AHA paper on cov. vac. - dramatic increase of cardiac risk markers

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Abstract 10712: Mrna COVID Vaccines Dramatically Increase Endothelial Inflammatory Markers and ACS Risk as Measured by the PULS Cardiac Test: a Warning

Steven R Gundry

Originally published8 Nov 2021Circulation. 2021;144:A10712

Quote: 

Abstract

Our group has been using the PLUS Cardiac Test (GD Biosciences, Inc, Irvine, CA) a clinically validated measurement of multiple protein biomarkers which generates a score predicting the 5 yr risk (percentage chance) of a new Acute Coronary Syndrome (ACS). The score is based on changes from the norm of multiple protein biomarkers including IL-16, a proinflammatory cytokine, soluble Fas, an inducer of apoptosis, and Hepatocyte Growth Factor (HGF)which serves as a marker for chemotaxis of T-cells into epithelium and cardiac tissue, among other markers. Elevation above the norm increases the PULS score, while decreases below the norm lowers the PULS score.The score has been measured every 3-6 months in our patient population for 8 years. Recently, with the advent of the mRNA COVID 19 vaccines (vac) by Moderna and Pfizer, dramatic changes in the PULS score became apparent in most patients.This report summarizes those results. A total of 566 pts, aged 28 to 97, M:F ratio 1:1 seen in a preventive cardiology practice had a new PULS test drawn from 2 to 10 weeks following the 2nd COVID shot and was compared to the previous PULS score drawn 3 to 5 months previously pre- shot. Baseline IL-16 increased from 35=/-20 above the norm to 82 =/- 75 above the norm post-vac; sFas increased from 22+/- 15 above the norm to 46=/-24 above the norm post-vac; HGF increased from 42+/-12 above the norm to 86+/-31 above the norm post-vac. These changes resulted in an increase of the PULS score from 11% 5 yr ACS risk to 25% 5 yr ACS risk. At the time of this report, these changes persist for at least 2.5 months post second dose of vac.We conclude that the mRNA vacs dramatically increase inflammation on the endothelium and T cell infiltration of cardiac muscle and may account for the observations of increased thrombosis, cardiomyopathy, and other vascular events following vaccination.

Sugar Industry and Coronary Heart Disease Research/A Historical Analysis

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"Sugar Industry and Coronary Heart Disease Research/A Historical Analysis of Internal Industry Documents" Cristin E. Kearns, Laura A. Schmidt, and Stanton A. Glantz, JAMA Intern Med. 2016 Nov 1; 176(11): 1680–1685.

Quote:

Results

SRF’s [Sugar Research Foundation] Interest in Promoting a Low-Fat Diet to Prevent CHD Sugar Research Foundation president Henry Hass’s 1954 speech, “What’s New in Sugar Research,”12 to the American Society of Sugar Beet Technologists identified a strategic opportunity for the sugar industry: increase sugar’s market share by getting Americans to eat a lower-fat diet:...
If the carbohydrate industries were to recapture this 20 percent of the calories in the US diet (the difference between the 40 percent which fat has and the 20 percent which it ought to have) and if sugar maintained its present share of the carbohydrate market, this change would mean an increase in the per capita consumption of sugar more than a third with a tremendous improvement in general health.
The industry would subsequently spend $600 000 ($5.3 million in 2016 dollars) to teach “people who had never had a course in biochemistry… that sugar is what keeps every human being alive and with energy to face our daily problems.” ..

Growing Evidence That Sucrose Elevates Serum Cholesterol Level

... Hickson proposed that the SRF “could embark on a major program” to counter Yudkin and other “negative attitudes toward sugar.”
... Finally, here commended that SRF fund CHD research: “There seems to be a question as to whether the [atherogenic] effects are due to the carbohydrate or to other nutrient imbalance. We should carefully review the reports, probably with a committee of nutrition specialists; see what weak points there are in the experimentation, and replicate the studies with appropriate corrections. Then we can publish the data and refute our detractors.” ...

SRF Funds Project 226: A Literature Review on Sugars, Fats, and CHD

... Nine months into the project, in April 1966, Hegsted told the SRF that the review had been delayed because of new evidence linking sugar to CHD: “Every time the Iowa group publishes a paper we have to rework a section in rebuttal [emphasis added].”44 The “Iowa group” included Alfredo Lopez, Robert Hodges, and Willard Krehl, who had reported a positive association between sugar consumption and elevated serum cholesterol level.

Discussion

These internal documents show that the SRF initiated CHD research in 1965 to protect market share and that its first project, a literature review, was published in NEJM in 1967 without disclosure of the sugar industry’s funding or role. The NEJM review served the sugar industry’s interests by arguing that epidemiologic, animal, and mechanistic studies associating sucrose with CHD were limited, implying they should not be included in an evidentiary assessment of the CHD risks of sucrose. Instead, the review argued that the only evidence modality needed to yield a definitive answer to the question of how to modify the American diet to prevent CHD was RCTs that exclusively used serum cholesterol level as a CHD biomarker. Randomized clinical trials using serum cholesterol level as the CHD biomarker made the high sucrose content of the American diet seem less hazardous than if the entire body of evidence had been considered.

Following the NEJM review, the sugar industry continued to fund research on CHD and other chronic diseases “as a main prop of the industry’s defense.”51 For example, in 1971, it influenced the National Institute of Dental Research’s National Caries Program to shift its emphasis to dental caries interventions other than restricting sucrose.8 The industry commissioned a review, “Sugar in the Diet of Man,” which it credited with, among other industry tactics, favorably influencing the 1976 US Food and Drug Administration evaluation of the safety of sugar.51 These findings, our analysis, and current Sugar Association criticisms of evidence linking sucrose to cardiovascular disease6,7 suggest the industry may have a long history of influencing federal policy.

animal fat is low cardio vascular risk, carbs are high risk

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A 2016 Czech study of 42 European countries

"Food consumption and the actual statistics of cardiovascular diseases: an epidemiological comparison of 42 European countries", by Pavel Grasgruber,* Martin Sebera, Eduard Hrazdira, Sylva Hrebickova, and Jan Cacek; Food Nutr Res. 2016; 60: 10.3402/fnr.v60.31694.

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The mean consumption of 62 food items from the FAOSTAT database (1993–2008) was compared with the actual statistics of five CVD [CVD=Cardio-Vascular Disease] indicators in 42 European countries. Several other exogenous factors (health expenditure, smoking, body mass index) and the historical stability of results were also examined.
...

The most significant dietary correlate of low CVD risk was high total fat and animal protein consumption.

Additional statistical analyses further highlighted citrus fruits, high-fat dairy (cheese) and tree nuts. Among other non-dietary factors, health expenditure showed by far the highest correlation coefficients.

The major correlate of high CVD risk was the proportion of energy from carbohydrates and alcohol, or from potato and cereal carbohydrates. Similar patterns were observed between food consumption and CVD statistics from the period 1980–2000, which shows that these relationships are stable over time.

...
Our results do not support the association between CVDs and saturated fat, which is still contained in official dietary guidelines. Instead, they agree with data accumulated from recent studies that link CVD risk with the high glycaemic index/load of carbohydrate-based diets. In the absence of any scientific evidence connecting saturated fat with CVDs, these findings show that current dietary recommendations regarding CVDs should be seriously reconsidered.
...

Low cholesterol levels correlate most strongly with the proportion of plant food energy in the diet (r=−0.87, p less than 0.001 in both sexes) and with sources of plant carbohydrates represented by items such as % PC CARB energy (r=−0.87 in men, r=−0.83 in women; p less than 0.001) (Fig. 2), % CA energy (r=−0.85 in men, r=−0.81 in women; p less than 0.001), and cereals (r=−0.74 in men, r=−0.73 in women; p less than 0.001). Smoking correlates quite strongly with lower cholesterol as well, but in men only (r=−0.62, p less than 0.001).

Remarkably, the relationship of raised cholesterol with CVD risk is always negative, especially in the case of total CVD mortality (r=−0.69 in men, r=−0.71 in women; p less than 0.001)

Most interesting is the discussion section at the end of the paper:

Discussion

Raised cholesterol correlates negatively with CVD risk

The results of our study show that animal fat (and especially its combination with animal protein) is a very strong predictor of raised cholesterol levels. This is in accordance with the meta-analyses of clinical trials, which show that saturated animal fat is the major trigger of raised cholesterol (6, 16). Interestingly, the relationship between raised cholesterol and CVD indicators in the present study is always negative. As shown in Figs. 3 and ​and Supplementary Figs. 1 and 2, this finding is visually less persuasive in the case of CVD mortality, where factors such as the quality of healthcare come to the foreground, but it is quite unambiguous in the case of women's raised blood pressure.

The negative relationship between raised cholesterol and CVD may seem counterintuitive, but it is not at variance with the available evidence. The largest of the recent worldwide meta-analyses dealing with cholesterol and CVD risk (17) observed a positive relationship between raised cholesterol and CVD mortality at younger ages, but this association gradually started to reverse in seniors, where the number of deaths is the highest. In fact, the relationship between raised cholesterol and stroke mortality in seniors was slightly negative. Both this study and other studies dealing with blood profiles of patients hospitalised with CVD events (18–22) demonstrate that low HDL (high-density lipoprotein associated) cholesterol (around ~1.0 mmol/L), or high total cholesterol: HDL-cholesterol ratio are the best indicators of CVD risk. Total cholesterol is usually normal or slightly elevated (4.5–5.5 mmol/L), and hence it cannot serve as a predictor of CVD events. Some other authors also point to high plasma triglycerides (which correlate with low HDL-cholesterol levels) (23), or to the ratio between triglycerides and HDL-cholesterol (24) as another useful risk indicators.

In this context it is important to note that saturated fat is not only the key trigger of high total cholesterol, but even high HDL-cholesterol and LDL (low-density lipoprotein associated)-cholesterol (16). Saturated fat also decreases triglyceride levels, but the total cholesterol: HDL-cholesterol ratio remains stable. The main sources of saturated fatty acids are red meat and milk products (whole fat milk, cheese, butter) (see Supplementary Table 1). Therefore, in Europe, where the consumption of animal products is the highest in the world, we can assume a strong connection between total cholesterol and HDL-cholesterol. Understandably, this relationship may not be so strong outside Europe and it may also vary depending on the individual diet. This could explain regional and individual differences in the relationship between total cholesterol and CVD risk.

Although the concurrent increase of LDL-cholesterol levels is often taken out of context and used as an argument against the intake of saturated fats in dietary recommendations (25), saturated fat is primarily tied to the less dense, large LDL particles (26), whereas cardiovascular risk is connected with the denser, small LDL particles (27), which accompany carbohydrate-based diets. There is also no evidence that the reduction of saturated fat intake (on its own) would decrease CVD risk (28). On the other hand, it is true, that so far, there is no clear evidence that saturated fat would be beneficial for the prevention of CVD. The only possible exception among the sources of saturated fat is dairy (29–31).

Major correlates of high CVD risk

Carbohydrates

The results of our study show that high-glycaemic carbohydrates or a high overall proportion of carbohydrates in the diet are the key ecological correlates of CVD risk. These findings strikingly contradict the traditional ‘saturated fat hypothesis’, but in reality, they are compatible with the evidence accumulated from observational studies that points to both high glycaemic index and high glycaemic load (the amount of consumed carbohydrates × their glycaemic index) as important triggers of CVDs (1, 32–34). The highest glycaemic indices (GI) out of all basic food sources can be found in potatoes and cereal products (Supplementary Table 2), which also have one of the highest food insulin indices (FII) that betray their ability to increase insulin levels.

The role of the high glycaemic index/load can be explained by the hypothesis linking CVD risk to inflammation resulting from the excessive spikes of blood glucose (‘post-prandial hyperglycaemia’) (35). Furthermore, multiple clinical trials have demonstrated that when compared with low-carbohydrate diets, a low-fat diet increases plasma triglyceride levels and decreases total cholesterol and HDL-cholesterol, which generally indicates a higher CVD risk (36, 37). Simultaneously, LDL-cholesterol decreases as well and the number of dense, small LDL particles increases at the expense of less dense, large LDL particles, which also indicates increased CVD risk (27). These findings are mirrored even in the present study because cereals and carbohydrates in general emerge as the strongest correlates of low cholesterol levels.

The authors discuss the reason behind the origin of the now discredited cholesterol-heart disease hypothesis prompted by Ancel Keyes' ‘Seven Countries Study’:

Discrepancy in the old statistics: The root of the ‘saturated fat hypothesis’?

The paradoxical results of our historical comparison (men's statistics from 1980 and 1990) have an interesting analogy in the ‘Seven Countries Study’, which stood behind the current ‘saturated fat paradigm’. The authors of this longitudinal ecological research, finished in the early 1980s, concluded that men's CHD [CHD=Coronary Heart Disease] mortality in seven countries correlated positively with high blood pressure, high cholesterol, and high saturated fat intake, but the relationship of high blood pressure and high cholesterol with men's stroke mortality (in 12 cohorts from six countries) was strongly negative (54). Because CHD mortality was the central CVD [CVD=Cardio-Vascular Disease] indicator in this study, we think that the authors did not pay sufficient attention to this discrepancy and they contented themselves with the fact that stroke mortality was positively associated with high blood pressure at the individual level. Ironically, in the following decades, the ecological relationship of CHD with risk factors completely reversed.

...Second, the effect of increased longevity in highly developed countries, after the eradication of serious infectious diseases after World War II, led to a temporary epidemic of CVDs, which also coincided with rapidly improving living standards and the increasing consumption of animal food. Because of the chronic nature of CVDs, this dietary change may have brought health benefits only after several decades and as a result, the relationship of CVD indicators to animal products has reversed with a certain delay (Supplementary Figs. 42–47). In the eastern half of Europe, this phenomenon started to fully manifest only very recently (possibly in combination with heavy alcohol drinking), which led to the increase of CVD rates.

The obvious fallacy of the ‘saturated fat hypothesis’ can be demonstrated by the example of France – a country with the highest intake of animal fat in the world and the second lowest CVD mortality (after Japan) (56). In fact, if we use a limited sample of 24 countries (without the former republics of USSR, Czechoslovakia and Yugoslavia, and Luxembourg), a summary mean of food consumption from the last half-century (1961–2008) produces very similar results like the mean for the period 1993–2008 (Table 4), reaching r=0.82 between % CA [CA=carbohydrates] energy and raised blood pressure in women.

A short summary of the paper can be read in the following article:

New study finds wheat and carbs biggest risk for heart disease, red meat and saturated fat has no direct effect

statins and cholesterol scam

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Do statins really work? Who benefits? Who has the power to cover up the side effects?,
By Aseem Malhotra , European Scientist - 03.09.2019,

Wiki

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Why It’s now time for a full public parliamentary inquiry into the controversial drug and fully expose the great cholesterol and statin con

Earlier this week, the Chair of the British Parliament Science and Technology Committee, Sir Norman Lamb MP made calls for a full investigation into cholesterol lowering statin drugs. It was instigated after a letter was written to him signed by a number of eminent international doctors including the editor of the BMJ, the Past President of the Royal College of Physicians and the Director of the Centre of Evidence Based Medicine in Brazil wrote a letter calling for a full parliamentary inquiry into the controversial medication[1]. It’s lead author Cardiologist Dr Aseem Malhotra makes the case for why’s there’s an urgent need for such an investigation in European Scientist.

A few weeks ago, an alarmed and confused patient in his late forties, who I shall call Mr Smith, came to see me for a consultation. Four years earlier he suffered a heart attack where severe blockages were found in his right coronary artery. These were opened up and kept open with metal stents.

He was prescribed atorvastatin, which is standard practice for heart attack patients regardless of cholesterol levels. Unfortunately, the atorvastatin caused severe muscle pains on exercise. Fortunately, his symptoms disappeared within a week of stopping the drug.

As an alternative to his statin, he decided to adopt an ultra-low fat vegan diet which he believed may halt, even reverse heart disease through lowering cholesterol. Within months he dropped his total cholesterol by 40% from 5.2mmol/L to 3.2, now placing his levels in the bottom five per cent of the population.

Despite sticking religiously to the diet, he began to develop chest pain when he did exercise, and a repeat heart scan showed a seventy per cent blockage in another artery, one that had been completely clear four years before. “How is this possible?” he asked me, clearly upset. ‘How could I develop more heart disease in such a short space of time with such low cholesterol?’

I explained to him his case was not unusual, nor inexplicable.
...

Rather than accept greater scrutiny, highly influential cardiologists are attacking those who question the benefits of statins. Those who believed that side effects are much more prevalent are denounced as peddlers of “fake news” or “fake science”. They are compared to “anti – vaxxers”.One Cardiologist, Ana Navar even wrote in a recent editorial in JAMA Cardiology that inappropriate fears about statin side effects are coming from social media wellness bloggers and that “lives lost from inappropriate concerns about statins may number in the millions” but this is not evidence based. The side effect literature and remarkably high discontinuation rate comes from very credible sources[21].

The largest statin survey in the United States exposes 75% of those prescribed the medication stop it within a year of prescription with 62% of those stating side effects as the reason

Even as far back as 2002 when there was no social media or public awareness of statin side effects a paper in JAMA of over 40,000 patients reveals that 60% of heart attack patients aged over 65 will stop the drug within 2 years (ref)

...

So how effective are statins in preventing and treating heart disease?

When one removes the industry funded PR and hype, the results are pretty underwhelming.

In 2015, new research published in BMJ Open revealed that despite tens of millions more people being prescribed statins across many European countries there was no evidence that this had any effect on cardiovascular mortality, over a twelve year period[24].

If you strip down the statin trials to their moving parts, the data actually reveals that, even in those who have established heart disease, the benefits are very small. Even in this high risk group, the average increase in life expectancy from taking the drug religiously for five years is a meagre four days[25].

...

We continue to have an epidemic of misinformed doctors and misinformed and unwittingly deceived and harmed patients. In large part this has been driven by a multi-billion-dollar food and drug industry that profits from the fear of cholesterol.

It’s now time for a full public parliamentary inquiry to push for the raw data on statins find out who really benefits, and to determine who has been manipulating and hiding data on the debilitating side effects that appear to possibly affect almost half taking the drug. Until then it’s better we focus healthcare resources in tackling the real root cause of heart disease through prioritising lifestyle changes. It’s finally time to stop falling for the great cholesterol and statin con.

Insulin resistance cause of cardio-vascular disease

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The following paper, based on literature review (not an independent study!) explains the mechanisms behind cardiovascular diseases: cardiomyopathy, endothelial dysfunction, atherosclerotic plaque formation and coronary heart disease. The main cause = insulin resistance!

"Association between insulin resistance and the development of cardiovascular disease", by
Valeska Ormazabal, Soumyalekshmi Nair, Omar Elfeky, Claudio Aguayo, Carlos Salomon and Felipe A. Zuñiga
Cardiovascular Diabetology201817:122


Quotes:

...epidemiological and pathophysiological studies suggest that hyperglycemia may be largely responsible for CVD. Blood glucose has been reported as an independent predictor of atherosclerosis and blood glucose level greater than 90 mg/dl can lead to atherosclerosis in the carotid artery [125]. Long-term follow up data from patients with type 1 and type 2 diabetes suggest that hyperglycemia is a risk factor for diabetes related diseases and CVDMoreover, it has been suggested by Salvin et al. [126] that a 1 unit increase in the total glycosylated hemoglobin or HbA1C, can increase the risk of CVD by up to 18%. Even in the absence of overt diabetes, impairment in the glucose homeostasis can affect the cardiac autonomic function leading to high risk of cardiac diseases [127].

...
In this sense, recently it has been shown that cyclic ketone bodies preserve “young cardiac phenotype” in old mice [167]. On the other hand, it has been reported that isocaloric ketogenic diet (very low in carbohydrates and high in fats and/or proteins) increases lifespan [168].


Overall, insulin resistance contributes to generate CVD via two independent pathways: (1) atheroma plaque formation and (2) ventricular hypertrophy and diastolic abnormality.

Non-compliant diabetics had lower CVD risk

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"Adherence to lipid-lowering medications and cardiovascular disease prevention in type 2 diabetes mellitus", by Karlsson, Sofia Axia, PhD thesis, University of Gothenburg, 7-Nov-2018


Quote:

Adjusted for potential confounders, risk of CV events was higher among patients with less than complete adherence to lipid lowering medications and that risk gradually increased as patient adherence declined, independent of prevention group.

Mediterranean diet is good, adding meat & dairy makes it better!

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as the following two studies have recently demonstrated:

1) "A Mediterranean-style eating pattern with lean, unprocessed red meat has cardiometabolic benefits for adults who are overweight or obese in a randomized, crossover, controlled feeding trial",
Lauren E O'Connor, Douglas Paddon-Jones, Amy J Wright, Wayne W Campbell,
The American Journal of Clinical Nutrition, Volume 108, Issue 1, 1 July 2018, Pages 33–40

Note: they used lean read meat. I predict a follow-up study titled "A Mediterranean-style eating pattern with fatty, unprocessed red meat has the greatest cardiometabolic benefits"!


2) "A Mediterranean diet supplemented with dairy foods improves markers of cardiovascular risk: results from the MedDairy randomized controlled trial",
Alexandra T Wade, Courtney R Davis, Kathryn A Dyer, Jonathan M Hodgson, Richard J Woodman, Karen J Murphy,
The American Journal of Clinical Nutrition, nqy207, https://doi.org/10.1093/ajcn/nqy207
Published: 22 October 2018


Quote:

Results
Compared with the LF intervention, the MedDairy intervention resulted in a significantly lower morning SBP (mean difference: −1.6 mm Hg; 95% CI: −2.8, −0.4 mm Hg; P = 0.01), lower morning diastolic blood pressure (mean difference: −1.0; 95% CI: −1.7, −0.2 mm Hg; P = 0.01) and clinic SBP (mean difference: −3.5 mm Hg; 95% CI: −6.4, −0.7 mm Hg; P = 0.02), significantly higher HDL cholesterol (mean difference: 0.04 mmol/L; 95% CI: 0.01, 0.06 mmol/L; P < 0.01), lower triglycerides (mean difference: = −0.05 mmol/L; 95% CI: −0.08, −0.01 mmol/L; P < 0.01), and lower ratio of total to HDL cholesterol (mean difference: −0.4; 95% CI: −0.6, −0.2; P < 0.001). No effects were observed for other outcome measures. Conclusions
Following a MedDiet with additional dairy foods led to significant changes in markers of cardiovascular risk over 8 wk. The MedDiet supplemented with dairy may be appropriate for an improvement in cardiovascular risk factors in a population at risk of CVD.

LDL does not cause heart disease

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Recent paper by Uffe Ravnskov (et al.) - the father of cholesterol "red-pilling"!

"LDL-C Does Not Cause Cardiovascular Disease: a comprehensive review of current literature",
Uffe Ravnskov et al., Taylor & Francis Online, 10 Sep 2018


Key issues (quoted):

• 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.

More Quotes (chapter headlines):

2.1 No association between TC and degree of atherosclerosis

2.2 No exposure-response

3.1 An idea supported by fraudulent reviews of the literature

4. Does high LDL-C cause atherosclerosis? 4.1 An idea based on selected patient groups

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

5.2 Elderly people with high LDL-C live the longest

6.1 No exposure-response in the statin trials

6.2 The benefit of statin treatment is exaggerated

6.3 The benefit from statin treatment has been questioned

6.4 Adverse effects from statin treatment

6.5 Does treatment with PCSK-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 (PCSK9), 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 [92]. 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 percent of FH [Familial Hypercholesterolemia] individuals die prematurely

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

8. Has CVD mortality decreased after the introduction of statin treatment? ...
American National Health and Nutrition Examination Survey [103] 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 [104].

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.

Quoting the captions for the figures!

Figure 2. The association between degree of LDL-C lowering and the absolute risk reduction of total mortality (per cent per year) in 26 statin trials, where total mortality was recorded and which were included in the study by Silverman et al. and in 11 ignored trials. ARR is weakly associated with degree of LDL-C lowering in the included trials (y = 0.28x + 0.06), but inversely associated in the excluded trials (y = - 0.49x - 0.81). Symbols: see figure 1.

According to Ference et al. [3] the most compelling clinical evidence for causality is provided by “the presence of more than 30 randomized cholesterol-lowering trials that consistently demonstrate that reducing LDL-C reduces the risk of CVD events proportional to the absolute reduction in LDL-C.” As previously noted, this is not true exposure-response. Furthermore, in their figure 5A, that illustrates the association, the authors have only included data from12 of the 30 trials they refer to. If all of the trials in table 1 are included, as we have done in figure 3, there is no association between LDL-C lowering and coronary event rate.

Figure 5. The association between the absolute risk reduction of total mortality in 26 statin trials included in the study by Silverman et al. and in 11 ignored trials; and the year where the trial protocols were published. The vertical line indicates the year where the new trial regulations were introduced. [penalizing publication of false results - the new trials show no risk reduction! commented by S.B.]

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added 5/10/2018


QJM. 2018 May 1;111(5):319-325. doi: 10.1093/qjmed/hcy043.
A longitudinal 20 years of follow up showed a decrease in the survival of heart failure patients who maintained low LDL cholesterol levels.
Charach G1

No benefit in LDL-C lowering, trend toward harm.

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Quote

No beneficial relationship was found between LDL-C lowering and cardiovascular events explored by meta-regression; instead, there was a trend toward harm.

The systematic review ...,Battaggia A, et al. Curr Med Res Opin. 2018.

Quote

CONCLUSIONS: The relationship between LDL-C lowering and cardiovascular events has not showed any significant association (and even a tendency toward harm), challenging the "lower the better" theory. A separate meta-analysis of trials recruiting familial hypercholesterolemia patients has showed a tendency to harm for all outcomes with PCSK9 antibodies. Therefore, at the moment, the data available from randomized trials does not clearly support the use of these antibodies.

salt and cardiovascular risk debunked

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It was a fake theory! Fake - I like this word.

A Canadian study, just published in The Lancet:
Urinary sodium excretion, blood pressure, cardiovascular disease, and mortality: a community-level prospective epidemiological cohort study
Andrew Menteet al., VOLUME 392, ISSUE 10146, P496-506, AUGUST 11, 2018

Quote:

The association between mean sodium intake and major cardiovascular events showed significant deviations from linearity (p=0.043) due to a significant inverse association in the lowest tertile of sodium intake (lowest tertile <4.43 g/day, mean intake 4.04 g/day, range 3.42-4.43; change -1.00 events per 1000 years,...

Sodium intake was associated with cardiovascular disease and strokes only in communities where mean intake was greater than 5 g/day.

Halite (rock salt) from the Wieliczka salt mine,

Note: "inverse" association means that lower sodium INCREASES the rate of disease. In this case the cutoff threshold for the inverse relation is about 4g per day. The recommended daily dose of sodium by the fake (I love it) medical authorities is about 2g/day. Also, the usage of the unit "minus one event per 1000 years" has to be interpreted such that statistically there is one event less than the average, per 1000 patients per year rather than having to wait 1000 years for one patient event.

Read also here:

Salt not as damaging to health as previously thought, says study

Quote:

The study suggests that very low levels of salt could lead to more heart attacks and suggests that moderate salt consumption may be protective.
...
The World Health Organization recommends cutting sodium intake to no more than 2g a day - the equivalent of 5g of salt - because of the link to increased blood pressure, which is in turn implicated in stroke.

American Heart Assoc. recommendations gave its own president heart attack!

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American Heart Association President Suffers Heart Attack at 52

Good article by Dr. Mercola. I like the fact that he is not mincing the words.

Story at-a-glance

• John Warner, cardiologist and president of the American Heart Association (AHA), recently suffered a heart attack in the middle of a health conference at the age of 52
• In all likelihood, Warner followed AHA recommendations, many of which can actually worsen or cause heart disease
• AHA supports ample grain consumption and recommends eating harmful fats such as canola, corn, soybean and sunflower oil, both of which are known to cause and/or contribute to cardiovascular problems
• Good heart health starts with your diet — what you eat and when you eat. A powerful treatment for heart disease is to work your way up to an intermittent fasting schedule where you’re fasting for 20 hours a day
• When you do eat, make sure you eat real food, and consider a cyclical ketogenic diet, high in healthy fats, low in net carbs with moderate protein. Once you’re comfortable with this intermittent fasting schedule, start doing a monthly water only fast, working your way up to multiple days

Many AHA Recommendations Worsen Heart Health

In all likelihood, Warner followed AHA recommendations, many of which are actually recipes for heart disease disaster. Of the foods scientifically proven to cause heart disease and clogged arteries, excess sugar and industrially processed omega-6 vegetable oils, found in nearly all processed foods, compete for space at the top the list. And what kinds of foods does the AHA recommend to protect your heart?

Not only does it support ample grain consumption, it also recommends eating harmful fats such as canola, corn, soybean and sunflower oil.5 “Blends or combinations of these oils, often sold under the name ‘vegetable oil,’ and cooking sprays made from these oils are also good choices,” the AHA says. Meanwhile, the association still insists saturated fats are to be avoided.

Just this past summer the AHA shocked health experts around the world by sending out a worldwide advisory6 saying saturated fats such as butter and coconut oil should be avoided to cut your risk of heart disease, and that replacing these fats with margarine and vegetable oil might cut your heart disease risk by as much as 30 percent. Overall, the AHA recommends limiting your daily saturated fat intake to 6 percent of daily calories or less.7

This is as backward as it gets, and if Warner was following this long-outdated advice, it’s no wonder he suffered a heart attack. In fact, it is to be expected. As noted by American science writer Gary Taubes in his extensive rebuttal to the AHA’s advisory,8 with this document, the AHA reveals its longstanding prejudice — and the method by which it reaches its flawed conclusions.

In short, the AHA simply excluded any and all contrary evidence. After this methodical cherry-picking, they were left with just four clinical trials published in the 1960s and early ‘70s — the eras when the low-fat myth was born and grew to take hold. The problem is nutritional science has made significant strides since then, and a number of significant studies have firmly disproven the hypothesis that saturated fat causes heart disease, finding no association whatsoever.

Low-salt diet increases insulin resistance in healthy subjects

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Interesting study:


Low-salt diet increases insulin resistance in healthy subjects.
Garg R1, Williams GH, Hurwitz S, Brown NJ, Hopkins PN, Adler GK., Metabolism. 2011 Jul;60(7)

From Wiki Salt

Quote:

Abstract
Low-salt (LS) diet activates the renin-angiotensin-aldosterone and sympathetic nervous systems, both of which can increase insulin resistance (IR). We investigated the hypothesis that LS diet is associated with an increase in IR in healthy subjects. Healthy individuals were studied after 7 days of LS diet (urine sodium < 20 mmol/d) and 7 days of high-salt (HS) diet (urine sodium > 150 mmol/d) in a random order. Insulin resistance was measured after each diet and compared statistically, unadjusted and adjusted for important covariates. One hundred fifty-two healthy men and women, aged 39.1 ± 12.5 years (range, 18-65) and with body mass index of 25.3 ± 4.0 kg/m(2), were included in this study. Mean (SD) homeostasis model assessment index was significantly higher on LS compared with HS diet (2.8 ± 1.6 vs 2.4 ± 1.7, P < .01). Serum aldosterone (21.0 ± 14.3 vs 3.4 ± 1.5 ng/dL, P <  .001), 24-hour urine aldosterone (63.0 ± 34.0 vs 9.5 ± 6.5 μg/d, P < .001), and 24-hour urine norepinephrine excretion (78.0 ± 36.7 vs 67.9 ± 39.8 μg/d, P < .05) were higher on LS diet compared with HS diet. Low-salt diet was significantly associated with higher homeostasis model assessment index independent of age, sex, blood pressure, body mass index, serum sodium and potassium, serum angiotensin II, plasma renin activity, serum and urine aldosterone, and urine epinephrine and norepinephrine. Low-salt diet is associated with an increase in IR [insulin resistance]. The impact of our findings on the pathogenesis of diabetes and cardiovascular disease needs further investigation.

Saturated fat does not clog the arteries

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Saturated fat does not clog the arteries: coronary heart disease is a chronic inflammatory condition, the risk of which can be effectively reduced from healthy lifestyle interventions FREE
Aseem Malhotra1⇑, Rita F Redberg2,3, Pascal Meier4,5

Quote:

Coronary artery disease pathogenesis and treatment urgently requires a paradigm shift. Despite popular belief among doctors and the public, the conceptual model of dietary saturated fat clogging a pipe is just plain wrong. A landmark systematic review and meta-analysis of observational studies showed no association between saturated fat consumption and (1) all-cause mortality, (2) coronary heart disease (CHD), (3) CHD mortality, (4) ischaemic stroke or (5) type 2 diabetes in healthy adults.1 Similarly in the secondary prevention of CHD there is no benefit from reduced fat, including saturated fat, on myocardial infarction, cardiovascular or all-cause mortality.2 It is instructive to note that in an angiographic study of postmenopausal women with CHD, greater intake of saturated fat was associated with less progression of atherosclerosis whereas carbohydrate and polyunsaturated fat intake were associated with greater progression.3

Study contradicts official guidelines promoting low salt intake

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Another mainstream medical theory bites the dust! Just like with the cholesterol-and-fat bull..t in the past - it will be interesting to find out what has gone wrong and who did it!   :)

Higher sodium intake associated with lower blood pressure.

PUBLIC RELEASE: 25-APR-2017
Low-sodium diet might not lower blood pressure
Findings from large, 16-year study contradict sodium limits in Dietary Guidelines for Americans

Quotes:

Chicago (April 25, 2017) - A new study that followed more than 2,600 men and women for 16 years found that consuming less sodium wasn't associated with lower blood pressure. The new findings call into question the sodium limits recommended by the current Dietary Guidelines for Americans.

Lynn L. Moore, DSc, associate professor of medicine at Boston University School of Medicine, will present the new research at the American Society for Nutrition Scientific Sessions and annual meeting during the Experimental Biology 2017 meeting, to be held April 22-26 in Chicago.

"We saw no evidence that a diet lower in sodium had any long-term beneficial effects on blood pressure," said Moore. "Our findings add to growing evidence that current recommendations for sodium intake may be misguided."

Potatoes and cereals are heart disease risk while dairy, fat and meat are good for you

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- says the new study: "FOOD CONSUMPTION AND THE ACTUAL STATISTICS OF CARDIOVASCULAR DISEASES: AN EPIDEMIOLOGICAL COMPARISON OF 42 EUROPEAN COUNTRIES" .

Results: ...The most significant dietary correlate of low CVD risk was high total fat and animal protein consumption. Additional statistical analyses further highlighted citrus fruits, high-fat dairy (cheese) and tree nuts. ... The major correlate of high CVD risk was the proportion of energy from carbohydrates and alcohol, or from potato and cereal carbohydrates.

Conclusion: Our results do not support the association between CVDs and saturated fat, which is still contained in official dietary guidelines. Instead, they agree with data accumulated from recent studies that link CVD risk with the high glycaemic index/load of carbohydrate-based diets. In the absence of any scientific evidence connecting saturated fat with CVDs, these findings show that current dietary recommendations regarding CVDs should be seriously reconsidered.

(CVD stands for "Cardio Vascular Disease")

by Cecilia Bleszynski (C) 2017

The first graph published in the paper:

is the most interesting in conjunction with the rest of the results, showing that the high consumption of animal fat and protein correlates very well with high blood cholesterol level and at the same time (see for example Fig.4 and 7) the high cholesterol and high consumption of animal fat and protein correlate consistently and strongly with the low cardiovascular and other diseases' risk! That is yet another nail to the coffin of the cholesterol-heart hypothesis and an indication that the blood cholesterol correlation with cardiovascular disease (+ or -) is secondary and spurious while the primary risk factor appears to be related to the carbohydrate contents of the diet! Note that some of the graphs refer to women some for men but the actual correlation factors are similar for men and momen (see Table 1) with the exception of correlations involving BMI and smoking which are opposite for women and men (that is another interesting subject).

Most of the results point consistently and strongly, see for example Fig.10 towards the carbohydrates contents of the diet as being the strongest positive correlator with the cardiovascular disease risk, where as the animal and most plant fats correlate most negatively (that is being protective) against cardiovascular disease, see Table 1, with the notable exception of sunflower oil which correlates strongly and positively with the CVD.

It is also interestingly to notice a strong linear correlation graph with very low data scatter, between the prevalence of raised blood glucose and consumption of carbohydrates plus alcohol ('CA' variable), on Fig.9:

Although diabetes risk was not directly measured in the study, Fig.9 appears to indicate that diabetes risk may be steeply correlated to the total consumption of carbohydrates plus alcohol, and strongly inversely correlated with the consumption of animal fat and protein (see Table 1). For example an increase of the dietary carbohydrate+alcohol contents from 42% to 68% seems to increase the prevalence of high blood glucose (and thus probably diabetes risk as well) by a factor of 3!

The overall results of this study are also remarkably consistent with the original China Study data as published on the Oxford University web site and  discussed on this blog (see my previous posts).

The study is also discussed in the following journalistic article:

"Potatoes and cereals are health risk, while dairy is good for you, says new study".

Fat and cholesterol-heart disease theory - worldwide hoax perpetrated by American Sugar Association!

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This is now official, documents found and published! If one thinks about the implications, scale and the length of time, it would probably not be surprizing if this were followed by some some serious Crime Against Humanity type investigation against the officials that were involved, and named!

NY Times: How the Sugar Industry Shifted Blame to Fat

The sugar industry paid scientists in the 1960s to play down the link between sugar and heart disease and promote saturated fat as the culprit instead, newly released historical documents show.

The internal sugar industry documents, recently discovered by a researcher at the University of California, San Francisco, and published Monday in JAMA Internal Medicine, suggest that five decades of research into the role of nutrition and heart disease, including many of today’s dietary recommendations, may have been largely shaped by the sugar industry.

“They were able to derail the discussion about sugar for decades,” said Stanton Glantz, a professor of medicine at U.C.S.F. and an author of the JAMA Internal Medicine paper.

The documents show that a trade group called the Sugar Research Foundation, known today as the Sugar Association, paid three Harvard scientists the equivalent of about $50,000 in today’s dollars to publish a 1967 review of research on sugar, fat and heart disease. The studies used in the review were handpicked by the sugar group, and the article, which was published in the prestigious New England Journal of Medicine, minimized the link between sugar and heart health and cast aspersions on the role of saturated fat.

...

In 1965, Mr. Hickson enlisted the Harvard researchers to write a review that would debunk the anti-sugar studies. He paid them a total of $6,500, the equivalent of $49,000 today. Mr. Hickson selected the papers for them to review and made it clear he wanted the result to favor sugar. Harvard’s Dr. Hegsted reassured the sugar executives. “We are well aware of your particular interest,” he wrote, “and will cover this as well as we can.”

JAMA paper: Sugar Industry and Coronary Heart Disease Research
A Historical Analysis of Internal Industry Documents

Abstract

Early warning signals of the coronary heart disease (CHD) risk of sugar (sucrose) emerged in the 1950s. We examined Sugar Research Foundation (SRF) internal documents, historical reports, and statements relevant to early debates about the dietary causes of CHD and assembled findings chronologically into a narrative case study. The SRF sponsored its first CHD research project in 1965, a literature review published in theNew England Journal of Medicine, which singled out fat and cholesterol as the dietary causes of CHD and downplayed evidence that sucrose consumption was also a risk factor. The SRF set the review’s objective, contributed articles for inclusion, and received drafts. The SRF’s funding and role was not disclosed. Together with other recent analyses of sugar industry documents, our findings suggest the industry sponsored a research program in the 1960s and 1970s that successfully cast doubt about the hazards of sucrose while promoting fat as the dietary culprit in CHD. Policymaking committees should consider giving less weight to food industry–funded studies and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development.

...
RESULTS

SRF’s Interest in Promoting a Low-Fat Diet to Prevent CHD

Sugar Research Foundation president Henry Hass’s 1954 speech, “What’s New in Sugar Research,”12 to the American Society of Sugar Beet Technologists identified a strategic opportunity for the sugar industry: increase sugar’s market share by getting Americans to eat a lower-fat diet: “Leading nutritionists are pointing out the chemical connection between [American’s] high-fat diet and the formation of cholesterol which partly plugs our arteries and capillaries, restricts the flow of blood, and causes high blood pressure and heart trouble… if you put [the middle-aged man] on a low-fat diet, it takes just five days for the blood cholesterol to get down to where it should be… If the carbohydrate industries were to recapture this 20 percent of the calories in the US diet (the difference between the 40 percent which fat has and the 20 percent which it ought to have) and if sugar maintained its present share of the carbohydrate market, this change would mean an increase in the per capita consumption of sugar more than a third with a tremendous improvement in general health.”12

The industry would subsequently spend $600 000 ($5.3 million in 2016 dollars) to teach “people who had never had a course in biochemistry… that sugar is what keeps every human being alive and with energy to face our daily problems.”12

...

The SRF’s vice president and director of research, John Hickson, started closely monitoring the field.15
In December 1964, Hickson reported to an SRF subcommittee15 that new CHD research was a cause for concern: “From a number of laboratories of greater or lesser repute, there are flowing reports that sugar is a less desirable dietary source of calories than other carbohydrates, eg,—Yudkin.”15 Since 1957, British physiologist John Yudkin16 had challenged population studies singling out saturated fat as the primary dietary cause of CHD and suggested that other factors, including sucrose, were at least equally important.17,18

Hickson proposed that the SRF “could embark on a major program” to counter Yudkin and other “negative attitudes toward sugar.”15 He recommended an opinion poll “to learn what public concepts we should reinforce and what ones we need to combat through our research and information and legislative programs” and a symposium to “bring detractors before a board of their peers where their fallacies could be unveiled.”15 Finally, he recommended that SRF fund CHD research: “There seems to be a question as to whether the [atherogenic] effects are due to the carbohydrate or to other nutrient imbalance. We should carefully review the reports, probably with a committee of nutrition specialists; see what weak points there are in the experimentation, and replicate the studies with appropriate corrections. Then we can publish the data and refute our detractors.”15

In 1965, the SRF asked Fredrick Stare, chair of the Harvard University School of Public Health Nutrition Department19 to join its SAB as an ad hoc member.20 Stare was an expert in dietary causes of CHD and had been consulted by the NAS,1 National Heart Institute,21 and AHA,22 as well as by food companies and trade groups.19 Stare’s industry-favorable positions and financial ties would not be widely questioned until the 1970s.23

....

SRF Funds Project 226: A Literature Review on Sugars, Fats, and CHD
On July 13, 1965, 2 days after the Tribune article, the SRF’s executive committee approved Project 226,31 a literature review on “Carbohydrates and Cholesterol Metabolism” by Hegsted and Robert McGandy, overseen by Stare.10 The SRF initially offered $500 ($3800 in 2016 dollars) to Hegsted and $1000 ($7500 in 2016 dollars) to McGandy, “half to be paid when you start work on the project, and the remainder when you inform me that the article has been accepted for publication.”31 Eventually, the SRF would pay them $650032 ($48 900 in 2016 dollars) for “a review article of the several papers which find some special metabolic peril in sucrose and, in particular, fructose.”31

High cholesterol does not cause heart disease new research finds...statins waste of time

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From US FDA

High cholesterol 'does not cause heart disease' new research finds, so treating with statins a 'waste of time'


Quote:

13 JUNE 2016 • 1:01AM
Cholesterol does not cause heart disease in the elderly and trying to reduce it with drugs like statins is a waste of time, an international group of experts has claimed.
A review of research involving nearly 70,000 people found there was no link between what has traditionally been considered “bad” cholesterol and the premature deaths of over 60-year-olds from cardiovascular disease.
Published in the BMJ Open journal, the new study found that 92 percent of people with a high cholesterol level lived longer.
Lowering cholesterol with medications is a total waste of time
Professor Sherif Sultan, University of Ireland
The authors have called for a re-evaluation of the guidelines for the prevention of cardiovascular disease and atherosclerosis, a hardening and narrowing of the arteries, because “the benefits from statin treatment have been exaggerated”.

Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review


Quote:

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.

Eating too little salt may increase your risk of a heart attack or stroke claims new research

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Daily Mail On-Line article:

Eating too LITTLE salt may INCREASE your risk of a heart attack or stroke, claims controversial new research

Wiki Salt

Nutritional heresy strikes back, some quotes:

The research was carried out by investigators at McMaster University and Hamilton Health Sciences.
They analyzed more than 130,000 people across 49 countries, focusing on whether the relationship between sodium (salt) intake and death, heart disease and stroke differs in people with high blood pressure compared to those with normal blood pressure.
Their findings showed that regardless of whether people have high blood pressure, low-salt intake is linked to a greater incidence of heart attacks, stroke, and deaths compared to average intake.
...

Dr Mente said that this suggests that the majority of individuals in Canada and most countries are consuming the right amount of salt.
He added that targeted salt reduction in those who are most susceptible because of hypertension and high salt consumption may be preferable to a population-wide approach to reducing sodium intake in most countries except those where the average sodium intake is very high, such as parts of central Asia or China.

He added that what is now generally recommended as a healthy daily ceiling for sodium consumption appears to be set too low, regardless of a person's blood pressure level.
'Low sodium intake reduces blood pressure modestly, compared to average intake, but low sodium intake also has other effects, including adverse elevations of certain hormones which may outweigh any benefits,' Dr Mente said.

'The key question is not whether blood pressure is lower with very low salt intake, instead it is whether it improves health.'

Dr Martin O'Donnell, a co-author on the study and an associate clinical professor at McMaster University and National University of Ireland Galway, said: 'This study adds to our understanding of the relationship between salt intake and health, and questions the appropriateness of current guidelines that recommend low sodium intake in the entire population.'

The study was funded from more than 50 sources, including the PHRI, the Heart and Stroke Foundation of Canada and the Canadian Institutes of Health Research.

-----

Reference:

A.Mente et al., The Lancet, 20/05/2016, "Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies"


Please note that the medical authorities have again been caught issuing inaccurate, perhaps harmful nutritional guidelines for half a century based on what appears to be the "treating the numbers" paradigm and experts' opinions rather than based on science. Is nobody responsible for the misconduct?

They finally proved correlation between saturated fat and heart disease...

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... and it is inverse!

From Wiki

In case you missed it, see the study link and the post on Diet Doctor.  See also an interesting post on the High Fat Hep-C Diet blog.  In a nutshell:

Each additional 5% of saturated fat (SFA) contents was associated with 17% lower risk of ischemic heart disease (IHD)  : Hazard Ratio 0.83 +/- 0.1.

RESULTS:
During 12 y of follow-up, 1807 IHD events occurred. Total SFA intake was associated with a lower IHD risk (HR per 5% of energy: 0.83; 95% CI: 0.74, 0.93). Substituting SFAs with animal protein, cis monounsaturated fatty acids, polyunsaturated fatty acids (PUFAs), or carbohydrates was significantly associated with higher IHD risks (HR per 5% of energy: 1.27-1.37). Slightly lower IHD risks were observed for higher intakes of the sum of butyric (4:0) through capric (10:0) acid (HRSD: 0.93; 95% CI: 0.89, 0.99), myristic acid (14:0) (HRSD: 0.90; 95% CI: 0.83, 0.97), the sum of pentadecylic (15:0) and margaric (17:0) acid (HRSD: 0.91: 95% CI: 0.83, 0.99), and for SFAs from dairy sources, including butter (HRSD: 0.94; 95% CI: 0.90, 0.99), cheese (HRSD: 0.91; 95% CI: 0.86, 0.97), and milk and milk products (HRSD: 0.92; 95% CI: 0.86, 0.97).

Interestingly, equal-caloric substitution of 5% of SFA in the diet with:

•  any carbohydrate type (low GI, medium GI or high GI),
•  mono-unsaturated fats,
•  polyunsaturated fats,
•  animal protein,

- correlated positively with IHD, while substitution of SFA with vegetable protein correlated negatively! (Correlation calculations were corrected against known confounding factors such as age, sex, BMI, waist circumference, educational level, physical activity level, smoking status, alcohol intake, energy-adjusted intakes of cholesterol, fiber, and vitamin C.

Stan (Heretic)

LDL cholesterol doesn't matter!

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According to this study (Framingham data):

Increased Small Low-Density Lipoprotein Particle Number

Compared with participants without the MetSyn [Metabolic Syndrome], those with the MetSyn had a higher CVD [Cardio Vascular Disease] event rate. However, among participants with the MetSyn, CVD rates were similar for groups with an elevated versus a lower number of small LDL particles (defined by the sex-specific median).

Conclusions— Small LDL particle number is elevated in the MetSyn, increases with the number of MetSyn components, and most prominently is correlated with triglycerides and HDL-C. Whereas increased small LDL particle number identified the MetSyn with high sensitivity, a higher small LDL particle number was not associated with greater CVD event rates in people with the MetSyn.

Putting it in simple terms: the common misconception that LDL correlates with cardio-vascular disease was caused by bad math! LDL correlated with MetSyn and MetSyn correlates with CVD.  Medical establishment leaders with insufficient mathematical training  incorrectly believed that correlation supposedly follows the "The law of syllogism"  (i.e. if LDL → MetSyn and MetSyn → CVD then LDL → CVD) - BUT IT DOES NOT!

 That study simply proved it by finding that in the sub-population of people who already had MetSyn, the number of small LDL particles did not matter!    Cholesterol theory is very dead and thoroughly debunked, case closed!  Fire them all and move on, next myth please...
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