statins and cholesterol scam

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

Wiki

Quote:

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

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

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

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

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

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

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

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

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

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

...

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

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

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

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

...

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

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

Short-sightedness may be tied to high-carbohydrate diet

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Old but actual.

New Scientist article:

"Short-sightedness may be tied to refined diet", By Douglas Fox, 5 April 2002

Based on Wiki Eye

Quote:

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.

...

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)

aspirin reduces the risk of death by 16-19%

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"Association of Aspirin Use With Mortality Risk Among Older Adult Participants in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial", by Holli A. Loomans-Kropp, et al.,
JAMA Netw Open. 2019;2(12); published December 4, 2019

Quote:

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).

Some people with schizophrenia may simply have B3 deficiency

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Some People With Schizophrenia May Simply Have a Vitamin Deficiency

Quote:

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.

Note that there is also a connection with the ketogenic diet.

Since NAPRT1 (Nicotinate phosphoribosyltransferase) is essential for increasing cellular NAD levels (preventing also oxidative stress of cells)
and NAD is also a precursor to SIRT6 which is also critical in DNA repair (thus longevity!)

See also


NAPRT1 (Nicotinate phosphoribosyltransferase) is essential for increasing cellular NAD levels and, thus, to prevent oxidative stress of cells. NAPRT1 converts Nicotinic acid (NA; niacin) to NA mononucleotide (NaMN), which is then converted to NA adenine dinucleotide (NaAD), and finally to nicotinamide adenine dinucleotide (NAD)

Ketogenic diet slows progression of 5 neuro degenerative diseases

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Source reference paper:

Letter to the editor/
Could a gene-environment interaction between NAPRT1 risk allele and pre-natal niacin deficiency explain 4 medical mysteries of schizophrenia research?/
Esme Fuller-Thomson, Rukshan Mehta; Schizophrenia Research
Available online 12 December 2019

keto diet against prostate and hyperinsulinemia

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"Complex relationship between sex hormones, insulin resistance and leptin in men with and without prostatic disease", by Halina Grosman et al., Journal The Aging Male, Volume 19, 2016 - Issue 1

Quote:

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.

See also the following case report:

Keto diet overcomes unfavorable ApoE4 Alzheimer's genetics

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Wiki Rostas

Wiki Fish

... better way to put it - ketogenic diet renders some of the genetical conditions such as ApoE4+  irrelevant or not endangering an individual survival chances! It appears ApoE4+ does represent a handicap ONLY on a high carbohydrate diet! It is probably similar with many other genetic impairments. It seems one needs to have a more than "perfect" genetics to be able to remain healthy until a very old age on a high carbohydrate diet!

"Ketogenic diet rescues cognition in ApoE4+ patient with mild Alzheimer's disease: A case study.", by Morrill SJ, Gibas KJ, Diabetes Metab Syndr., March-April 2019


Quotes:

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.

UPDATE

Within a short time from posting the above, the following comments were posted on Twitter.
(BTW - Thanks Tucker Goodrich and Shaza!)

Indeed, it turns out that it is not the keto diet per-se but rather the improved DHA contents of such a diet that is the critical factor, not just the low carbohydrates aspect of it!    Tsimane (Bolivian natives) diet is high carbohydrate (vegetable & fruit) and low protein (16%), low fat but also most of the protein comes from fish.  The paper on "DHA brain uptake..." of ApoE4 versus non-ApoE4 carriers confirms that the critical factor is abundance of DHA in food for the ApoE4 carriers. In return they have a higher mass of grey matter in the brain than non-ApoE4, which appears to be confirmed by cognition tests [add study refs]. In return for having higher grey matter mass, the uptake of DHA is 20% higher for ApoE4 carriers, making them more vulnerable to DHA starvation.

It seems that this story has evolved in a direction that I did not expect. Perhaps the ApoE4 rather than being a mildly inconvenient adaptation requiring high fat/high fish diet, turns out to be a very beneficial genetic evolutionary trait helping in brain development and achieving higher IQ - which is clearly a survival advantage. Especially for navigation over the high seas or in the Arctic!

Nuts against dementia

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Study: A Daily Dose Of Nuts Could Be Key To Staying Sharp In Old Age

From Wiki Nut (fruit)-
By Sage Ross- Own work,
CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=30392736

Study release report (March 2019):

A nutty solution for improving brain health

Quote:

Long-term, high nut consumption could be the key to better cognitive health in older people according to new research from the University of South Australia.

In a study of 4822 Chinese adults aged 55+ years, researchers found that eating more than 10 grams of nuts a day was positively associated with better mental functioning, including improved thinking, reasoning and memory.

Lead researcher, UniSA’s Dr Ming Li, says the study is the first to report an association between cognition and nut intake in older Chinese adults, providing important insights into increasing mental health issues (including dementia) faced by an ageing population.

“Population aging is one of the most substantial challenges of the twenty-first century. Not only are people living longer, but as they age, they require additional health support which is placing unprecedented pressure on aged-care and health services,” Dr Li says.

Reference:

A Prospective Association of Nut Consumption with Cognitive Function in Chinese Adults Aged 55+ _ China Health and Nutrition Survey

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.

How ketogenic diet protects against vascular aging

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It has been noticed that ketone bodies producing diets such as calorie-restricted diet and ketogenic diets exert some anti-aging effects (on test animals). This study, see the article linked below, pinpoints the mechanism of this effect to the specific ketone body molecule: β-Hydroxybutyrate.

Natural “Fasting” Molecule Exerts Anti-Aging Effects to Protect Vascular System
By NutritonReview.org - May 16, 2019


Quote:

In their study, the research team explores the link between calorie restriction (eating less or fasting) and delaying aging, which is unknown and has been poorly studied. The findings are published in the journal Molecular Cell.

The researchers identified an important, small molecule that is produced during fasting or calorie restriction conditions. The molecule, β-Hydroxybutyrate, is one type of a ketone body, or a water-soluble molecule that contains a ketone group and is produced by the liver from fatty acids during periods of low food intake, carbohydrate restrictive diets, starvation and prolonged intense exercise.

The researchers reported that β-Hydroxybutyrate delays vascular aging by providing a chemical link between calorie restriction and fasting and the anti-aging effect.

This compound can delay vascular aging of the endothelial cells, which line the interior surface of blood vessels and lymphatic vessels, preventing a type of cell aging called senescence, or cellular aging.

Senescent cells can no longer multiple and divide. The researchers found β-Hydroxybutyrate can promote cell division and prevent these cells from becoming old. Because this molecule is produced during calorie restriction or fasting, when people overeat or become obese this molecule is possibly suppressed, which would accelerate aging.

In addition, the researchers found when β-Hydroxybutyrate binds to a certain RNA-binding protein, this increases activity of a stem cell factor called Octamer-binding transcriptional factor (Oct4) in vascular smooth muscle and endothelial cells in mice.

Stem cell factor Oct4 increases a key factor against DNA damage-induced senescence, which can keep blood vessels young.

Reference:

1. "β-Hydroxybutyrate Prevents Vascular Senescence through hnRNP A1-Mediated Upregulation of Oct4",
Young-min Han et al., Molecular Cell, VOLUME 71, ISSUE 6, P1064-1078.E5, SEPTEMBER 20, 2018.

Example of a ketogenic (high fat low carb) dish.  Ketogenic diet has been described by some as BBB diet, meaning Butter, Bacon and Brie.  It is not limited to that!  

How Carbohydrates and Not Protein Promote Aging

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Interesting article:

How Carbohydrates and Not Protein Promote Aging

Denise Minger's different kinds of magic

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I love her presentation!

Probably not true!

Who is a bastard who wrote "why"?

Magic rocks!   :)

I highly recommend to listen to her video. She is reviewing some old studies showing therapeutic effects of the very low fat high carbohydrate diets (VLFHC). Low fat means well below 10% preferably about 2%. When I begun my high fat low carb experiment back in 1999, which grew into my ongoing lifestyle nutrition to this day, I was aware that the very low fat natural food diet has been successfully used in halting progression of coronary heart disease and MS. I was familiar about Pritikin and Dr. Swank work. Prior to 1999 I was experimenting with vegetarian nutrition but I found it unpalatable, unless a sufficient amount of fat was added. More than 10%. So for me finding dr. Kwasniewski's Optimal Diet was a "gift from God", or I should say a gift from a friend of mine (Andrew S.)! Kwasniewski's Optimal Diet is high animal fat low carb diet (HFLC). After noticing back then that the VLFHC diets have some therapeutic property, I had many questions (i.e. "question everything"). One of them is about the long term viability and the side effects. Like with every therapy, there may be side effects. Are there side effects of VLFHC diets? How do people do on such nutrition scheme fare in the long term? Longevity issue? Longevity with a robust health or not so well? The same question can also be asked about any other diet, including the HFLC diet.

Unlike most other low carb promoters at that time (1970-ties - 1990-ties), dr. Kwasniewski did acknowledge that a high carbohydrate diet may also be healthy, quoting Japanese rice based diet as an example. He also insisted that, on such a diet (1) fat intake must be limited to abut 10% and (2) a sufficient amount of (lean) protein must be consumed. Insulin sensitivity is very high on such a diet because the intake of fat is very low but the pancreatic insulin secretion is medium. Insulin cannot be too low, due to carbohydrate-based metabolism. Typically it amounts to about 20-30 iu per day, based on my understanding and from reports by t1 diabetics (quoting from memory so verify this before you requote me!)

Dr. Kwasniewski also noticed, based on his patients record, that a particular proportion of macronutrients, consisting of about 35-45% of fat (by calories) and about 45-35% of carbohydrates is particulary unhealthy and makes people prone to developing diabetes and atherosclerotic heart disease. Kwasniewski also noticed that it causes a peculiar form of neuro-degeneration for people in their 40-ties and 50-ties manifesting itself in form character disorder (psychopathy). He called that dietary zone "dangerous middle zone". Pancreatic insulin secretion has to be very high (typically 40-60 iu/day or more) on such a diet in order to overcome the insulin insensitivity induced by the high fat intake.

He also noticed that as soon as you up the total fat intake to above 50% of calories then these pathological effects gradually subside and the diet becomes healthy again, even therapeutically healthy. The widely popular diet he publicized in the 1980-ties, arrived at the macronutrient proportions P:F:C (Protein to Fat to Carbohydrates) in gram per day per 1kg of ideal body weight of 1:3-3.5:0.8 to 1:2-2.5:0.5 . This typically works out at way over 60% (typ about 85%) of fat by calories. Notice that fat has 9kcal/g, glucose 4.5kcal/g and protein 3.5kcal/g (or less if used anabolically). Interestingly, Kwasniewski also found that his patients with coronary heart disease begun reversing and recovering. So his patients with many autoimmune disease such as asthma, rheumatoid arthritis, MS, IBS, and other - also recovered on his diet! Even though the HFLC diet is the exact opposite of the VLFHC diet, it nevertheless produced surprisingly similar (if not greater) therapeutic effects! Notice that the insulin sensitivity (and the effect of fat upon it) becomes irrelevant due to very low intake of carbohydrates. Kwasniewski quoted insulin requirement at this point, to be about 6-10 iu/day. How did he measured it? By observing his type 1 diabetic patients!

What Denise Minger has done, is rediscovering and publicizing that fact that there are 2 dietary zones that have therapeutic properties, not just one diet!

What I would disagree with, is her presumption that the VLFHC diet would:

- "results in healthier gut microbiome long term"

There is not proof or comparison studies done for VLFHC vs HFLC on that, while there is enough reports indicating the long term gut flora deterioration among vegans (I would put refs to Dr. Stanley Bass and Dr. Gian-Cursio reports on Natural Hygienists).

- "may do best for ApoE4 carriers"

No proof either, other than high serum cholesterol which does not always translate to a health risk, except for people eating in the dangerous middle zone.

- "may be able to restore and heal glucose tolerance which does not happen on the high fat..."

This is not true based on my personal observation. Initially yes, HFLC diet did not restore my glucose tolerance, it only allowed my body to bypass the issue by not showering my body with the excess carbohydrates. Whenever I tried to eat a little bit more than 50g of carbohydrates in a day, I would inevitably come to regret it! Carb-headache and nausea. Beer was especially bad for me. However, after about 2 years I noticed that I was able to increase that limit and add more than previously and after about 6-7 years I noticed that my carbohydrates tolerance has been totally restored! For example I can now consume a high carb dinner if I have no other choice without any adverse side effects. I don't do it often, but it is nice to know that my metabolism has completely been restored. I suspect it has to do with the mitochondrial regeneration. It takes about 7 years to regrow and renew most of our muscular tissues from our stem cells. I also found it that initially I had to watch not only the total carbohydrates intake, but I also had to limit the overall caloric intake from fat as well. Initially the total limit was about 1800kcal. Believe it or not that is actually perfectly sufficient for an adult leading an active life on the high fat diet, without any problems (I was 43 in 1999 when I begun HFLC and I weigh 64k, 173cm height) It was as if my metabolic channels were impaired for both macronutrients, for carbs as well as for fat, except the metabolism of fat, being more effective, allowed me to live better and have more energy in spite of the limitations. Again, that restriction is no longer applicable and lifted itself after about 7 years.

Stan (Heretic) Bleszynski

People with low cholesterol dying like flies

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"Serum total cholesterol and risk of cardiovascular and non-cardiovascular mortality in old age: a population-based study", Yajun LiangEmail author, Davide Liborio Vetrano and Chengxuan QiuEmail,
BMC Geriatrics, 2017/17:294

First graph from the above paper.

Quote:

Results

During 23,196 person-years of follow-up (median per person, 7.5 years), 1059 (34.3%) participants died. Compared to normal total cholesterol (<5.18 mmol/l), borderline-high (5.18-6.21 mmol/l) and high (≥6.22 mmol/l) total cholesterol were associated with a decreased risk of all-cause mortality, with the multiple-adjusted hazard ratio (95% confidence interval, CI) of 0.71 (0.61–0.83) and 0.68 (0.57–0.80), respectively (P for trend <0.001). The competing risk regression models revealed that the reduced all-cause mortality associated with high total cholesterol (≥6.22 mmol/l)) was mainly due to the reduced risk of non-cardiovascular mortality (hazard ratio = 0.67, 95% CI = 0.51-0.88). These associations were statistically evident only among individuals without use of cholesterol-lowering medications.

Conclusions

The inverse association between high total cholesterol and reduced all-cause mortality in older adults is primarily due to non-cardiovascular mortality, especially among those who are not treated with cholesterol-lowering medications.

Telomere length correlates with red meat consumption

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Blog article:

Unexpected relationship between Red Meat Diet and PBMC Telomere Length, Sep 28, 2016 1:30:54 AM / by Stacy Matthews Branch, DVM, PhD

Update 15-Jan-2020

500% extension for C.Elegans by TOR and Insulin IIS signaling modification:
Pathways that extend lifespan by 500 percent identified Discovery of cellular mechanisms could open door to more effective anti-aging therapies, Date:January 8, 2020, Mount Desert Island Biological Laboratory

Quote:

The new research uses a double mutant in which the insulin signaling (IIS) and TOR pathways have been genetically altered. Because alteration of the IIS pathways yields a 100 percent increase in lifespan and alteration of the TOR pathway yields a 30 percent increase, the double mutant would be expected to live 130 percent longer. But instead, its lifespan was amplified by 500 percent.

Reference:

"The relationship between peripheral blood mononuclear cells telomere length and diet - unexpected effect of red meat.", Kasielski M, Eusebio MO, Pietruczuk M, Nowak D., Nutr J. 2016 Jul 14;15(1)

Fig.1 from the paper above.

Mount Desert Island Biological Laboratory. "Pathways that extend lifespan by 500 percent identified: Discovery of cellular mechanisms could open door to more effective anti-aging therapies." ScienceDaily. ScienceDaily, 8 January 2020.

Jianfeng Lan, Jarod A. Rollins, Xiao Zang, Di Wu, Lina Zou, Zi Wang, Chang Ye, Zixing Wu, Pankaj Kapahi, Aric N. Rogers, Di Chen. Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity. Cell Reports, 2019; 28 (4): 1050 DOI: 10.1016/j.celrep.2019.06.078

Schizophrenia put into remission on keto diet

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Chronic Schizophrenia Put Into Remission Without Medication/New research suggests ketogenic diet may play a role in treating schizophrenia.
by Chris Palmer, M.D., Apr 06, 2019

Quotes

An 82 year old woman with chronic paranoid schizophrenia since age 17

The first patient documented in the Schizophrenia Research article is a woman who spent nearly her whole life suffering chronic, treatment-resistant schizophrenia. For more than 50 years, she endured paranoia, disorganized speech, visual and auditory hallucinations. By the time she was 70, she was suicidal and had been hospitalized repeatedly for psychosis or suicide attempts. She had been treated with over ten different antipsychotic and mood stabilizing medications, including regular antipsychotic injections. None of them helped her symptoms. She was unable to care for herself and had a court-appointed guardian and home health services.

At the age of 70, weighing 330 pounds, she went to a medical weight loss clinic and was started on a ketogenic diet. Within two weeks of starting the diet, she reported a noticeable reduction not only in her weight but also her psychotic symptoms. Within several months, she started to feel so much better that she was able to stop taking her psychiatric medications while remaining on the diet. Over time, her mood stabilized, and her hallucinations and paranoia remitted completely. She was no longer suicidal. Her case was first reported in 2009.

Today, 12 years later, she has lost a total of 150 pounds and remains on the ketogenic diet. She takes no medications and remains symptom-free. She was able to regain her independence, no longer requiring the guardian and the home health care team. When I recently spoke with her, she recalled her decades of suffering and hopelessness, and said that since starting the diet, she has had a "new life," and is happy to be alive.

A 39 year old woman with schizophrenia for 20 years

The second patient described in the article is a thirty-nine year old woman who suffered from depression, anxiety, anorexia nervosa, hallucinations and paranoia since her teens. As patients sometimes do, she concealed her psychotic symptoms when she was initially treated for depression and anorexia. When she finally reported her psychotic symptoms later in her twenties, she was diagnosed with schizophrenia. For the next ten years, she was treated with 7 different antipsychotic medications—including clozapine (called the “gold standard antipsychotic medication”) - along with antidepressants and anti-anxiety medications. Nevertheless, she continued to have symptoms.

She was having chronic gastrointestinal problems, so she saw a doctor who recommended the ketogenic diet. Noticing some improvement of her symptoms and being frustrated with all of her psychiatric medications, she unwisely stopped taking all 14 of her medications “cold turkey.” This sent her into severe psychosis requiring an extended hospitalization. In the hospital, she was re-medicated with Haldol-decanoate (an injectable medication which had not worked for her previously) and she continued the ketogenic diet. Within a month on both Haldol and the ketogenic diet, she reported complete remission of her psychotic symptoms for the first time since she was 14. Over the following year, she slowly tapered off Haldol, and remained free of psychotic symptoms. Of note, she lost 70 pounds from the diet, which exacerbated her anorexia. She has since regained 30 of those pounds and maintains a healthy weight today. 5 years after starting the ketogenic diet, she is off all antipsychotic medications, remains on the diet, and is free of all psychotic symptoms. She has since finished graduate school and now works full time.

Interestingly, these aren’t the first reports of the ketogenic diet for schizophrenia
While inspiring, these two case reports join a growing body of evidence supporting the use of the ketogenic diet in the treatment of schizophrenia.

Schizophrenia in 1965

In 1965, ten women hospitalized with schizophrenia who were already receiving medications and electroconvulsive therapy (ECT or “shock therapy”) were also placed on the ketogenic diet for a month. The researchers reported that their symptoms improved after two weeks on the diet, but then returned back to their baseline level of symptoms after the diet was stopped.

Schizoaffective disorder in 2017

In 2017, I reported two other cases of schizoaffective disorder improving significantly on the ketogenic diet. Schizoaffective disorder is a diagnosis that includes both a mix of schizophrenia and a mood disorder, often bipolar disorder. One man and one woman, both in their 30’s, had suffered treatment-resistant schizoaffective disorder for years. On the diet, their symptoms were greatly improved, and they both lost significant amounts of weight. Off the diet, their symptoms returned.

Schizophrenia in Ecuador

In 2018, two Ecuadorian twins, one male and one female, diagnosed with schizophrenia since the ages of 14 and 18 were started on a 6-week trial of the ketogenic diet. This study had a psychiatrist rate each twin’s symptoms while being unaware of their diet status. Interestingly, only when the patients were compliant with the diet did their symptoms improve. They also both lost weight. When they stopped the diet at the end of the study, their symptoms returned to their baseline level.

Stan's comments: - who were the medical criminals who stopped their patients' treatment as the article described, in spite of the clear improvement and despite of no viable alternatives? Why there was no information published and made available over the years, to other patients suffering from this debilitating disease, and their families? It is very symptomatic of a very serious disease rotting the medical system from within, in all countries. What have the government departments in charge of public health policies done to make that treatment available? Why did the judicial system refrain from punishing the people involved in maintaining this information hidden or even actively discouraging it by denigrating all ketogenic diets, all high fat low carbohydrate diets publicly and in the media? Who were the people, and who financed those who campaigned in the media smearing Drs. Yudkin, Atkins, Bernstein and others and why did public prosecutors and politicians allowed that to continue?

More connections between metabolic disorder and psychiatric/neurological conditions:

"Impaired insulin signaling in unaffected siblings and patients with first episode psychosis", by Virginie-Anne Chouinard et al., Mol Psychiatry. 2018 Mar 9


Quote

Patients with psychotic disorders are at high risk for type 2 diabetes mellitus, and there is increasing evidence that patients display glucose metabolism abnormalities before significant antipsychotic medication exposure. In the present study, we examined insulin action by quantifying insulin sensitivity in first episode psychosis (FEP) patients and unaffected siblings, compared to healthy individuals, using a physiological-based model and comprehensive assessment battery. Twenty-two unaffected siblings, 18 FEP patients and 15 healthy unrelated controls were evaluated using a 2-hour oral glucose tolerance test (OGTT), with 7 samples of plasma glucose and serum insulin concentration measurements. Insulin sensitivity was quantified using the oral minimal model method. Lipid, leptin, free fatty acids and inflammatory marker levels were also measured. Anthropometric, nutrient and activity assessments were conducted; total body composition and fat distribution were determined using whole-body dual energy x-ray absorptiometry. Insulin sensitivity significantly differed among groups (F=6.01, P=0.004), with patients and siblings showing lower insulin sensitivity, compared to controls (P=0.006, and P=0.002, respectively).

Comment: Comparison between people diagnosed with psychiatric disorder and their sibling who were not diagnosed and therefore not affected by psychiatric drugs, showed the common underlying metabolic disorder involving insulin insensitivity and high risk of developing diabetes type 2.

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Update 11/04/2019 Another interesting paper on this subject. A different angle:

"Psychosis and Symbiosis: Microbiome and Schizophrenia. Fascinating new research links the gut and brain in sickness and health.", by Emily Deans M.D., Posted Mar 31, 2019

Quote:

Those mice that received the transplants from schizophrenic patients had higher levels of glutamine in the serum and hippocampus, decreased glutamate in the hippocampus, and increased GABA in the hippocampus. These difference were localized to areas of the brain particularly rich in glutamate and its metabolites (i.e., the outer shell of the brain and the hippocampus). This means that a transplant of a different microbiome led to different GABA-glutamate-glutamine neurotransmission in mouse brains. Corresponding human brain areas are related to memory, neuron repair, and executive functioning, all significantly impacted in schizophrenia.

In addition, the schizophrenia microbiome recipient mice had different behaviors than the healthy control mice, with exaggerated startle response and increased activity.

Optimal sodium is 3-5g/day and potassium above 2g/day

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- in order to minimize the risk of cardio-vascular disease. This is based on thew recent study:
"Joint association of urinary sodium and potassium excretion with cardiovascular events and mortality: prospective cohort study", by Martin O’Donnell et al., BMJ 2019; 364

These guidelines are significantly higher than the existing WHO recommendations.

Fig 3

Heat map of risk for composite of cardiovascular events or death showing lowest risk in region of moderate sodium intake 3-5 g/day and higher potassium intake and highest risk in region of extremes of sodium excretion and low potassium excretion. The reference hazard for these hazard ratios was set at a value of sodium daily excretion/intake of 5.00 g and potassium daily excretion/intake of 2.25 g (median excretion of sodium and potassium), marked as X. The overlaid lines represent joint distribution quartiles; each region contains a quarter of the analysed participants. r=0.34

Non-compliant diabetics had lower CVD risk

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


Quote:

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

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.

many top scientists believe global warming theory is fraud

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1000 Scientists Declare Man Made Global Warming Climate Change a Complete Fraud / Hoax

German Professor: NASA Has Fiddled Climate Data On ‘Unbelievable’ Scale


Quote:

Professor Dr. Friedrich Karl Ewert is a retired geologist and data computation expert. He has painstakingly examined and tabulated all NASA GISS’s temperature data series, taken from 1153 stations and going back to 1881. His conclusion: that if you look at the raw data, as opposed to NASA’s revisions, you’ll find that since 1940 the planet has been cooling, not warming.

New cancer treatment with rosiglitazone+trametinib

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Cancer Cells Transformed into Harmless Fat in Mouse Study, By Rachael Rettner, January 15, 2019

Quote:

Then, the researchers treated the mice with two drugs: rosiglitazone, which is used in people to treat type 2 diabetes, and trametinib, an anti-cancer drug that inhibits the growth and spread of cancer cells. (Rosiglitazone belongs to a class of drugs known as thiazolidinediones, which bind to receptors that are found mainly in fat tissue and that play a role in a number of biological processes, including the formation of mature fat cells, according to a 2005 paper on the topic. People with diabetes are given the drug because the receptors that it binds to also help increase sensitivity to the hormone insulin, which is involved in regulating blood sugar levels.) The researchers in the new study found that when mice received this drug combination, the cancer cells that had broken free from the initial tumor (called "invasive cancer" cells) changed into fat cells. The drugs also suppressed the growth of the tumor and prevented further metastasis.