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COVID-19: Montreal Heart Institute concludes colchicine tablet is effectivePatients involved needed to be over the age of 40 and have at least one risk factor for possible complications. The results showed the medication helped reduce hospitalizations by a quarter, the need for mechanical ventilation by half and deaths by 44 per cent.
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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.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.
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This is reposted from facebook,Introduction. So called “optimal diet” – a low-carbohydrate, high-fat
diet, different from Atkins diet – has become very popular in Poland
during the last 20 years. It is very controversial; official dietetics in
Poland claim it is extremely noxious.
Aim [Objectives]. To check what are the effects of so-called “optimal diet” on
health status, frame of mind of people, their physical activity and
diseases including type 2 diabetes.
Material and methods. 436 persons aged 20-75 years, both
women (247) and men (189) were examined. 231 of them applied
“optimal diet” and 205 did not. 86 confirmed they suffered from
type 2 diabetes. All examined persons were inquired with our own
questionnaire.
Results. Quite a lot of statistically significant dependencies were
found to exist. They show us that persons applying the “optimal
diet” might be physically active longer than the persons not applying
it. The majority of the “optimal diet” users claim they got rid of
overweight owing to this diet. Quite many of them claim they
cured themselves of the diabetes or at least the diabetes distress
has distinctly diminished.
Conclusions. The persons applying the “optimal diet” claim they
got rid of overweight or even cured themselves of the diabetes
owing to the diet. Our data do seem to confirm the last reports
(Al-Khalifa et al. 2009).
"Over half of the respondents were able (in their opinion)-----
to heal themselves of diabetes using the so-called optimal diet [OD], but it was not possible for anyone (according to respondents' opinions) who did not follow the OD."
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SARS-CoV-2 has some unexplained pathogenic features that might be related to the table of putative pathogenic priming peptides. Exposure to these specific peptides - via either infection or vaccination - might prime patients for increased risk of enhanced pathogenicity during future exposure due either to future pandemic or outbreaks or via universal vaccination programs. While the mechanisms pathogenesis of COVID-19 are still poorly understood, the morbidity and mortality of SARS has been extensively studied. Thus, the involvement of pathogenic priming in re-infection by COVID-19 is a theoretical possibility; of course no vaccine against SARS-CoV-2 has yet been tested in animals and therefore we do not yet know if pathogenic priming is in fact expected. Such studies should be undertaken before use of any vaccine against SARS-CoV-2 is used in humans.
"In English this says, the Covid 19 virus has only one sequence that does not have links to human proteins. Thus any part of the virus used in a vaccine could potentially make the vaccine fatal to the humans injected with it."
The immunity you get from the actual disease is much more enduring, robust, durable and broader spectrum than the immunity you get from vaccines. So there is more protection with immunity derived from the actual disease. There are two types of antibodies produced in an immune response: neutralizing antibodies and binding antibodies. The danger with Coronavirus vaccines is a phenomenon called 'pathogenic priming'.
Neutralizing antibodies are good. Binding antibodies however, are produced when you try to vaccinate against a Coronavirus. These binding antibodies act like Velcro on your cells' receptors. So the virus sticks to the cells and makes you much more sick.
If you get exposed to Coronavirus through the vaccine, it actually 'primes' your system. So you get much sicker the next time the virus comes around. For example, in the 1960's a MERS (Coronavirus) vaccine was tested on children. But when they were actually challenged by disease itself, they all became horrendously sick and two of them died.
In 2014 Sanofi worked with the NIH to develop a Dengue vaccine. And they saw some of those same pathogenic priming signals during the clinical trials. But ignored them. They gave that vaccine to hundreds of thousands of kids in the Philippines and they all got an immune response. But when the Dengue came back around, the kids who were vaccinated were devastated and 600 of them died. There are criminal charges right now in the Philippines trying public health officials, who were involved in that decision.
Additionally, vaccine manufacturers are free from liability. So they can't be sued, even if things go dreadfully wrong. And there is no adequate safety testing done. Because it's costly and manufacturers don't do it, bcz they are not required to. This 'pathogenic priming' effect is the single most important and dangerous issue when it comes to a Coronavirus vaccine. As no one knows how devastating it can turn out to be.
ABSTRACT The present invention provides methods and compositions for the treatment of DNA damage related disorders. One embodiment is a method for the inhibition of Side effects asSociated with chemotherapeutic and radiotherapeutic agents using chloroquine compounds. Another embodiment is a method for treatment and/or prevention of lethal or Sub-lethal radiation toxicities associated with terrorist acts or war.
BRIEF DESCRIPTION OF THE FIGURES 0007 FIG. 1 shows a Kaplan-Meier survival curve of C57/BL6 mice after exposure to 8 Gy total body irradiation (TBI). Half of the cohort received a dose of chloroquine (dashed line) by either i.p. injection (1.75 mg/kg or 3.5 mg/kg) or in their drinking water (3.5 mg/kg or 7 mg/kg) the day before the TBI. The one mouse which died in the chloroquine-treated group received 1.75 mg/kg by i.p. injection.
0008 FIG. 2 shows that chloroquine treatment enhances survival after TBI by enhancing recovery of hematopoietic progenitor cells. Five mice received 3.5 mg/kg chloroquine (C) by i.p. injection 24 and 4 hours prior to TBI (bars with diagonal Stripes). Five mice received no chloroquine (stippled bars). Fourteen days after irradiation, the cellular ity (open bars) of hematopoietic tissues (spleen, thymus, bone marrow) was assessed by a blinded observer on a scale of 0-3 with 3 being normal cellularity. The bars represent the average cellularity of the tissues from the 5 mice in each group.
0009 FIG.3 shows a Kaplan-Meier survival curve of AT mice after exposure to 8 GyTBI. Half of the cohort received a dose of 3.5 mg/kg chloroquine (CHL; dashed line) by i.p. injection 24 and 4 hours prior to the TBI.
0010 FIG. 4 demonstrates that chloroquine treatment prevents the development of tumors in Eul-myc mice. After weaning, a cohort of transgenic mice expressing the c-myc oncogene were started on chloroquine (CHL) at 7.0 mg/kg in the drinking water ((+), solid line). Within 100 days, all of the mice with no drug in the water had died of leukemia, while none of the cohort of mice on drug had Succumbed. The latter group of mice was then divided into two groups (timing of this event depicted by heavy arrow), one group of which was taken off of chloroquine ((-), dashed line) and the other group of which was started on i.p. injections of 3.5 mg/kg of chloroquine once a week. Within a month, all of the mice taken off of chloroquine had developed malignan cies and all of the mice on the weekly i.p. injections remained tumor-free for months.
0011 FIG. 5 illustrates that chloroquine treatment reduces the development of tumors in mice injected with the potent chemical carcinogen, 3-methylcholanthrene (3-MC). Chloroquine (CHL, 3.5 mg/kg) was given by i.p. injection 24 and 4 hours prior to 3-MC injection in 30 mice and 30 mice received the carcinogen with no chloroquine pretreat ment. The percentage of animals remaining tumor-free is plotted. Statistical significance, log rank test P-0.0001.
0012 FIG. 6 demonstrates that chloroquine treatment reduces the development of tumors in mice exposed to ionizing radiation in a protocol that induces thymic lym phomas. Chloroquine (CHL, 3.5 mg/kg) was given by i.p. injection 24 and 4 hours prior to irradiation in four Successive weeks and animals were subsequently observed for the development of tumors. Statistical Significance, log rank test P=0.0012.
0013 FIG. 7 shows tumor incidence in wildtype mice receiving either placebo or CHQ before 3-MC injection. CHQ markedly protects from tumor development.
0014 FIG. 8 shows tumor incidence in ATM-null mice receiving either placebo or CHQ before 3 MC injection. CHQ does not protect from tumor development.
0015 FIG. 9 shows tumor incidence in p53-null mice receiving either placebo or CHQ before 3 MC injection. CHQ does not protect from tumor development.
0016 FIG. 10 demonstrates the efficacy of two chloroquine compounds in preventing, in Varying degree, the change in coat color in mice treated with 8 GY radiation.
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Abstract
Objective: To describe outcomes of patients with coronavirus disease 2019 (COVID-19) in the outpatient setting after early treatment with zinc, low dose hydroxychloroquine, and azithromycin (the triple therapy) dependent on risk stratification. Design: Retrospective case series study. Setting: General practice. Participants: 141 COVID-19 patients with laboratory confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections in the year 2020. Main Outcome Measures: Risk-stratified treatment decision, rate of hospitalization and all-cause death. Results: Of 335 positively PCR-tested COVID-19 patients, 127 were treated with the triple therapy. 104 of 127 met the defined risk stratification criteria and were included in the analysis. In addition, 37 treated and eligible patients who were confirmed by IgG tests were included in the treatment group (total N=141). 208 of the 335 patients did not meet the risk stratification criteria and were not treated. After 4 days (median, IQR 3-6, available for N=66/141) of onset of symptoms, 141 patients (median age 58 years, IQR 40-60; 73% male) got a prescription for the triple therapy for 5 days. Independent public reference data from 377 confirmed COVID-19 patients of the same community were used as untreated control. 4 of 141 treated patients (2.8%) were hospitalized, which was significantly less (p less than 0.001) compared with 58 of 377 untreated patients (15.4%) (odds ratio 0.16, 95% CI 0.06-0.5). Therefore, the odds of hospitalization of treated patients were 84% less than in the untreated group. One patient (0.7%) died in the treatment group versus 13 patients (3.5%) in the untreated group (odds ratio 0.2, 95% CI 0.03-1.5; p=0.16). There were no cardiac side effects. Conclusions: Risk stratification-based treatment of COVID-19 outpatients as early as possible after symptom onset with the used triple therapy, including the combination of zinc with low dose hydroxychloroquine, was associated with significantly less hospitalizations and 5 times less all-cause deaths.
(CNN)A surprising new study found the controversial antimalarial drug hydroxychloroquine helped patients better survive in the hospital. But the findings, like the federal government's use of the drug itself, were disputed.
A team at Henry Ford Health System in southeast Michigan said Thursday their study of 2,541 hospitalized patients found that those given hydroxychloroquine were much less likely to die.
Dr. Marcus Zervos, division head of infectious disease for Henry Ford Health System, said 26% of those not given hydroxychloroquine died, compared to 13% of those who got the drug. The team looked back at everyone treated in the hospital system since the first patient in March.
"Overall crude mortality rates were 18.1% in the entire cohort, 13.5% in the hydroxychloroquine alone group, 20.1% among those receiving hydroxychloroquine plus azithromycin, 22.4% among the azithromycin alone group, and 26.4% for neither drug," the team wrote in a report published in the International Journal of Infectious Diseases.
...
It's a surprising finding because several other studies have found no benefit from hydroxychloroquine, a drug originally developed to treat and prevent malaria. President Donald Trump touted the drug heavily, but later studies found not only did patients not do better if they got the drug, they were more likely to suffer cardiac side effects....
...Treatment with HCQ-AZ was associated with a decreased risk of transfer to ICU or death (Hazard ratio (HR) 0.18 0.11–0.27), decreased risk of hospitalization ≥10 days (odds ratios 95% CI 0.38 0.27–0.54) and shorter duration of viral shedding (time to negative PCR: HR 1.29 1.17–1.42). QTc prolongation (greater than 60 ms) was observed in 25 patients (0.67%) leading to the cessation of treatment in 12 cases including 3 cases with QTc greater than 500 ms. No cases of torsade de pointe or sudden death were observed.
Conclusion
Although this is a retrospective analysis, results suggest that early diagnosis, early isolation and early treatment of COVID-19 patients, with at least 3 days of HCQ-AZ lead to a significantly better clinical outcome and a faster viral load reduction than other treatments.
Studies Designed To Fail
As Doctor Jim Meehan conjectures, these studies are designed to fail. He believes this is being done to contrive a message to manipulate, mislead and deceive the masses, and that public health is being subverted by commercial bias and political agendas. ...
And these excessive doses are not only making it impossible to assess the therapeutic benefits of HCQ for COVID-19 patients accurately. They are clearly hastening the deaths of many in the study who have been unaccountably administered dangerous amounts of a highly effective drug with a 70-year record of safety and efficacy. A highly salient point made by Del Bigtree of ICAN is that well over 5 million doses of hydroxychloroquine were taken in the United States in 2107 [2017?] for the treatment of lupus, arthritis, and malaria. If the FDA is so concerned about adverse effects associated with HCQ, why wait until now to revoke its use when it was used so widely and so effectively just a few years ago? ...
Small early terminated late stage (60% on oxygen) RCT in France showing 46% lower mortality. mortality at 28 days relative risk RR 0.54 [0.21-1.42] combined mortality/intubation at 28 days relative risk RR 0.74 [0.33-1.70]
Abstract
Since cancer cells depend on glucose more than normal cells, we compared the effects of low carbohydrate (CHO) diets to a Western diet on the growth rate of tumors in mice. To avoid caloric restriction–induced effects, we designed the low CHO diets isocaloric with the Western diet by increasing protein rather than fat levels because of the reported tumor-promoting effects of high fat and the immune-stimulating effects of high protein. We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein. There was no weight difference between the tumor-bearing mice on the low CHO or Western diets.
Additionally, the low CHO-fed mice exhibited lower blood glucose, insulin, and lactate levels. Additive antitumor effects with the low CHO diets were observed with the mTOR inhibitor CCI-779 and especially with the COX-2 inhibitor Celebrex, a potent anti-inflammatory drug. Strikingly, in a genetically engineered mouse model of HER-2/neu–induced mammary cancer, tumor penetrance in mice on a Western diet was nearly 50% by the age of 1 year whereas no tumors were detected in mice on the low CHO diet. This difference was associated with weight gains in mice on the Western diet not observed in mice on the low CHO diet. Moreover, whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low CHO diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression. Cancer Res; 71(13); 4484–93. ©2011 AACR.
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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.
“Patient Five” was in his late 50s when a trip to the doctors changed his life.
He had diabetes, and he had signed up for a study to see if taking a “statin” – a kind of cholesterol-lowering drug – might help. So far, so normal.
But soon after he began the treatment, his wife began to notice a sinister transformation. A previously reasonable man, he became explosively angry and – out of nowhere – developed a tendency for road rage. During one memorable episode, he warned his family to keep away, lest he put them in hospital.
Out of fear of what might happen, Patient Five stopped driving. Even as a passenger, his outbursts often forced his wife to abandon their journeys and turn back. Afterwards, she’d leave him alone to watch TV and calm down. She became increasingly fearful for her own safety.
Then one day, Patient Five had an epiphany. “He was like, ‘Wow, it really seems that these problems started when I enrolled in this study’,” says Beatrice Golomb, who leads a research group at the University of California, San Diego.
... Over the years, Golomb has collected reports from patients across the United States – tales of broken marriages, destroyed careers, and a surprising number of men who have come unnervingly close to murdering their wives. In almost every case, the symptoms began when they started taking statins, then promptly returned to normal when they stopped; one man repeated this cycle five times before he realised what was going on.
Golomb first suspected a connection between statins and personality changes nearly two decades ago, after a series of mysterious discoveries, such as that people with lower cholesterol levels are more likely to die violent deaths. Then one day, she was chatting to a cholesterol expert about the potential link in the hallway at her work, when he brushed it off as obviously nonsense. “And I said ‘how do we know that?’,” she says.
Filled with fresh determination, Golomb scoured the scientific and medical literature for clues. “There was shockingly more evidence than I had imagined,” she says. For one thing, she uncovered findings that if you put primates on a low-cholesterol diet, they become more aggressive.
Golomb remains convinced that lower cholesterol can cause behavioural changes in both men and women
There was even a potential mechanism: lowering the animals’ cholesterol seemed to affect their levels of serotonin, an important brain chemical thought to be involved in regulating mood and social behaviour in animals. Even fruit flies start fighting if you mess up their serotonin levels, but it also has some unpleasant effects in people – studies have linked it to violence, impulsivity, suicide and murder.
If statins were affecting people’s brains, this was likely to be a direct consequence of their ability to lower cholesterol.
Since then, more direct evidence has emerged. Several studies have supported a potential link between irritability and statins, including a randomised controlled trial – the gold-standard of scientific research – that Golomb led, involving more than 1,000 people. It found that the drug increased aggression in post-menopausal women though, oddly, not in men.
In 2018, a study uncovered the same effect in fish. Giving statins to Nile tilapia made them more confrontational and – crucially – altered the levels of serotonin in their brains. This suggests that the mechanism that links cholesterol and violence may have been around for millions of years.
Golomb remains convinced that lower cholesterol, and, by extension, statins, can cause behavioural changes in both men and women, though the strength of the effect varies drastically from person to person. “There are lines of evidence converging,” she says, citing a study she conducted in Sweden, which involved comparing a database of the cholesterol levels of 250,000 people with local crime records. “Even adjusting for confounding factors, it was still the case that people with lower cholesterol at baseline were significantly more likely to be arrested for violent crimes.”.
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.
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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.
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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)
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.
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.
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UCLA scientists have identified specific gut bacteria that play an essential role in the anti-seizure effects of the high-fat, low-carbohydrate ketogenic diet. The study, published today in the journal Cell, is the first to establish a causal link between seizure susceptibility and the gut microbiota—the 100 trillion or so bacteria and other microbes that reside in the human body's intestines.
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In a study of mice as a model to more thoroughly understand epilepsy, the researchers found that the diet substantially altered the gut microbiota in fewer than four days, and mice on the diet had significantly fewer seizures.
To test whether the microbiota is important for protection against seizures, the researchers analyzed the effects of the ketogenic diet on two types of mice: those reared as germ-free in a sterile laboratory environment and mice treated with antibiotics to deplete gut microbes.
"In both cases, we found the ketogenic diet was no longer effective in protecting against seizures," said lead author Christine Olson, a UCLA graduate student in Hsiao's laboratory. "This suggests that the gut microbiota is required for the diet to effectively reduce seizures."
The biologists identified the precise order of organic molecules known as nucleotides from the DNA of gut microbiota to determine which bacteria were present and at what levels after the diet was administered. They identified two types of bacteria that were elevated by the diet and play a key role in providing this protection: Akkermansia muciniphila and Parabacteroides species.
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How do the bacteria do this? "The bacteria increased brain levels of GABA—a neurotransmitter that silences neurons—relative to brain levels of glutamate, a neurotransmitter that activates neurons to fire," said co-author Helen Vuong, a postdoctoral scholar in Hsiao's laboratory.
"This study inspires us to study whether similar roles for gut microbes are seen in people that are on the ketogenic diet," Vuong said.
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| Wiki |
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.
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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)
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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].
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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.
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| Based on Wiki Eye |
Diets high in refined starches such as breads and cereals increase insulin levels. This affects the development of the eyeball, making it abnormally long and causing short-sightedness, suggests a team led by Loren Cordain, an evolutionary biologist at Colorado State University in Fort Collins, and Jennie Brand Miller, a nutrition scientist at the University of Sydney.
The theory could help explain the dramatic increase in myopia in developed countries over the past 200 years. It now affects 30 per cent of people of European descent, for example.
“The rate of starch digestion is faster with modern processed breads and cereals,” says Brand Miller. In response to this rapid digestion, the pancreas pumps out more insulin. High insulin is known to lead to a fall in levels of insulin-like binding protein-3, the team points out.
That could disturb the delicate choreography that normally coordinates eyeball lengthening and lens growth. And if the eyeball grows too long, the lens can no longer flatten itself enough to focus a sharp image on the retina, they suggest.
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But while reading may play a role, it does not explain why the incidence of myopia has remained low in societies that have adopted Western lifestyles but not Western diets, says Cordain.
“In the islands of Vanuatu they have eight hours of compulsory schooling a day,” he says, “yet the rate of myopia in these children is only two per cent.” The difference is that Vanuatuans eat fish, yam and coconut rather than white bread and cereals.
The theory is also consistent with observations that people are more likely to develop myopia if they are overweight or have adult-onset diabetes, both of which involve elevated insulin levels. The progression of myopia has also been shown to be slower in children whose protein consumption is increased.
Journal reference: Acta Ophthalmologica Scandinavica (vol 80, p 125)
Findings
This cohort study included 146152 individuals from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial and found that aspirin use 3 or more times per week was associated with reduced risk of all-cause, cancer, gastrointestinal cancer, and colorectal cancer mortality.
Results
A total of 146152 individuals (mean [SD] age at baseline, 66.3 [2.4] years; 74742 [51.1%] women; 129446 [88.6%] non-Hispanic white) were included in analysis. The median (interquartile range) follow-up time was 12.5 (8.7-16.4) years, encompassing 1822164 person-years. Compared with no use, aspirin use 1 to 3 times per month was associated with reduced risk of all-cause mortality (HR, 0.84; 95% CI, 0.80-0.88; P less than .001) and cancer mortality (HR, 0.87; 95% CI, 0.81-0.94; P less than .001). Aspirin use 3 or more times per week was associated with decreased risk of mortality of all causes (HR, 0.81; 95% CI, 0.80-0.83; P less than .001), any cancer (HR, 0.85; 95% CI, 0.81-0.88; P less than .001), GI cancer (HR, 0.75; 95% CI, 0.66-0.84; P less than .001), and CRC (HR, 0.71; 95% CI, 0.61-0.84; P less than .001).
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The idea behind the hypothesis occurred to Esme Fuller-Thomson, professor at the University of Toronto’s Factor-Inwentash Faculty of Social Work (FIFSW) after learning about recent research conducted in South India. This study newly identified a link between schizophrenia and a variant of the gene NAPRT1, which lowers the body’s ability to use niacin, or Vitamin B3, which naturally occurs in meat, poultry, fish, and eggs.
“When I read this study a light bulb went on in my head,” says Fuller-Thomson, who published the hypothesis in the journal Schizophrenia Research this month with doctoral student, Rukshan Mehta. “This seems to be the missing link that explains all these medical mysteries.”
The researchers speculate that there is a critical interaction between an expectant mother’s prenatal niacin deficiency due to malnourishment and the NAPRT1 variant that impedes the fetus’ ability to use niacin. This interaction between the gene and the prenatal environment may predispose the offspring to develop a psychotic disorder.
Several studies indicate that the offspring of mothers who experience famine in their first trimester of pregnancy have double the chance of developing schizophrenia. Most researchers assume nutrient deficiency must be playing a role, but the particular nutrient has yet to be identified. Fuller Thomson now speculates that niacin may be the key nutrient involved.
Results: Prostate cancer and BPH patients presented higher total, fT and bT levels than CG. IGF-1, insulin and HOMA index were higher in BPH than in the other two groups.
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| Wiki Fish |
Abstract
It has been established that there is a correlation between Alzheimer's disease and apolipoprotein E, specifically the ApoE4 genetic variant. However, the correlation between Apoe4, insulin resistance and metabolic syndrome (MetS) pathologies still remains elusive. As apolipoprotein E has many important physiological functions, individuals with the ApoE4 allele variant, also known as the Alzheimer's disease gene, are primarily at a greater risk for physiological consequences, specifically cognitive impairment (Chan et al., 2016). In this case study, a 71-year old female, heterozygous for ApoE4 with a family history of Alzheimer's Disease (AD) and the dual diagnosis of mild AD/metabolic syndrome (MetS) was placed on a 10-week nutrition protocol purposed at raising plasma ketones through carbohyrdrate restricted, high fat ketogenic diet (KD), time- restricted eating and physical/cognitive exercise. Primary biomarkers for MetS were measured pre/mid-/post intervention. The MoCA (Montreal Cognitive Assessment) was administered pre/post intervention by a licensed clinical therapist. The results were statistically significant. The HOMA-IR decreased by 75% from 13.9 to 3.48. Triglycerides decreased by 50% from 170mg/dL to 85mg/dL. VLDL dropped by 50% from 34mg/dL to 17mg/dL, and HgA1c decreased from 5.7% to 4.9%. The baseline MoCA score was 21/30; post treatment score was 28/30. The significant results in both MetS biomarkers and the MoCA score suggest that a ketogenic diet may serve to rescue cognition in patients with mild AD. The results of this case study are particularly compelling for ApoE4 positive (ApoE4+) subjects as ketogenic protocols extend hope and promise for AD prevention.
