DOBBS – HOW CLOSE IS AMERICA TO SAYING “TO HELL WITH THIS CORRUPT GOVT?” — tomfernandez28’s Blog


By Rick Wells Detailing the corruption and grim prospects for salvaging our federal govt without Trump taking matters into his own hands, Dobbs asks if America is ready to say… The Lou Dobbs interview of Chris Farrell begins with them coming to an easy agreement that James Comey is nauseating, that he’s a disgrace and […]

via DOBBS – HOW CLOSE IS AMERICA TO SAYING “TO HELL WITH THIS CORRUPT GOVT?” — tomfernandez28’s Blog

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As the Whistle-Blowers who were former CIA agents come forward their disclosures will be worse than thought


Best description on what is going on, that I have read yet!
Thanks

Jim Campbell's

By Jim Campbell

May 12, 2018

As the Whistle-Blowers come forward the disclosures are really terrible.

This person, a former CIA operative, distinguishes between the Deep State and the Shadow Government.

The Deep State is alleged to operate with money, power and greed.

Do I personally believe in the Deep State or the Dark State?

After reading Area 51 a true documentary of CIA unclassified documents I will never consider what the government is doing for us especially when its run by Democrats, then think what it is actually doing “To US.”

That being said, this entire article must be taken with a grain of salt.

As far as governments go, the bottom line is that government is just too damn big,

WAY too big.  It needs to be cut back and pruned drastically  and Trump is just the guy to do it, he has already made a good start…

View original post 2,464 more words

The Donald’s Done — The Deep State Wins Its War On America First; written by david stockman wednesday may 9, 2018


The Donald’s Done — The Deep State Wins Its War On America First
written by david stockman wednesday may 9, 2018
http://www.ronpaulinstitute.org/archives/featured-articles/2018/may/09/the-donalds-done-the-deep-state-wins-its-war-on-america-first/

The Donald’s action to ash-can the Iranian nuclear deal marks the War Party’s complete and baleful triumph. There is now nothing much left of America First.

Trump’s reckless, unwarranted and utterly irrational action will pull Washington ever deeper into an incendiary middle eastern vortex of political and religious conflict that has absolutely nothing to do with the safety and security of the America people.

To the contrary, picking a fight with Tehran is an exercise in unprovoked Imperial aggression. The Iranian regime has no means to attack America militarily and has never threatened to do so. Nor has it invaded any other country in the region where it was not invited by a sovereign government host.

Even Iran’s minor skirmishes with American forces in recent years have been owing to the happenstance of Washington’s far-flung imperial ventures.

For example, Washington destroyed Saddam’s Sunni/secular government in Iraq and installed a Shiite regime in Baghdad, thereby leaving the Sunni lands of western Iraq in chaos. Only then did Baghdad invite their shiite co-religionists from Iran to help excise the scourge of ISIS that formed from the remnants of Saddam’s army and government.

Likewise, Washington and its allies sent thousands of jihadist warriors and billions of aid and supplies into Syria to topple its dully elected government. Only then did the Alawite (Shiite) Assad regime invite help from its confessional compatriots in Tehran.

And you can’t find any more ludicrous example of the cat calling the kettle black than the Donald’s claim that Iran is a terrorist state because it is aligned with the Shiite population of Lebanon represented by Hezbollah.

For crying out loud. The War Party pretends Washington has turned much of the middle east into rubble and barbarism in order to spread democracy — whether they wanted it or not, and whether they were ready for it or not.

But Lebanon is a serviceable democracy and last weekend Hezbollah and its allies — including certain Sunni factions — won an overwhelming election victory. They now control a clear majority in its legislature, where Hezbollah will have the power to name a new Prime Minister (a Sunni) and Speaker of the Parliament (a Shiite) — both of whom will be pledged to work with the country’s Christian president.

That particular outcome of democracy the War Party can’t abide. But it fairly violates the english language itself to call it state sponsored terrorism.

In a similar vein, the Houthi tribe of Shiites have dominated much of northern and western Yemen for centuries. So when a Washington installed government in Sana’a was overthrown, the Houthi took power in northern Yemen — as had been the case during the long expanse from 1918-1990 when the two Yemens were finally unified.


But it is the Houthis who are the victims of aggression by the brutal Saudi bombing campaign that has left more than 10,000 civilians dead and the land plagued with famine, cholera, rubble, and economic collapse.

There is no telling which faction in Yemen’s fratricidal civil war and invasion by Saudi Arabia is the more barbaric, but the modest aid provided by Iran to its Shiite kinsman in northern Yemen is absolutely not a case of state sponsored terrorism.

In a word, the Donald has fallen hook, line and sinker for the War Party’s lie- and propaganda-filled demonization of the Iranian regime. We have debunked this false history elsewhere, but suffice to say that it boils down to two very imperialist propositions.

To wit, that Iran is not entitled to have its own foreign policy via alliances with Iraq, Syria, the dominant party of Lebanon, or the official government in Sana’a Yemen because Washington (and Israel) say so; and that it’s not allowed to have even intermediate and medium range missiles (that can’t reach either the US or most of Europe) to defend itself — even though Washington has armed its far wealthier Sunni rival across the Persian Gulf with upwards of $250 billion of America’s most advanced warplanes, attack helicopters, missiles, drones and sundry other accoutrements of war.

And that is to say nothing of a tiny residual capacity to enrich uranium to 3.5 percent purity (compared to 90 percent weapons grade) for civilian power reactors on fewer than one-fifth of the oldest and slowest centrifuges it had before the 2015 nuke deal.

Nor does it consider that all 17 US intelligence agencies certified in an official NIE (national intelligence estimate) in 2007 and again in 2011 that Iran only had a small weaponization research program between 1999 and 2003, which was then abandoned and never restarted.

Moreover, the documentary proof of that was thoroughly investigated by the IAEA after the 2015 deal, which then re-validated that the Iranian weapons program was indeed disbanded in 2003.

In short, the Donald has fallen for a pack of lies and distortions that are only remotely plausible if the aim is to find enemies and territories around the planet to police, occupy or otherwise hegemonize. And to thereby keep the Warfare State in business, its $800 billion budget funded, and the Imperial City’s vast beehive of think-tanks, contractors, NGOs, lobbyists, and racketeers in clover.

The invincible grip on power of the above — the Deep State for short-hand purposes — has now been proven. And that’s a full-on tragedy because the Donald’s inchoate notion of America First was an incipient challenge to its power — the only one since the end of the cold war.

To be sure, Donald Trump never had a coherent or articulated notion of America First. But all of his impulses were in the right direction.

Perhaps like renegade Sarah Palin before him, for example, he could see Russia from his airy on the 68th floor of Trump Tower and recognize that it is no threat whatsoever to America’s security.

That is, from his perch the Donald could gaze upon metro New York’s $1.6 trillion of GDP, which is greater than the entirety of Russia’s economy ($1.5 trillion GDP); and whether he knew the precise numbers or not, his impulse toward rapprochement with Putin was spot on.

Likewise, whether he had gotten George Bush’s folly in Iraq right on day one or not — he was loud and clear in his consistent denunciation years before Hillary sprouted her dawkish feathers.

Nor was he any less correct when he averred that NATO was obsolete. After all, the GDP of the EU-29 is 10X larger than Russia’s, and their combined military spending is 4X greater.

If you’re not a prisoner of Imperial Washington’s twisted group think you cannot possibly believe that Russia’s supremely rational leader — Cool Hand Vlad — intends to militarily assault his European neighbors. He’d like to supply their markets, not occupy their cities — something that anyone except the demented, self-serving bureaucrats of NATO can easily understand.

Ditto for Afghanistan, Syria, Yemen, Libya, Somalia et. al. They aren’t cold war “dominoes” because the Soviet Union slithered off the pages of history 27 years ago; they don’t threaten America directly, either, because they don’t have two dimes to rub together economically or militarily; and whether they affiliate with the Saudi-Sunni axis or the Iran-Shiite crescent makes not one damn bit of difference for the safety and security of American citizens in Lincoln NE or Springfield MA.

In the case of the Korean Peninsula, the Donald also rightly questioned why we are still funding 29,000 US troops when the war there ended 65 years ago.

The truth is, it is a war that never should have been fought in the first place because the now open Soviet archives show both Stalin and Mao were against it. US national security was never at stake.

Rather than a domino, it originated purely as a civil war between the communist/nationalists under Kim II-sung, who had fought the Japanese occupiers to the death, and a puppet government in the South under Syngman Rhee.

The latter was an aristocratic dandy who moved to the US in 1904 and spent most of the next 40 years hob-knobbing in Washington. So doing, he promoted endless schemes to install himself in power back in Korea, which finally happened when Japan’s 35-year long occupation was ended in August 1945.

At length, the two Korean political rivals got into a war that the north would have handily won — and might well have turned itself into a cheap labor based export platform just as did Mao’s heirs on the mainland. It might even have become a darling of Wall Street — just as the Red Suzerains of Beijing are today.

That is to say, there was exactly nothing at stake in June 1950 — until the rabid cold warriors in Washington persuaded Truman to intervene.

So doing, the US military launched the most destructive and vicious bombing campaign in history under the blood-thirsty top Air Force general, Curtis LeMay. By the 1953 armistice, North Korea had become a bombed-out wasteland with hardly a city or town not reduced to rubble and with millions of civilians dead or starving.

But it was not merely a pointless war and waste of American blood and treasure; it also became forever embraced by the people of the north as the patriotic war of resistance that paved the way for six decades of the brutal Kim family dictatorship and a life of poverty and misery for its 25 million people, who could otherwise be working in Apple factories and auto plants today.

Needless to say, Imperial Washington has no regard for honest history — only its own self-serving narrative and imperative need for enemies and missions to justify nearly $800 billion per year for the machinery of war and empire. In the case of North Korea, in fact, its imperial pretensions and penchant for “regime change” under the neocons in recent decades, unleashed a veritable monster.

That is, a drive by the Kim family to obtain nuclear weapons, thereby hoping to avoid Saddam’s fate at the end of a rope or Khadafy’s bloody demise with a shive up his rectum.

Fortunately, the Donald has been blessed with a historic serendipity. His military bluster and name-calling apparently caused Kim Jong-un to stage so many nuclear bomb tests culminating in a huge (for N. Korea) 160 kiloton explosion last September that the Fat Boy of Pyongyang has literally destroyed the mountains which house his Punggye-ri test site.

A recent authoritative study actually warns that if North Korea were to use the same area for another test it could cause an “environmental catastrophe.”

North Korea’s past tests have altered the tectonic stress in the region to the extent that previously inactive tectonic faults in the region have reached their state of critical failure. Any further disturbance from a future test could generate earthquakes that may be damaging by their own force or crack the nuclear test sites of the past or the present.
Of course, Kim Jong-un is now attempting to make a virtue out of necessity by ostentatiously shuttering the no longer useable site and inviting the world to witness its entombment. But if that leads to a denuclearization of the Korean peninsula, so be it.

And let it also be an occasion to reverse the mistake of June 1950, and get American forces off the peninsula once and for all: Return Korea to the Koreans to work out their own governance as they see fit!

Yet even on this matter, where the Donald has recently tried to explore a drastic reduction, if not complete removal, of US troops as part of the pending deal with Kim Jong-un, the Deep State has come down on him with all fours.

In that regard, here is what former “peace” candidate Barack Obama’s leading advisor on the topic had this to say:

Kelly E. Magsamen, a top Asia policy official at the Pentagon during the Obama administration, said, ‘U.S. presence in South Korea is a sacrosanct part of our alliance.’
In fact, apparently the entire global empire of Washington is sacrosanct — including the ridiculous fact that in the year 2018 Washington still has military bases in the defeated powers of World War II. Yet neither Japan nor Germany have any mortal military enemies and both are utterly dependent on the trade custom of the US for their high standard of living.

So the Deep State now owns the Donald and America First is not even a slogan. It’s inoperative, Nixon-style.

Indeed, it’s only a matter of time before the Donald gets the ultimate Nixon treatment — now that he has done the Deep State’s dirty work and ash-canned the deal that could have opened a broad avenue toward peace in the world and drastic retrenchment of the fiscally bankrupting Warfare State at home.

That is to say, at length the ingrates of the Deep State will put the Donald on the Dick Nixon Memorial Helicopter for his final ride to Gonesville.

To paraphrase the great Randolph Bourne, Demonization of the Unwilling is the Health of the Deep State.

At least that much the Donald has now, regrettably, confirmed with his sophomoric attack on Iran.

So doing he has also lurched America drastically forward on the path to a monumental financial catastrophe. That’s because taken together the Warfare State and the Welfare State are also the fiscal demise of the state.

One of these days even the lemmings of Wall Street — which took day’s calamitous news in stride — will finally get the memo, too.

Reprinted with permission from David Stockman’s Contra Corner.

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
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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


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The Event Chronicle: 82-Year-Old Woman With Dementia Gets Her Memory Back



82-Year-Old Woman With Dementia Gets Her Memory Back After Changing Her Diet
By Editor May 2, 2018 No Comments

http://www.theeventchronicle.com/health/82-year-old-woman-with-dementia-gets-her-memory-back-after-changing-her-diet-2/

82-Year-Old Woman With Dementia Gets Her Memory Back After Changing Her Diet

By Alanna Ketler

Recently, an 82-year-old woman who suffered from dementia, who couldn’t recognize her own son has miraculously got her memory back after changing her diet.

When his mother’s condition became so severe that for her own safety she had to be kept in the hospital, Mark Hatzer almost came to terms with losing another parent.

Sylvia had lost her memory and parts of her mind, she had even phoned the police once accusing the nurse who were caring for her of kidnap.

A change in diet, which was comprised of high amounts of blueberries and walnuts, has proven to have had a strong impact on Sylvia’s condition that her recipes are now being shared by the Alzheimer’s Society.

Sylvia also began incorporating other health foods, including broccoli, kale, spinach, sunflower seeds, green tea, oats, sweet potatoes and even dark chocolate with a high percentage of cacoa. All of these foods are known to be beneficial for brain health.

Mark and Sylvia devised to diet together after deciding that the medication on it’s own was not enough, they looked into the research showing that rates of dementia are much lower in mediterranean countries and copied a lot of their eating habits.

According to Mirror.co.uk“

Mark, whose brother Brent also died in 1977, said: “When my mum was in hospital she thought it was a hotel – but the worst one she had ever been in.

“She didn’t recognise me and phoned the police as she thought she’d been kidnapped.

“Since my dad and brother died we have always been a very close little family unit, just me and my mum, so for her to not know who I was was devastating.

“We were a double act that went everywhere together. I despaired and never felt so alone as I had no other family to turn to.

“Overnight we went from a happy family to one in crisis.

“When she left hospital, instead of prescribed medication we thought we’d perhaps try alternative treatment.

“In certain countries Alzheimer’s is virtually unheard of because of their diet.

“Everyone knows about fish but there is also blueberries, strawberries, Brazil nuts and walnuts – these are apparently shaped like a brain to give us a sign that they are good for the brain.”

There were also some cognitive exercises that Mark and his mother would do together like jigsaw puzzles crosswords and meeting people in social situations, Sylvia would also exercise by using a pedaling device outfitted for her chair.

Mark said, “It wasn’t an overnight miracle, but after a couple of months she began remembering things like birthdays and was becoming her old self again, more alert, more engaged..

“People think that once you get a diagnosis your life is at an end. You will have good and bad days, but it doesn’t have to be the end. For an 82-year-old she does very well, she looks 10 years younger and if you met her you would not know she had gone through all of this.

“She had to have help with all sorts of things, now she is turning it round. We are living to the older age in this country, but we are not necessarily living healthier.”

The Body’s Ability To Heal Is Greater Than Anyone Has Permitted You To Believe

This story just goes to show how resilient our bodies really are if given the right environment. Most of these types of diseases are often related to diet in the first place so that means that they can indeed be reversed with a proper diet. Sure, some of them are genetic and you might be a carrier of the gene, but that is not a guarantee that it will become active, there are things you can do to minimize the risk. Our health is our greatest wealth. We have to realize that we do have a say in our lives and what our fate is.

We have covered the topic before of how aluminum build up in the brain is directly related to dementia and more specifically Alzheimer’s disease, being able to identify this as a cause is important because recognizing this means we can do our part to limit the exposure and to also detoxify our brains and bodies from this damaging heavy metal.

In an article titled, Strong evidence linking Aluminum to Alzheimer’s, recently published in The Hippocratic Post website, Exley explained that:

“We already know that the aluminium content of brain tissue in late-onset or sporadic Alzheimer’s disease is significantly higher than is found in age-matched controls. So, individuals who develop Alzheimer’s disease in their late sixties and older also accumulate more aluminium in their brain tissue than individuals of the same age without the disease.

Even higher levels of aluminium have been found in the brains of individuals, diagnosed with an early-onset form of sporadic (usually late onset) Alzheimer’s disease, who have experienced an unusually high exposure to aluminium through the environment (e.g. Camelford) or through their workplace. This means that Alzheimer’s disease has a much earlier age of onset, for example, fifties or early sixties, in individuals who have been exposed to unusually high levels of aluminium in their everyday lives.”

His most recent study, published by the Journal of Trace Elements in Medicine and Biology in December 2016, titled: Aluminium in brain tissue in familial Alzheimer’s disease, is one of the many studies that he and his team have conducted on the subject of aluminum over the years. However, this study in particular is believed to be of significant value, because it is the first time that scientists have measured the level of aluminum in the brain tissue of individuals diagnosed with familial Alzheimer’s disease. (Alzheimer’s disease or AD is considered to be familial if two or more people in a family suffer from the disease.)

According to their paper, the concentrations of aluminum found in brain tissue donated by individuals who died with a diagnosis of familial AD, was the highest level ever measured in human brain tissue.

Professor Exley wrote:

“We now show that some of the highest levels of aluminium ever measured in human brain tissue are found in individuals who have died with a diagnosis of familial Alzheimer’s disease.

The levels of aluminium in brain tissue from individuals with familial Alzheimer’s disease are similar to those recorded in individuals who died of an aluminium-induced encephalopathy while undergoing renal dialysis.”

He explained that:

“Familial Alzheimer’s disease is an early-onset form of the disease with first symptoms occurring as early as 30 or 40 years of age. It is extremely rare, perhaps 2-3% of all cases of Alzheimer’s disease. Its bases are genetic mutations associated with a protein called amyloid-beta, a protein which has been heavily linked with the cause of all forms of Alzheimer’s disease.

Individuals with familial Alzheimer’s disease produce more amyloid beta and the onset of the symptoms of Alzheimer’s disease are much earlier in life.”
The First Step Towards Change Is By Raising Awareness

As more and more awareness grows involving the true causes of these neurodegenerative brain disorders, the more we can do our part to prevent and even treat them and hopefully, eventually eliminate things such as aluminum and other chemicals in our foods to prevent this disease from happening altogether.

Please share this article with anyone you know who knows someone who is suffering from dementia or Alzheimer’s.

This article (82-Year-Old Woman With Dementia Gets Her Memory Back After Changing Her Diet) was originally published on Collective Evolution and syndicated by The Event Chronicle.
———————————-

Apparently the reason Aluminum has been found in the Chemtrails that allegedly don’t exist! “They” are not only trying to kill us, and make us dumb, they want us to succumb to dementia…

Fukushima is Now Officially the Worst Nuclear Power Disaster in History


Move Over Chernobyl, Fukushima is Now Officially the Worst Nuclear Power Disaster in History

 

The radiation dispersed into the environment by the three reactor meltdowns at Fukushima-Daiichi in Japan has exceeded that of the April 26, 1986 Chernobyl catastrophe, so we may stop calling it the “second worst” nuclear power disaster in history. Total atmospheric releases from Fukushima are estimated to be between 5.6 and 8.1 times that of Chernobyl, according to the 2013 World Nuclear Industry Status Report. Professor Komei Hosokawa, who wrote the report’s Fukushima section, told London’s Channel 4 News then, “Almost every day new things happen, and there is no sign that they will control the situation in the next few months or years.”

Tokyo Electric Power Co. has estimated that about 900 peta-becquerels have spewed from Fukushima, and the updated 2016 TORCH Report estimates that Chernobyl dispersed 110 peta-becquerels.[1](A Becquerel is one atomic disintegration per second. The “peta-becquerel” is a quadrillion, or a thousand trillion Becquerels.)

Chernobyl’s reactor No. 4 in Ukraine suffered several explosions, blew apart and burned for 40 days, sending clouds of radioactive materials high into the atmosphere, and spreading fallout across the whole of the Northern Hemisphere — depositing cesium-137 in Minnesota’s milk.[2]

The likelihood of similar or worse reactor disasters was estimated by James Asselstine of the Nuclear Regulatory Commission (NRC), who testified to Congress in 1986: “We can expect to see a core meltdown accident within the next 20 years, and it … could result in off-site releases of radiation … as large as or larger than the releases … at Chernobyl.[3] Fukushima-Daiichi came 25 years later.

Contamination of soil, vegetation and water is so widespread in Japan that evacuating all the at-risk populations could collapse the economy, much as Chernobyl did to the former Soviet Union. For this reason, the Japanese government standard for decontaminating soil there is far less stringent than the standard used in Ukraine after Chernobyl.

Fukushima’s Cesium-137 Release Tops Chernobyl’s

The Korea Atomic Energy Research (KAER) Institute outside of Seoul reported in July 2014 that Fukushima-Daiichi’s three reactor meltdowns may have emitted two to four times as much cesium-137 as the reactor catastrophe at Chernobyl.[4]

To determine its estimate of the cesium-137 that was released into the environment from Fukushima, the Cesium-137 release fraction (4% to the atmosphere, 16% to the ocean) was multiplied by the cesium-137 inventory in the uranium fuel inside the three melted reactors (760 to 820 quadrillion Becquerel, or Bq), with these results:

Ocean release of cesium-137 from Fukushima (the worst ever recorded): 121.6 to 131.2 quadrillion Becquerel (16% x 760 to 820 quadrillion Bq). Atmospheric release of Cesium-137 from Fukushima: 30.4 to 32.8 quadrillion Becquerel (4% x 760 to 820 quadrillion Bq).

Total release of Cesium-137 to the environment from Fukushima: 152 to 164 quadrillion Becquerel. Total release of Cesium-137 into the environment from Chernobyl: between 70 and 110 quadrillion Bq.

The Fukushima-Daiichi reactors’ estimated inventory of 760 to 820 quadrillion Bq (petabecquerels) of Cesium-137 used by the KAER Institute is significantly lower than the US Department of Energy’s estimate of 1,300 quadrillion Bq. It is possible the Korean institute’s estimates of radioactive releases are low.

In Chernobyl, 30 years after its explosions and fire, what the Wall St. Journal last year called “the $2.45 billion shelter implementation plan” was finally completed in November 2016. A huge metal cover was moved into place over the wreckage of the reactor and its crumbling, hastily erected cement tomb. The giant new cover is 350 feet high, and engineers say it should last 100 years — far short of the 250,000-year radiation hazard underneath.

The first cover was going to work for a century too, but by 1996 was riddled with cracks and in danger of collapsing. Designers went to work then engineering a cover-for-the-cover, and after 20 years of work, the smoking radioactive waste monstrosity of Chernobyl has a new “tin chapeau.” But with extreme weather, tornadoes, earth tremors, corrosion and radiation-induced embrittlement it could need replacing about 2,500 times.

John Laforge’s field guide to the new generation of nuclear weapons is featured in the March/April 2018 issue of CounterPunch magazine.

Notes.

[1]Duluth News-Tribune & Herald, “Slight rise in radioactivity found again in state milk,” May 22, 1986; St. Paul Pioneer Press & Dispatch, “Radiation kills Chernobyl firemen,” May 17, 1986; Minneapolis StarTribune, “Low radiation dose found in area milk,” May 17, 1986.

[2]Ian Fairlie, “TORCH-2016: An independent scientific evaluation of the health-related effects of the Chernobyl nuclear disaster,” March 2016 (https://www.global2000.at/sites/global/files/GLOBAL_TORCH%202016_rz_WEB_KORR.pdf).

[3]James K. Asselstine, Commissioner, US Nuclear Regulatory Commission, Testimony in Nuclear Reactor Safety: Hearings before the Subcommittee on Energy Conservation and Power of the Committee on Energy and Commerce, House of Representatives, May 22 and July 16, 1986, Serial No. 99-177, Washington, DC: Government Printing Office, 1987.

[4] Progress in Nuclear Energy, Vol. 74, July 2014, pp. 61-70; ENENews.org, Oct. 20, 2014.

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