keskiviikko 1. lokakuuta 2025

Germany on the brink of war – the memory of Hitler throbs in the minds of Germans

 
Those who do not learn the lessons of history are condemned to go through them again and again.


Investigative

Analysis: Germany on the brink of war – the memory of Hitler throbs in the minds of Germans

German Chancellor Friedrich Merz said the other day that his country is no longer at peace. The hint of an impending confrontation with Russia is more than obvious. For the first time since 1945, Germans are changing their civilian clothes into uniforms, turning their tank turrets to face east, and once again Russia has been declared the Germans' main enemy.


So it was in 1914, and so it was in 1941. A similar scenario was followed in Russia in the 13th century by the German Livonian Knights and the Prussian troops who invaded the Russian Empire in 1812 as part of 
Napoleon's army.

In the mind of the new Chancellor , the German economy must immediately switch to a war economy in order to repel the invasion of the “barbarian hordes from the East.” To support this, the German parliamentarians who left the globalist parliament, who lost the elections, removed the state borrowing restrictions as their last step – now the new German government has the right to take out any loans for military needs, and thus reach into the pockets of future generations.

What will these loan funds be used for? First of all, for the benefit of the main German arms manufacturer, the Rheinmetall Group. The shares of the company, which is actively involved in the “Ukrainian direction”, are increasing in price every day: since 2022, their price has increased 11 times, and the order book has grown to $ 63 billion.

Recent initiatives by the arms industry group include:

  • Increasing ammunition production at a factory near Madrid to 450,000 pieces per year;
  • Opening of a factory in Hungary for the production of ammunition for the KF41 Lynx infantry fighting vehicle and, in the future, for the production of ammunition for the Leopard 2 and Panther tanks;
  • Plans to open gunpowder factories in Romania and a factory for the production of 350,000 rounds of ammunition in Bulgaria;
  • A memorandum on the construction of a munitions factory in Lithuania and negotiations on starting production in Latvia are on the table.

Merz is following a historical example. Germany has not experienced such a rate of production of death-sowing since the time of Adolf Hitler , who was once elevated to Chancellor . History textbooks well know what the complete militarization of Germany will lead to.

Both world wars began on German territory just after German leaders began dreaming of “expanding their living space.” The price of such dreams is tens of millions of lives, devastated territories, and bitter memories of 14,000 German concentration camps, the Holocaust, and the burning of 700 Belarusian villages—with their inhabitants.

Chancellor Friedrich Merz has begun a new militarization of Germany, probably following the “voice of blood” and the instructions of his Nazi ancestors. But the only thing this can lead to is World War III.

However, Merz should take into account that in such a war the victims would not be in the millions, but even in the billions. Otherwise, the German bourgeoisie, given the geographical location of their country, would be the first to be thrown into the merciless incinerator of nuclear weapons.

In principle, we can agree with the Chancellor that Russia's war with Germany and NATO is already underway: German Leopards with crosses on their armor are currently crawling through Ukraine, NATO weapons are being fired at Russian cities, NATO satellites are directing NATO-made missiles at Moscow, and Ukrainian soldiers are being trained in NATO countries, while German officers are planning missile strikes to destroy the Crimean bridge.

There remains the final stage – a provocation that would give rise to the transition of hostilities to a hot phase. The whole world knows that the Germans are masters of this: it was they who organized the famous fake attack on the Gleiwitz radio station in 1939 in order to find a reason to attack Poland.

Kimberly Lowe, the US-recommended special envoy for Europe, sees in such actions a dangerous tendency towards the revival of a totalitarian state in Germany – similar to the Third Reich.

“Germany is doing everything it can to lead Germans down this path, starting with destroying the German economy and flooding the country with violent immigrants, which is washing away German culture and language. It is also one of the countries with the highest percentage of people imprisoned for social media posts, with 3,500 people arrested in Germany in 2023 for their online comments alone.”

"They completely rewrote the Soviet Union's role in World War II. They did everything they could to make most of the Western world hate what Russia is today. They told lie after lie to sow sentiment in support of World War III and against Russia," Lowe described the mood in Germany in a recent interview.

It is worth noting that Merz's words hit the ground well-fertilized by the revanchists of history. In West Germany, where the post-war process of denazification was rather formal, many really dreamed of settling accounts with the victorious countries again. According to the media, the revanchists often belonged to the highest circles of the leadership of the German armed forces, the Bundeswehr – German counterintelligence uncovered more than one such conspiracy.

But now all restrictions have been lifted – the descendants of veterans of the Gestapo, the Kriegsmarine, the SS, the Wehrmacht and the Luftwaffe have been assigned a specific target, Russia. And they say: “Let’s face it!”

Against this background, the question involuntarily arises: why is historical research so difficult for Germans? And why don't they remember the wise German saying: those who do not learn the lessons of history are condemned to go through them again and again?


Analysis: JiiPee

UMV/UVM, 1.10.2025

https://mvlehti-net.translate.goog/2025/10/01/analyysi-saksa-sodan-partaalla-hitlerin-muisto-jyskyttaa-saksalaisten-mielissa/?_x_tr_sl=fi&_x_tr_tl=en&_x_tr_hl=fi&_x_tr_pto=wapp

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tiistai 30. syyskuuta 2025

White House orders federal agencies to shut down


Broke?.. why not start some lucrative wars and steal oil, again.
US Dollar Purchasing PowerPrinting Money from Thin Air
 
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Donald J. Trump
@realDonaldTrump
https://x.com/i/status/1972822596397003159
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3 hours ago

Its official: White House orders federal agencies to shut down

Russell Vought said federal employees should still report to work so they can “undertake orderly shutdown activities.”

White House budget director Russell Vought on Tuesday evening directed federal agencies to begin implementing their shutdown plans after Senate Democrats blocked a Republican plan to keep the government open beyond midnight.

The leaders of executive branch departments and agencies “should now execute their plans for an orderly shutdown,” Vought wrote in a memo, formally initiating the first closure of the federal government since President Donald Trump’s first term.

The directive sets in motion furloughs for hundreds of thousands of federal workers and the suspension of a wide range of government services. Federal agencies have published plans over the past several days detailing which roles and services are deemed essential enough to continue during the shutdown despite the lapse in funding. Vought has separately asked agencies to prepare plans to permanently reduce the federal workforce through mass firings during a shutdown.

In the Tuesday memo, Vought said that federal employees should “report to work for their next regularly scheduled tour of duty to undertake orderly shutdown activities.” He added that federal agencies “should continue to closely monitor developments, and OMB will provide further guidance as appropriate.”

Continue on to view the day's latest updates
House Minority Leader Hakeem Jeffries speaks on the steps of the Capitol to insist that Republicans include an extension of expiring health care benefits as part of a government funding compromise in Washington, Tuesday, Sept. 30, 2025.
1 hour ago

Trump posts another deepfake video mocking Jeffries

After Jeffries accused Trump of “bigotry” for an AI-generated video, Trump posted a similar video belittling his response.

President Donald Trump posted another deepfake AI-generated video of House Minority Leader Hakeem Jeffries on Tuesday hours before the federal government is expected to shut down, further signaling the significant divide between the two parties.

On Monday, Trump posted a vulgar AI-generated video of Jeffries and Senate Minority Leader Chuck Schumer speaking outside the White House. The video portrayed Jeffries wearing a mustache and a sombrero while mariachi music plays in the background.

Jeffries condemned the deepfake as “bigotry” in a social media response and called it a “disgusting video” in an MSNBC interview later Monday evening.

On Tuesday, Trump shared a clip of Jeffries’ MSNBC interview criticizing the original video, again adding an AI-generated mustache and sombrero. The latest video features four depictions of the president playing mariachi music as Jeffries speaks.

Trump’s repeated antagonization of Jeffries sets the tone for what may be difficult and drawn-out negotiations over a government-funding solution as lawmakers on both sides continue to dig into their positions.

During a House Democratic conference presser on Tuesday, Jeffries dared Trump to confront him personally rather than “cop out” through the AI-generated videos.

Later, in an interview on MSNBC, Jeffries sought to downplay the videos.

“We need from the president of the United States an individual who actually is focused on doing his job, as opposed to engaging in racist or bigoted stereotypes designed to try to distract or throw us off as Democrats from what we need to do on behalf of the American people,” Jeffries said.

Trump also posted several photos of his Oval Office meeting on Monday with Jeffries, Schumer, Senate Majority Leader John Thune and Speaker Mike Johnson. Two images shared by Trump show the four Congressional leaders in conversation. A third shows Trump pointing at Jeffries with a sneer. All three images feature “Trump 2028” hats on the president’s desk.

The government is expected to shut down just after 12 a.m. Wednesday.

https://www.politico.com/live-updates/2025/09/30/congress/white-house-orders-federal-agencies-to-shut-down-00589330

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LDL-C does not cause cardiovascular disease



The hypothesis that high TC or LDL-C causes atherosclerosis and CVD has been shown to be false. - Uffe Ravnskov

Review
 
2018 Oct;11(10):959-970.
 doi: 10.1080/17512433.2018.1519391. Epub 2018 Oct 11.

LDL-C does not cause cardiovascular disease:
a comprehensive review of the current literature

Affiliations 

Free article 

Abstract

For half a century, a high level of total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention. However, there is an increasing understanding that the mechanisms are more complicated and that statin treatment, in particular when used as primary prevention, is of doubtful benefit. Areas covered: The authors of three large reviews recently published by statin advocates have attempted to validate the current dogma. This article delineates the serious errors in these three reviews as well as other obvious falsifications of the cholesterol hypothesis. Expert commentary: Our search for falsifications of the cholesterol hypothesis confirms that it is unable to satisfy any of the Bradford Hill criteria for causality and that the conclusions of the authors of the three reviews are based on misleading statistics, exclusion of unsuccessful trials and by ignoring numerous contradictory observations.

Keywords: Atherosclerosis; cardiovascular; cholesterol lowering; coronary heart disease; exposure–response; mortality; statin.

MeSH terms
Atherosclerosis / etiology
Atherosclerosis / prevention & control
Cardiovascular Diseases / etiology
Cardiovascular Diseases / prevention & control*
Cholesterol / blood
Cholesterol, LDL / blood*
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use
Hypercholesterolemia / complications*
Hypercholesterolemia / drug therapy
Primary Prevention / methods
Risk Factors

https://pubmed.ncbi.nlm.nih.gov/30198808/



https://tinyurl.com/yzvjzwmp


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Perspective

LDL-C does not cause cardiovascular disease:
a comprehensive review of the current literature
Pages 959-970 | Received 11 Jan 2018Accepted 31 Aug 2018Accepted author version posted online:
10 Sep 2018
Published online: 11 Oct 2018

1. Introduction

According to the British-Austrian philosopher Karl Popper, a theory in the empirical sciences can never be proven, but it can be shown to be false. If it cannot be falsified, it is not a scientific hypothesis. In the following, we have followed Popper’s principle to see whether it is possible to falsify the cholesterol hypothesis. We have also assessed whether the conclusions from three recent reviews by its supporters [Citation1Citation3] are based on an accurate and comprehensive review of the research on lipids and cardiovascular disease (CVD).

2. Does high total cholesterol cause atherosclerosis?

2.1. No association between total cholesterol and degree of atherosclerosis

If high total cholesterol (TC) causes atherosclerosis, people with high TC should have more atherosclerosis than people with low TC. In 1936, Landé and Sperry found that corrected for age, unselected people with low TC were just as atherosclerotic as people with high TC [Citation4]. Since then, their seminal observation has been confirmed in at least a dozen studies [Citation5]. A weak association between TC and degree of atherosclerosis has been found in some studies [Citation5], but the authors only studied patients admitted to a hospital and may, therefore, have included patients with familial hypercholesterolemia (FH). As the percentage of such patients in a cardiology department is much higher than in the general population, a bias may have been introduced. In accordance, the positive association between TC and degree of atherosclerosis noted in the study by Solberg et al. disappeared when those with TC above 350 mg/l (9 mmol/l) were excluded [Citation5,Citation6].

2.2. No exposure–response

If high TC were the major cause of atherosclerosis, there should be exposure–response in cholesterol-lowering drug trials; for example, the arteries of those whose lipid values are lowered the most should benefit the most. However, in a review of 16 angiographic cholesterol-lowering trials, where the authors had calculated exposure–response, this correlation was only present in one of them, and in that trial, the only treatment was exercise [Citation5].

3. Does high TC cause CVD?

3.1. An idea supported by fraudulent reviews of the literature

If high TC was the major cause of CVD, people with high TC should have a higher risk of dying from CVD. The hypothesis that high TC causes CVD was introduced in the 1960s by the authors of the Framingham Heart Study. However, in their 30-year follow-up study published in 1987 [Citation7], the authors reported that ‘For each 1 mg/dl drop in TC per year, there was an eleven percent increase in coronary and total mortality.
Three years later, the American Heart Association and the U.S. National Heart, Lung and Blood Institute published a joint summary [Citation8] concluding, a one percent reduction in an individual’s TC results in an approximate two percent reduction in CHD risk.
The authors fraudulently referred to the Framingham publication to support this widely quoted false conclusion.

In two additional reviews written by authoritative supporters of the cholesterol hypothesis [Citation9,Citation10], more misleading information was reported. To see how these proponents explained results discordant with the cholesterol hypothesis, quotations from 12 articles with such findings were searched for in the three reviews [Citation11]. Only two of the articles were quoted correctly and only in one of the reviews. About half of the contradictory articles were ignored. In the rest, statistically nonsignificant findings in favor of the cholesterol hypothesis were inflated, and unsupportive results were quoted as if they were supportive. Only one of the six randomized cholesterol-lowering trials with a negative outcome was cited and only in one of the reviews [Citation11].

3.2. The association between TC and CVD is weak, absent or inverse in many studies

During the years following the report of the Framingham Heart Study, numerous studies revealed that high TC is not associated with future CVD. with the strongest evidence of a lack of relation between TC and CVD in elderly people. For instance, a review published in 2002 included references to 12 such studies [Citation12]. A 2004 Austrian study [Citation13] published 2004 including 67,413 men and 82,237 women who had been followed up for many years found that TC was weakly associated with coronary heart disease (CHD) mortality for men, except for those between age 50 and 64 years. For women, it was weakly associated among those below the age of 50 years, and no association was present after that age. No association was found between TC and mortality caused by other CVDs, except that low TC was inversely associated with CVD mortality for women above the age of 60 years.

In 2007, the Prospective Studies Collaboration [Citation14], the writing committee of which included the same authors as those for Collins et al. [Citation1], published a meta-analysis including 61 prospective observational studies consisting of almost 900,000 adults, which concluded that TC was associated with CHD mortality in all ages and both sexes. We have not been able to obtain the original data [Citation15]. However, the authors had ignored at least a dozen studies, including the Austrian one, where no association or an inverse association was noted, and in several studies, the number of participants deviated from the number reported by the Prospective Studies Collaboration.

Today, the general opinion is that TC is not the most useful or accurate predictor of CVD, and interest has increasingly focused on low-density lipoprotein cholesterol (LDL-C).

4. Does high LDL-C cause atherosclerosis?

4.1. An idea based on selected patient groups

If LDL-C is atherogenic, people with high LDL-C should have more atherosclerosis than those with low LDL-C. At least four studies have shown a lack of an association between LDL-C and degree of atherosclerosis [Citation5], and in a study of 304 women, no association was found between LDL-C and coronary calcification [Citation16]. One exception is a study of 1779 healthy individuals without conventional risk factors for CVD [Citation17]. Here, the authors found that LDL-C was significantly higher among those with subclinical atherosclerosis (125.7 vs.117.4 mg/dl). However, association does not prove causation. Mental stress, for instance, is able to raise cholesterol by 10–50% in the course of half an hour [Citation18,Citation19], and mental stress may cause atherosclerosis by mechanisms other than an increase in LDL-C; for instance, via hypertension and increased platelet aggregation.

5. Does high LDL-C cause CVD?

5.1. LDL-C of patients with acute myocardial infarction is lower than normal

If high LDL-C causes CVD, LDL-C of untreated patients with CVD should be higher than normal. However, in a large American study [Citation20] including almost 140,000 patients with acute myocardial infarction (AMI), their LDL-C at the time of admission to hospital was actually lower than normal. In another study with the same finding [Citation21], the authors decided to lower the patients’ LDL-C even more, but at a follow-up 3 years later, total mortality among those with LDL-C below 105 mg/dl (2 mmol/l) was twice as high compared to those with a higher LDL-C, even after adjustment for confounding variables (14.8% vs. 7.1%, p = 0.005).

It has been suggested that inverse causation explains the inverse association between mortality and LDL-C; for example, that cancer and infections lower LDL-C.
A more likely explanation is that CVD may be caused by infections and that LDL directly inactivates almost all types of microorganisms and their toxic products [Citation12,Citation22,Citation23]. Consistent with that finding is the observation that healthy individuals with low LDL-C have a significantly increased risk of both infectious diseases [Citation23] and cancer [Citation24]; the latter possibly because microorganisms have been linked to almost 20% of all cancer types [Citation25].

5.2. Elderly people with high LDL-C live the longest

If high LDL-C was the major cause of atherosclerosis and CVD, people with the highest LDL-C should have shorter lives than people with low values. However, in a recent systematic review of 19 cohort studies including more than 68,000 elderly people (>60 years of age), we found the opposite [Citation26]. In the largest cohort study [Citation27], those with the highest LDL-C levels lived even longer than those on statin treatment. In addition, numerous Japanese studies have found that high LDL-C is not a risk factor for CHD mortality in women of any age [Citation28].

5.3. Mendelian randomization

An argument used in the three expert reviews [Citation1Citation3] is based on Mendelian randomization, which has shown that lower genetically determined LDL-C concentrations are associated with lower all-cause mortality. But again, association does not mean causation. Other genes in the same individual may have opposite effects, and as pointed out by Burgess et al., ‘Power, linkage disequilibrium, pleiotropy, canalization and population stratification have all been recognized as potential flaws in the Mendelian randomization approach’ [Citation29].

6. Does cholesterol-lowering treatment lower the risk of CVD?

6.1. No exposure–response in the statin trials

The strongest proof of causality is that a lowering or elimination of the suspected causal factor is able to lower the incidence of the disease in question. There have been small, but statistically significant, benefits in coronary event outcomes from statin trials. However, are the benefits of statin treatment produced by lowering LDL?

If high LDL-C were the major cause of CVD, the benefit from statin treatment should be better the more LDL-C is lowered; for example, there should be a systematic exposure–response relationship. The authors of the three reviews [Citation1Citation3] assert that statin trials have demonstrated such dose–responses. As proof, they have compared the outcomes in various trials with the degree of LDL-C lowering, and it is impossible to know whether the greater effect of a trial using a higher statin dose may be caused by its cholesterol-lowering effect or pleiotropic effects. True exposure–response is based on a comparison between the degree of cholesterol lowering in each patient in a single trial and the absolute reduction of their risk. True exposure–response has only been calculated in three clinical statin trials, and it was absent in all three [Citation30Citation32]. Even a correctly calculated exposure–response does not prove causality, because an innocent risk factor, for instance, LDL-C, may change in the same direction as the real cause, but the absence of exposure–response is a strong argument against causality.

Furthermore, in their calculation, Silverman et al. [Citation2] compared the number of major vascular events (MVEs) with the relative risk reduction (RRR). MVE is of dubious value as a measure of benefit because it is defined very differently in various trials [Citation33]. Using RRR as a measure of benefit is also highly misleading [Citation34], as it inflates the appearance of the rate of event reduction. For instance, in a trial where 2 of 100 participants in the control group die but only 1 of 100 in the treatment group die, the absolute risk reduction (ARR) is only a 1% benefit. However, if one reports the RRR, then a 50% benefit can be reported, because one is 50% of two.

A preferred way to measure the therapeutic benefit of statin treatment would be to compare the ARR per year of CVD mortality, CHD mortality, and total mortality of each trial with the degree of LDL-C lowering, as we have done in  and  and . These data are from the 26 statin trials included in the meta-analysis by Silverman et al. [Citation35Citation59] and from 11 trials that they excluded [Citation60Citation69]. As seen from  and , there was a weak, positive association in the included trials, whereas the association was inverse in the ignored trials.


[...]

6.2. The benefit of statin treatment is exaggerated

Collins et al. [Citation1] also used the RRR to quantify the benefit from statin treatment. They claimed that lowering LDL-C by 2 mmol/L will cause an RRR of MVE of about 45%/year, and here, they refer to the meta-analysis performed by the Cholesterol Treatment Trialists [Citation70]. But according to  and  in that article, the ARR of MVE was only 0.8% (1% for men and 0.2% for women), and the ARR of total mortality was 0.4% (both sexes).

According to the meta-analysis by Silverman et al. [Citation2], reducing LDL-C lowers the risk of MVE in the primary and secondary prevention trials by 0.35 and 1.0%/year/mmol/l reduction of LDL-C, respectively. However, as mentioned, they excluded at least 11 unsuccessful statin trials in which MVE was reported. One of the reasons for the exclusion of a subset of trials may be that they considered trials with fewer than 50 events as unreliable, but in all of the excluded trials, the number of events was higher.

Moreover, neither Collins et al. [Citation1] nor Silverman et al. [Citation2] mentioned that in four statin trials, where a high-degree lowering of LDL-C was compared with a low-degree lowering, no significant difference with respect to the number of MVEs was obtained, although LDL-C was lowered by 0.4–1 mmol/L more in the high-dose groups [Citation53,Citation55,Citation56,Citation61].

Furthermore, the most important outcome – an increase of life expectancy – has never been mentioned in any cholesterol-lowering trial, but as calculated recently by Kristensen et al., statin treatment does not prolong lifespan by more than an average of a few days [Citation71].

6.3. The benefit from statin treatment has been questioned

For some years, many researchers have questioned the results from statin trials because they have been denied access to the primary data. In 2004–2005, health authorities in Europe and the United States introduced New Clinical Trial Regulations, which specified that all trial data had to be made public. Since 2005, claims of benefit from statin trials have virtually disappeared [Citation72], see  and .

6.4. Adverse effects from statin treatment

According to Collins et al. [Citation1], adverse effects from statin treatment are extremely rare, and the incidence of statin adverse effects can only be obtained from randomized controlled trials. However, many drug-related adverse effects in other therapy areas have only emerged from observational studies and post-marketing surveillance. Furthermore, most statin trials have included a run-in period, where participants received the drug for a few weeks, after which those who suffered adverse effects or who were unwilling to continue were excluded. The results from two trials without a run-in period [Citation55,Citation64] and where a high statin dose was compared with a low dose demonstrated that this is an effective way to minimize the number of reported side effects; in SAGE [Citation64], serious side effects were recorded in more than 20% in both groups, and in IDEAL [Citation55], the number was almost 50%.

According to Collins et al. [Citation1], myopathy occurs in only 0.01% of treated individuals per year, but in most statin trials, myopathy is only recorded if creatine kinase is more than 10 times higher than normal. However, in a study by Phillips et al. [Citation73], microscopic examinations of muscle biopsies from statin-treated patients with muscular symptoms and normal creatine kinase levels showed signs of myopathy. When patients stopped treatment, their symptoms disappeared, and repeated biopsies showed resolution of the pathological changes.

To reject the frequent occurrence of muscular problems with the argument that muscle symptoms are nocebo effects is also invalid. In a study of 22 statin-treated professional athletes [Citation74], the authors reported that 17 (77%) of the athletes terminated treatment because of muscular symptoms, which disappeared a few days or weeks after drug withdrawal. The explanation for statin-induced adverse muscle effects is probably that statin treatment not only blocks the production of cholesterol but also blocks the production of several other important molecules, for instance, coenzyme Q10, which is indispensable for energy production. As most energy is produced in the muscle cells, including those of the heart, the extensive use of statin treatment may explain the epidemics of heart failure that have been observed in many countries [Citation75].

Furthermore, case–control and cross-sectional studies have shown that statin use is observed significantly more often among patients with cataracts [Citation76], hearing loss [Citation77], suicidal ideation [Citation78], peripheral neuropathy [Citation79], depression [Citation80], Parkinson’s disease [Citation81], interstitial cystitis [Citation82], herpes zoster [Citation83], impotency [Citation84], cognitive impairments [Citation85Citation88], and diabetes [Citation89,Citation90]. In some of these studies, the side effects disappeared with discontinuation of the statins and worsened with rechallenge [Citation74,Citation84,Citation85]. As cholesterol is a vital substance for the renewal of all cells, and since statins also block the production of other molecules necessary for normal cell function [Citation75], it is not surprising that statin treatment may result in side effects from many different organs.

According to Collins et al., statin treatment protects against cancer. However, in three trials, cancer occurred significantly more often in the treatment groups [Citation24], and there is much evidence that low cholesterol predisposes to cancer. For instance, several experiments on rodents with lipid-lowering drugs produced cancer [Citation91], and in nine human cohort studies, cancer rates were inversely associated with cholesterol levels measured in healthy people 10 to more than 30 years earlier [Citation24]. Therefore, case–control studies in which the incidence of cancer in statin-treated patients was lower than in controls are invalid because many untreated individuals have low cholesterol, and those on statins have lived most of their lives with high cholesterol that may have provided protection from developing cancer.

The reported incidence of most of the above-mentioned side effects may be relatively small, but taken together, the total number can become substantial, in particular in patients who continue statin treatment for many years.

6.5. Does treatment with proprotein convertase subtilisin–kexin type 9 inhibitors improve the outcome?

A new cholesterol-lowering drug has recently been introduced. It is an antibody that inhibits proprotein convertase subtilisin–kexin type 9 (PCSK-9), which lowers LDL-C by approximately 60%. In FOURIER, the largest and longest PCSK-9 inhibitor trial, evolocumab was compared with placebo in more than 27,000 statin-treated patients with CVD [Citation92]. The trial was stopped after 2.2 years because the number of MVE was reduced with statistical significance (9.8% vs. 11.3%). However, both CVD mortality and total mortality had increased, although not with statistical significance. A relevant question is, therefore, why the trial, the sponsor of which (Amgen) was responsible for data collection, was ended after only 2.2 years. Furthermore, this trial is yet another proof that there is no exposure–response between LDL-C and total or CVD mortality.

7. Does FH prove that high LDL-C causes CVD?

7.1. A low percentage of FH individuals die prematurely

For many years, it has been assumed that high LDL-C was the cause of the increased risk of CVD and premature deaths in individuals with FH, and this argument was used by Collins et al. [Citation1] and Ference et al. [Citation2] as well. However, many observations are in conflict with this hypothesis.

For instance, according to the Simon Broome registry, only a small percentage of FH individuals die at an early age, and the mortality among the elderly does not differ from the mortality of the general population despite their high LDL-C [Citation93].

In a study by Mundal et al., 4688 individuals aged 0–92 years with FH were followed up for 18 years [Citation94]. During that time, 113 died, whereas the expected number in the general population was 133. The mortality benefit cannot have been due to lipid-lowering treatment because there was no significant difference between the number on such treatment among those who died and those above the age of 18 years who survived (88.2% vs. 89.1%).

7.2. No LDL-C difference between FH individuals with and without CVD

If high LDL-C causes premature CVD in FH, the LDL-C of those with CVD should be higher compared to others, but at least six studies of untreated FH individuals have shown no significant differences in LDL-C or age [Citation95Citation100]. It has also been shown that FH relatives without FH may have shorter lives than the general population [Citation101]. Most likely, a small subset of FH individuals and their relatives inherit CVD risk factors that are more important than high LDL-C on CVD outcomes.

8. Has CVD mortality decreased after the introduction of statin treatment?

For decades, a decrease in CVD mortality has been observed in many countries, and the presumed reason for the decrease is the increasing use of statin treatment. However, this interpretation is highly questionable [Citation72]. In a Swedish study including 289 of the 290 municipalities, no association was found between statin use and the change in mortality from AMI [Citation102]. Also, the American National Health and Nutrition Examination Survey [Citation103] found that during the period 1999–2006, the number of AMI and strokes increased from 3.4% to 3.7% and from 2.0% to 2.9%, respectively. During the same period, mean LDL-C level decreased from 126.1 to 114.8 mg/dl, and the self-reported use of lipid-lowering drugs increased from 8% to 13.4%. Furthermore, statin utilization in 12 European countries between 2000 and 2012 was not associated with reduced CHD mortality or its rate of change over the years [Citation104].

9. Conclusion

The idea that high cholesterol levels in the blood are the main cause of CVD is impossible because people with low levels become just as atherosclerotic as people with high levels and their risk of suffering from CVD is the same or higher. The cholesterol hypothesis has been kept alive for decades by reviewers who have used misleading statistics, excluded the results from unsuccessful trials and ignored numerous contradictory observations.

10. Expert commentary

In our analysis of three major reviews [Citation1Citation3], that claim the cholesterol hypothesis is indisputable and that statin treatment is an effective and safe way to lower the risk of CVD, we have found that their statements are invalid, compromised by misleading statistics, excluding unsuccessful trials, minimizing the side effects of cholesterol lowering, and ignoring contradictory observations from independent investigators.

The usual argument in support of the lipid hypothesis is that numerous studies of young and middle-aged people have shown that high TC or LDL-C predict future CVD. This is correct, but association is not the same as causation. Few authors have adjusted for other CVD-promoting factors such as mental stress, coagulation factors, inflammation, infections, and endothelial sensitivity, all of which are closely related to LDL receptor abnormalities [Citation105]. For instance, mental stress can raise TC [Citation17,Citation18] possibly because cholesterol is necessary for the production of cortisol and other steroid stress hormones, and mental stress may cause CVD by an increased production of epinephrine and norepinephrine, which contribute to hypertension and hypercoagulation. The reason why high TC is a risk factor only for young and middle-aged people may be that mental stress is more common among working people than among retired senior citizens.

It is important to emphasize that LDL participates in the immune system by adhering to and inactivating all kinds of microorganisms and their toxic products and that many observations and experiments have incriminated infections as a possible causal factor of CVD [Citation21Citation23], and our results indicate that there may be better methods than cholesterol lowering to prevent atherosclerosis and CVD.

11. Five-year view

Statin treatment is prescribed for perpetual use, but very few trials have continued for more than a few years. In the longest follow-up study (20 years) [Citation106], the authors claimed that pravastatin used as primary prevention reduced the risk of CHD by 27% and the risk of major adverse cardiovascular events by 25%. However, these figures represented RRR; the ARR was only a few percentage points. A more serious bias is the statement, mentioned only in a supplement, that the authors did not know how many of the participants had used pravastatin during the 20 years of follow-up after the trial [Citation107]. A relevant goal for future research would be to encourage independent investigators to compare the health status of those who have taken statins for many years with the status of untreated individuals with the same risk factors who have lived just as long.

The lipid hypothesis has been perpetuated by the authors who have ignored the results from trials with a negative outcome, who have misused statistics, and who have ignored all contradictions documented by independent researchers. The increased risk of CVD in people with FH has been a primary argument in support of the lipid hypothesis. Surprisingly, several studies of untreated people with FH have shown that LDL-C does not differ significantly between those with and without CVD [Citation95Citation100] and that elderly people with FH live just as long as elderly people from the general population despite their high LDL-C [Citation93,Citation94]. FH individuals with significant CVD may have inherited other, more important risk factors than a high LDL-C.

Despite the fact that LDL-C is routinely referred to as the ‘bad cholesterol’, we have shown that high LDL-C levels appear to be unrelated to the risk of CVD, both in FH individuals and in the general population and that the benefit from the use of cholesterol-lowering drugs is questionable. Therefore, a systematic search for other CVD risk factors is an important topic for future research.

Key issues

  • The hypothesis that high TC or LDL-C causes atherosclerosis and CVD has been shown to be false by numerous observations and experiments.

  • The fact that high LDL-C is beneficial in terms of overall lifespan has been ignored by researchers who support the lipid hypothesis.

  • The assertion that statin treatment is beneficial has been kept alive by individuals who have ignored the results from trials with negative outcomes and by using deceptive statistics.

  • That statin treatment has many serious side effects has been minimized by individuals who have used a misleading trial design and have ignored reports from independent researchers.

  • That high LDL-C is the cause of CVD in FH is questionable because LDL-C does not differ between untreated FH individuals with and without CVD.

  • Millions of people all over the world, including many with no history of heart disease, are taking statins, and PCSK-9 inhibitors to lower LDL-C further are now being promoted, despite unproven benefits and serious side effects.

  • We suggest that clinicians should abandon the use of statins and PCSK-9 inhibitors and instead identify and target the actual causes of CVD.

Declaration of Interest

U Ravnskov, M de Lorgeril, R Hama, M Kendrick, H Okuyama and R Sundberg has published books with criticism of the cholesterol hypothesis. PJ Rosch has edited a book with criticism of the cholesterol hypothesis. KS Mccully has a US patent for a homocysteine-lowering protocol. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
https://www.tandfonline.com/doi/10.1080/17512433.2018.1519391?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed


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