If you can't tolerate aspirin you can't tolerate hydroxychloroquine

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Covid-19 – a case for medical detectives", by WOLFGANG WODARG, 2-May-2020

Quotes:

...
The Nigerian dead in Sweden

I was aware of such a case with the same puzzling symptoms, which had been described in 2014 by Swedish pneumologists in a young patient from Nigeria who had died of the disease. At that time, an enzyme deficiency was suspected and actually found to be a possible cause after death, which occurs in many regions of Africa in 20 - 30% of the population.

It is the so-called glucose-6-dehydrogenase deficiency, or "G6PD deficiency", one of the most common genetic peculiarities, which can lead to threatening haemolysis (dissolution of red blood cells), mainly in men, when certain drugs or chemicals are taken. The following map shows the distribution of this deficiency (Source and explanations here).

[pic]

This hereditary trait is particularly common among ethnic groups living in areas with malaria. The modified G6PD gene offers advantages in the tropics. It makes its carriers resistant to malaria pathogens. However, G6PD deficiency is also dangerous if those affected come into contact with certain substances found in, for example, field beans, currants, peas and a number of medicines.

These include acetylsalicylic acid, metamizole, sulfonamides, vitamin K, naphthalene, aniline, malaria drugs and nitrofurans. The G6PD deficiency then leads to a disruption of the biochemical processes in the red blood cells and – depending on the dose – to mild to life-threatening haemolysis. The debris of the burst erythrocytes subsequently leads to microemboli, which block small vessels throughout the organs. What had caused the illness and death of the young man from Nigeria remained unclear at the time.

An alarming discovery

I looked at the drugs that can cause severe hemolysis in G6PD deficiency and got really scared. One of the substances that is called very dangerous in all forms of this enzyme deficiency is the anti-malarial drug hydroxychloroquine (HCQ).

But this is precisely the substance that Chinese researchers in Wuhan have been recommending against SARS since 2003. Along with the virus from Wuhan, HCQ now came back to us as one of the therapeutic options and was accepted as such. At the same time, HCQ was recommended as a promising agent against Covid-19 for further clinical trials with the support of WHO and other agencies.

According to reports, production of this drug is to be increased in Cameroon, Nigeria and other African countries. India is the largest producer of HCQ and exports it to 55 countries. Werner Baumann, Chairman of the Board of Management of Bayer AG, announced at the beginning of April that "various investigations in laboratories and clinics" had provided first indications that chloroquine might be suitable for the treatment of corona patients. The company then provided several million tablets.

There are now hundreds of trials worldwide, planned or ongoing by different sponsors, in which HCQ is used alone or together with other drugs. When I looked at some large studies to see if patients with G6PD deficiency were excluded, I found no evidence of this in most study plans. In the USA, for example, a large multi-center study with 4,000 volunteers from healthy medical staff is being prepared. Here, however, the term "hypersensitivity" is only used in general terms, as is the case with all drugs with regard to allergic reactions. In a chloroquine/hydroxychloroquine study by Oxford University (NCT04303507) with a planned 40,000 participants, the risk of G6PD deficiency is also not mentioned. In another large study by the Pentagon, though, there is an explicit warning to exclude G6PD deficiency patients from the study.

The following graph, based on information from the WHO database, shows how many studies on Covid-19 and HCQ have been initiated – and how few of them take enzyme deficiency into account.

[pic]

Mostly only the cardiac complications of chloroquine or hydroxychloroquine are mentioned, which in Brazil led to the premature termination of a study with 11 deaths of 81 subjects. However, it seems that worldwide little attention is paid to this further serious side effect. In addition, due to the lack of alternatives, HCQ has been tolerated and massively applied in many countries since the beginning of the year as part of a so-called "compassionate use". In medicine, compassionate use refers to the use of not yet approved drugs in emergency situations.

Conspicuous clusters

During this research, more and more results of more precise evaluations of the deaths in especially affected cities were received. In New York and other cities in the USA, it was reported that the vast majority of fatalities were African Americans – twice as many as could be expected based on the proportion of the population.

Also from England, where the mortality data from Euromomo shows an increasing death rate since the beginning of April, it was reported that 35% of about 2000 seriously ill people, twice as many as expected, came from ethnic "minorities" ("black, Asian or other ethnic minority"), including doctors and medical staff.

A major doctor's death in Italy remains in urgent need of clarification. The death of about 150 doctors and only a few female doctors is associated with Covid-19. Although age may have played a role in many of these cases, it should be noted that a high prevalence of G6PD deficiency has also been described for some regions of Italy and that in Italy up to 71% of those who tested positive with PCR, as well as the staff, had a prophylactic high level of HCQ. The same applies to Spain. Among the first 15 Covid-19 deaths in Sweden, there were 6 younger migrants from Somalia.

Deadly combination

Therefore the frightening result of my research is that typical severe courses with haemolysis, microthrombi and shortness of breath without typical signs of pneumonia occur more frequently where two factors come together:

Many patients with ancestors from malaria countries with G6PD deficiency
Prophylactic or therapeutic use of high-dose HCQ
This is exactly what is to be expected in Africa, and this is already the case everywhere where migration is causing a large proportion of the population coming from malaria countries. The following diagram shows the process flow schematically.

[pic]

Cities such as New York, Chicago, New Orleans, London, or even large cities in Holland, Belgium, Spain and France are such centers. If the test is widely used in these migration hotspots and is expected to be positive in about 10 to 20% of the population, many people from the G6PD countries will also be among them. If they are then treated with high-dose HCQ, either prophylactically or as part of a "compassionate" use, as planned, then those severe clinical pictures will also be evoked in young people, as has been presented to us by the sensational press, and which keep our fear of Covid-19 alive.

It is unknown how many times this deadly combination has already led to victims. There has been no discussion of the issue among those responsible in the WHO and in governments. There is also a frightening lack of knowledge and sense of responsibility among doctors who are accountable for the treatment of Covid-19 patients or for the staff treating them.

Once again: This connection applies not only to Africa, but also to large parts of Asia, South and Central America, Arabia and the Mediterranean region.

However, the cases mentioned have nothing to do with Covid-19 disease. A PCR test result leading to the prophylactic prescription of HCQ is sufficient to cause severe disease in up to one third of the people from high-risk populations treated in this way.

HCQ treatment for G6PD deficiency is a dangerous malpractice

This could be remedied immediately if all treating physicians worldwide were informed about the contraindication of HCQ. However, the WHO, the CDC, the ECDC, the Chinese SARS specialists, the medical associations, the drug authorities and the German government and its advisors are carelessly neglecting to inform the public. In view of the ongoing programmes, this appears to be gross negligence.

It is a malpractice to treat people with G6PD deficiency with high-dose chloroquine derivatives or other drugs known to be dangerous for them. Under the WHO label "'Solidarity' clinical trial for COVID-19 treatments", healthy people are exposed in a hurry to authorised, life-threatening experiments. Hundreds of clinical trials, mostly worthless observational studies with parallel approaches, very often also run with HCQ as one of the alternatives.

German drug legislation prohibits the use of unauthorised drugs, but the government still encourages this. A non-validated test that is not approved for diagnostic purposes provides the pretext for the use of life-threatening medication – given an infectious disease where there is still no evidence that it poses serious risks beyond the risk of the annual flu epidemic.

At full throttle into the catastrophe

The dangers of this epidemic are presented with the help of scientific imposture. An unsuitable test from Berlin provides the pretext for deadly measures all over the world. The consequences of these mistakes lead to emergencies in many regions, which are attributed to an epidemic. This creates precisely the wave of fear so many in business and politics are now riding and which threatens to bury our fundamental rights.

The public, the media and the medical community hardly seem to be surprised that in New York and other centres more than twice as many "African Americans" die as would be expected due to their population share. Even in the studies of deaths in the USA and elsewhere, the risk posed by G6PD deficiency is almost always ignored or forgotten.

When sought-after virologists and other experts have been announcing for a long time that there will be a wave of deaths and terrible conditions in the cities in Africa, do they know about these connections? Or are there other provable reasons that justify such momentous prophecies? Finally: Is all this just a matter for science or also for public prosecutors and courts?

Note from the editor: Further information and graphics can be found on the author's website.

About the author: Dr. med. Wolfgang Wodarg, born in 1947, is an internist and pulmonary physician, specialist for hygiene and environmental medicine as well as for public health and social medicine. After his clinical activity as an internist, he was, among other things, a public health officer in Schleswig-Holstein, Germany for 13 years, at the same time lecturer at universities and technical colleges and chairman of the expert committee for health-related environmental protection at the Schleswig-Holstein Medical Association; in 1991 he received a scholarship at the Johns Hopkins University, Baltimore, USA (epidemiology).

As a member of the German Federal Parliament from 1994 to 2009, he was initiator and speaker in the Enquête Commission "Ethics and Law of Modern Medicine", member of the Parliamentary Assembly of the Council of Europe, where he was chairman of the Subcommittee on Health and deputy chairman of the Committee on Culture, Education and Science. In 2009, he initiated the Committee of Inquiry into WHO's role in H1N1 (swine flu) in Strasbourg, where he remained as a scientific expert after leaving Parliament. Since 2011 he has been working as a freelance university lecturer, doctor and health scientist and was a volunteer member of the board and head of the health working group at Transparency International Germany until 2020.

Connection between immune system, microbiome and psychiatric disorders

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"He Got Schizophrenia. He Got Cancer. And Then He Got Cured." by Moises Velasquez-Manoff, NYT, Sept. 29, 2018

Quotes:

...A year later, the man’s condition worsened. He developed fatigue, fever and shortness of breath, and it turned out he had a cancer of the blood called acute myeloid leukemia. He’d need a bone-marrow transplant to survive. After the procedure came the miracle. The man’s delusions and paranoia almost completely disappeared. His schizophrenia seemingly vanished.

Years later, “he is completely off all medication and shows no psychiatric symptoms,” Dr. Miyaoka told me in an email. Somehow the transplant cured the man’s schizophrenia.

A bone-marrow transplant essentially reboots the immune system. Chemotherapy kills off your old white blood cells, and new ones sprout from the donor’s transplanted blood stem cells. It’s unwise to extrapolate too much from a single case study, and it’s possible it was the drugs the man took as part of the transplant procedure that helped him. But his recovery suggests that his immune system was somehow driving his psychiatric symptoms.

...


In the late 19th century, physicians noticed that when infections tore through psychiatric wards, the resulting fevers seemed to cause an improvement in some mentally ill and even catatonic patients.

Inspired by these observations, the Austrian physician Julius Wagner-Jauregg developed a method of deliberate infection of psychiatric patients with malaria to induce fever. Some of his patients died from the treatment, but many others recovered. He won a Nobel Prize in 1927.

One much more recent case study relates how a woman’s psychotic symptoms — she had schizoaffective disorder, which combines symptoms of schizophrenia and a mood disorder such as depression — were gone after a severe infection with high fever.

...

Indeed, in the past 15 years or so, a new field has emerged called autoimmune neurology. Some two dozen autoimmune diseases of the brain and nervous system have been described. The best known is probably anti-NMDA-receptor encephalitis, made famous by Susannah Cahalan’s memoir “Brain on Fire.” These disorders can resemble bipolar disorder, epilepsy, even dementia — and that’s often how they’re diagnosed initially. But when promptly treated with powerful immune-suppressing therapies, what looks like dementia often reverses. Psychosis evaporates. Epilepsy stops. Patients who just a decade ago might have been institutionalized, or even died, get better and go home.

...

Dr. Robert Yolken, a professor of developmental neurovirology at Johns Hopkins, estimates that about a third of schizophrenia patients show some evidence of immune disturbance. “The role of immune activation in serious psychiatric disorders is probably the most interesting new thing to know about these disorders,” he told me.

Studies on the role of genes in schizophrenia also suggest immune involvement, a finding that, for Dr. Yolken, helps to resolve an old puzzle. People with schizophrenia tend not to have many children. So how have the genes that increase the risk of schizophrenia, assuming they exist, persisted in populations over time? One possibility is that we retain genes that might increase the risk of schizophrenia because those genes helped humans fight off pathogens in the past. Some psychiatric illness may be an inadvertent consequence, in part, of having an aggressive immune system.

...

Another case study from the Netherlands highlights this still-mysterious relationship. In this study, on which Dr. Yolken is a co-author, a man with leukemia received a bone-marrow transplant from a schizophrenic brother. He beat the cancer but developed schizophrenia. Once he had the same immune system, he developed similar psychiatric symptoms.

...

And there may be other, softer interventions. A decade ago, Dr. Miyaoka accidentally discovered one. He treated two schizophrenia patients who were both institutionalized, and practically catatonic, with minocycline, an old antibiotic usually used for acne. Both completely normalized on the antibiotic. When Dr. Miyaoka stopped it, their psychosis returned. So he prescribed the patients a low dose on a continuing basis and discharged them.

Minocycline has since been studied by others. Larger trials suggest that it’s an effective add-on treatment for schizophrenia. Some have argued that it works because it tamps down inflammation in the brain. But it’s also possible that it affects the microbiome — the community of microbes in the human body — and thus changes how the immune system works.

...

The study is preliminary, but it suggests that targeting immune function may improve mental health outcomes and that tinkering with the microbiome might be a practical, cost-effective way to do this.

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.

Ketogenic diet protects against chemotherapy

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"β-Hydroxybutyrate, a ketone body, reduces the cytotoxic effect of cisplatin via activation of HDAC5 in human renal cortical epithelial cells", Daisuke Mikami et al., Life Sciences
Volume 222, 1 April 2019, Pages 125-132

Quote:

Main methods

In this study, we used human renal cortical epithelial (HRCE) cells. The anti-apoptotic effect of βOHB was evaluated using flow cytometry analysis. The expression of apoptosis-related proteins and HDACs was evaluated by western immunoblot.

Key findings

The results showed that βOHB significantly reduced cisplatin-induced apoptosis in HRCE cells. Furthermore, βOHB significantly reduced cisplatin-induced cleavage of caspase-3, acetylation of histone H3, and phosphorylation of AMP-activated kinase. This anti-apoptotic effect of βOHB was markedly attenuated by an inhibitor of HDAC4/5, and βOHB-mediated suppression of cleavage of caspase3 was significantly blocked by siRNA-induced gene silencing of HDAC5.

Significance

βOHB attenuates cisplatin-induced apoptosis by activation of HDAC5 in HRCE cells, suggesting that βOHB may be a new therapeutic agent for cisplatin nephropathy.

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.]

-------
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

New anti-viral melanoma therapy

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TV interview with medical doctor prof Andrzej Mackiewicz (in Polish)

Quote:

Oncologist prof. Andrzej Mackiewicz, creator of the melanoma vaccine, was a guest of "Dzien Dobry" ["Good Morning"] TVN program. It is a vaccine that heals, not just prevents melanoma! It could have helped several hundred sick people each year if it was officially registered and approved, however that is very expensive. Why is the melanoma vaccine not available to all patients? - We are scientists who have developed a medicine that works, and that seems to pose a huge problem for certain people or authorities - said prof. Mackiewicz on Good Morning TVN.

Non-interferon Hepatitis-C therapy

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Article (in Polish)

Quote (translated):

2. What is non-interferon therapy?

The non-interferon therapy involves the use of drugs that contain substances such as ombitasvir, paritaprevir, ritonavir (1 EAN code) and dasabuvu, which have maximum efficacy in the treatment of hepatitis C.

These modern drugs can be used in patients of all ages, regardless of the stage at which they have the disease. The patient requires constant medical supervision, however, hospitalization is not needed. This means that the patient is not exposed to stress and can undergo the therapy, which lasts from 12 to 24 weeks and costs about 60,000 zl (about 17600 US$). The therapy is completely safe and does not cause side effects, and most importantly - eliminates the virus in 90 to 100 percent of patients.

Older hepatitis C treatment therapies are much longer and more expensive - they last up to 72 weeks, and their cost often exceeds 160,000zl (47,200 US$).
In addition, they cause severe side effects - patients complain of very high fever, hair loss and skin problems. The success rate of healing hepatitis C with these older therapies is 70%.

Vigorous exercizing increases macular degeneration risk

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... by 54% in the high group and 28% in the moderate group!


A Nationwide Cohort Study on the Association Between Past Physical Activity and Neovascular Age-Related Macular Degeneration in an East Asian Population, by Tyler Hyungtaek Rim, Hong Kyu Kim, Ji Won Kim, et al, JAMA Ophthalmol. Published online December 14, 2017.


Quote:

Findings
In a propensity score–matched cohort of 211 960 participants, self-reported past vigorous physical activity in men aged 45 to 64 years of age was associated with an increased risk for neovascular age-related macular degeneration, compared with the no physical activity group.

Wiki 

Sanofi dengue vaccine "worsens" the disease!

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Duterte vows to get to the bottom of dengue vaccine 'health scam'

Medicine in the new Middle Ages! How any more ridiculous it can get?

Quote:

MANILA - The office of the Philippine president on Sunday vowed to hold accountable those responsible for a suspended dengue immunization program, which it said placed thousands of lives at risk.
The Department of Health (DOH) halted on Friday the use of a dengue vaccine made by Sanofi after the company said its use must be strictly limited due to evidence it can worsen the disease in people who have not previously been exposed to the infection.

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.

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."

Lack of benefits from blood glucose-lowering diabetes treatment, doctors confused

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This is the key conclusion from the recently published study.

Glycemic Control for Patients With Type 2 Diabetes Mellitus
Our Evolving Faith in the Face of Evidence

Abstract

...We searched in top general medicine and specialty journals for articles referring to glycemic control appearing between 2006 and 2015 and identified the latest practice guidelines.
...
We identified 16 guidelines and 328 statements. The body of evidence produced estimates warranting moderate confidence. This evidence reported no significant impact of tight glycemic control on the risk of dialysis/transplantation/renal death, blindness, or neuropathy. In the past decade, however, most published statements (77%–100%) and guidelines (95%) unequivocally endorsed benefit. There is also no significant effect on all-cause mortality, cardiovascular mortality, or stroke; however, there is a consistent 15% relative-risk reduction of nonfatal myocardial infarction. Between 2006 and 2008, most statements (47%–83%) endorsed the benefit; after 2008 (ACCORD), only a minority (21%–36%) did.

Conclusions — Discordance exists between the research evidence and academic and clinical policy statements about the value of tight glycemic control to reduce micro- and macrovascular complications.

And journalistic commentary, from the CBC:

New study questions Type 2 diabetes treatment
No evidence glucose-lowering drugs help ward off long-term complications, researchers say

It's a curious case of missing evidence. When a diabetes specialist searched the medical literature looking for proof to support the use of glucose-lowering drugs for Type 2 diabetes, he couldn't find it.

...
His conclusions challenge the conventional wisdom of many medical specialists, and contradict most clinical practice guidelines.

...
"Over 90 per cent of experts were saying that controlling blood sugars tightly was associated with a reduction in your risk of going blind or of needing dialysis or having to undergo an amputation," Montori said. "But when we looked at the evidence for that, we could not see any signal that would suggest that is true despite the question being asked at least since the 1970s."
...
The finding reveals a divergence in professional opinion based on the same set of facts, and it exposes a dilemma in the science of Type 2 diabetes — that doctors don't completely understand the relationship between blood sugar and the disease.

My comments:

1) The lack of benefits from glucose lowering therapies may be explained by the primary cause of the damage being the total carbohydrate overload (Glycemic Load) rather than the blood glucose level.

2) The results are consistent with the research published by R.W.Stout (Lancet, 1969) demonstrating arteriosclerotic plaque production stimulated by glucose and insulin. Reduction of carbohydrate consumption therefore reduces both glycemic load and insulin secretion, reducing the overall risk, especially cardiovascular. Some glucose level controlling drugs only push glucose from one location (blood) into another (tissues) without generally affecting insulin secretion and therefore unchanging the risk, while some other drugs that do increase insulin would also increase the risk.

3) Confusion among medical professionals stems from their attachment to the Western food and lifestyle, unable to consider a possibility that the high carbohydrate nutrition may by itself be the main trigger (if not the cause) of diabetes. In my personal opinion, best remedy would be to allow more free play and competition in the medical field, enabling doctors trained in other countries that may not be subject to the above described mind blocks, to practice legally world-wide, as it is already being widely accepted in other professions such as engineering, scientific research and art.

Stan (Heretic)

They tried really really hard...

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.. to prove that cholesterol and eggs were supposed to be harmful, in the most recent Finnish study:

Associations of egg and cholesterol intakes with carotid intima-media thickness and risk of incident coronary artery disease according to apolipoprotein E phenotype in men: the Kuopio Ischaemic Heart Disease Risk Factor Study

I respect persistence, dedication, efforts and resources devoted by the world medical establishment to their long term goals. I believe that no civilian scientific project ever, in the history of science, commanded more time, efforts and money than attempting to prove Ancel Keys' cholesterol theory of the 1950-ties! Probably more so, if we include the R&D efforts by the pharmaceutical companies, than even the space programs.

Quote:

Conclusion: Egg or cholesterol intakes were not associated with increased CAD risk, even in ApoE4 carriers (i.e., in highly susceptible individuals).

(Thanks JC for the link alert)

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)

Insulin, Glucose, Grim Reaper and Sweet Sixteen gene

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Sugar (wiki)

Important new reasearch published just recently by Cynthia Kenyon, University of California, described in the following Oct-26,2010 Daily Mail article (Jerome Burne):

Can cutting carbohydrates from your diet make you live longer?

Quotes:

She made her remarkable breakthrough after studying roundworms, specifically the C.elegans, a worm just a millimetre in size that lives in soil in temperate climates all over the world. By tweaking some of their genes she has been able to help these worms live up to six times longer than normal. 'Not only that, but we also know how to make them stay healthy all that time as well,' she told an audience at the Wellcome Collection in London earlier this month.
...
Scientists already knew how to make laboratory animals live longer and healthier lives - you just cut back their calories to about three-quarters of their normal amount.  ... But what Professor Kenyon found out was why ­drastically reducing calories has such a remarkable effect. She discovered that it changed the way two crucial genes behaved. It turned down the gene that controls insulin, which in turn switched on another gene, which acted like an elixir of life.  'We jokingly called the first gene the Grim Reaper because when it’s switched on, the lifespan is fairly short,' she explains.  The ­second 'elixir' gene seems to bring all the anti-ageing benefits - its proper name is DAF 16, but it was quickly nicknamed 'Sweet Sixteen' because it turned the worms into teenagers.
...
Discovering the Grim Reaper gene has prompted the professor to ­dramatically alter her own diet, ­cutting right back on carbohydrates. That’s because carbs make your body produce more insulin (to mop up the extra blood sugar carbs ­produce); and more insulin means a more active Grim Reaper.  So the vital second gene, the 'elixir' one, won't get turned on.

To test this, last year she added a tiny amount of ­sugary glucose to the normal diet of some of her worms that had had their genes engineered so they were living much longer, healthier lives.  'The effect was remarkable,' she says. 'The sugary glucose blocked the ''youthful'' genes and they lost most of the health gains.'
...
Following Kenyon’s lead, other researchers started looking for the Grim Reaper/ Sweet Sixteen combination in other animals — and of course in humans.

They found it.

One clue came from a small remote community of dwarves living in northern Ecuador who are cancer-free. They are missing the part of the Grim Reaper gene that controls a hormone called insulin-like growth factor. The downside is they only grow to 4ft tall because the hormone is needed for growth.  But this missing bit of the Grim Reaper gene also means they don’t develop cancer and are less likely to suffer from heart disease or obesity.

Professor Jeff Holly, who specialises in insulin-like growth factor, confirms that it is linked to cancer of the prostate, breast and colon.  In fact raised insulin levels, triggered by high carbohydrate ­consumption, could be what ­connects many of our big killers. Research is at its early stage, but raised insulin triggers an increase in cholesterol production in the liver, makes the walls of blood vessels ­contract so blood pressure goes up and stimulates the release of fats called triglycerides (linked to heart disease).
...
'Carbo­hydrates, and especially refined ones like sugar, make you produce lots of extra insulin. I’ve been keeping my intake really low ever since I discovered this. I've cut out all starch such as potatoes, noodles, rice, bread and pasta. Instead I have salads, but no sweet dressing, lots of olive oil and nuts, tons of green vegetables along with cheese, chicken and eggs. I'll have a hamburger without a bun and fish without batter or chips. I eat some fruit every day, but not too much and almost no processed food. I stay away from sweets, except 80 per cent chocolate.'

--------------

Refs (older, not this one):

http://kenyonlab.ucsf.edu/html/history.html

http://kenyonlab.ucsf.edu/Kenyon_et_al_Nature.pdf




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China Study - Raw Data - more plant food = more heart disease!

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At last! Finally the Raw Data behind the infamous "The China Study..." book by Dr. TC Campbell from Cornell University has emmerged out of some obscure "unobtainium" publication and became available on-line on the Clinical Trial Service Unit at Oxford University web site!

http://www.ctsu.ox.ac.uk/~china/monograph/chdata.htm

Below are the links to blogs and sources.

#1. Denise Minger on China Study - long and in depth analysis of the raw data with graphs. See also her article on Tuoli county the only county in the China Study that consumed a high fat medium carb diet:

http://rawfoodsos.com/2010/07/07/the-china-study-fact-or-fallac/

http://rawfoodsos.com/2010/06/23/tuoli-chinas-mysterious-milk-drinkers/

According to our prominent vegan theorists such as Drs Campbel, Ornish, McDougall, Esselstyne et al, the Tuoli people ought to have been very sick or dead. As you can read from Denise analysis nothing is farthest from truth. Tuoli seems to be healthier than in most other China counties!

#2. Fantastic comment by Richard Kroeker on Amazon forum,
- giving his own analyzis of the raw date similar to and corroborationg an analysis by Denise Minger.  Note: you should start reading from that post and then move on to #1 above, since Kroeker's article is much shorter.

http://www.amazon.com/Analyzing-the-China-Study-Dataset/forum/Fx1YJPR95OHW08P/TxY4S5EZD8Y2XE/1/ref=cm_cd_dp_ef_tft_tp?_encoding=UTF8&s=books&asin=1932100660&store=books

Quote:

... This is not at all what Campbell's book implied the data said. As I said above, I am an engineer (with a PhD) with heart disease simply trying to find out what to eat. You do the math...

My day-job is analyzing hard drive failure statistics that result from usage and stress testing; I get paid to make the problems being studied "go away". I have also recently had a triple bypass, ...

For instance, the people who ate the most animal protein had 68.9% less heart disease (at 95% confidence) than those people who ate the least animal protein. The people who ate the most plant protein had 64.9% more heart disease (at 89% confidence) than those people who ate the least plant protein.

I am quoting here some interesting correlation (actually the risk ratio between the extreme sample bins for a given variable, '-' means improvement, '+' means harm) from Kroeker's post, the first column numbers are univariate (single-variable, uncorrected against possible confounders) risk ratios in %, the most negative numbers (blue) = low mortality, the most positive numbers (red) = high mortality. The second number in brackets are the "confidence" estimates in % as per Kroeker's definition (see here in his methodology document). This is for mortality of all vascular disease age 35-69.



RISK% (CONFIDENCE%) - INDEPENDENT VARIABLE

-70.7% (93%) - PERCENTAGE OF CALORIC INTAKE FROM FAT
-68.9% (95%) - PERCENTAGE ANIMAL PROTEIN INTAKE
-60.8% (92%) - HDLCHOL plasma HIGH DENSITY LIPOPROTEIN CHOLESTEROL (mg/dL)
-57.0% (89%) - PERCENTAGE OF CALORIC INTAKE FROM ANIMAL
-55.6% (90%) - ANIMAL FOOD INTAKE (g/day/ref)
-55.1% (94%) - FOLATE plasma FOLATE (ng/mL)
-54.8% (89%) - ANIMAL PROTEIN INTAKE (g/day/ref)
-54.1% (90%) - FISH INTAKE (g/day/ref)

-49.5% (84%) - TOTAL LIPID INTAKE (g/day/reference man)
-49.1% (87%) - PERCENTAGE ANIMAL FOOD INTAKE (for refere
-48.4% (83%) - MEAT INTAKE (red meat and poultry) (g/day
-48.0% (83%) - CHOLESTEROL INTAKE (mg/day/reference man)
-46.6% (81%) - RED MEAT (pork, beef, mutton) INTAKE (g/d
-42.2% (82%) - SATURATED FATTY ACID INTAKE (g/day/ref)
-40.7% (89%) - RICE INTAKE (g/day/reference man, air-dry
-38.0% (84%) - TOTAL CAROTENOID INTAKE (retinol equivale
-36.0% (84%) - POULTRY INTAKE (g/day/reference man, as-c
-42.9% (82%) - Se plasma SELENIUM (ug/dL)
-42.8% (85%) - TOTPROT plasma 1989 TOTAL PROTEIN (g/dL)
-42.6% (86%) - APOA1 plasma APOLIPOPROTEIN A1 (mg/dL) (non-pooled analysis
-40.7% (88%) - Zn plasma ZINC (mg/dL)
-38.7% (76%) - B-CAROT plasma BETA CAROTENE (ug/dL)
-38.0% (82%) - ANHYDLUT plasma ANHYDRO LUTEIN (ug/dL)
-34.6% (81%) - TOTCHOL plasma TOTAL CHOLESTEROL (mg/dL)
-34.1% (79%) - NON-HDL plasma CHOLEST.(mg/dL)[=LDL+Trig/5]

...

32.4% (79%) - plasma LDL to HDL ratio
35.6% (75%) - PLANT FOOD INTAKE (g/day/reference man)
37.5% (82%) - POTASSIUM INTAKE (mg/day/ref)
39.3% (76%) - SPICE INTAKE (g/day/ref)
39.6% (84%) - TOTAL NEUTRAL DETERGENT FIBRE INTAKE (g/d/ref)
40.0% (84%) - MAGNESIUM INTAKE (mg/day/ref)
42.2% (80%) - MANGANESE INTAKE (mg/day/ref)
43.0% (90%) - OTHER CEREAL INTAKE (g/day/ref)
46.4% (93%) - TOTAL PROTEIN INTAKE (g/day/ref)
47.7% (91%) - COPPER INTAKE (mg/day/ref)

50.5% (87%) - IRON INTAKE (mg/day/ref)
54.3% (91%) - PERCENTAGE OF CALORIC INTAKE FROM CARBOHYDRATES
56.0% (87%) - PERCENTAGE PLANT FOOD INTAKE
58.9% (95%) - PLANT PROTEIN INTAKE (g/day/reference man)
62.4% (97%) - WHEAT FLOUR INTAKE (g/day/reference man)
64.9% (89%) - PERCENTAGE PLANT PROTEIN INTAKE (for ref)
65.7% (95%) - PERCENTAGE OF CALORIC INTAKE FROM PLANT PROTEIN

#3. Richard Nikoley's blog where I found the original links (thanks):

http://freetheanimal.com/2010/07/t-colin-campbells-the-china-study-finally-exhaustively-discredited.html

Stan (Heretic)

-----------------------------------

Update 13-July-2010


HILLARIOUS response (and also the comment #505 here (*) that is  http://rawfoodsos.com/2010/07/07/the-china-study-fact-or-fallac/#comment-505   ) by Dr. TC Campbell of Cornell University to Denise Minger!

No discussion of the data, instead plenty of ad-hominem attacks, pointing out her age, questioning her character integrity and weaving some conspiracy theory implying backing by some lobbying organization having "untold financial resources" such as Weston A. Price Foundation!   :)

Dr. TC Campbell of Cornell U. (probably) wrote:

"I find it very puzzling that someone with virtually no training in this science can do such a lengthy and detailed analysis in their supposedly spare time. I know how agricultural lobbying organizations do it–like the Weston A Price Foundation with many chapters around the country and untold amounts of financial resources. Someone takes the lead in doing a draft of an article, then has access to a large number of commentators to check out the details, technical and literal, of the drafts as they are produced. I have no proof, of course, whether this young girl is anything other than who she says she is, but I find it very difficult to accept her statement that this was her innocent and objective reasoning, and hers alone. If she did this alone, based on her personal experiences from age 7 (as she describes it), I am more than impressed."

- I am not!
H.

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*) If someone figured it out how to link to a comment by its number, on wordpress blog please let me know. Nothing obvious such as ?comment=505 etc seems to work.

Update 17-July-2010

Reordering and reformatting. It is interesting to notice that in China Study the higher total cholesterol, and the higher LDL+Triglycerides correlated with LOWER cardiovascular mortality; while higher HDL level correlated very strongly with lower cardiovascular mortality!

Update 29-July-2010

Added confidence levels in brackets (%) and a link to Rich Kroeker's methodology document.

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