Sunday, October 4, 2015

Did a psychiatric drug or did guns trigger mass shooting?

This is speculative but the question must be asked in public and then must be answered by the authorities entrusted in regulatory duties.  No it is not about guns!

Michael Moore - Reveals the real cause of Columbine. (watch minute 1:30)


... Eli Lilly for nearly 15 years covered up their own internal investigation that anyone on Prozac is 12 times more likely to commit suicide than on other anti-depressant.

See also this:

Oregon: Another Mass Shooting, Another Psychiatric Drug? 35 School Shootings/Mass Stabbings Tied to Psychiatric Drugs


According to an article posted in the Oregonian, “There are a number of indications that Mercer had mental health or behavioral issues. His screen name on some social media sites was ‘lithium love.’ Lithium is a psychiatric medication.

The question is what a particular drug or a class of drugs may be triggering it?

Thursday, September 24, 2015

It is the fettered capitalism that is the problem!


From Wiki

It is the "fettered" capitalism which sucks and taxes capital out of individuals and small businesses, taking from people who work and create wealth giving it to governments and corporate/banking oligarchs.

Pope calls unfettered capitalism 'the dung of the devil'

I disagree, I think the Pope is mistaken.   "Unfettered" capitalism, when it still existed, created the wealthiest country in the world by allowing the poor European peasant refugees who came here with nothing to keep the money they earned, to reinvest it to grow their own businesses.

No country in Europe including the part of Italy that was ruled by Vatican for long period of time,  allowed their poorest working class people to accumulate capital and become rich, they were always taxed out of their surplus income.   If that is the Pope's solution against poverty than no thanks.  I prefer the unfettered capitalism.  If I could only find one somewhere...


Saturday, September 19, 2015

Longevity genes, glucose and insulin sensitivity

Some of the most interesting longevity research concerns FOXO3A (homozygotic GG) and SIRT6 genes. In the case of FOXO3A, it seem to be associated also with the improved insulin sensitivity (thus allowing the body to maintain consistently LOW insulin level, reducing the risk of insulin resistance, metabolic factor and diabetes t2) throughout one's life. In the case of SIRT6 which plays a major role in DNA repair process, it appears to be upregulated with lower glucose consumption. Insulin and carbohydrates, carbohydrates and insulin...

Lots of unanswered questions: is the link accidental or not? Which is the primary and which is the secondary factor in the longevity?
Is (a) FOXO3A the primary cause of longevity while in addition improving also the insulin sensitivity? - Or, (b) is the improved insulin sensitivity and low glucose caused by the gene (or by whatever other factors...) - the primary longevity factor?

So far, the second answer (b) seems to be already demonstrated for the SIRT6 while there seems to be a growing suspicion that it is may be so for the FOXO3A as well!

This situation reminds me that the life forms may deals with any adverse environmental threat in the two-fold fashion: - either evolving a special resistance against a threat or simply avoiding the threat (in this case by not consuming the excessive carbohydrates...)

So, you either may already have the protective genes and in this case you can safely consume whatever high carbohydrate food is being marketed your way, or you minimize or avoid that stuff altogether. Everybody has a choice - and that's excellent news!

More links:

Bradley Willcox et al., "FOXO3A genotype is strongly associated with human longevity", PNAS, September 16, 2008, vol. 105 no. 37


Human longevity is a complex phenotype with a significant familial component, yet little is known about its genetic antecedents. Increasing evidence from animal models suggests that the insulin/IGF-1 signaling (IIS) pathway is an important, evolutionarily conserved biological pathway that influences aging and longevity.
Long-lived men also exhibited several biological markers indicative of greater insulin sensitivity and this was associated with homozygosity for the FOXO3A GG genotype.

I also posted on this subject in post. See the following quote from this article about the SIRT6 gene:


One explanation for this failure may relate to SIRT6’s critical role in DNA repair. Several studies have indicated that SIRT6 helps catalyze repair of the damage at numerous types of DNA lesions, including single- and double-strand breaks. A characteristic feature of aging cells is an increase in the amount of DNA damage.
While overexpression of SIRT6 may not be tractable in a therapeutic context, SIRT6 activity can be increased by caloric restriction, reducing glucose consumption, or increasing NAD+ bioavailability (**) - interventions that have already shown promise in increasing longevity in animal models. (Such interventions are also showing promise in slowing the progress of some age-related neurodegenerative disorders.

Sunday, August 2, 2015

'Cool' teenagers at higher risk of becoming losers or criminals



This is what the recent study has found:

"Whatever Happened to the Cool Kids?", published in the journal Child Development by researchers at the University of Virginia


Pseudomature behavior—ranging from minor delinquency to precocious romantic involvement—is widely viewed as a nearly normative feature of adolescence. When such behavior occurs early in adolescence, however, it was hypothesized to reflect a misguided overemphasis upon impressing peers and was considered likely to predict long-term adjustment problems. In a multimethod, multireporter study following a community sample of 184 adolescents from ages 13 to 23, early adolescent pseudomature behavior was linked cross-sectionally to a heightened desire for peer popularity and to short-term success with peers. Longitudinal results, however, supported the study's central hypothesis: Early adolescent pseudomature behavior predicted long-term difficulties in close relationships, as well as significant problems with alcohol and substance use, and elevated levels of criminal behavior.

The abstract seems to be slightly toned down, while the actual correlation figures (see Table 1) are quite high and significant! For example, some correlation factors (age range in brackets):

"1.Pseudomature behavior (13-15)" versus "12.Problems related to substance use (21–23)", Correlation=50%.

"4.Precocious romantic behavior (13–15)" versus "12.Problems related to substance use (21–23)", Correlation=33%.

"1.Pseudomature behavior (13-15)" versus "14.Criminal behavior (21–23)", Correlation=27%.

"4.Precocious romantic behavior (13–15)" versus "14.Criminal behavior (21–23)", Correlation=31%.

Interestingly, both substance abuse and criminality appear to be also correlated with early puberty!

More reading:

The Independent article: 'Cool kids' can go on to become losers in later life, study finds

My essays on social regression and anthropology.

Saturday, July 25, 2015

Myth of increasing interest rates


A recent news headline "US Fed data leak shows staff expect interest rate to increase"


Data accidentally published on the US Federal Reserve website shows that staff economists at the central bank expect an about 25 basis point increase in interest rates in 2015.

I think they are probably lying!

1) It was not an accidental leak but an intentionally planted disinformation like many times before.

2) Interest rates will not significantly increase any time soon, under the present monetary system, because neither the government, central banks nor large corporations can afford the consequences of such a move! There is only one way the interest rates can go at the moment: down!

(see this graph)


Many times in the last couple of years I have witnessed various banking or governmental officials, here in Canada and elsewhere, talking of some imminent interest rate increases - which never seem to materialize!

 Why are they misleading the people? My guess is that they are trying to cool off the property market and preempt the speculative bubbles. If the investors would suddenly rush to buy bonds believing the yields (and interest rates) to go down, then the yields and interest rate would come down faster than anticipated prior to the actual announcement, which would deprive the central banks and the governments of an advantage of being the prime movers.

Interest rates cannot go up, under the current monetary system, because it would probably bankrupt all government (addicted to cheap financing at low interests), most large corporations (ditto) and would instantaneously devalue almost all banking collateral (note: bonds and property go down in value if interest rates go up!).

added 2/07/2015 - There is a better way of putting it:
Lowering of interest rates is inflationary (short term), while increasing them is deflationary (also short term).  Governments and banks cannot afford to initiate a deflationary move (of increasing the rates) under an already deflationary and stagnating economy, given a risk of recession!

I think that the authorities – governments, public sector institutions, large corporations and banks, cannot allow the capital market system to naturally correct towards the higher yields while at the same time obliterating the total value of their personal wealth, value of the entire banking collateral and devaluing most paper "assets"! This process (towards the higher yields) will certainly be opposed by the authorities as hard as they can, because it would render them poorer and less powerful!

The establishment have a very tight control over the system and will not allow that! Not unless they have an alternative. I don’t think they have an alternative at the moment - thus, the interest rates have only one way to go – down, asymptotically to zero!

This is the scenario similar to a classical deflationary spiral with decreasing yields (and profit margins), with diminishing velocity of money counteracted by an expansion of monetary mass. Deflationary trend caused by diminishing yields seems to be masked by an expansion of monetary mass (through credit and debt expansion i.e. "Quantitative Easing") that mitigates the deflationary effects and keeps the average prices more stable than they would have been otherwise.

The biggest drawback of this system, in my opinion, lies in the fact that the benefits of the monetary mass expansion apply to governments, large centralized institutions and large corporations, where as the recessionary hardship of the diminishing velocity of money is being felt on the lower and local market level. The current system is unbalanced and I think it will probably not improve much until an additional local multiple-currency system is introduced, that will balance that out and will reverse a recessionary pressure felt by the local markets.

I also suspect that the presence of the local currencies (at the township level, not countries!) may alter the entire dynamics of the central banks and the governments, but we won't know for sure until it is tried and tested.


Friday, June 26, 2015

After 9 years on statins - 2.5 times more diabetes with complications!

Found and published in this recent study titled: Statins and New-Onset Diabetes Mellitus and Diabetic Complications: A Retrospective Cohort Study of US Healthy Adults..


A total of 25,970 patients (3982 statin users and 21,988 nonusers) were identified as healthy adults at baseline. Of these, 3351 statins users and 3351 nonusers were propensity score-matched. Statin users had higher odds of new-onset diabetes (odds ratio [OR] 1.87; 95 % confidence interval [95 % CI] 1.67-2.01), diabetes with complications (OR 2.50; 95 % CI 1.88-3.32), and overweight/obesity (OR 1.14; 95 % CI 1.04-1.25). Secondary and sensitivity analyses demonstrated similar findings.

From Wiki

A summary of the study is also published on the Daily Reckoning site under the title: New Concern About Cholesterol Drugs and Diabetes.  Unfortunately, at the end of the abstract, the authors are promoting another non-statin replacement toxins drugs that have not yet been found to kill patients.

Tuesday, May 19, 2015

Anti-Iodine conspiracy - Wolff-Chaikoff medical myth

"Sample of iodine" by LHcheM - Own work. Licensed under CC BY-SA 3.0 via Wikimedia Commons 

Much of the following information, studies, links and inspiration is based on Jerzy Zięba's 2015 book "Ukryte Terapie" ("Hidden Cures"). Highly recommended!

Basically, Wolff and Chaikoff (Wolff J, Chaikoff IL "Plasma inorganic iodide as a homeostatic regulator of thyroid function", J.Biol Chem, 1948) destroyed the previously widespread and largely successful thyroid disease therapies based on iodine supplementation (*) by claiming that the excess iodine blocks thyroid hormone production. However, what their study did actually measure was the effect of stopped absorption of radioactive iodine in to iodine-saturated rat's thyroid tissue. They did not measure thyroid hormones production! Furtheromre, they used unrealistically high iodine tissue dosage, corresponding to an oral intake of 50 grams of Iodine a day (if it were done for humans)

This one study has became the basis of discontinuation of the time-proven previous iodine supplementation therapies in favor of treating thyroid disorders with thyroid hormonal supplements or with surgery.

*) Using Iodine in Potassium-Iodide (Lugol) solution, for both hypothyroid and hyperthyroid conditions. The claimed success rate was close to 90% of the cases!

A compilation/review study of prior thyroid therapies using inorganic iodine supplementation can be read here:
Kelly FC, "Iodine in medicine and pharmacy since its discovery - 1811-1961", Proc R Soc Med, 1961, 54:831-836

Interesting overview of the conspiratorial aspect of the story can be found here:

Guy E. Abraham "The History of Iodine in Medicine Part III; Thyroid Fixation and Medical Iodophobia", The Original Internist, June 2006


From Guy E. Abraham "The History of Iodine in Medicine Part III

Sunday, May 3, 2015

Give us NOT our daily bread with gluten!

Unless you want to increase your risk of diabetes and probably many other diseases, according to this study (on mice):

Gluten-free diet reduces adiposity, inflammation and insulin resistance associated with the induction of PPAR-alpha and PPAR-gamma expression.


Our data support the beneficial effects of gluten-free diets in reducing adiposity gain, inflammation and insulin resistance. The data suggests that diet gluten exclusion should be tested as a new dietary approach to prevent the development of obesity and metabolic disorders.


More and more studies indicate deleterious effect of wheat consumption. The problem is not only in the very high concentration of carbohydrates, 60-80% by weight which is nearly as high as in pure sugar, but the presence of several other harmful compounds such as auto-immune triggering low molecular mass wheat proteins, nutrient-blocking lectins (agglutins), mood-altering addictive exorphins and other plant poisons.

 (Source: Wiki)

Thursday, April 23, 2015

Diet not exercize the best way to lose weight

According to the recent editorial published in British Journal of Sports Medicine/BMJ:

A. Malhotra, T. Noakes, S. Phinney, "It is time to bust the myth of physical inactivity and obesity: you cannot outrun a bad diet", Br J Sports Med doi:10.1136/bjsports-2015-094911


According to the Lancet global burden of disease reports, poor diet now generates more disease than physical inactivity, alcohol and smoking combined.
Instead, members of the public are drowned by an unhelpful message about maintaining a ‘healthy weight’ through calorie counting, and many still wrongly believe that obesity is entirely due to lack of exercise. This false perception is rooted in the Food Industry's Public Relations machinery, which uses tactics chillingly similar to those of big tobacco. The tobacco industry successfully stalled government intervention for 50 years starting from when the first links between smoking and lung cancer were published. This sabotage was achieved using a ‘corporate playbook’ of denial, doubt, confusing the public and even buying the loyalty of bent scientists, at the cost of millions of lives. [4,5]

Coca Cola, who spent $3.3 billion on advertising in 2013, pushes a message that ‘all calories count’; they associate their products with sport, suggesting it is ok to consume their drinks as long as you exercise. However science tells us this is misleading and wrong. It is where the calories come from that is crucial. Sugar calories promote fat storage and hunger. Fat calories induce fullness or ‘satiation’.

A large econometric analysis of worldwide sugar availability, revealed that for every excess 150 calories of sugar (say, one can of cola), there was an 11-fold increase in the prevalence of type 2 diabetes, in comparison to an identical 150 calories obtained from fat or protein.

And this was independent of the person's weight and physical activity level; this study fulfils the Bradford Hill Criteria for causation.[6]

A recently published critical review in nutrition concluded that dietary carbohydrate restriction is the single most effective intervention for reducing all the features of the metabolic syndrome and should be the first approach in diabetes management, with benefits occurring even without weight loss.[7]


[4] Brownell KD, Warner KE . "The perils of ignoring history: big tobacco played dirty and millions died. How similar is big food?" Milbank Q 2009;87: 259–94. doi:10.1111/j.1468-0009.2009.00555.x

[5] Gornall J. "Sugar: spinning a web of influence." BMJ 2015;350:h231. doi:10.1136/bmj.h231

[6] Basu S, Yoffe P, Hills N, et al . "The relationship of sugar to population-level diabetes prevalence: an econometric analysis of repeated cross-sectional data." PLoS ONE 2013;8:e57873.

[7] Richard D. Feinman et al., "Dietary carbohydrate restriction as the first approach in diabetes
management: Critical review and evidence base", Nutrition 31 (2015) 1–13

See also:

"Exercise 'not key to obesity fight'" By Nick Triggle, BBC Health, 23 April 2015

(Note: highlights are mine)

Tuesday, April 21, 2015

Human brain size is shrinking!


From uncyclopedia.

Human brain (average 1100 to 1300cm^3) seem to have deteriorated at least in size, in the last couple of hundred thousands years.   How does that decline translate to intelligence?  Not sure but I would speculate that it probably does correlate!

As to the cause, anthropologists seem to be rather in agreement that nutrition may have had something to do with that.  Humankind seemed to have regressed from very healthy nomadic lifestyle based on hunting and fishing to a settled one based on farming and consuming starchy plant based food.  Which correlated with the deterioration of physical health, body size and brain size.  [add refs later]

According to this research.  Neanderthal did not have to use fire to cook their exclusively animal based meals.  My thought is that they must also have consumed plenty of DHA from animal brains and spinal cords, together with all the fats to grow and feed their very large brains of average volume 1600 cm^3 (some sources give bigger estimates) .   Ability to use fire gave Cro-Magnon (average brain volume 1500 or 1600 cm^3) an advantage when game became scarce and food versatility became useful, by the end of the last ice age.

Sunday, April 19, 2015

Lariam medical drug scandal, manslaughter by authorities against their own own soldiers!

The title is not an exaggeration! - Manslaughter being defined as an action causing death. This is fully supported by many years of published data!

This is a very sad story that appears to explain the true cause behind the last couple of decades' "epidemics" of severe cases of PTSD (post-traumatic stress-disorder) among soldiers returning home from active duty. It appears that the US, British and probably other governments' officials were putting their own soldiers over many years, on anti-malaria drug Lariam (mefloquine, manufactured originally by Hoffmann–La Roche), ignoring the drug's known neurological side effects. The less severe neurological side effects seem to occur in about a quarter of the soldiers taking them, according to some unconfirmed reports, but in some smaller percentage cases the drug is known to induce what looks like a permanent brain damage triggering homicidal and suicidal psychotic episodes, lasting long after discontinuation of taking the drug, causing death or requiring patient's lock-up in a psychiatric azylum!

Published last week:

Lariam: Hundreds of British soldiers suffering from mental illness after being given anti-malarial drug


The Ministry of Defence (MoD) has been accused of knowingly risking the mental health of its own soldiers after new figures showed that nearly 1,000 British servicemen and women have required psychiatric treatment after taking a discredited anti-malarial drug.

Psychosis, suicidal thoughts, depression and hallucinations are among the mental-health problems associated with Lariam, also known as mefloquine.

But the MoD has rejected all appeals to stop giving the drug to troops posted overseas – to the mounting fury of relatives, politicians and retired military figures who fear it could be responsible for an epidemic of psychiatric illness in Britain’s Armed Forces.

The Independent can reveal that a retired major-general who was given Lariam prior to a deployment to Sierra Leone is among those struggling with the after-effects.

Maj-Gen Alastair Duncan, who commanded British forces in Bosnia, is currently in a secure psychiatric unit after a post-traumatic stress disorder (PTSD) episode over Christmas.

His wife, Ellen, told The Independent: “Like others, I believe that this is a scandal. If 1,000 troops have reported the effects then you can be sure there are others who have not.

It makes me wonder since it does look to me as if some government officials of the countries involved appear to be above the law since almost nothing is being done in spite of the repetitive warnings. As if there were an intention to cover it up. For example, there is an article published on the same subject over a year ago (September 2013):

Exclusive: The Lariam scandal - MoD ‘ignored decades of warnings about dangers of suicide drug’


Amid mounting concerns about the dangers of the drug – which has been linked with a string of suicides and murders – the US military acted this month to ban its use among special forces. The decision came after it was linked to the massacre of 16 Afghan civilians by a US soldier.

Speaking to The Independent, a former senior medical officer accused the MoD of ignoring repeated warnings over the dangers of the drug. Lt-Col Ashley Croft, who served for more than 25 years in the Royal Army Medical Corps and is an expert on malaria, said: “For the past 12 years I was saying this is potentially a dangerous drug – most people can take it without problems but a few people will experience difficulties and of those a small number will become psychotic and because there are other alternatives that are safer and just as effective we should move to them but my words fell on deaf ears.”

Lt Col Ashcroft, who retired in April, accused the MoD of being in “denial mode”. He added: “The problem is that it can make people have psychotic thoughts and therefore act in an irrational manner and potentially a manner that is dangerous to themselves or their colleagues, or civilians.”

Doxycycline and malarone are safer drugs which are as effective in preventing malaria, according to the retired officer. “Really the only people that get it [Lariam] now are the poor old soldiers and they have no choice.”

An order issued earlier this month by the US Special Forces Command states: “medical personnel will immediately cease the prescribing and use of mefloquine for malaria prophylaxis”. It adds: “Hallucinations and psychotic behaviour can occur and continue for months or years after mefloquine use; cases of suicidal ideation and suicide have been reported.”

The neurotoxicity of Lariam has been known for years and written about in the media, yet nothing has been done to stop it! Going back in time, see for example this 2003 article: The dark side of Lariam

Last summer, four soldiers from Ft. Bragg were accused of killing their wives. Two of the men committed suicide, and the other two await trial. So many brutal crimes, so similar, so close in time – raised questions, and the army sent a team to investigate.

One possible suspect was mefloquine - brand name Lariam, an anti-malarial drug. It was invented by the U.S. Army and is routinely given to soldiers deployed overseas. In scientific terms, Lariam can cause neuropsychiatric adverse events. In plain language, it can make lose your mind.


Saturday, April 18, 2015

Alzheimer's and lack of arginine


Arginine is especially abundant in common food such as dairy products, meat, nuts and chickpeas!

(from Dairy Council of California)
Recent study described here:

Alzheimer's breakthrough: Scientists may have found potential cause of the disease in the behaviour of immune cells..


They observed that in Alzheimer’s, immune cells that normally protect the brain instead begin to consume a vital nutrient called arginine.

My comment:

Probably because arginine is an essential nutrient for all cells including immune cells. If there is not enough, immune cells will sequester what is available.

Arginine is an amino acid and an essential nutrient for several bodily processes, including cell division, healing and immune responses.

It is found in food, including dairy products, meat, nuts and chickpeas, but the team at Duke said that their study did not suggest eating more arginine would have an impact on Alzheimer’s risk. The blood-brain barrier regulates how much arginine can enter the brain, and the immune response that breaks down arginine would remain the same even if confronted with higher levels of the nutrient.
Really?  Dr. Pickett must be a very wise man knowing that upfront and thus excluding that therapeutic option by his statement, without doing any testing!

“The study suggests that low levels of arginine in the brain could contribute to the death of nerve cells in Alzheimer’s, but there is much more we still need to understand about how and why nerve cells die in the disease,” she added.


Friday, April 10, 2015

LDL cholesterol doesn't matter!

According to this study (Framingham data):

Increased Small Low-Density Lipoprotein Particle Number

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

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

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

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

Sunday, March 29, 2015

Bose Einstein condensate and quantum physics in the living systems

This is a short memo triggered by this paper to alert us to some new ideas emerging in the boundary zone between biology and quantum physics. It could be the next big breakthrough in biology or it it could be off the mark! We shall see.

From Wiki 

See my write-up here:
"Bose Einstein condensate - cold fusion, cellular membranes and neurons."

I have to stress that the above text is a compilation of some speculative ideas and references, not a proof of anything!

For people with a sufficient scientific background, I strongly recommend to read the following references:

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

E. Del Giudice, S. Doglia, M. Milani, C. W. Smith, G. Vitiello, “Magnetic Flux Quantization and Josephson Behaviour in Living Systems”; Physica Scripta. Vol. 40, 786-791, 1989.

(P.S. thanks to Edward E. for the links!)

Wednesday, March 4, 2015

Ketogenic diet slows progression of 5 neuro degenerative diseases


Slowing down of neuro-degenerative disease by ketogenic diet was claimed in the recent paper:
Nourishing the Aging Brain, By Morten Scheibye-Knudsen,  The Scientist, March 2015

( in pdf format )

Quotes (see here ):

Increased basal metabolism
Caloric restriction exacerbates progression
Ketogenic diet slows progression

Normal or lowered basal metabolism
Caloric restriction slows progression
Ketogenic diet slows progression

Increased basal metabolism
Caloric restriction slows progression
Ketogenic diet slows progression

Increased basal metabolism
Caloric restriction may slow progression
Ketogenic diet slows progression

COCKAYNE SYNDROME [accelerated aging disease]:
Increased basal metabolism
Caloric restriction exacerbates progression
Ketogenic diet slows progression

[added on 6/03/2015, from the same source]

And the low carbohydrate (or low glucose) nutrition appears to contribute to longevity by increasing the SIRT6 activity (*), according to this paper, from the same issue of The Scientist magazine:

Wrangling Retrotransposons, by Michael Van Meter, Andrei Seluanov, and Vera Gorbunova | March 1, 2015


Perhaps the best evidence for the retrotransposon’s role in aging comes from the link between the activity of a longevity gene, SIRT6, and the repression of L1 in somatic tissues. SIRT6 encodes an enzyme critical to the forestallment of aging: it maintains telomere length, promotes DNA repair, regulates metabolism, opposes tumorigenesis, and attenuates inflammation—all processes associated with the prevention of age-related decline. Mice lacking SIRT6 suffer from a severe premature aging syndrome, while mice that overexpress SIRT6 enjoy extended life spans.


One explanation for this failure may relate to SIRT6’s critical role in DNA repair. Several studies have indicated that SIRT6 helps catalyze repair of the damage at numerous types of DNA lesions, including single- and double-strand breaks. A characteristic feature of aging cells is an increase in the amount of DNA damage.


While overexpression of SIRT6 may not be tractable in a therapeutic context, SIRT6 activity can be increased by caloric restriction, reducing glucose consumption, or increasing NAD+ bioavailability (**) - interventions that have already shown promise in increasing longevity in animal models. (Such interventions are also showing promise in slowing the progress of some age-related neurodegenerative disorders.


*) Underexpression or removal of SIRT6 gene is linked to accelerated aging disease, while overexpression of SIRT6 has been shown to extend the lifespan, in mice studies, see Wiki.

**) Niacin is one of the precursors of NAD+, another one is tryptophan.


Saturday, February 28, 2015

Bad science and politically motivated low fat dietary guidelines finally exposed and ditched!


Recent (20/02/2015) New York Times article by Nina Teicholz (**):

The Government’s Bad Diet Advice

First, last fall, experts on the committee that develops the country’s dietary guidelines acknowledged that they had ditched the low-fat diet. On Thursday, that committee’s report was released, with an even bigger change: It lifted the longstanding caps on dietary cholesterol, saying there was “no appreciable relationship” between dietary cholesterol and blood cholesterol.
Instead of accepting that this evidence was inadequate to give sound advice, strong-willed scientists overstated the significance of their studies.
Much of the epidemiological data underpinning the government’s dietary advice comes from studies run by Harvard’s school of public health. In 2011, directors of the National Institute of Statistical Sciences analyzed many of Harvard’s most important findings and found that they could not be reproduced in clinical trials.
In 2013, government advice to reduce salt intake (which remains in the current report) was contradicted by an authoritative Institute of Medicine study[*]. And several recent meta-analyses have cast serious doubt on whether saturated fats are linked to heart disease, as the dietary guidelines continue to assert.

Uncertain science should no longer guide our nutrition policy. Indeed, cutting fat and cholesterol, as Americans have conscientiously done, may have even worsened our health. In clearing our plates of meat, eggs and cheese (fat and protein), we ate more grains, pasta and starchy vegetables (carbohydrates). Over the past 50 years, we cut fat intake by 25 percent and increased carbohydrates by more than 30 percent, according to a new analysis of government data. Yet recent science has increasingly shown that a high-carb diet rich in sugar and refined grains increases the risk of obesity, diabetes and heart disease — much more so than a diet high in fat and cholesterol.

It’s not that health authorities weren’t warned. “They are not acting on the basis of scientific evidence, but on the basis of a plausible but untested idea,” Dr. Edward H. Ahrens Jr., a top specialist at Rockefeller University and prominent critic of the growing doctrine on dietary fats and cholesterol, cautioned back in the ’80s.
Since the very first nutritional guidelines to restrict saturated fat and cholesterol were released by the American Heart Association in 1961, Americans have been the subjects of a vast, uncontrolled diet experiment with disastrous consequences. We have to start looking more skeptically at epidemiological studies and rethinking nutrition policy from the ground up.
Until then, we would be wise to return to what worked better for previous generations: a diet that included fewer grains, less sugar and more animal foods like meat, full-fat dairy and eggs.

Other links:

*) She probably meant this report: Sodium Intake in Populations: Assessment of Evidence (14/05/2015)

**) Nina Teicholz, author of “The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet.”


Tuesday, February 17, 2015

US to drop anti-cholesterol food guidelines!

Cholesterol in food is "no longer a concern"!   It is now OK to eat bacon and eggs!

From Commons.Wiki 

U.S. may lower cholesterol's level of threat to health: report

WASHINGTON (Reuters) - A U.S. advisory panel reviewing national dietary guidelines has decided to drop its caution against eating cholesterol-laden food, the Washington Post reported on Tuesday.

At a December meeting, the Dietary Guidelines Advisory Committee discussed its decision to no longer deem cholesterol a "nutrient of concern," according to the Washington Post.

What happened to those scientists and medical doctors who, for many decades have been signing and propagating the anti-cholesterol guidelines?  I wonder, what could be the overall health damage estimate, caused by those recommendations, to date?

Tuesday, February 10, 2015

Useless low fat dietary guidelines by governments, no scientific justification!

Open Heart/BMJ just published a meta-study:

Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis

Objectives National dietary guidelines were introduced in 1977 and 1983, by the US and UK governments, respectively, with the ambition of reducing coronary heart disease (CHD) by reducing fat intake. ...


Dietary recommendations were introduced for 220 million US and 56 million UK citizens by 1983, in the absence of supporting evidence from RCTs.

The main findings of the present meta-analysis of the six RCTs [Randomized Controlled Trials] available at the time of issuing dietary guidelines in the US and UK indicate that all-cause mortality was identical at 370 in the intervention and control groups. There was no statistically significant difference in deaths from CHD. The reductions in mean serum cholesterol levels were significantly higher in the intervention groups; this did not result in significant differences in CHD or all-cause mortality.
It is a widely held view that reductions in cholesterol are healthful per se. The original RCTs did not find any relationship between dietary fat intake and deaths from CHD or all-causes, despite significant reductions in cholesterol levels in the intervention and control groups. This undermines the role of serum cholesterol levels as an intermediary to the development of CHD and contravenes the theory that reducing dietary fat generally and saturated fat particularly potentiates a reduction in CHD.
There was best practice, randomised controlled trial, evidence available to the dietary committees, which was not considered and should have been. The results of the present meta-analysis support the hypothesis that the available RCTs did not support the introduction of dietary fat recommendations in order to reduce CHD risk or related mortality. Two recent publications have questioned the alleged relationship between saturated fat and CHD and called for dietary guidelines to be reconsidered.31 ,32 The present review concludes that dietary advice not merely needs review; it should not have been introduced.
Actual data from the publication:

References and links:

Interestingly, the original studies at that time produced similar similar conclusions of non-supporting the reduction of dietary fat.  The following quotes are from Zoë Harcombe's blog (one of the main author of the above quoted study):

The studies’ own conclusions.  These are the verbatim conclusions from each of the studies:

1965 Rose Corn and olive oil: “It is concluded that under the circumstances of this trial corn oil cannot be recommended as a treatment of ischaemic heart disease. It is most unlikely to be beneficial, and it is possibly harmful.” (ref 9)

1965 Research Committee Low-fat diet: “A low-fat diet has no place in the treatment of myocardial infarction” (ref 10) [heart attack].

1968 MRC soya-bean oil: “There is no evidence from the London trial that the relapse-rate in myocardial infarction is materially affected by the unsaturated fat content of the diet used.” (ref 11)

1969 Dayton LA Veterans study: “Total longevity was not affected favorably in any measurable or significant degree… For this reason, and because of the unresolved question concerning toxicity, we consider our own trial, with or without the support of other published data, to have fallen short of providing a definitive and final answer concerning dietary prevention of heart disease.” (ref 12)

1970 Leren Oslo Diet Heart study: “Epidemiological studies have demonstrated several factors associated with the risk of developing first manifestations of coronary heart disease. Blood lipids, blood pressure and cigarette smoking are such risk variables… In spite of the small numbers this observation lends some support to the view that the multi-factorial approach is the best way to the solution of the coronary heart disease problem.”(ref 13)

1978 Woodhill Sydney Diet Heart Study: “Survival was significantly better in the P [control] Group.” “It must be concluded that the lipid hypothesis has gained little support from secondary intervention studies.” (ref 14)