL-C and mortality was present in all studies.

We may not have included studies where an evaluation of LDL-C as a risk factor for mortality was performed but where it was not mentioned in the title or in the abstract.

We may have overlooked relevant studies because we have only searched PubMed.

Minor errors may be present because some of the authors may not have adjusted LDL-C by appropriate risk factors.

Some of the participants with high LDL-C may have started statin treatment during the observation period and, in this way, may have added a longer life to the group with high LDL-C and some of them may have started with a diet able to influence the risk of mortality.

We may have overlooked a small number of relevant studies because we only searched papers in English.

Introduction
Rationale

For decades, the mainstream view has been that an elevated level of total cholesterol (TC) is a primary cause of atherosclerosis and cardiovascular disease (CVD). There are several contradictions to this view, however. No study of unselected people has found an association between TC and degree of atherosclerosis.1 Moreover, in most of the Japanese epidemiological studies, high TC is not a risk factor for stroke, and further, there is an inverse association between TC and all-cause mortality, irrespective of age and sex.2

In a recent meta-analysis performed by the Prospective Studies Collaboration, there was an association between TC and CV mortality in all ages and in both sexes.3 However, even in this analysis, the risk decreased with increasing age and became minimal after the age of 80 years. Since atherosclerosis and CVD are mainly diseases of the elderly, the cholesterol hypothesis predicts that the association between CV mortality and TC should be at least as strong in the elderly as in young people. There may be a confounding influence in these studies, however, because TC includes high-density lipoprotein cholestrol (HDL-C), and multiple studies have shown that a high level of HDL-C is associated with a lower risk of CVD.
Objectives

We examined the literature assessing low-density lipoprotein cholesterol (LDL-C) as a risk factor for mortality in elderly people. Since the definition of CVD varies considerably in the scientific literature, we have chosen to focus on the association between LDL-C and all-cause and CVD mortality, because mortality has the least risk of bias among all outcome measures. If Goldstein and Brown’s recent statement that LDL-C is ‘the essential causative agent’ of CVD4 is correct, then we should find that LDL-C is a strong risk factor for mortality in elderly people.


Methods
Search strategy

UR and RS searched PubMed independently from initial to 17 December 2015. The following keywords were used: ‘lipoprotein AND (old OR elderly) AND mortality NOT animal NOT trial’. We also retrieved the references in the publications so as not to miss any relevant studies. The search was limited to studies in English.
Inclusion and exclusion criteria

All included studies should meet the following criteria: the study should be a cohort study of people aged 60 years or older selected randomly from the general population, or a study where the authors had found no significant differences between the participants and the source population’s demographic characteristics. The studies should include an initial assessment of LDL-C levels, the length of the observation time and information about all-cause and/or cardiovascular mortality at the end of follow-up. The studies should also include information about the association between LDL-C and all-cause and/or CVD mortality. We excluded studies that did not represent the general population (eg, case–control studies; case reports; studies that included patients only); studies where data about elderly people were not given separately, and studies without multivariate correction for the association between LDL-C and all-cause and/or CV mortality. We accepted studies where the authors had excluded patients with serious diseases or individuals who had died during the first year.
Study selection, data items and extraction

Studies where the title or abstract indicated that they might include LDL-C data of elderly people, were read in full, and the relevant data were extracted by at least three of the authors, for example, year of publication, total number of participants, sex, length of observation time, exclusion criteria, LDL-C measured at the start and the association between initial LDL-C and risk of all-cause and/or at follow-up. When more than one adjusted HR was reported, the HR with the most fully adjusted model was selected.

Quality assessment

The design of the study satisfies almost all points of reliability and validity according to the Newcastle Ottawa Scale as regards selection, comparability and exposure.5 Thus, all studies represented elderly people only; ascertainness of exposure (eg, measurement of LDL-C) was present in all studies, and outcome was unknown at the start. It can be questioned if all of the studies represented the general population because, as shown below, in some of them various types of disease groups were excluded.

Results
Study selection

Our search gave 2894 hits. We excluded 160 studies, which were not in English, and 2452 studies because, judged from the abstract, it was obvious that they were irrelevant.

The rest of the papers were read in full; 263 of these studies were excluded for the following reasons: (1) the participants did not represent the general population; (2) LDL-C was not measured at the start; (3) follow-up information was not given for the elderly separately; or (4) no information was present about mortality during the observation period (figure 1). One of the studies6 was excluded because it included the same individuals as in a previous study.7
Figure 1

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Figure 1

Flow Chart. CV, cardiovascular; LDL-C, low-density lipoprotein cholesterol.
Study characteristics

The remaining 19 studies including 30 cohorts with a total of 68 094 participants met the inclusion criteria (figure 1). All-cause mortality was recorded in 28 cohorts. In 16 of these cohorts (representing 92% of the individuals), the association was inverse and with statistical significance in 14; in 1 of the cohorts, the association was mirror-J-formed with the lowest risk in the highest quartile; in the rest of the papers, no association was found. CV mortality was recorded in nine cohorts; in one of them, the association was almost U-shaped with the lowest risk in the highest quartile (curvilinear fit: p=0.001); in one of them, the association was mirror-J-formed and also with the lowest risk in the highest quartile (curvilinear fit: p=0.03); in the other seven cohorts, no association was found (table 1).

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Table 1

Association between LDL-C and all-cause mortality and CVD mortality, respectively, in 19 studies including 30 cohorts with 68 094 individuals from the general population above the age of 60 years
Risk of bias across studies

One explanation for the increased risk of mortality among people with low cholesterol is that serious diseases may lower cholesterol soon before death occurs. Evidence to support this hypothesis may be obtained from 10 of the studies in which no exclusions were made for individuals with terminal illnesses. However, in four of the studies, participants with a terminal illness or who had died during the first observation year were excluded. In one of those studies,8 LDL-C was not associated with all-cause mortality; in the three others,16 ,20 ,24 which included more than 70% of the total number of participants in our review, LDL-C was inversely associated with all-cause mortality and with statistical significance. Thus, there is little support for the hypothesis that our analysis is biased by end of life changes in LDL-C levels.

It is also potentially relevant that all studies did not correct for the same risk factors, and some of them did not inform the reader about which risk factors they corrected for. However, taking all studies together, 50 different risk factors were corrected for in the Cox analyses (table 2).

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Table 2

Factors corrected for in the multifactorial analyses of each study

It is worth considering that some of the participants with high LDL-C may have started statin treatment during the observation period. Such treatment may have increased the lifespan for the group with high LDL-C. However, any beneficial effects of statins on mortality would have been minimal because most statin trials have had little effect on CVD and all-cause mortality, with a maximum reduction of mortality of two percentage points. It is therefore relevant that the 4-year mortality among those with the highest LDL-C in the included cohorts was up to 36% lower than among those with the lowest LDL-C. Furthermore, in the largest study20 that included about two-thirds of the total number of participants in our study, the risk was lower among those with the highest LDL-C than among those on statin treatment.

It is also possible that those with the highest LDL-C were put on a different diet than those with low LDL-C. However, this potential bias in mortality outcomes could have gone in both directions. Some of the individuals with high LDL-C may have followed the official dietary guidelines and exchanged saturated fat with vegetable oils rich in linoleic acid. In a recent study, the authors reported that among participants who were older than 65 at baseline, a 30 mg/dL decrease in serum cholesterol was associated with a higher risk of death (HR 1.35, 95% CI 1.18 to 1.54).26 If applied to the general population, this finding suggests that the conventional dietary treatment for high cholesterol with vegetable oil replacing saturated fat may actually increase mortality in those individuals with high LDL-C. Thus, the lack of an association between LDL-C and mortality may have been even stronger than reported since the dietary intervention may have been counterproductive.

Finally, it is potentially relevant that we limited our literature search to PubMed. In preliminary searches with PubMed, OVID and EMBASE, we identified 17 relevant studies in PubMed, but only 2 in OVID and EMBASE, and these 2 studies were found in PubMed as well. Therefore, it is highly unlikely that there are studies with findings with divergent results from those we have reported here, as all of them reported either no association or an inverse association between LDL-C and mortality.
Discussion

Assessments of the association between serum cholesterol and mortality have been studied for decades, and extensive research has shown a weak association between total cholesterol and mortality in the elderly; several studies have even shown an inverse association. It is therefore surprising that there is an absence of a review of the literature on mortality and levels of LDL-C, which is routinely referred to as a causal agent in producing CVD4 and is a target of pharmacological treatment of CVD.

Our literature review has revealed either a lack of an association or an inverse association between LDL-C and mortality among people older than 60 years. In almost 80% of the total number of individuals, LDL-C was inversely associated with all-cause mortality and with statistical significance.

These findings provide a paradoxical contradiction to the cholesterol hypothesis. As atherosclerosis starts mainly in middle-aged people and becomes more pronounced with increasing age, the cholesterol hypothesis would predict that there should be a cumulative atherosclerotic burden, which would be expressed as greater CVD and all-cause mortality, in elderly people with high LDL-C levels.

Our results raise several relevant questions for future research. Why is high TC a risk factor for CVD in the young and middle-aged, but not in elderly people? Why does a subset of elderly people with high LDL-C live longer than people with low LDL-C? If high LDL-C is potentially beneficial for the elderly, then why does cholesterol-lowering treatment lower the risk of cardiovascular mortality? In the following we have tried to address some of these questions.
Inverse causation

A common argument to explain why low lipid values are associated with an increased mortality is inverse causation, meaning that serious diseases cause low cholesterol. However, this is not a likely explanation, because in five of the studies in table 1 terminal disease and mortality during the first years of observation were excluded. In spite of that, three of them showed that the highest mortality was seen among those with the lowest initial LDL-C with statistical significance.18 ,20 ,24
Is high LDL-C beneficial?

One hypothesis to address the inverse association between LDL-C and mortality is that low LDL-C increases susceptibility to fatal diseases. Support for this hypothesis is provided by animal and laboratory experiments from more than a dozen research groups which have shown that LDL binds to and inactivates a broad range of microorganisms and their toxic products.27 Diseases caused or aggravated by microorganisms may therefore occur more often in people with low cholesterol, as observed in many studies.28 In a meta-analysis of 19 cohort studies, for instance, performed by the National Heart, Lung and Blood Institute and including 68 406 deaths, TC was inversely associated with mortality from respiratory and gastrointestinal diseases, most of which are of an infectious origin.29 It is unlikely that these diseases caused the low TC, because the associations remained after the exclusion of deaths occurring during the first 5 years. In a study by Iribarren et al, more than 100 000 healthy individuals were followed for 15 years. At follow-up, those whose initial cholesterol level was lowest at the start had been hospitalised significantly more often because of an infectious disease that occurred later during the 15-year follow-up period.30 This study provides strong evidence that low cholesterol, recorded at a time when these people were healthy, could not have been caused by a disease they had not yet encountered.

Another explanation for an inverse association between LDL-C and mortality is that high cholesterol, and therefore high LDL-C, may protect against cancer. The reason may be that many cancer types are caused by viruses.31 Nine cohort studies including more than 140 000 individuals followed for 10–30 years have found an inverse association between cancer and TC measured at the start of the study, even after excluding deaths that occurred during the first 4 years.32 Furthermore, cholesterol-lowering experiments on rodents have resulted in cancer,33 and in several case–control studies of patients with cancer and controls matched for age and sex, significantly more patients with cancer have been on cholesterol-lowering treatment.32 In agreement with these findings, cancer mortality is significantly lower in individuals with familial hypercholesterolaemia.34

That high LDL-C may be protective is in accordance with the finding that LDL-C is lower than normal in patients with acute myocardial infarction. This has been documented repeatedly without a reasonable explanation.35–37 In one of the studies,37 the authors concluded that LDL-C evidently should be lowered even more, but at a follow-up 3 years later mortality was twice as high among those whose LDL-C had been lowered the most compared with those whose cholesterol was unchanged or lowered only a little. If high LDL-C were the cause, the effect should have been the opposite.
Conclusions

Our review provides the first comprehensive analysis of the literature about the association between LDL-C and mortality in the elderly. Since the main goal of prevention of disease is prolongation of life, all-cause mortality is the most important outcome, and is also the most easily defined outcome and least subject to bias. The cholesterol hypothesis predicts that LDL-C will be associated with increased all-cause and CV mortality. Our review has shown either a lack of an association or an inverse association between LDL-C and both all-cause and CV mortality. The cholesterol hypothesis seems to be in conflict with most of Bradford Hill’s criteria for causation, because of its lack of consistency, biological gradient and coherence. Our review provides the basis for more research about the cause of atherosclerosis and CVD and also for a re-evaluation of the guidelines for cardiovascular prevention, in particular because the benefits from statin treatment have been exaggerated.38–40
Acknowledgments

The study has been supported by a grant from Western Vascular Institute.
References


Ravnskov U. Is atherosclerosis caused by high cholesterol? QJM 2002;95:397–403. doi:10.1093/qjmed/95.6.397
FREE Full TextGoogle Scholar

Hamazaki T, Okuyama H, Ogushi Y, et al. Towards a paradigm shift in cholesterol treatment—a re-examination of the cholesterol issue in Japan. Ann Nutr Metab 2015;66(Suppl 4):1–116. doi:10.1159/000381654
Google Scholar

Lewington S, Whitlock G, Clarke R, et alProspective Studies CollaborationLewington S, Whitlock G, Clarke R, et al. Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths. Lancet 2007;370:1829–39. doi:10.1016/S0140-6736(07)61778-4
CrossRefPubMedWeb of ScienceGoogle Scholar

Goldstein JL, Brown MS. A century of cholesterol and coronaries: from plaques to genes to statins. Cell 2015;161:161–72. doi:10.1016/j.cell.2015.01.036
CrossRefPubMedGoogle Scholar

Stang A. Critical evaluation of the Newcastle-Ottawa scale for the assessment of the quality of nonrandomized studies in meta-analyses. Eur J Epidemiol 2010;25:603–5. doi:10.1007/s10654-010-9491-z
CrossRefPubMedWeb of ScienceGoogle Scholar

Psaty BM, Anderson M, Kronmal RA, et al. The association between lipid levels and the risks of incident myocardial infarction, stroke, and total mortality: the Cardiovascular Health Study. J Am Geriatr Soc 2004;52:1639–47. doi:10.1111/j.1532-5415.2004.52455.x
CrossRefPubMedWeb of ScienceGoogle Scholar

Fried LP, Kronmal RA, Newman AB, et al. Risk factors for 5-year mortality in older adults: the Cardiovascular Health Study. JAMA 1998;279:585–92. doi:10.1001/jama.279.8.585
CrossRefPubMedWeb of ScienceGoogle Scholar

Zimetbaum P, Frishman WH, Ooi WL, et al. Plasma lipids and lipoproteins and the incidence of cardiovascular disease in the very elderly: the Bronx Aging Study. Arterioscler Thromb 1992;12:416–23. doi:10.1161/01.ATV.12.4.416
Abstract/FREE Full TextGoogle Scholar
Kronmal RA, Cain KC, Ye Z, et al. Total serum cholesterol levels and mortality risk as a function of age. A report based on the Framingham data. Arch Intern Med 1993;153:1065–73. doi:10.1001/archinte.1993.00410090025004
CrossRefPubMedWeb of ScienceGoogle Scholar
Räihä I, Marniemi J, Puukka P, et al. Effect of serum lipids, lipoproteins, and apolipoproteins on vascular and nonvascular mortality in the elderly. Arterioscler Thromb Vasc Biol 1997;17:1224–32. doi:10.1161/01.ATV.17.7.1224
Abstract/FREE Full TextGoogle Scholar
Chyou PH, Eaker ED. Serum cholesterol concentrations and all-cause mortality in older people. Age Ageing 2000;29:69–74. doi:10.1093/ageing/29.1.69
Abstract/FREE Full TextGoogle Scholar
Weverling-Rijnsburger AW, Jonkers IJ, van Exel E, et al. High-density vs low-density lipoprotein cholesterol as the risk factor for coronary artery disease and stroke in old age. Arch Intern Med 2003;163:1549–54. doi:10.1001/archinte.163.13.1549
CrossRefPubMedWeb of ScienceGoogle Scholar
Schupf N, Costa R, Luchsinger J, et al. Relationship between plasma lipids and all-cause mortality in nondemented elderly. J Am Geriatr Soc 2005;53:219–26. doi:10.1111/j.1532-5415.2005.53106.x
CrossRefPubMedWeb of ScienceGoogle Scholar
Tikhonoff V, Casiglia E, Mazza A, et al. Low-density lipoprotein cholesterol and mortality in older people. J Amer Geriatr Soc 2005;53:2159–64. doi:10.1111/j.1532-5415.2005.00492.x
CrossRefPubMedWeb of ScienceGoogle Scholar
Störk S, Feelders RA, van den Beld AW, et al. Prediction of mortality risk in the elderly. Am J Med 2006;119:519–25. doi:10.1016/j.amjmed.2005.10.062
CrossRefPubMedWeb of ScienceGoogle Scholar

Akerblom JL, Costa R, Luchsinger JA, et al. Relation of plasma lipids to all-cause mortality in Caucasian, African-American and Hispanic elders. Age Ageing 2008;37:207–13. doi:10.1093/ageing/afn017
Abstract/FREE Full TextGoogle Scholar
Upmeier E, Lavonius S, Lehtonen A, et al. Serum lipids and their association with mortality in the elderly: a prospective cohort study. Aging Clin Exp Res 2009;21:424–30. doi:10.1007/BF03327441
CrossRefPubMedWeb of ScienceGoogle Scholar

Nilsson G, Ohrvik J, Lönnberg I, et al. Ten-year survival in 75-year-old men and women: predictive ability of total cholesterol, HDL-C, and LDL-C. Curr Gerontol Geriatr Res 2009:158425. doi:10.1155/2009/158425doi:10.1155/2009/158425
Google Scholar
Werle MH, Moriguchi E, Fuchs SC, et al. Risk factors for cardiovascular disease in the very elderly: results of a cohort study in a city in southern Brazil. Eur J Cardiovasc Prev Rehabil 2011;18:369–77. doi:10.1177/1741826710389405
CrossRefPubMedWeb of ScienceGoogle Scholar

Bathum L, Depont Christensen R, Engers Pedersen L, et al. Association of lipoprotein levels with mortality in subjects aged 50+without previous diabetes or cardiovascular disease: a population-based register study. Scand J Prim Health Care 2013;31:172–80. doi:10.3109/02813432.2013.824157
Google Scholar
Linna M, Ahotupa M, Löppönen MK, et al. Circulating oxidised LDL lipids, when proportioned to HDL-C emerged as a risk factor of all-cause mortality in a population-based survival study. Age Ageing 2013;42:110–13. doi:10.1093/ageing/afs074
Abstract/FREE Full TextGoogle Scholar
Jacobs JM, Cohen A, Ein-Mor E, et al. Cholesterol, statins, and longevity from age 70 to 90 years. J Am Med Dir Assoc 2013;14:883–8. doi:10.1016/j.jamda.2013.08.012
CrossRefPubMedGoogle Scholar
Takata Y, Ansai T, Soh I, et al. Serum total cholesterol concentration and 10-year mortality in an 85-year-old population. Clin Interv Aging 2014;9:293–300. doi:10.2147/CIA.S53754
Google Scholar

Lv YB, Yin ZX, Chei CL, et al. Low-density lipoprotein cholesterol was inversely associated with 3-year all-cause mortality among Chinese oldest old: data from the Chinese Longitudinal Healthy Longevity Survey. Atherosclerosis 2015;239: 137–42. doi:10.1016/j.atherosclerosis.2015.01.002
Google Scholar
Blekkenhorst LC, Prince RL, Hodgson JM, et al. Dietary saturated fat intake and atherosclerotic vascular disease mortality in elderly women: a prospective cohort study. Am J Clin Nutr 2015;101:1263–8. doi:10.3945/ajcn.114.102392
Abstract/FREE Full TextGoogle Scholar

Ramsden CE, Zamora D, Majchrzak-Hong S, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968–73). BMJ 2016;353:i1246. doi:10.1136/bmj.i1246
Abstract/FREE Full TextGoogle Scholar

Ravnskov U, McCully KS. Vulnerable plaque formation from obstruction of vasa vasorum by homocysteinylated and oxidized lipoprotein aggregates complexed with microbial remnants and LDL autoantibodies. Ann Clin Lab Sci 2009;39:3–16.
Abstract/FREE Full TextGoogle Scholar

Ravnskov U. High cholesterol may protect against infections and atherosclerosis. QJM 2003;96:927–34. doi:10.1093/qjmed/hcg150
FREE Full TextGoogle Scholar

Jacobs D, Blackburn H, Higgins M, et al. Report of the conference on low blood cholesterol: mortality associations. Circulation 1992;86:1046–60. doi:10.1161/01.CIR.86.3.1046
Abstract/FREE Full TextGoogle Scholar

Iribarren C, Jacobs DR Jr., Sidney S, et al. Cohort study of serum total cholesterol and in-hospital incidence of infectious diseases. Epidemiol Infect 1998;121:335–47. doi:10.1017/S0950268898001435
CrossRefPubMedGoogle Scholar

Read SA, Douglas MW. Virus induced inflammation and cancer development. Cancer Lett 2014;345:174–81. doi:10.1016/j.canlet.2013.07.030
CrossRefPubMedGoogle Scholar

Ravnskov U, McCully KS, Rosch PJ. The statin-low cholesterol-cancer conundrum. QJM 2012;105:383–8. doi:10.1093/qjmed/hcr243
FREE Full TextGoogle Scholar

Newman TB, Hulley SB. Carcinogenicity of lipid-lowering drugs. JAMA 1996;275:55–60. doi:10.1001/jama.1996.03530250059028
CrossRefPubMedWeb of ScienceGoogle Scholar

Neil HA, Hawkins MM, Durrington PN, et al. Non-coronary heart disease mortality and risk of fatal cancer in patients with treated heterozygous familial hypercholesterolaemia: a prospective registry study. Atherosclerosis 2005;179:293–7. doi:10.1016/j.atherosclerosis.2004.10.011
CrossRefPubMedWeb of ScienceGoogle Scholar

Reddy VS, Bui QT, Jacobs JR, et al. Relationship between serum low-density lipoprotein cholesterol and In-hospital mortality following acute myocardial infarction (The lipid paradox). Am J Cardiol 2015;115:557–62. doi:10.1016/j.amjcard.2014.12.006
CrossRefPubMedGoogle Scholar

Sachdeva A, Cannon CP, Deedwania PC, et al. Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in get with the guidelines. Am Heart J 2009;157:111–17. doi:10.1016/j.ahj.2008.08.010
CrossRefPubMedWeb of ScienceGoogle Scholar

Al-Mallah MH, Hatahet H, Cavalcante JL, et al. Low admission LDL-cholesterol is associated with increased 3-year all-cause mortality in patients with non ST segment elevation myocardial infarction. Cardiol J 2009;16:227–33.
PubMedGoogle Scholar

Diamond DM, Ravnskov U. How statistical deception created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease. Expert Rev Clin Pharmacol 2015;8:201–10. doi:10.1586/17512433.2015.1012494
Google Scholar

Kristensen ML, Christensen PM, Hallas J. The effect of statins on average survival in randomised trials, an analysis of end point postponement. BMJ Open 2015;5:e007118. doi:10.1136/bmjopen-2014-007118
Abstract/FREE Full TextGoogle Scholar

de Lorgeril M, Rabaeus M. Beyond confusion and controversy, Can we evaluate the real efficacy and safety of cholesterol-lowering with statins? J Controversies Biomed Res 2015;1:67–92. doi:10.15586/jcbmr.2015.11
Google Scholar