The further a society drifts from the truth, the more it will hate those who speak it. ... In a time of deceit, telling the truth is a revolutionary act. George Orwell

Friday, February 24, 2017

High fat diet appears to regenerate diabetic pancreas

Is this possibly a cure for diabetes type 1 ?    According to this BBC article and the quoted study, it may be so!

Interestingly, dr. Jan Kwasniewski , creator of the "Optimal Diet" has always claimed that such diet can virtually cure about 9 out of 10 of diabetes type 1, based on his personal patient's records from his own medical practice during 1970-ties and 1980-ties. The reason, according to him, is that in most cases, there are at least residual 10% of the pancreatic beta cells still intact allowing the patient to survive on the high fat diet, on about 6 insulin units per day, which is about 10% of the normal (on a high carb diet) insulin production. Such low insulin requirements is only attainable on a diet that is very low in carbohydrates, low in protein and therefore - high in fat. Dr. Kwasniewski always recommended to eat mostly animal fat and saturated fats, with a minimal to none contents of polyunsaturated vegetable oils. This is interesting because that was back in the days when the  negative impact of polyunsaturated oils upon health was not as widely known as it is now. I always admired his medical insights ever since I learned about and adopted his diet in 1999. Since I don't normally trust opinions and always try to "touch the wound", so to speak, I always made efforts to verify and test all his claims. Every time when I thought he may have been wrong about some details such as vegetable fats issue or his preference on saturated fats, or insistence that cholesterol is a good thing and egg yolks are the best food (back in the 1970-ties!) - sooner or later he turned out to have been correct!


Monday, February 20, 2017

Quantum processing in brain via phosphorus nucleons' spin

There is a revolution in physics going on, regarding research on the nature of consciousness, neural transmission and signal processing in the brain.  This seems like a very  important paper:

by Matthew Fisher



Fisher's theory of quantum entanglement in the brain starts with the chemical compound pyrophosphate.

Known to be essential for cellular function, pyrophosphate is made of two bonded phosphates, each made up of phosphorus (which has a nuclear spin of ½) and oxygen (which has a spin of zero).

When pyrophosphate is broken down by enzymes, the bonded pair of phosphate ions separates.

Pairs of spin-½ particles can combine in one of four ways. Three combinations lead to a total spin of one, and these are called triplet states. The fourth leads to a spin of zero, or a "singlet state," which is a special state of entanglement often referred to as the currency of quantum computing.

The enzyme catalysis of pyrophosphate occurs more often, and possibly only, if the bonded phosphate ions are in a singlet state. These entangled ions could then be "taken up" by nanometre-diameter-sized Posner molecules. Made up of six phosphate ions bound to nine calcium ions, Posner molecules have been identified in simulated body fluid and are thought to be present in the body.

The other ingredients in Posner molecules – calcium and oxygen – do not have a nuclear spin, and the small molecules are very spherical, thus are expected to tumble rapidly in water. This means the quantum entanglement of the phosphate ions is expected to be highly protected from its environment, and could remain coherent for a day or much longer.

With Posner molecules serving as a "qubit memory," the end result could lead to non-local quantum correlations – what Einstein called "spooky action at a distance" – in neurotransmitter release and postsynaptic firing across multiple neurons. This is what Fisher calls quantum cognition.

See also

Neural qubits: Quantum cognition based on synaptic nuclear spins
August 27, 2015 by John Hewitt report


Can Quantum Physics Explain Consciousness?
A new approach to a once far fetched theory is making it plausible that the brain functions like a quantum computer.


From Atlantic, Nov-2016


Quantum Cognition: The possibility of processing with nuclear spins in the brain

Matthew P. A. Fisher
(Submitted on 19 Aug 2015 (v1), last revised 29 Aug 2015 (this version, v2))


The possibility that quantum processing with nuclear spins might be operative in the brain is proposed and then explored. Phosphorus is identified as the unique biological element with a nuclear spin that can serve as a qubit for such putative quantum processing - a neural qubit - while the phosphate ion is the only possible qubit-transporter. We identify the "Posner molecule", Ca9(PO4)6, as the unique molecule that can protect the neural qubits on very long times and thereby serve as a (working) quantum-memory. A central requirement for quantum-processing is quantum entanglement. It is argued that the enzyme catalyzed chemical reaction which breaks a pyrophosphate ion into two phosphate ions can quantum entangle pairs of qubits. Posner molecules, formed by binding such phosphate pairs with extracellular calcium ions, will inherit the nuclear spin entanglement. A mechanism for transporting Posner molecules into presynaptic neurons during a "kiss and run" exocytosis, which releases neurotransmitters into the synaptic cleft, is proposed. Quantum measurements can occur when a pair of Posner molecules chemically bind and subsequently melt, releasing a shower of intra-cellular calcium ions that can trigger further neurotransmitter release and enhance the probability of post-synaptic neuron firing. Multiple entangled Posner molecules, triggering non-local quantum correlations of neuron firing rates, would provide the key mechanism for neural quantum processing. Implications, both in vitro and in vivo, are briefly mentioned.


Saturday, January 21, 2017

Was the Climate Action Plan a population reduction in disguise?

The new US president is said to have removed all references to global warming/curbing carbon emission initiative, from the government website!

Had the world governments succeeded depleting carbon dioxide, it would speed up the coming of the new ice age. It may still happen. Ice age is the greatest threat to humanity and the biosphere, since a cold climate means not only more ice but it means also a dry climate!

Double whammy - first the Earth would loose most of the agricultural viable land in the Northern temperate climates, then it would cause desertification of the tropical areas causing a further damage to agriculture. Result: dramatic reduction of the human and animal population due to starvation! I would like to make Carbon Curbers and my other progressive friends think if that may have been perhaps the original hidden intention?

Stan (Heretic)



1. Humanity be proud!

 "Human emissions of carbon dioxide have saved life on Earth from inevitable starvation and extinction due to lack of CO2"

October 2015 Annual GWPF Lecture, Institution of Mechanical Engineers, London.

2. Honestly...

Global Warming data fiddle:

3. After the dust settles

There is a consistent ice-core evidence suggesting that each time before an ice age ended, there was a large spike of atmospheric dust. This may suggest that the dust spike may have been in fact the main trigger of glacial meltdown. Where does the dust came from?  Not sure - volcanic perhaps or was the dust blown off the arid deserts of the continental interiors?  I would probably be more inclined towards the latter since the ice age climate is known to have been much drier thus turning the vast areas of land into deserts.  This would also present an automatic feedback mechanism were upon at some point the cooling off of the Earth, the cold climate creates so much continental deserts that the amount of dust blown over the glaciers causes their melt-down.  In this picture a paradoxical carbon-dioxide time lag with respect to the temperature data can be explained by the CO2 (and methane!) out-gassing from the warming oceans, this being the result of the climate warming rather than the cause.

Picture from the above-linked article with my comments:

Update (6-Feb-2017):

Sunday, October 16, 2016

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


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

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

(CVD stands for "Cardio Vascular Disease")

by Cecilia Bleszynski (C) 2017

The first graph published in the paper:

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

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

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

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

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

The study is also discussed in the following journalistic article:

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

Thursday, September 15, 2016

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

This is the key conclusion from the recently published study.

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


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

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

And journalistic commentary, from the CBC:

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

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

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

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

My comments:

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

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

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

Stan (Heretic)

Tuesday, September 13, 2016

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


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

NY Times: How the Sugar Industry Shifted Blame to Fat

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

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

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

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


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

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


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


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

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

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


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

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

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


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

Thursday, September 1, 2016

Diets higher in protein are associated with lower adiposity and do not impair kidney function

Another myth bites the dust. It appears protein-kidney scare was a BS all along...

The recently published paper:

Diets higher in animal and plant protein are associated with lower adiposity and do not impair kidney function in US adults

Conclusions: Diets higher in plant and animal protein, independent of other dietary factors, are associated with cardiometabolic benefits, particularly improved central adiposity, with no apparent impairment of kidney function.

Tuesday, August 9, 2016

DHA forming BE quantum condensate in the living organisms

It is a good time for some nutty speculative science stuff, for a change. 8-:) This post was inspired by the following paper:

"A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signalling throughout evolution";
by Michael A. Crawford, Kebreab Ghebremeskel, C. Leigh Broadhurst, Walter F. Schmidt, Martin Guest;
Published in: Prostaglandins, Leukotrienes and Essential Fatty Acids 88 (2013) 5–13,

The paper above is postulating that the DHA (docosehexaenoic acid) has a special role in the living organism since the beginning of Life on Earth, and must have certain unique properties so that it has never been supplanted by any other molecule.

I came to a very similar conclusions regarding DHA except that I think the primary drive behind the evolutionary use of DHA was not only the neural conduction or photosensitivity/vision as stipulated in the paper, but rather much more fundamental property of the DHA-composed cellullar membranes. That is the ability to establish quantum coherency involving very large number of ions or pseudoparticles (polarons etc) trapped on the membrane, forming the so-called Bose-Einsten Condensate (BEC). For example, a polarized DHA membrane with with H+ on one side and and e- on the opposite side, may form (H+)--(e-) integral spin pseudo atoms stretched across the membrane, which may and probably do form Bose-Einstein Condensate (BEC). I think BEC explains neatly the fact that biochemical reactions involving several electron-volt of chemical potential can be driven by only a tiny ~180mV cellullar membrane potential.

It seems that the reason neural propagation appears to be extremely fast, probably instantanous, is because the quantum change of the BEC state takes place instantaneously regardless of the spacial extent of the underlying structure. Similar physics is probably taking place in the mitochondrial membranes except the purpose there would be chemical synthesis rather than signal propagation and quantum logic.

Even more speculative.

The primary evolutionary drive behind DHA could have been an ability of Bose-Einstein Condensate (BEC) of accelerating decay of naturally occurring radioactive Potassium-40 isotope, to Calcium 40 by creating BEC of both elements on the DHA membrane. By exposing of the BEC composed of Calcium 40 that is (one of) the end-product of Potassium 40 decay, to the original Potassium 40 nuclei in the initial quantum state, it would increase the probability of the K40-->Ca40 transistion. This is statistical property of bosons making them more likely to transition into a particular state if there are already bosons residing in that state. This effect is behind the well-known effect (to physicists) of "stimulated emission of radiation" in lasers, as opposed to "spontaneous emission".

If that is true then this effect could have greatly facilitated production of energy through stimulated radioactivity on the early Earth, in the primordial environment deep underground or at the bottom of the ocean, that were devoid of light and lacking other readily available sources of energy. This would probably be taking place in the first one billion years of the Earth evolution when the abundance of Potassium-40 was much higher than it is now.

There are other interesting and equally speculative possibilities to explore, involving BCE phenomena on the membranes and thin layers,
see for example this proposal.

Stan Bleszynski, August 2016.

Update 31-Aug-2016

Interesting link, an article on quantum processes in biology.

Thursday, July 28, 2016

A long-time vegan guru changes from fatophobic to favoring saturated fat!


Plant Oils Are Not a Healthy Alternative to Saturated Fat
By T. Colin Campbell, PhD July 21, 2016

My take on Dr. TCC's change of opinion about saturated fat:  I think his claims of expertise and consistency in terms of understanding the effects of various fats are not true, and it can be very easily checked by looking at his academic papers, popular publications and articles. He has always been the low fat exclusively plant-based diet promoter discouraging his followers against consuming any kinds of fats, especially dairy and animal fat. I would not be surprised if we shall soon witness a similar complete re-evaluation of his anti-animal protein beliefs as well, by himself or his colleagues.

In the last 15 years I have been warning many professional low fat vegan diet promoters on various forums, to bail out of their belief system earlier while they still could, rather than later. Not only to prevent hurting their  followers but also to minimize the damage to their own professional careers. The best time of jumping the sinking ship of low fat vegetarianism was a few years ago before it begun getting discredited rather than now when it is sinking like a boat anchor.

It is too late for Dr. TCC and others. He appeared to have sacrificed the truth about fats for short term career benefits in the past several decades of his work and now all that is coming back to bite him. However, all the pseudo-scientific anti-fat vegan garbage that various gurus have been spewing out in the mass media, on-line websites and in printed popular literature over the years is out there for all to re-read and ponder... - It cannot be undone!

(Thanks for the link, JC)

Quote (from somebody):
It's is not what is taken into one's mouth that can can be most harmful, it is what comes out!

Wiki Butter

Monday, June 13, 2016

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


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

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

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

Objective It is well known that total cholesterol becomes less of a risk factor or not at all for all-cause and cardiovascular (CV) mortality with increasing age, but as little is known as to whether low-density lipoprotein cholesterol (LDL-C), one component of total cholesterol, is associated with mortality in the elderly, we decided to investigate this issue.
Setting, participants and outcome measures We sought PubMed for cohort studies, where LDL-C had been investigated as a risk factor for all-cause and/or CV mortality in individuals ≥60 years from the general population.
Results We identified 19 cohort studies including 30 cohorts with a total of 68 094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found.
Conclusions High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.

Monday, May 23, 2016

New Battle of Fat in the British media

British National Obesity Forum and the Public Health Collaboration have just issued a damning report accusing public health bodies of colluding with the food industry, blaming them for contributing to the obesity epidemics and calling for a complete overhaul of the present low fat dietary reccomendations.

Mainstream health "authorities" have fired their salvo accusing the authors of the report of irresponsibility.

(Illustration by Cecilia Bleszynski)

The report is described here, titled "'Eating fat does not make you fat,' says UK health report".


Focus on low fat diets fails to address obesity, return to whole foods like meat, dairy needed.
Urging people to follow low fat diets and to lower their cholesterol is having "disastrous health consequences", a health charity has warned.
In a damning report that accuses major public health bodies of colluding with the food industry, the National Obesity Forum and the Public Health Collaboration call for a “major overhaul” of current dietary guidelines.
They say the focus on low fat diets is failing to address Britain’s obesity crisis, while snacking between meals is making people fat.
Instead, they call for a return to "whole foods" such as meat, fish and dairy, as well as high fat healthy foods including avocados, arguing that "eating fat does not make you fat".
The report — which has caused a huge backlash amongst the scientific community - also argues that saturated fat does not cause heart disease while full fat diary — including milk, yoghurt and cheese — can actually protect the heart.

Processed foods labelled "low fat", "lite", "low cholesterol" or "proven to lower cholesterol" should be avoided at all costs
and people with Type 2 diabetes should eat a fat-rich diet rather than one based on carbohydrates.
The report also said sugar should be avoided, people should stop counting calories and the idea that exercise can help you “outrun a bad diet” is a myth.

The authors of the report also argue that the science of food has also been “corrupted by commercial influences”.
Just as big tobacco companies bought the “loyalty of scientists” when a link was made between smoking and lung cancer, the influence of the food industry represents a “significant threat to public health”, they argued.
They said the recent Eatwell Guide from Public Health England (PHE) was produced with a large number of people from the food and drink industry.

Professor David Haslam, chairman of the National Obesity Forum, said: “As a clinician, treating patients all day every day, I quickly realised that guidelines from on high, suggesting high carbohydrate, low fat diets were the universal panacea, were deeply flawed.
“Current efforts have failed — the proof being that obesity levels are higher than they have ever been, and show no chance of reducing despite the best efforts of Government and scientists.”
Dr Aseem Malhotra, consultant cardiologist and founding member of the Public Health Collaboration, a group of medics, said dietary guidelines promoting low fat foods “is perhaps the biggest mistake in modern medical history resulting in devastating consequences for public health.
“Sadly this unhelpful advice continues to be perpetuated. The current Eatwell guide from Public Health England is in my view more like a metabolic timebomb than a dietary pattern conducive for good health.

Professor Iain Broom, from Robert Gordon University in Aberdeen, said: “The continuation of a food policy recommending high carbohydrate, low fat, low calorie intakes as ‘healthy eating’ is fatally flawed.
“Our populations for almost 40 years, have been subjected to an uncontrolled global experiment that has gone drastically wrong.”

A counterattack has been launched through the BBC by Public Health England "Advice to eat more fat 'irresponsible'":


Advice to eat more fat is irresponsible and potentially deadly, Public Health England's chief nutritionist has said.
Dr Alison Tedstone was responding to a report by the National Obesity Forum, which suggests eating fat could help cut obesity and type 2 diabetes.
The charity said promoting low-fat food had had "disastrous health consequences" and should be reversed.
Other experts have also criticised the report saying it cherry-picked and misquoted evidence.

But the report has been criticised for not going though scientific peer review.
Dr Tedstone responded to the publication by saying: "In the face of all the evidence, calling for people to eat more fat, cut out carbs and ignore calories is irresponsible."
She said thousands of scientific studies were considered as part of the official guidance adopted throughout the UK, whereas the National Obesity Forum quoted just 43 studies, some of which were comment pieces.

She praised the call to lower refined carbohydrates, but said the overall message to cut carbs ignored the issue of quality as "we do need wholegrain carbs and fibre in out diet".

Prof Tom Sanders from King's College London said: "It is not helpful to slag off the sensible dietary advice.
"The harsh criticism of current dietary guidelines meted out in this report is not justified as few people adhere to these guidelines anyway.

I need to help the readers who may have difficulty uderstanding or comprehending Prof Sanders statement. Let me translate it to a language that the working class people may understand.

According to Prof Sanders its OK to tell the public questionable theories bullshit because people don't listen anyway so there is no harm done.

On the side note, for people who did happen to listen, perhaps accidentally, who may have by a chance taken his dietary theories seriously, and got fat - please contact King's College London.

Update 1/07/2016 - a follow-up study published:

US and UK dietary advice on fats “should not have been introduced” Part 2

Evidence from prospective cohort studies did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review Zoƫ Harcombe1, Julien S Baker1, Bruce Davies2

Saturday, May 21, 2016

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

Daily Mail On-Line article:

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

Wiki Salt

Nutritional heresy strikes back, some quotes:

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

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

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

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

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

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



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

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

Sunday, April 24, 2016

Environmental predictions of the 1970-ties

Interestingly, some environmentalists and climate researchers of the 1960-ties and 70-ties seemed to have believed that the Earth climate faces imminent catastrophic cooling rather than "global warming", and they were backing it up with research and studies. There is an interesting reference article on the Wiki Earth Day. Quote:

Predictions from Earth Day 1970

During the 1970 Earth Day, given assumptions of continued exponential annual population growth of 2% or more[12] and unchanged or increasing climate impact per person, the following predictions were made:[13]

  • Denis Hayes, the chief organizer for the first Earth Day, wrote, "It is already too late to avoid mass starvation."
  • Senator Gaylord Nelson, the founder of Earth Day, stated, "Dr. S. Dillon Ripley, secretary of the Smithsonian Institution, believes that in 25 years, somewhere between 75 and 80 percent of all the species of living animals will be extinct."
  • Peter Gunter, a professor at North Texas State University, stated, "... by 1975 widespread famines will begin in India; these will spread by 1990 to include all of India, Pakistan, China and the Near East, Africa. By the year 2000, or conceivably sooner, South and Central America will exist under famine conditions.... By the year 2000, thirty years from now, the entire world, with the exception of Western Europe, North America, and Australia, will be in famine."
  • Paul Ehrlich, author of The Population Bomb, predicted that between 1980 and 1989, 4 billion people, including 65 million Americans, would starve to death.
  • Life Magazine wrote, "... by 1985 air pollution will have reduced the amount of sunlight reaching earth by one half."
  • Ecologist Kenneth Watt stated, "The world has been chilling sharply for about twenty years. If present trends continue, the world will be about four degrees colder for the global mean temperature in 1990, but eleven degrees colder in the year 2000. This is about twice what it would take to put us into an ice age."
  • Watt also stated, "By the year 2000, if present trends continue, we will be using up crude oil at such a rate…that there won’t be any more crude oil."

More on the professional environmental "prophecy of doom" business and the achievements of some of its greatest academic spin-masters, read this article:
Earth Day, Then and Now / The planet's future has never looked better. Here's why. (by Ronald Bailey, May.1,2000)


Earth Day 1970 provoked a torrent of apocalyptic predictions. "We have about five more years at the outside to do something," ecologist Kenneth Watt declared to a Swarthmore College audience on April 19, 1970. Harvard biologist George Wald estimated that "civilization will end within 15 or 30 years unless immediate action is taken against problems facing mankind." "We are in an environmental crisis which threatens the survival of this nation, and of the world as a suitable place of human habitation," wrote Washington University biologist Barry Commoner in the Earth Day issue of the scholarly journal Environment. The day after Earth Day, even the staid New York Times editorial page warned, "Man must stop pollution and conserve his resources, not merely to enhance existence but to save the race from intolerable deterioration and possible extinction." Very Apocalypse Now.

Three decades later, of course, the world hasn't come to an end; if anything, the planet's ecological future has never looked so promising. With half a billion people suiting up around the globe for Earth Day 2000, now is a good time to look back on the predictions made at the first Earth Day and see how they've held up and what we can learn from them. The short answer: The prophets of doom were not simply wrong, but spectacularly wrong.
Of course, the biggest environmental crisis facing humanity nowadays is supposed to be global warming. Not surprisingly, worries about the future climate were a common theme among alarmists on the first Earth Day. However, they couldn't agree on what direction the earth's temperature was going to take.

"The greenhouse theorists contend the world is threatened with a rise in average temperature, which if it reached 4 or 5 degrees, could melt the polar ice caps, raise sea level by as much as 300 feet and cause a worldwide flood," explained Newsweek in its special January 26, 1970, report on "The Ravaged Environment." In the service of balance, however, the magazine also noted that many other scientists saw temperatures dropping: "This theory assumes that the earth's cloud cover will continue to thicken as more dust, fumes, and water vapor are belched into the atmosphere by industrial smokestacks and jet planes. Screened from the sun's heat, the planet will cool, the water vapor will fall and freeze, and a new Ice Age will be born."

Kenneth Watt was less equivocal in his Swarthmore speech about Earth's temperature. "The world has been chilling sharply for about twenty years," he declared. "If present trends continue, the world will be about four degrees colder for the global mean temperature in 1990, but eleven degrees colder in the year 2000. This is about twice what it would take to put us into an ice age."

Watt was wrong. Global temperatures didn't fall, and fears of a new ice age dissolved like frost on an early-autumn morning. Since 1988, when government climatologist James Hansen testified before the Senate Energy and Natural Resource committee that he had detected global warming, climate doomsters have switched almost entirely to worrying about global warming. The theory is straightforward--burning fossil fuels like coal and oil puts excess carbon dioxide in the atmosphere; the carbon dioxide traps heat from the sun and re-radiates it, heating up the atmosphere.

It's generally agreed that the earth's average temperature has indeed gone up by 1 degree Fahrenheit or so in the past century. The question now is, How much man-made warming can we expect in the 21st century? Computer climate models originally predicted that atmospheric temperatures might increase between 3 to 5 degrees centigrade by 2100. However, as the models have been refined, their estimates of how much warming might occur have been declining--the range is now down to 1.5 degrees centigrade to 3.5 by 2100. A recent report from the National Research Council noted that "the surface apparently warmed by 0.25 C to 0.4 C since 1979." Remarkably, the NRC panel also estimates the change in the temperature of the atmosphere as being between 0 C to 0.2 C during the same period. In other words, the atmosphere may not have warmed at all since 1979. This is an odd conclusion because the climate computer models have never predicted that the surface would warm first or faster than the atmosphere--in fact, they predict the opposite. Consequently, this gap between surface temperatures and atmospheric temperatures calls the predictive accuracy of the models into serious question.
Indeed, a far greater threat for the next century comes from environmental activists. To counteract global warming, they essentially want to plan the energy future of the entire world for the next 100 years. They are enacting the plan through the U.N. Convention on Climate Change and the Kyoto Protocol. The absurdity (and arrogance) of that type of planning becomes clear when one imagines the same exercise taking place in 1900. The best scientific panel available in 1900 would simply not have been able to plan for millions of automobiles and trucks, ubiquitous electric lighting in millions of houses and office buildings, fuel for thousands of jet planes, and millions of refrigerators, air-conditioners, and the like. Virtually none of the devices on this nearly endless list had even been invented by 1900. Given the increasing rate of technological innovation, we undoubtedly have even less chance of foreseeing the future than people in 1900.

Why So Wrong?

How did the doomsters get so many predictions so wrong on the first Earth Day? Their mistake can be handily summed up in Paul Ehrlich and John Holdern's infamous I=PAT equation. Impact (always negative) equals Population x Affluence x Technology, they declared. More people were always worse, by definition. Affluence meant that rich people were consuming more of the earth's resources, a concept that was regularly illustrated by claiming that the birth of each additional baby in America was worse for the environment than 25, 50, or even 60 babies born on the Indian subcontinent. And technology was bad because it meant that humans were pouring more poisons into the biosphere, drawing down more nonrenewable resources and destroying more of the remaining wilderness.

We now know that Ehrlich and his fellow travelers got it backwards. If population were necessarily bad, then Brazil, with less than three-quarters the population density of the U.S., should be the wealthier society. As far as affluence goes, it is clearly the case that the richer the country, the cleaner the water, the clearer the air, and the more protected the forests. Additionally, richer countries also boast less hunger, longer lifespans, lower fertility rates, and more land set aside for nature. Relatively poor people can't afford to care overmuch for the state of the natural world.

With regards to technology, Ehrlich and other activists often claim that economists simply don't understand the simple facts of ecology. But it's the doomsters who need to update their economics - things have changed since the appearance of Thomas Malthus' 200-year-old An Essay on the Principle of Population, the basic text that continues to underwrite much apocalyptic rhetoric. Malthus hypothesized that while population increases geometrically, food and other resources increased arithmetically, leading to a world in which food was always in short supply. Nowadays, we understand that wealth is not created simply by combining land and labor. Rather, technological innovations greatly raise positive outputs in all sorts of ways while minimizing pollution and other negative outputs.

As side note, below is Bailey's other fascinating interview, enjoy!

Sunday, April 17, 2016

Rediscovery of Discount Rate


This post deals with economy and bond market pricing rather than medical heresies. I am posting it because the article is somewhat heretical and is pointing out some (probably intentionally) forgotten aspects of the bond investing that may soon become very important.

Rediscovery of Discount Rate.


Some implications of bond discounting under negative interest rate policy (NIRP) are as follows:

* Banks will not be able to avoid discounting of their own held government-issued bonds (otherwise they would be risking their own insolvency)

* Collateral assets held by the banking system will be loosing value (since the discounting would have to be accounted for).

* Total market capital value of the entire bond market will probably keep growing faster in relation to monetary mass in circulation, due to discounting mechanism applied during the roll-over refinancing at maturity. (At roll-over a borrower must re-pay the principal amount by issuing a higher nominal amount of bonds to offset the discounting). .

* Bond market will have to be made working under the truly open market rules controlled by supply and demand rather than by market administrators. Under NIRP the market will probably not be able to tolerate mispricing or distorsions in the discounting mechanism, because it requires accounting for cash losses or gains upfront leaving very little scope for market losses deferrals and creative accounting. Any attempts at manipulating the discount rate back towards 0, would result in buyers (even government buyers) walking away otherwise they would have to book losses immediately.

Wednesday, March 30, 2016

Vegetarian diet causes genetic adaptation that raises risk of heart disease and cancer

- which was found by an Indian/American study "Positive selection on a regulatory insertion-deletion polymorphism in FADS2 influences apparent endogenous synthesis of arachidonic acid" published in Mol Biol Evol (2016) doi: 10.1093/molbev/msw049 on March 29, 2016.

The study found a specific genetic adaptation to vegetarian diet that is detrimental to cardiovascular health and causes higher susceptability to cancer, due to enhanced production of arachidonic acid. Such adaption is not observed among populations consuming diets that are not exclusively plant-based.

From Wiki 
More discussion of the study can be found in:

Science Daily / Are we what we eat?
Evidence of vegetarian diet permanently shaping human genome to change individual risk of cancer, heart disease


In a new evolutionary proof of the old adage, 'we are what we eat,' scientists have found tantalizing evidence that a vegetarian diet has led to a mutation that -- if they stray from a balanced omega-6 to omega-3 diet -- may make people more susceptible to inflammation, and by association, increased risk of heart disease and colon cancer.

Daily Mail - Vegetarian diet 'raises risk of heart disease and cancer'


Vegetarianism over generations can result in genetic mutations which increase the risk of heart disease and cancer.
Researchers found a long-term vegetarian diet means populations are more likely to carry DNA that makes them vulnerable to inflammation.
The mutation is believed to make it easier for vegetarians to absorb necessary fatty acids from plants, but also boosts their production of arachidonic acid, which increases inflammatory disease and cancer.

Added 2/04/2016

This is an important study because it is not only describing statistical correlation which may or may not reflect the real causes, but it also described specific biochemical and genetical mechanisms underlying the effects they have observed. I am tempted to draw the following conclusions, some of them may be a bit stretched, some not. Time will tell.

1) The key factor in the chronic diseases are polyunsaturated fats - not the carbohydrates and not the other types of fats (for example not the mono-unsaturated or saturated fats).

2) Adaptation to a low fat plant based nutrition takes place over many generations of people, works through epigenetic mechanisms, predisposing such populations to efficiently process and convert the little amount of total and mostly polyunsaturated plant fat that they eat. This adaptation allows them to very efficiently convert the small amounts of vegetable oils they consume to some essential fatty acids required for the body, preventing malnutrition related deficiency diseases.

3) The same adaptation allowing low fat plant based food eaters to survive, causes chronic diseases risk once they add too much polyunsaturated fat into their diet, due to hyperactivity of metabolic pathway involving arachidonic acid and prostaglandins. The threshold is probably 5-10% of calories. This threshold applies to polyunsaturated fats of all kinds, including fish fat - BUT IT DOES NOT APPLY TO SATURATED FATS!

4) Both population groups - the one adapted to a low fat plant based diet and the one unadapted could safely consume larger amounts of saturated fats (i.e animal saturated fat, dairy fats, coconut fat etc) if they choose so, without a detriment to their health because saturated fats do not partake in the biochemical pathways involving arachidonic acid and prostaglandins.

5) Population adapted to low fat plant based diet should not consume more than a few percent (in total calories) of polyunsaturated fats such as vegetable oils (and fish oil!), otherwise the risk of chronic diseases increases.

6) Population not adapted to low fat plant based diet, not only can but should consume somewhat higher amounts of polyunsaturated fats including fish fat. How much would be OK and how high is too high? This is to be determined, I am not sure! This will ensure adequate supply of some essential polyunsaturated fatty acids, that their bodies cannot synthesize as efficiently as the adapted group! At the same time, the non-adaptation to low fat makes this group particularly well adapted to consuming larger amounts of polyunsaturated fish fat!

7) For the people who are not adapted to a low fat plant based diet, or those who tried it but could not or would not do it, I would say this: - a high animal fat diet will automatically make it low to moderate in polyunsaturated fats (suitable to both adapted and non-adapted) as long as you avoid using vegetable oils! If in addition, you avoid also consuming excessive amounts of carbohydrates then you will avoid other risk factors involving metabolic dysfunctions involving hyper-insulinemia and glucose overload.

8) Last but not least, I am directing this message to my vegetarian on-line friends and real life friends: - if you find yourself thriving on a low fat plant based diet then you are probably genetically adapted to it, therefore ABSOLUTELY avoid consuming more than a few % of daily calories in form of plant oils and fish (or fish fat)! Stay with it - it will probably work for you, however you most likely DO NOT NEED TO AVOID SATURATED FAT! You do not need to avoid meat, dairy and poultry either but watch out for the polyunsaturated contents of some animal fat! In this respect, if you wanted to add meat to your low fat plant based diet, you are probably better off adding beef rather than chicken or fish!


9) Limiting consumption of polyunsaturated oils, especially Linoleic Acid present in commercial vegetable oils, will likely reduce mitochondrial damage alleviating the risk of metabolic syndrome, even on a high carbohydrate diet. This is key point of the Cardiolipin hypothesis that postulates that the primary cause of metabolic syndrome is mitochondrial degeneration due to incorporation of the linoleic acid into cardiolipin molecules, which makes mitochondria exceedingly vulnerable to oxidative damage. Such oxidative damage may be triggered be glucose overload as in a high carbohydrate diet, or by other factors. This is a two step process the primary factor (a) being the linoleic acid making mitochondria vulnerable and in the second stage (b) carbohydrate overload (or other toxins) actually damages the mitochondria. For further details on Cardiolipin hypothesis read Tucker Goodrich comments under my previous post and this blog.
I thoroughly enjoyed this article by Dr. Kendrick, very much on the topic of polyunsaturated fats: "Greater Cholesterol lowering increases the risk of death" , I hope you too. Here are some quotes:

The original researchers who set up and ran the SDHS did not fully publish their data at the time (one can only speculate as to why this may be so). When this current group of researchers finally managed to get hold of the full data from the SHDS, it was found that replacing saturated fat with polyunsaturated fat did lower cholesterol, however:

and another one:

The Minnesota Coronary Experiment (MCE), a randomized controlled trial conducted in 1968-73, was the largest (n=9570) and perhaps the most rigorously executed dietary trial of cholesterol lowering by replacement of saturated fat with vegetable oil rich in linoleic acid.
Now, a few years later, the researchers who re-analysed the Sydney Diet Heart Study decided to try and find all the unpublished data from the Minnesota Coronary Experiment (MCE). (One can again only speculate as to why the original researchers did not reveal all of their data). The main points from this re-analysis were the following

* Though the MCE intervention lowered serum cholesterol, this did not translate to improved survival

* Paradoxically, MCE participants who had greater reductions in serum cholesterol had a higher, rather than lower, risk of death

Stan (Heretic)

Saturday, March 5, 2016

They tried really really hard...

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

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

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

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

(Thanks JC for the link alert)

Thursday, February 4, 2016

Zika virus, GM mosquitoes or TDAP vaccine?


More controversies and more "known unknowns"...

Zika Virus – What They Are Not Telling You

While the Brazilian government rushes to blame the Zika virus for this huge rise in abnormal birth defects, causation remains unclear. Only a small number of babies with birth defects, who died, had the virus in their brain or in the mother’s placenta. This means a large number of the babies who died had no Zika virus in their brain. Hard to blame Zika then, which has been around since before 1948 and has never been known to cause birth defects and/or death. In fact, Zika makes only one in five people get “mildly” sick with flu-like symptoms, with no symptoms at all in 4 out of 5 people. So why are they quick to blame a generally benign Zika virus?

In late 2014, the Brazilian minister of health announced that a new Tdap shot would be mandatory for all expectant mothers starting in 2015. Since it’s mandatory, mothers with birth defect babies received this newly formulated vaccine while pregnant. The timeliness of the Tdap vaccine and the sudden rise in birth defects is more than just a little coincidental. The consequences of this untested vaccine is being swept under the rug.

More links (far out warning - not for mainstream believer types!):

The CDC / Its agents run global covert ops / The virus hunters

Zika Outbreak Epicenter ... in Same Area where GM Mosquitoes were Released in 2015

Is the Dreaded Zika Virus Another Giant Scam?

Update 13/02/2016

A dissenting voice of reason. By Anonymous:


Zika virus damages babies when pregnant women initially become infected for the FIRST time. A mother who was previously exposed to Zika has natural immunity. Zika is native to West Africa, NOT to South America. Women in west Africa have natural immunity since they are exposed to it as children. But Zika was brought to Brazil by the World Cup a few years ago and introduced to a population that was not exposed to it before, leading to a LARGE number of first infections, many of whom were pregnant women.

In other words, a West African woman is unlikely to have her first Zika exposure while she is pregnant and her children will be protected by her already-developed immunity. However, South American women are NOT exposed to Zika endemically and therefore a first infection for them is catastrophic. Zika does its damage in the first 1-2 weeks of exposure, after which the body develops antibodies and fights it off so it is undetectable. This is why many pregnant women and children with microcephaly will not show signs of active Zika infection; the damage has already been done during the initial course of infection, which has resolved and been cleared by the immune system by the time of testing (testing for ANY virus outside of its initial symptomatic outbreak is not very effective, e.g. herpes simplex). Zika causes microcephaly through widespread clotting in the brain during the early weeks of fetal development. Infection with Zika resolves quickly for the mother.

TDAP has never been associated with these specific birth defects. It is in fact a very well tested vaccine which has never demonstrated an increase in microcephaly anywhere it has been used, e.g. in the Western world where it has been administered routinely for decades. Additionally, a 2015 rollout of TDAP would not have produced the massive increase in microcephaly incidence in time for it to be noticed this year (the data that showed the increase in microcephaly is from 2014 onwards). - paper from 2009 detailing difficulty of accurately assessing Zika infection r/t cross-reactivity of tests with other dengue fever viruses. Also contains data on antibodies vs. Zika in endemic populations.  - paper from 2015 detailing clinical cases of Zika in women in Rio. Interestingly, many pts positive for Zika had not been exposed to dengue, an endemic cousin of Zika which may have granted partial cross-immunity?  - the CDC has a great, sourced write-up on guidelines for pregnant women concerned about Zika.

Added 20/02/2016:
Zika Virus Associated with Microcephaly


My comments:

There are still some doubts about TDAP vaccine in pregnancy, although the risk may be presumed but not proven.

For example this:


The truth is that the Tdap shot has never been proven safe for use during pregnancy. In fact, Tdap is classified by the FDA as a Class C drug.

The definition of a Class C drug which is how the Tdap shot is classified:

Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks.

Sanofi Pasteur Adacel (TDAP) safety sheet (FDA document):


Safety and effectiveness of Adacel vaccine have not been established in pregnant women. (8.1)


* from Advisory Committee on Immunization Practices (ACIP) Summary Report February 23-24, 2011 minutes (p. 34-35)

"From January 1, 2005 through June 30, 2010, of 10,350 reports after Tdap vaccines, 129 involved pregnant women who submitted a report to VAERS. Although there were reports of 20 spontaneous abortions, 2 stillbirths, and 2 congenital anomalies, VAERS is not designed to assess whether a vaccine caused an adverse event. A review of VAERS reports in pregnant women who received Tdap vaccines revealed no elevated frequency or unusual patterns. Both GSK and sanofi pasteur maintain vaccination pregnancy registries to collect data on pregnancy outcomes and newborn health status outcomes following vaccination. Both were kind enough to allow Dr. Liang to present on their behalf. The work group reviewed their data in detail, and she provided the summary points. Boostrix® was licensed in 2005 for 10 through 18 year olds, and in 2008 for adults. GSK maintains a registry to collect data on pregnancy outcomes and newborn health status outcomes following vaccination. From its U.S. market launch in 2005 through August 2, 2010, 33 pregnancies were prospectively registered. Of these pregnancies, 18 were lost to follow-up. Outcomes were reported for seven pregnancies, and consisted of six live infants born without birth defects and one spontaneous abortion at seven weeks gestation. The remaining eight pregnancies were on-going at the time of last contact. In addition to the prospective reports of pregnancy received to the pregnancy registry from the U.S., GSK has received 13 reports from other countries. Just over half of these reported normal outcomes. The rest are on-going or were lost to follow-up. There have been no birth defects after Boostrix® vaccination reported to GSK."

Stan (Heretic)

Thursday, January 28, 2016

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


... and it is inverse!

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

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

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

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

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

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

Stan (Heretic)

Tuesday, January 26, 2016

Manufacturing of fake profits by some corporations

(Note: I rarely post that kind of analyses but this time it is probably important to know about, and interesting to watch).  

From Wiki
Surprized by the booming US stock market in the past few years 2012-2015 in spite of rotten business fundamentals and no growth?

How to transfer cheap credit into fake profit and create an illusion of growth, simple:

  • borrow a few billions of dollars at near zero interest rate
  • buy your own corporate stock back, which allows the company to increases dividend per free trading share without incurring extra costs or improving anything nor adding anything of value. It also triggers a buying momentum on the stock market, which other "investors" tend to follow. 
  • wait until stock price increases due to higher dividend yield and due to momentum investing.  This will also increase a value of the previously purchased corporate stock held as the asset, making it available to use as a collateral for future loans.  
  • repeat the above, roll-over the old loans if necessary.

In fact, one can argue that it makes no sense whatsoever to invest in production if stock buyback brings more return on “investment” and quicker since the lag is much shorter then a new product development cycle.

What can go wrong?

  • if interest rates go up too much then rolling over the old loans would drain the cash and bankrupt the companies.  This is highly unlikely since the central banks are well aware of that kind of systemic risk and will not raise the interest rates substantially, any time soon.
  • if the stock prices decline in spite of buybacks due to market correction or declining fundamentals (as in case of mining & energy sectors and some banks) , then the own corporate stock held as a collateral must also decline which may trigger the calls on the existing loans and may make it more difficult to borrow  and to roll-over the old debt.  This may potentially expose the company to a liquidity crisis.  We will probably see some interesting examples of this phenomenon in 2016, beginning with the mining sector  and some oil companies and then possibly some banks exposed to bad loans. Previously, the governments fought it by issuing another QE (“quantitative easing” of credit), will it work this time?  We shall see.     It will cause US dollar exchange rate to rapidly go down as it happened during 2008-9, which may trigger an outflow of capital out of the US stock and bond market, again as in 2008-9 (this time into the currencies of countries that are not exposed to deflationary risk of mining and energy markets).   This will exacerbate the stock market rout in the US.  Note that the above mechanisms are not self-correcting, they form a positive feedback loop, that is a movement in one direction, up or down tends to amplify itself reinforcing the trend.     
Stan (Heretic)

Updated 9/02/2016:

Big companies have lost billions buying their own shares

And it's not just a few big corporate losers accounting for all the pain. The group includes 229 companies in the Standard and Poor's 500 index, nearly half of the companies in the study prepared by FactSet for The Associated Press. When a company shells out money to buy its own shares, Wall Street usually cheers. The move makes the company's profit per share look better, and many think buybacks have played a key role pushing stocks higher in the seven-year bull market.

Updated 10/02/2016:

Why Stock Buybacks Won’t Save The Market This Time

There's a reason investors have blindly trusted Wall Street's "buy the dips" mantra since 2009. In fact… there are 2.3 trillion reasons. That's because since 2009 U.S. companies spent more than $2.3 trillion buying back their own shares, according to a report by Aranca Investment Research Services. All that buying acted as a floor for stocks and launched the major indices to new heights.
Fundamentally, spending cash on or debt-financing buybacks is touted by management as "returning cash to shareholders" by reducing share count, which reduces the number of shares the company's earnings are divided across. So, by reducing shares through buybacks, earnings per share can rise even if actual earnings are flat or falling. And that's a source of positive sentiment for those holding those stocks.

Update 14/03/2016:

There is only one buyer keeping S&P 500 bull alive

When The Prop Drops - Company Share Buybacks Accounted For 100% of New Stock Market Cash Since 2010