Monday, May 22, 2017

FRSP Week 7 #3 Ep 15 | Rocking that Heart Rate!

In episode 15 of the Full Range Strength Series, I reach 83% of my maximum heart rate after just 4 strength training exercise sets, and I evaluate this months straddle split progress.

Graecopithecus Casts Doubt on "Out of Africa" Story of Human Origins

As reported in PLOS | One today, a 7.2 million year old fossil named Graecopithecus, from late Miocene Europe, suggests that the human line may have originated in the Eastern Mediterranean (i.e. Europe), not Africa.  
"In this study, we propose based on root morphology a new possible candidate for the hominin clade, Graecopithecus freybergi from Europe. " [...]
"In contrast to the Ponginae, Graecopithecus shares derived characters with African apes (ventrally shallow roots, buccolingually broad molar roots; [32, 75]). Therefore, we consider four principle alternative interpretations of its phylogenetic position: Graecopithecus is a stem-hominine (last common ancestor of African apes and Homo), a gorillin, a panin, or a hominin." [...]
"Accordingly, the most parsimonious interpretation of the phylogenetic position of Graecopithecus is that it is a hominin, although we acknowledge that the known sample of fossil hominin root configurations is too small for definitive conclusions."[...]
"Taken at face value, the derived characters of Graecopithecus (p4 root morphology and possibly canine root length) may indicate the presence of a hominin in the Balkans at 7.2 Ma." [...]
"Therefore, we submit that the dental root attributes of Graecopithecus suggest hominin affinities, such that its hominin status cannot be excluded. If this status is confirmed by additional fossil evidence, Graecopithecus would be the oldest known hominin and the oldest known crown hominine, as the evidence for the gorillin status of Chororapithecus is much weaker than the hominin status of Graecopithecus [8]. More fossils are needed but at this point it seems likely that the Eastern Mediterranean needs to be considered as just as likely a place of hominine diversification and hominin origins as tropical Africa." provides more information on Graecopithecus: apparently the species inhabited a savannah habitat and remains were found with large grass-feeding herbivores.
"The phytolith record provides evidence of severe droughts, and the charcoal analysis indicates recurring vegetation fires," said Böhme. "In summary, we reconstruct a savannah, which fits with the giraffes, gazelles, antelopes, and rhinoceroses that were found together with Graecopithecus," Spassov added.
"The incipient formation of a desert in North Africa more than seven million years ago and the spread of savannahs in Southern Europe may have played a central role in the splitting of the human and chimpanzee lineages," said Böhme. She calls this hypothesis the North Side Story, recalling the thesis of Yves Coppens, known as East Side Story.
More information: Potential hominin affinities of Graecopithecus from the Late Miocene of Europe, PLOS ONE (2017).
Messinian age and savannah environment of the possible hominin Graecopithecus from Europe, PLOS ONE (2017).

Read more at:
 The full text is "Messinian age and savannah environment of the possible hominin Graecopithecus from Europe" at PLOS | One.

This might support my suggestion that humans are descended not from a chimpanzee-like frugivore, but a savannah-dwelling largely or heavily insectivorous (i.e. carnivorous) ancestor .  As I wrote there:

....before there existed some putative pre-human (i.e. non-human) ancestors who ate plant-based diets, the ancestors of the primate line were insectivores, i.e. carnivores who specialized in eating insects.  From
"Transitional primate-like creatures were evolving by the end of the Mesozoic Era (ca. 65.5 million years ago)....The few placental mammals that existed at that time mainly consisted of the insectivore ancestors of primates."
These carnivorous ancestors of primates continued until about 55 million years ago when some creatures resembling modern prosimians emerged.  But notes:
"Among the numerous Miocene primate species were the ancestors of all modern apes and humans.  By 14 million years ago, the group of apes that included our ancestors was apparently in the process of adapting to life on the edges of the expanding savannas in Southern Europe." 
[Graecopithecus was found in Southern Europe.]

The human line descends from those primates that specialized in living on the savannas, not those – like the ancestors of chimps – that specialized in the arboreal habitats.  On savannas, the predominant form of plant-life is grass, while fruits are relatively scarce, especially during Ice Ages.  Thus, an animal can thrive on a savanna only if it eats grass, or animals that eat grass.  Humans are obviously not grass-eaters – we don't have the multi-compartment guts adapted to fiber fermentation that is typical of grass-eating animals.  But an insectivore can find plenty of grass-eating insects, such as grasshoppers, caterpillars, moth larvae, grubs, crickets, and billbug larvae.  It can also find small grass-eating molluscs like snails.

The nutritional profile of insects is quite similar to wild game:

Insects are wild game.  Therefore an insectivore is already a predator adapted to eating wild game.  Insectivores have simple, carnivore-type guts.   An insectivorous species would have to evolve new behaviors or gut features – hindgut fermentation vats – to become predominantly frugivorous and deal with the fiber abundant in plants, as has occurred in the great apes but not in humans. The great apes have enormous guts adapted to fermenting fiber to convert it into saturated fats, mostly butyrate; healthy humans do not:

We have strong evidence that early Pleistocene humans – definite members of our genus – were ambush predators 2 million years ago.   We know that all definitely human ancestors –  from Homo habilis 2 mya to present – were hunters and meat-eaters.  Dunn could justify his claim only by referring to the putative habits of ancient species who were not human and are only suspected human ancestors (e.g. Australpiths), while ignoring the heavy meat-eating habits of those species that we know were human.  Is that scientifically honest?

The truth is all known human ancestors of modern humans, i.e. Homo habilis, Homo erectus, Neanderthals, and Denisovans were predators, not vegetarians.  Only non-human species that might have been part of the human lineage,  such as Austalopiths, were largely plant-eaters.  The hypothesis that human ancestors were nearly all vegetarians can't explain what we know about human evolution, and does not align with what we know about the Earth's climate, flora and fauna changes during the period of time when the human lineage evolved and moved out of Africa. 

An insectivore is a hunter, a predator.  Humans have been deliberate predators for at least 2 million years.  Which is the most likely evolutionary scenario: 


While the savannas are expanding and forests shrinking during the millions of predominantly Ice Age years, natural selection acts on an insectivorous savanna species to favor those that prefer to eat fruits and vegetables that don't exist on the savanna and are disappearing due to the cold and dry climate, ultimately converting that insectivore with a simple carnivore-type gut into a frugivorous, hindgut fermenter arboreal species; then natural selection changes course completely, starts favoring the savanna-dwelling meat-eaters among those fruit-eaters, progressively selects against the hindgut fermenters and eventually changes the members of this lineage back into a savanna-dwelling apex predator species with a relatively simple, reduced volume carnivore-type gut with gastric acidity greater than most carnivores and comparable to scavenger species (the human line starting at least 2 mya with Homo habilis).

Source:  Voegtlin, The Stone Age Diet, p. 44
Source:  Voegtlin, The Stone Age Diet, p. 45

While the savannas are expanding and forests shrinking (starting towards the end of the Miocene, up to ~ 6 mya), natural selection favors the reproduction of those members of an  insectivorous savanna species who capitalize on the increasing abundance of grass-eating insects, then favors those who can capture and eat the even more energy-dense grass-eating mammals (various rodents such as rabbits and gerbils), then among those favors the individuals who are able to capture larger and larger, more and more energy-dense, fat-rich game, ultimately transforming the originally puny predatory primate (the insectivore) into a mega-primate, the most predatory ape of all, the human, who hunted elephants for a living?

It seems to me that the second scenario is far more likely to be what happened.  In fact, due to the biological leaps and outright reversals (in dentition and intestinal form and function) required, I would venture that the probability of the first scenario is near zero.  If chimps and humans have a common ancestor, that ancestor was likely primarily an insectivore (chimps still are somewhat insectivorous).  The chimp line likely represents the descendants of that last common ancestor (LCA) who chose to specialize in an arboreal habitat.  The descendants of the LCA who specialized in a savanna habitat retained their dominant predatory way of life, and this line slowly graduated from insects and worms to snakes, amphibians and other small animals, then to larger and larger savanna animals until finally the highly carnivorous human emerged by 2 mya.


More information: Potential hominin affinities of Graecopithecus from the Late Miocene of Europe, PLOS ONE (2017).
Messinian age and savannah environment of the possible hominin Graecopithecus from Europe, PLOS ONE (2017).

Read more at:

Sunday, May 21, 2017

Tooth decay bacteria evolved as diet changed › News in Science (ABC Science)

Tooth decay bacteria evolved as diet changed › News in Science (ABC Science)

"Mesolithic hunter-gatherers living on a meat-dominated, grain-free diet
had much healthier mouths that we have today, with almost no cavities
and gum disease-associated bacteria, a genetic study of ancient dental
plaque has revealed."

"What we found was that the early [hunter-gatherer] groups really had
a lot lower frequencies of any of the disease-associated bacteria
compared to what you see today [and] that the number of species per
person's mouth, or the diversity, was much higher in the past," says
"If they've got more [bacterial] diversity that means that those
people's mouths were more resilient to stresses, and probably less
likely to develop disease."

"Gum disease and heart health

"However, while the researchers noted that bacteria associated with dental cavities such as S. mutans
became dominant around the time of the Industrial Revolution, the
frequency of bacteria associated with periodontal diseases such as
gingivitis has not changed much since farming began.
"This may have implications for the notion that gum disease and
associated bacteria are a significant contributor to the recent increase
in conditions such as cardiovascular disease and atherosclerotic
plaques, says co-author Professor Alan Cooper, director of the
Australian Centre for Ancient DNA.
"It has been suggested that the presence of this permanent
inflammation state along the gums was promoting an immune inflammatory
response, which in turn leads to cardiovascular disease," says Cooper.

Saturday, May 20, 2017

Policy Does Not Equal Science: Development of U.S. Dietary Guidelines, A...

Very interesting lecture.  It covers:

  • Historical changes in the U.S. diet
  • The impact of the U.S.D.A.'s dietary guidelines on the weight and health of the U.S. population and the viability of family farms.
  • The science (or lack of science) behind the dietary guidelines.
  • The interesting but unintended alignment of those who promote plant-based diets with the goals of food corporation.
Mrs. Hite's discussion of data will certainly raise questions about the rational basis for the U.S.D.A.'s progressive promotion of more and more plant-based diets. 

Tuesday, May 16, 2017

The Cost of Carbohydrates Versus Fats: Not What It Seems?

When we went shopping at the Scottsdale farmers' market a couple of weeks ago, Tracy wanted to get some spring mix from McClendon farms to make a salad for our wedding anniversary dinner.  While getting the greens, we noticed that McClendon Farms also had some artisnal butter that they were selling for 6.99 for a half pound.

We didn't get any of the butter, but Tracy got a small bag, about a quart, of spring mix.  When we got to the check out, the cashier announced that we were to pay $8 for the quart of spring mix.

The moment I heard that, I thought that we could be getting the half pound of butter for $7 and we'd get a lot more calories for our money.

A quart of spring mix supplies about 52 calories.  At $8 per quart, that works out to $0.15 per calorie.

A half-pound of butter supplies about 1626 calories, 31 times the calories found in a quart of spring mix.  At $7 per half-pound, that works out to $0.004 per calorie.

Hence, on a per calorie basis, spring mix is 38 times more expensive than butter.

I wanted to trade in the spring mix for the much tastier butter!

That got me curious about the cost of commonly consumed plant foods on a per calorie basis.

After the market, we went to Trader Joe's to get some supplies, and on the way I decided I would do some cost-per-calorie comparison shopping.

TJ's organic carrot juice costs $3.99 for a quart.

The whole quart supplies 320 calories:

That works out to $0.012 per calorie for the carrot juice.

TJ's pint of organic heavy whipping cream also costs $3.99.

The pint supplies 1600 calories:

That works out to $0.0025 per calorie for the organic cream.

Per calorie, the organic carrot juice is 4.8 times more expensive than the organic heavy cream.

TJ's has conventional cream from animals not treated with r-BST for $3.29 per pint:

Of course it supplies the same number of calories per pint as the organic cream:

The cost per calorie from this cream is $0.0021.

If you're on a budget, trying to meet your energy needs, cream is a far better value than carrot juice, or for that matter, any fruit or vegetable.

TJ's regular butter costs only $3.19 per pound, which supplies 3252 calories, about what a physically active young man needs for an entire day.  That works out to about $0.001 per calorie.

Let's postulate that a young man gets 50% of his energy from butter and cream daily.  One stick of TJ's butter is going to provide him 813 calories for about $0.78 per day, and 8 ounces of heavy cream will provide another 800 calories for $1.65, for a total of 1613 calories at a cost of $2.43.

Now let's have him eat 3 eggs and 300 g of ground beef daily.

Three large (50 g) eggs supplies 233 calories, and 300 g of 80% lean ground beef.  He could once a week replace 100 g of that ground beef with pork or beef liver.  Three eggs and 300 g of beef will provide him with a generous 92 g of protein.

Fairly high quality eggs are going for about $3.00-$4.00 per dozen, or about $0.30 per egg.  Grass-fed ground beef is going for $6.99 per pound (454 g) at our local Sprouts store, so 300 g cost $4.62.

So this hypothetical young man can meet his calorie and nutrient needs on a high fat, animal-based diet, using eggs rich in omega-3 fats and beef from grass-fed animals, for about $7.95 per day.

Add  $1.05 for a teaspoon of nutritional yeast, a medium (131 g) orange ($0.35), a large (150 g) onion (0.31) and third of a bunch of spinach and he's good to go for $9.00 per day.

Source:  Numbeo

According to Numbeo, this is only $0.44 more than the average cost of food for an individual eating a standard Western diet in Phoenix:

If he's on a tighter budget he could choose conventional eggs and beef.   This week, Fry's Market in Scottsdale advertised ground beef for $2.99 per pound and pork loin roast or turkey breast for $1.49 per pound.

As noted above, the average cost for eggs in the Phoenix area is $2.26 per dozen, or just $0.19 per egg.  If he ate 150 g of ground beef ($0.99), 150 g of pork loin or turkey breast ($0.49), and 3 conventional eggs, the meat and egg portion of his low carbohydrate diet would cost  $2.05, and the butter and cream portion $2.43, for a total of $4.48.  Now he should substitute ~100 g of liver for one of the other meats once or twice weekly, and he can (if he wants) spend $1.52 daily for fruit, vegetables, and little nutritional yeast, and he is eating very well for $6.00 per day, $2.50 LESS than expected average costs (only $180 per month). 

If you do the cost per calorie calculation for any fruit or vegetable compared to the above deals for ground beef, turkey breast or pork loin, you will find the animal products are cheaper.

Here's another ad from Fry's:

Strawberries, at $2.00 and only 145 calories per pound, cost $0.014 per calorie.

Grapes, at $1.99 and 313 calories per pound, cost $0.0064 per calorie, half that of strawberries. 

Grass-fed ground beef, at $6.99 and 898 calories per pound, costs $0.008 per calorie, almost half the cost of strawberries and only 25 percent more than the grapes.

Conventional ground beef, at $2.99 and 898 calories per pound, costs $0.0033 per calorie, one-quarter the cost of strawberries and one-half the cost of grapes, and more nutrient dense as well.

Pork loin roast, at $1.49 and 1143 calories per pound (if you eat all visible fat), costs only $0.0013 per calorie, ONE-TENTH the cost of strawberries and one-fifth the cost of the grapes.

In summary, a meat- and fat- based diet is not necessarily more expensive than a carbohydrate-based diet in the short-term, and it may be less expensive in the long-term by saving you lots of costs in dental work (carbohydrates promote tooth decay and periodontal disease, protein and fat do not) as well as diabetes and other modern, sugar-related diseases.

Humphrey et al. "present evidence linking a high prevalence of caries to reliance on highly cariogenic wild plant foods in Pleistocene hunter-gatherers from North Africa, predating other high caries populations and the first signs of food production by several thousand years. Archaeological deposits at Grotte des Pigeons in Morocco document extensive evidence for human occupation during the Middle Stone Age and Later Stone Age (Iberomaurusian), and incorporate numerous human burials representing the earliest known cemetery in the Maghreb. Macrobotanical remains from occupational deposits dated between 15,000 and 13,700 cal B.P. provide evidence for systematic harvesting and processing of edible wild plants, including acorns and pine nuts. Analysis of oral pathology reveals an exceptionally high prevalence of caries (51.2% of teeth in adult dentitions), comparable to modern industrialized populations with a diet high in refined sugars and processed cereals. We infer that increased reliance on wild plants rich in fermentable carbohydrates and changes in food processing caused an early shift toward a disease-associated oral microbiota in this population."  [Italics added.]

Thus, even wild foods high in unrefined carbohydrate causes a high incidence of dental pathology.

Since a mammal can not survive without teeth, it seems impossible that natural selection could have favored reproduction of individuals whose internal organs demanded consumption of a high carbohydrate diet that progressively destroyed the individual's teeth from a very early age. 

Hamasaki et al. report:  "Multivariate analysis revealed that the percentage of calories from fat was a nutrient factor associated with periodontal disease, with the percentage of calories from fat being significantly lower in the group with advanced periodontal disease."   In other words, for modern humans, high carbohydrate diets promote – and high fat diets prevent – periodontal disease.  That's because carbohydrate feeds the growth of pathogenic oral bacteria, which can't metabolize fats for energy.

Thus it is clear that natural selection has not yet produced a human species that in the absence of modern dentistry can remain free of dental disease while eating a high carbohydrate diet.  In fact the practice of dentistry prevents such adaptation from taking place.  In nature the loss of teeth through decay would lead to malnutrition and an unattractive appearance that would prevent reproduction and cause early death. 

Can a diet that causes progressive dental disease (in the absence of modern prophylactic and remedial dentistry) really be good for the gut or the rest of the body?

Dr. Philippe P. Hujoel, professor of dental public health sciences at the University of Washington  School of Dentistry reviewed the relationships between diet, dental disease, and chronic systemic illness in a report published July 1, 2009 in The Journal of Dental Research.  As reported by Leila Gray of the University of Washington

"He weighed two contradictory viewpoints on the role of dietary carbohydrates in health and disease. The debate surrounds fermentable carbohydates: foods that turn into simple sugars in the mouth. Fermentable carbohydrates are not just sweets like cookies, doughnuts, cake and candy. They also include bananas and several tropical fruits, sticky fruits like raisins and other dried fruits, and starchy foods like potatoes, refined wheat flour, yams, rice, pasta, pretzels, bread, and corn.....
"Hujoel observed that the dental harms of fermentable carbohydrates have been recognized by what looks like every major health organization. Even those fermentable carbohydrates assumed to be good for systemic health break down into simple sugars in the mouth and promote tooth decay. All fermentable carbohydrates have the potential to induce dental decay, Hujoel notes.

"But what if fermentable carbohydrates are also bad for systemic health? Hujoel asks. What if dietary guidelines would start incorporating the slew of clinical trial results suggesting that a diet low in fermentable carbohydrates improves cardiovascular markers of disease and decreases body fat? Such a change in perspective on fermentable carbohydrates, and by extension, on people’s diets, could have a significant impact on the dental profession, as a diet higher in fat and protein does not cause dental diseases, he notes. Dentists would no longer be pressed to recommend to patients diets that are bad for teeth or remain mum when it comes to dietary advice. Dentists often have been reluctant, Hujoel says, to challenge the prevailing thinking on nutrition. Advising patients to reduce the amount or frequency of fermentable carbohydrate consumption is difficult when official guidelines suggested the opposite.

"The close correlation between the biological mechanisms that cause dental decay and the factors responsible for high average levels of glucose in the blood is intriguing. Hujoel explains that eating sugar or fermentable carbohydrates drops the acidity levels of dental plaque and is considered an initiating cause of dental decay.

“Eating these same foods, he says, is also associated with spikes in blood sugar levels. There is fascinating evidence that suggests that the higher the glycemic level of a food, the more it will drop the acidity of dental plaque, and the higher it will raise blood sugar. So, possibly, dental decay may really be a marker for the chronic high-glycemic diets that lead to both dental decay and chronic systemic diseases. This puts a whole new light on studies that have linked dental diseases to such diverse illnesses as Alzheimer’s disease and pancreatic cancer.

"The correlations between dental diseases and systemic disease, he adds, provide indirect support for those researchers who have suggested that Alzheimer’s disease and pancreatic cancer are due to an abnormal blood glucose metabolism.

"The hypotheses on dental diseases as a marker for the diseases of civilization were postulated back in the mid-20th century by two physicians: Thomas Cleave and John Yudkin. Tragically, their work, although supported by epidemiological evidence, became largely forgotten, Hujoel notes. This is unfortunate, he adds, because dental diseases really may be the most noticeable and rapid warning sign to an individual that something is going awry with his or her diet.

“'Dental problems from poor dietary habits appear in a few weeks to a few years,' Hujoel explains. 'Dental improvement can be rapid when habits are corrected. For example, reducing sugar intake can often improve gingivitis scores (a measurement of gum disease) in a couple of weeks. Dental disease reveals very early on that eating habits are putting a person at risk for systemic disease. Since chronic medical disease takes decades to become severe enough to be detected in screening tests, dental diseases may provide plenty of lead-time to change harmful eating habits and thereby decrease the risk of developing the other diseases of civilization.'

"In planning a daily or weekly menu, Hujoel suggests: 'What’s good for your oral health looks increasingly likely to also benefit your overall health.'"  [Bold and italics added.]
And what's good for your oral health?  Hujoel said it:  "a diet higher in fat and protein does not cause dental diseases."

Full Range Strength Series Week 7 Ep 13 | High Intensity Calisthenics |...

Monday, May 15, 2017

VLCHF Diet for Psoriasis Experiment Week 2 Report

I have been eating very low carbohydrate, high fat for two weeks now.  My digestible (net) carbohydrate intake has been below 50 g on most days, provided by oranges, berries, onions, beets, carrots, winter squash, and greens (mostly spinach, lettuce, kale).

I've continued to eat 300-400 g of meat daily, mostly beef (roast, brisket, sirloin steak, ground), with some pork, chicken, and sardines.  I had at least half a dozen eggs over the week.  My protein intake has been in the range of 120-140 g per day.  I have found my desire for protein is less than my desire for fat.

I have gotten roughly 65-70% of my calories from fats, mostly clarified butter, bacon drippings, fat naturally occurring on meats (all saved), heavy cream, coconut cream, and nuts, with some tallow, olive oil, high-oleic sunflower oil, and liquid fish oil (~1-1.5 tsp. daily).  I've been getting around 150 g total fat in a day, with about 55 g of that from saturated fatty acids.  My cholesterol intake has ranged from about 350 to 1000 mg per day, mostly depending on egg yolk intake.

So, what has happened to my skin?  Take a look.
I find this photo of my eye remarkable.  The skin above the eye is much healthier, but the eye itself has changed.  The sclera is whiter with less blood vessels visible.  The iris is a bluer green and more clearly defined around the edges. I can't recall my iris ever being this blue-green.  In the April 30 and May 8 photos, there is a brown area around and especially above the pupil, which has greatly reduced in area.  Iridology identifies that area around the pupil as indicative of the condition of the intestine, with the yellow-brown discoloration indicating inflammation. 

The left ear has always been had the most severe visible lesion.  In the past week it has reduced by more than half, perhaps 75%, from May 8, and its reduced by at least 90% since April 30.

On the right ear, the visible lesion looks to me to have changed very little in the past week.  However, not visible in this photo is the improved condition inside the ear, particularly on the inside of the tragus (the flap over the ear canal). 

On the scalp, the size of the area with thickened, flaking skin has reduced by an estimated 50%.  The skin is not as thick, and there are no large flakes coming off anymore, only fine dust.  It still itches some, but not as much as two weeks ago, I'll estimate about a 75% reduction in itching, which is now primarily confined to an area about 2.5" in diameter encompassing but offset to the left of the occipital protuberance. 

The lesion on my tailbone has also improved.  The surface area affected has reduced by about 40-50%.  

My digestion and elimination have been functioning very smoothly.  My sleep has been sounder than before starting VLCHF.   I have had an abundance of physical and mental energy, more than when I was eating a high carbohydrate diet.  I am less irritable and more energetic and capable of mental focus toward the end of my daily ~16 hour fasts. 

Food preparation is quick and easy.   Food costs have decreased somewhat because we aren't spending on large hauls of low calorie fruits and vegetables.  As I will show in an upcoming post, on a cost per calorie basis, animal fats are far more economical than fruits and vegetables.

I've been making progress in both strength and mobility training.  The residual swelling and stiffness in my left knee (injured in September 2015, when I was eating a vegan high carbohydrate low fat whole foods plant based diet) has reduced and I can now sit in a full squat position for 14 minutes straight and sit on my heels for 5 minutes straight with tolerable discomfort in that knee (sitting on my heels was impossible for 17 months while still eating the plant-based diet).

One other tentative observation:  It seems that I may have less underarm odor.  During the past 5 years I have had a problem with strong underarm odor and staining of white shirts.  When I would eat a lot of brown rice, my underarms would emit the odor of rice, then turn sour.  Underarm odor is caused by bacterial growth, and bacteria thrive in sugar-laden mediums.  I have the hypothesis that this diet has reduced my blood sugar level, which has reduced the amount of sugar in my skin, which in turn has reduced the growth of bacteria that produce odorous compounds.  This needs further observation for confirmation. 

I am very pleased with these results so far, and most impressed with the change in the whites and irises of my eyes, and the apparent improvement in my body odor.  I look forward to seeing what occurs over the next week. 

Sunday, May 14, 2017

FRSP Ep 12 | Week 6 High Intensity Calisthenics | FULL STRADDLE SPLIT TR...

Episode 12 of the Full Range Strength Project features another high intensity, brief calisthenics routine, a high post-training heart rate, and demonstration of my full straddle split routine. 

Study: "Those with a lower cholesterol experienced a higher mortality than those with a higher cholesterol."

The full text of this report is behind a pay wall, so I haven't read the whole thing. Nevertheless, I have comments on the contents of the abstract, assuming it correctly represents the data collected.

"Those with a lower cholesterol experienced a higher mortality" mostly from cancers and two respiratory diseases:  tuberculosis and cor pulmonale.

Most advocates of the cholesterol hypothesis explain away this association not by saying it does not exist but by attributing it to reverse causality.  Their idea is that cancer and respiratory disease processes reduce serum cholesterol.  I previously uncritically accepted the reverse causality hypothesis myself.  However, I now believe I was wrong to do so.

If you accept the reverse causality hypothesis, then you must believe that in this group of 11,121 men, there existed a large number of individuals who had undetected cancer and respiratory diseases (pulmonary tuberculosis and cor pulmonale) at baseline, which diseases were causing those individuals to have low serum cholesterol.  You have to believe that the physicians who examined these subjects at baseline were not doing their jobs very well.

"Cor pulmonale is a common type of heart disease, as a result of its close association with COPD which has emerged, in recent years, as a leading cause of disability and death."[1]  Chronic obstructive pulmonary disease (COPD) is the most common cause of pulmonary hypertension and cor pulmonale.  It seems unlikely that the physicians who first examined the subjects of this study failed to detect COPD or a high risk thereof in subjects who were declared healthy at baseline but within 7 years died from cor pulmonale.

Further, you have to accept that this Yugoslavia Cardiovascular Disease Study data supports this premise:  Low cholesterol in an otherwise apparently healthy individual is a possible or probable sign of occult, not-yet-discovered cancer, tuberculosis, or chronic obstructive pulmonary disease.

This puts advocates of the cholesterol-heart hypothesis in a bind.  They maintain that low cholesterol is health-promoting, because it reduces your risk of cardiovascular disease mortality.  Yet as soon as they postulate their reverse causation explanation for findings like this, they are also asserting that low cholesterol may be a sign of undiagnosed cancer, tuberculosis, or chronic obstructive pulmonary disease.

So, which is it?  Is low cholesterol a sign that you are healthy and destined for a long life, or is it a sign you are or may be very sick and on the verge of death from cancer or respiratory disease?

From the perspective of a student of philosophy of science like myself, this type of contradiction signals that the reverse causality hypothesis is an ad hoc hypothesis.  The Latin phrase means "formed, arranged, or done for a particular purpose only."  In this case, the purpose of the reverse causation hypothesis is to save the cholesterol hypothesis in the face of data that contradicts or refutes that hypothesis.

Has anyone ever produced convincing evidence – not just a convincing hypothesis – that the finding of higher mortality from cancer and respiratory diseases in this specific population was just a result of the failure of the involved physicians to detect latent cancer, tuberculosis and cor pulmonale in the individuals involved at the baseline examination?  No.

It would be impossible to do so, as providing such evidence would require turning back the hands of time, and re-examining all subjects at baseline with every tool available in order to detect or rule out latent cancer, tuberculosis, and cor pulmonale.  You would have to provide evidence that at baseline these people who had low cholesterol had or were on the path to having those diseases and that those diseases were the cause of their having low serum cholesterol at baseline.  Only then could you say with confidence that the low cholesterol levels of those who died from cancer or respiratory diseases were caused by those diseases.

Since we are not able to travel back in time to confirm the reverse causation hypothesis, it is an in principle not testable, ad hoc hypothesis.

If your hypothesis is not testable by experiment, its not empirical science.  

The reverse causation "explanation" has two purposes.  First, it is designed to relieve cognitive dissonance among proponents of the cholesterol hypothesis when they encounter evidence indicating that people who have supposedly healthy low serum cholesterol have an increased risk of death.  Second, it is designed save the lipid hypothesis from contrary evidence.

The people who postulated reverse causation to explain away the findings that are contrary to the lipid hypothesis are attached to the cholesterol hypothesis as an explanation for cardiovascular disease.  They have difficulty entertaining the possibility that they are wrong about cholesterol, especially if their income depends on sales of cholesterol-lowering drugs.

They don't want to consider the possibility that their campaign to lower cholesterol may make some people more susceptible to cancer, respiratory diseases, or other maladies, and wipe out any benefit gained in reduced risk for coronary heart disease mortality.

The mind wants to be right and righteous.  Many people have great difficulty admitting they have erred, whether in matters of fact or matters of morality.  It is hard to lose face (speaking from plenty of experience). 

You see, the alternative is to entertain the possibility that this and a large amount of other research suggests: that having low cholesterol makes one more susceptible to mortality from cancer or respiratory diseases.  And also the possibility that people who have very low cholesterol might have a low rate of death from cardiovascular disease because they are more likely to die of cancer or respiratory diseases first.

In The China Study, T. Colin Campbell, PhD, classifies coronary heart disease, hypertension and cancer as diseases of affluence, and classifies the following as diseases of poverty:
"Pneumonia, intestinal obstruction, peptic ulcer, digestive disease, pulmonary tuberculosis, parasitic disease, rheumatic heart disease, metabolic and endocrine disease other than diabetes, diseases of pregnancy and many others."[1, italics added]
Thus, from Campbell's point of view, according to the above report from the Yugoslavia Cardiovascular Disease Study, Slavic men who have low cholesterol have a greater mortality from both two diseases of affluence – cancer and cor pulmonale – and a disease of poverty – pulmonary tuberculosis.

But according to Campbell, most diseases of affluence are caused by eating animal foods and consequently having high serum cholesterol.  In other words, according to Campbell's hypothesis, the Slavic men who died of cor pulmonale should have had high cholesterol at baseline, not low.

And from the other angle: Who wants to trade dying relatively young from tuberculosis, as an alternative to dying from coronary heart disease when old?  Most deaths from coronary heart disease happen to people who are well past 65 years of age; while according to WHO, "Tuberculosis mostly affects adults in their most productive years."[3]

If it is a fact that high serum cholesterol is more common among people who die of coronary heart disease, or those that have progressive atherosclerosis, and even if it is true that high LDL accelerates the progression of atherosclerosis, this doesn't directly imply that high serum cholesterol is the cause for the atherosclerotic process.

Everywhere you find a cut, you find a scab.  Does that mean that scabs cause the cuts?  Of course not. Atherosclerosis is like a scab.  Cholesterol is needed to make these scabs, but what makes the artery need a scab?

Inflammation.  In the American Journal of Clinical Nutrition, Libby [4] writes:

 Inflammation is involved in all stages of the atherosclerotic process:

There exists evidence that lipid-reducing drugs like statins are anti-inflammatory.
"If lipid-lowering therapy is antiinflammatory and statins decrease lipid concentrations and reduce cardiovascular disease risk, statin therapy should produce a parallel decrease in CRP as well. Indeed, that is exactly what happens: CRP concentrations decrease 15–50% with statin therapy (44-52). This is a class effect; the entire family of lipid-lowering drugs decreases inflammation." [4]
Although statins have a direct effect of reducing the liver's cholesterol production by inhibiting HMG-CoA reductase, it also appears that by reducing inflammation, they reduce the peripheral tissue's demand for cholesterol from the liver. 
"The observed benefit of statin therapy, however, may be larger in these trials than that expected on the basis of lipid lowering alone. Emerging evidence from both clinical trials and basic science studies suggest that statins have anti-inflammatory properties, which may additionally lead to clinical efficacy."[5]
Statins have little effect on atherosclerosis (i.e. they don't clear plaque from the arteries to any marked degree):
"Despite large reductions in cardiac event rates, the absolute angiographic change in arterial narrowing observed with statin therapy is small [6]. Second, several trials suggest that the observed clinical benefit of statin therapy is greater than that expected on the basis of low density lipoprotein (LDL) reduction alone"[5]
We have evidence that inhibition of HMG-CoA reductase directly inhibits inflammation by reducing macrophage secretion of metalloproteinase (MMP), which in turn improves the stability of atheromatous plaques, which reduces the risk of thrombosis and myocardial infarction (heart attack).
"Numerous studies suggest important effects of statins on macrophage function. Macrophages are capable of degrading the extracellular matrix and, by secreting matrix metalloproteinase (MMP), may weaken the fibrous cap and thus predispose an atheromatous plaque to rupture. Fluvastatin and simvastatin have recently been shown to inhibit MMP-9 (gelatinase B) activity and secretion by macrophages [18]. This effect is reversed by the addition of mevalonate, suggesting that it is mediated by HMGCoA reductase inhibition."[5]
 Hence it is possible that elevated high-density LDL cholesterol and the laying of atherosclerotic lesions are responses to inflammation.

In which case cholesterol does not cause atherosclerosis, it merely participates in a process which the body uses to cope with inflammation.

So, what causes the inflammation?  A likely suspect is excess blood glucose (from eating starchy and sugar-rich foods including fruits):
"Sugary foods, notoriously bad for your teeth, also may be bad for your blood vessels and many other areas of the body, University at Buffalo endocrinologists have found.

"Their study, published in the August issue of The Journal of Clinical Endocrinology and Metabolism, shows that excess sugar in the bloodstream stimulates the generation of free radicals, the oxygen molecules known to damage cells lining blood vessels and many other organs.

"In blood vessels, free-radical injury causes inflammation and initiates the accumulation of plaque that can lead to blocked arteries and cardiovascular disease....
"To test his hypothesis, Dandona and colleagues selected glucose, the nutrient with the most direct impact on diabetics. They gave 14 healthy men and women who had fasted for 12 hours a drink composed of 75 grams of glucose -- the simplest form of sugar -- dissolved in 300 milliliters of water -- a little more than one cup. This amount of glucose is roughly equivalent to the sugar content in two cans of a cola drink, Dandona said.
"Another six participants, who served as controls, drank a water-saccharin solution.
Researchers took blood samples from all participants before the glucose challenge and at one, two and three hours after.
"Results showed there was no change in free-radical generation in samples taken from controls. However, in samples from subjects who drank the sugar water, free-radical generation increased significantly at one hour and more than doubled at two hours. The analysis also showed an increase in the key protein component of an enzyme that promotes free-radical generation.
"At the same time, levels of a-tocopherol, the active form of vitamin E and a powerful antioxidant, fell about 4 percent by hour two and remained depressed at hour three."[6]
The typical physically active male needs at least 2500 kcal per day.  If his diet is just 50% of energy from carbohydrate, he is getting 417 g of glucose daily.  Spread over 3 meals, that is 139 g of glucose at a meal, 64 g more than tested in this experiment.

No, there is no difference between glucose from whole grains and glucose as a simple sugar solution.  None.  The glucose behaves exactly the same once it arrives in the blood.  Exactly. The. Same.  Anyone who says otherwise does not understand chemistry, has a mystical view of reality.  (I was once seduced by this mystical view of nutritional reality.)

The problem is, many people have a really hard time thinking of whole grains, legumes, and starchy vegetables as packs of sugar.  I know that I did.  But that is what they are.  As soon as you put any whole food starch in your mouth, your salivary amylase immediately starts converting it to the simple sugar glucose. 
Thus a significant portion of the starch you eat is already turned to simple sugar – glucose – before it even reaches your stomach.  Then, when whatever is left makes it into the small intestine, the pancreas releases more amylase to make sure that it is all converted to sugar.  This is not controversial.  It is a simple, well established fact of human physiology and biochemistry.

Therefore, dietary carbohydrate is dietary sugar.  An 80% starch diet is an 80% sugar diet. That's a simple biochemical fact.

Anyway, back to the abstract.  The Yugoslavia Cardiovascular Disease Study appears to have produced evidence that casts doubt on the idea that reducing cholesterol is desirable, and the ad hoc reverse causation hypothesis does not and in principle can not save the cholesterol hypothesis from this challenge.


1. Weitzenblum, Emmanuel. “CHRONIC COR PULMONALE.” Heart 89.2 (2003): 225–230. Print.

2. Campbell TC, The China Study (BenBella Books, 2006), p. 76.
4. Libby P, "Inflammation and Cardiovascular Disease Mechanisms," AJCN 2006 Feb;83(2):456S-460S. 
5.  Blake, Gavin J, and Paul M Ridker. “Are Statins Anti-Inflammatory?” Current Controlled Trials in Cardiovascular Medicine 1.3 (2000): 161–165. PMC. Web. 10 May 2017.  

Saturday, May 13, 2017

FRSP Ep 11 | Wk 6 #2 | D3 High Intenstiy Calisthenics | D4 Bridge Training

Full range strength project Episode 11 features straight arm high intensity calisthenics and bridge training from week 6 days 3 and 4.

FRSP Ep 10 | D1 High Intensity Calisthenics | D2 Pike Training & Progress

Full Range Strength Project Episode 10 includes training from days 1 and 2 of week 6.  Day 1 features fat-fueled high intensity calisthenics, day 2 features pike mobility training and progress.

High Animal Protein Intake Reduces Frailty and Increases Survival In Japanese & Okinawan Elders

In a previous blog I discussed how natural selection has favored both strength and longevity in humans, and argued that evidence suggests that humans' increased intake of animal foods and restricted intake of plant foods during the Pleistocene probably played an important role in favoring the natural selection of longer life spans in humans compared to the other great apes.

In that blog I mentioned that we have evidence that animal protein is more effective than plant protein for maintaining muscle mass in humans, particularly people more than 65 years of age.

Yet it is sometimes claimed that Japanese live long and health because they eat little protein, especially animal protein.  This claim is a myth.

  Kobayashi et al report:
"Protein intake has been inversely associated with frailty. However, no study has examined the effect of the difference of protein sources (animal or plant) or the amino acid composing the protein on frailty. Therefore, we examined the association of protein and amino acid intakes with frailty among elderly Japanese women."
"Total protein intake was significantly inversely associated with frailty in elderly Japanese women. The association of total protein with frailty may be observed regardless of the source of protein and the amino acid composing the protein."
 In table 3 we find that women who ate the most animal protein, at least 54.8 g per day (fifth quintile), had the lowest absolute incidence of frailty, the lowest age-adjusted risk of frailty, and the second lowest multivariate adjusted odds risk of frailty, just slightly higher than the fourth quintile of the population, which consumed 45.6-54.8 g of animal protein daily.  The fifth quintile level of animal protein intake is equivalent to about 8 ounces of meat, fish or poultry; the fourth quintile range was 45.6-54.8 g per day, which is 6.5 to 8 ounces daily.

The positive association between plant protein and reduced frailty was less linear than the association between animal protein and reduced frailty.  Quintiles 3 and 5 for plant protein intake had lower odds ratios than quintiles 2 and 4. 

The table also shows a linear positive relationship between increased intake of branched chain amino acids (BCAAs) and sulphur amino acids and reduced frailty.  The best sources of BCAAs and sulphur amino acids are meat, chicken, fish, dairy products and eggs.  

The table also shows intake of at least 1.8 g/d of methionine was also associated with the lowest risks for frailty.  Animal proteins are the best sources of methionine.  This might call into question the idea that methionine restriction is a viable method for promotion of life span.  Such restriction may lead to frailty, which leads to premature disability and often death from falling.

This study resonates with the research by Shibata et al., which found that Okinawan centenarians eat more animal protein and fat and less carbohydrate than average Japanese (I have previously discussed Shibata et al. here.)

Since frailty impairs longevity, and animal protein reduces frailty, it follows that animal protein promotes longevity.  As it most likely did for our ancestors during the Pleistocene

Friday, May 12, 2017

A Life Saving Diet - The Ketogenic Diet REVERSES Diabetic Kidney Disease

Researchers have shown that a ketogenic diet reverses diabetic kidney disease in animals. 
"Diabetic nephropathy, as indicated by albumin/creatinine ratios as well as expression of stress-induced genes, was completely reversed by 2 months maintenance on a ketogenic diet....Whether reduced glucose metabolism mediates the protective effects of the ketogenic diet remains to be determined." (1)
Further, the researchers determined that the reversal of cellular dysfunction was brought about by ketones protecting the cells from glucose-induced oxidative stress.
"To further assess potential mechanisms mediating the protective effects of the ketogenic diet, and since glucose toxicity in diabetes is thought to be mediated by glucose-induced oxidative stress, we assessed if the ketone 3-OHB would protect cells from oxidative stress enhanced by either high or low glucose. As shown in Figure 6, ,3-OHB3-OHB produced a dose-responsive cytoprotective effect at both elevated and reduced glucose." (1)
No other dietary approach has ever done this.  The conventional diet for kidney disease is low protein, but protein restriction has never been reported to reverse the disorder. 

However, in the video interview of the researchers (below), they say that they don't want diabetics to adopt a ketogenic diet.  They claim to be worried that eating a high fat diet could cause other problems.  Instead, they want to create a drug to replicate the effects of the diet.

What "other problems" are they afraid of?  Are they really worried about your health?  Or are they warning you away from the diet in order to preserve their customer base for the drug they want to create?  What if a ketogenic diet reversed diabetes?
"By 10 weeks, 133/234 (56.8%) individuals had one or more diabetes medications reduced or eliminated. At follow-up, 47.7% of participants (125/262) achieved an HbA1c level of less than 6.5% while taking metformin only (n=86) or no diabetes medications (n=39). Mean body mass reduction was 7.2% (SD 3.7%; 95% CI 5.8% to 7.7%, P less than .001) from baseline (117, SD 26, kg).
"These initial results indicate that an individualized program delivered and supported remotely that incorporates nutritional ketosis can be highly effective in improving glycemic control and weight loss in adults with T2D while significantly decreasing medication use."(2)
Reducing or eliminating medications?  Now that's a problem for a drug company or someone who wants to cash in by developing a drug to sell to a drug company.  We can't have people curing their diabetes or kidney disease with a ketogenic diet, that would cut into pharmaceutical profits.

So you better be really, really scared of eating fat.   

Can you say "conflict of interest?" 

When you fast, your body eats your own animal fat.  That human body fat is about 43% saturated and 47% monounsaturated fatty acids.  It is very similar to the fat in all other mammals.  If you eat a high carbohydrate diet, your liver will convert the vast majority of your dietary carbohydrate into saturated and monounsaturated fats in that proportion. (It can't produce polyunsaturated fats.)

It has no other choice.  A high carbohydrate meal contains too much sugar to safely allow into the blood stream.  So insulin is released to cause the body to convert the glucose into fatty acids, and those are stored in your adipose, from which they are released between meals. 

Why was Nature so stupid to store such a toxic substance (saturated fat) for fuel IN ALL MAMMALS?

Burning dietary animal fats is no more dangerous than burning your own body fat during a fast (which a lot of people would love to do).

Our ancestors were fat hunters and could not have survived the Pleistocene without eating a fat-based diet.

Yet these scientists are programmed to think high fat diets are dangerous, or at least they want to program you to think so!

Would you rather eat a ketogenic diet and reverse your diabetes or kidney disease, or be on dialysis?


1.  Poplawski, Michal M. et al. “Reversal of Diabetic Nephropathy by a Ketogenic Diet.” Ed. Krisztian Stadler. PLoS ONE 6.4 (2011): e18604. PMC. Web. 10 May 2017. 

2. McKenzie AL, Hallberg SJ, Creighton BC, Volk BM, Link TM, Abner MK, Glon RM, McCarter JP, Volek JS, Phinney SD.  A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes
JMIR Diabetes 2017;2(1):e5

Thursday, May 11, 2017

Okinawan Centenarians Eat More Animal Proteins and Fats and Less Carbohydrates Than Average Japanese

"Japanese Okinawan centenarians eat diets low in animal protein."  Is that true?  

Not according to Shibata et al.:

According to Shibata et al.

1. Nutrient intakes in 94 Japanese centenarians investigated between 1972 and 1973 showed a higher proportion of animal protein to total proteins than in contemporary average Japanese.
2. High intakes of milk and fats and oils had favorable effects on 10-year (1976-1986) survivorship in 422 urban residents aged 69-71. The survivors revealed a longitudinal increase in intakes of animal foods such as eggs, milk, fish and meat over the 10 years.
3. Nutrient intakes were compared, based on 24-hour dietary records, between a sample from Okinawa Prefecture where life expectancies at birth and 65 were the longest in Japan, and a sample from Akita Prefecture where the life expectancies were much shorter. Intakes of Ca, Fe, vitamins A, B1, B2, C, and the proportion of energy from proteins and fats were significantly higher in the former [Okinawa] than in the latter [Akita]. Intakes of carbohydrates and NaCl were lower.

If its still not clear, read it again.  Japanese centenarians ate more animal protein and fats and less carbohydrates and salt than average Japanese.  Survivors had high intakes of milk, fats, and oils and an increase in intakes of animal foods such as eggs, milk, fish and meat over the ten years of this study. 

More animal protein and fat and less carbohydrate was found beneficial for life span in Okinawa, which supports what may be my unique theory that humans' increased intake of animal foods and restricted intake of plant foods during the Pleistocene probably played an important role in favoring the natural selection of longer life spans in humans compared to the other great apes.

Wednesday, May 10, 2017

Studies: Saturated fats don't impair vascular endothelial function, but starch and sugar do

Many people will think first that this study was funded by the meat and dairy industry.  Nice try, but it wasn't.  The authors are from the Diabetes and Nutritional Sciences Division and British Heart Foundation Centre of King's College London. 

They simply "tested the effects of replacing SFAs with monounsaturated fatty acids (MUFAs) or carbohydrates on endothelial function and arterial stiffness."

The subjects were moderately insulin resistant but not diabetic.  This would characterize a large portion of the general population.  

The authors wrote: "We set out to test the hypothesis that decreasing SFA intake would improve vascular function. Our hypothesis was based on the belief that decreasing SFA intake would improve insulin sensitivity, which the main report (17) showed not to be the case."

Put otherwise: Before doing this study, they believed that reducing saturated fat would improve insulin sensitivity and improve vascular function.   If they had a bias, it was against saturated fat.  They fully expected that removing saturated fat from the diet would improve vascular function. 

They measured vascular function after 1 month of consumption of a high-SFA (HS) diet and after 24 week after random assignment to the high saturated (HS) fat diet or diets that contained  less than 10% saturated fatty acids and were high in either monounsaturated fatty acids (HM) or carbohydrates (HC). The primary outcome was a change in flow-mediated dilation (FMD), and secondary outcomes were changes in carotid to femoral pulse wave velocity (PWV) and plasma 8-isoprostane F-III concentrations.

The HS reference diet used full-fat milk (3.8 g/100 mL) and cheese (35 g/100 g), whereas these were replaced with skimmed milk (0.1 g fat/100 g) and half-fat cheese (18 g/100 g) in HM and HC diets.  Those on the HS diet also consumed palm oil. 

On the HM diet, the MUFA was provided by refined high oleic sunflower oil and nuts.

With the HC diet, participants were advised to consume additional portions of bread, potatoes, and rice to compensate for the energy reduction that resulted from decreased fat intake, thus it was a high starch diet, not a high sugar diet. 

They found the opposite of what they expected to find.  To their credit, they reported results contrary to their expectations: 
"In the current study, we were unable to show any benefit on vascular function from replacing SFAs with MUFAs or carbohydrates."

Replacing saturated fats with either MUFAs or starch was not beneficial to mildly hyperinsulinemic, prediabetic subjects.


In contrast, another research team tested the effects of starch and sugar on endothelial function:
'Using 56 healthy volunteers, the researchers looked at four groups. One group ate a cornflake mush mixed with milk, a second a pure sugar mixture, the third bran flakes, while the last group was given a placebo (water). Over four weeks, Dr. Shechter applied his method of "brachial reactive testing" to each group. The test uses a cuff on the arm, like those used to measure blood pressure, which can visualize arterial function in real time."

"The results were dramatic. Before any of the patients ate, arterial function was essentially the same. After eating, except for the placebo group, all had reduced functioning."
 The lead author commented:
"We knew high glycemic foods were bad for the heart. Now we have a mechanism that shows how," says Dr. Shechter. "Foods like cornflakes, white bread, french fries, and sweetened soda all put undue stress on our arteries. We've explained for the first time how high glycemic carbs can affect the progression of heart disease." 
 The article continues:
Endothelial health can be traced back to almost every disorder and disease in the body. It is "the riskiest of the risk factors," says Dr. Shechter, who practices at the Chaim Sheba Medical Center — Tel Hashomer Hospital... 
The take-away message? Dr. Shechter says to stick to foods like oatmeal, fruits and vegetables, legumes and nuts, which have a low glycemic index. Exercising every day for at least 30 minutes, he adds, is an extra heart-smart action to take.
 Schecter neglects to mention that greens, nuts, fats and meats are the foods with the lowest glycemic index: 0. Zero. Zip.

Look at the glycemic indices listed by the Harvard School of Public Health for the foods Schecter tested or mentions as harmful:

cornflakes, 81
milk, 31
All Bran, 44

white bread, 70-75
french fries, 80-114

And, again from Harvard, sweetened soda, 60-70:

Now the foods he recommends:

oatmeal,  55
whole grain wheat breads, 51-69 
whole grain pasta, 42
100% whole rye bread, 65
brown rice, 50
quinoa, 53
fruits, 22-72
roots and tubers, 51-111 (baked potato is 111, sweet potato is 70)
legumes (excluding peanuts), 10-40
nuts (except cashews), 0

Schecter's experiment revealed that bran flakes, with a GI of only 44, impaired endothelial function. 

White potatoes (80-111), sweet potatoes (70), whole rye bread (65), whole grain wheat bread (51), oatmeal (55), quinoa (53), and brown rice (50) all have glycemic impact slightly or markedly GREATER than the bran flakes.

Therefore it can be expected that eating these foods would have a negative effect on the endothelium similar to eating bran flakes.

These whole plant foods all have an impact on blood sugar of the same order of magnitude as white bread, Coca Cola and Fanta soft drinks. 

Note that the glycemic indices of many low sugar fruits are actually lower than those of starches.

Thus, it is not true that restricting fruits and increasing whole plant food starches in their stead (recommended by some advocates of plant-based diets) reduces your exposure to sugar or blood sugar variations. 

However, it is also true the most of the listed fruits have a glycemic index about the same as bran flakes.  Therefore, if the glycemic effect is the driver of the phenomenon observed by Schecter, it can be expected that eating any of these fruits in sufficient quantity would have a negative impact on vascular function similar to the bran flakes. 

Compare the whole foods to snacks and candy bars:

The only snack foods listed that have a higher glycemic index than sweet potato are pretzels and fruit roll ups.  Corn chips, M&Ms, popcorn, potato chips, and Snickers Bar all have similar or less impact on blood sugar than oatmeal, brown rice, whole wheat bread, whole rye bread, and quinoa.  Corn chips have a GI similar to bran flakes.

Thus, according to Harvard School of Public Health, many so-called "low glycemic" whole grains, roots, tubers, and legumes release sugar into the blood at a rate similar to or greater than these junk foods.

The glycemic impact of the recommended whole plant foods is  at a minimum 10 and a maximum a little more than 100 times that of greens, nuts, fats and meats, if we assign those a false value of 1.  However, since greens, nuts, fats and meats actually have zero impact on blood sugar, there is no comparison.  Items that have no effect on blood sugar can't have even 0.00000000000001 percent of the effects down stream from post-meal blood sugar elevation, such as the impairment of vascular endothelial function observed by Schecter. 


Schecter's findings are not surprising to any serious student of basic biochemistry. It is well known from studies of diabetics that glucose – abundantly provided by starchy foods – does a lot of damage. 

After meals, the liver converts excess dietary carbohydrate into saturated and monounsaturated fats, which enter the bloodstream as triglycerides and LDL.[1] (This is why high carbohydrate diets typically produce high triglyceride levels compared to low fat diets.)  LDL then delivers the fats to cells where they will be stored or burned. (This is why LDL is not "bad;" without it cells would not get the fuel they need.)

The liver does this because high blood sugar (hyperglycemia) is very toxic:
"It's important to treat hyperglycemia, because if left untreated, hyperglycemia can become severe and lead to serious complications requiring emergency care, such as a diabetic coma. In the long term, persistent hyperglycemia, even if not severe, can lead to complications affecting your eyes, kidneys, nerves and heart."[2]
Prolonged hyperglycemia causes kidney damage, neurological damage, cardiovascular damage, damage to the retina or damage to feet and legs.  Thus, the liver turns any unnecessary dietary glucose into the much safer saturated fats.  Remember, there is no dietary requirement for glucose.  Thus, all dietary glucose is unnecessary dietary glucose.

In contrast,  SFA and MUFA are essential to health. They are used to make cell walls resistant to penetration by parasites, viruses, and bacteria. The fat pads that protect bony surfaces (palms, soles, sitting bones) and fat deposits that cushion the internal organs are made up largely of saturated fat.
Saturated fats are also very important in the nervous system and brain. The gray matter of the nervous system is made up largely of sphingomyelin, a compound that incorporates 1 fatty acid, most commonly saturated stearic acid or palmitic acid (the same as in palm oil).(3, 4) The white matter of the brain is composed largely of phospholipids incorporating palmitic or stearic acids.(5) All told, about a third of the brain’s fat is saturated.

Am I to believe that Nature chose to construct my brain of a substance that causes heart disease?

Human body fat has a saturated fat composition similar to beef tallow and lard,  about 43% SFA, 47% MUFA, and 10% PUFA:

When you fast – between meals, overnight, or longer – your body releases saturated and monounsaturated fats from fat stores into the blood stream to satisfy ongoing energy demands.  On an ongoing basis, these body fats supply about 60-70% of total body energy expenditure (6). 

Fatty acids are the main fuels for muscles at rest; muscles prefer glucose only during very high intensity activities (such as middle distance sprinting):
"The major fuels for muscle are glucose, fatty acids, and ketone bodies....muscle retains glucose, its preferred fuel for bursts of activity...The metabolic pattern of resting muscle is quite different. In resting muscle, fatty acids are the major fuel, meeting 85% of the energy needs."[1]
Muscles get about 70% of their energy from fats during aerobic activities.  As stated, they only rely on glycolysis when the activity incurs an oxygen-debt.

Thus, contrary to oft-made claim, fats – saturated and monounsaturated – are the body's predominant, hence preferred fuel source. 

More importantly, saturated and monounsaturated fats are the principle fuel source for the cardiac muscle, and the heart muscle actually prefers the ketone body acetoacetate to glucose.
"Unlike skeletal muscle, heart muscle functions almost exclusively aerobically, as evidenced by the density of mitochondria in heart muscle. Moreover, the heart has virtually no glycogen reserves. Fatty acids are the heart's main source of fuel, although ketone bodies as well as lactate can serve as fuel for heart muscle. In fact, heart muscle consumes acetoacetate in preference to glucose."(1)
So the heart is primarily fueled by saturated and monounsaturated fats on an ongoing basis, and yes, it prefers ketones to glucose.  So, if you want your heart to function well, why would you try to force it to run on glucose?

Since glucose suppresses ketosis, this basic biochemistry knowledge indicates that the heart prefers a high fat, ketogenic diet to a glucose-based diet, because glucose-rich foods – starches and fruits – suppress fat metabolism and ketosis through raising insulin level.

The hypothesis that fats are harmful to health can't provide a cogent explanation for why not only humans but all mammals use saturated fats as one of the primary fuel sources at all times and also store large amounts of this supposedly toxic stuff all over the body to serve as a reserve between meals.  (Even a lean individual stores minimally 30 times as much fat as glucose in the form of glycogen, 15 kg vs a maximum of 0.5 kg).

The hypothesis that dietary saturated fats harm and dietary starches (glucose) benefit the heart can not accommodate the well-proven fact that fat and ketones are the preferred fuels of the heart.   

To support the hypothesis that fat is harmful to the heart, you would have to produce a refutation of facts well-established by basic biochemistry research.


In conclusion, saturated fats are intrinsic to the human body, unavoidable because our own liver produces them on an ongoing basis.  Since the liver converts excess dietary glucose into either saturated or monounsaturated fats as quickly as possible, to prevent hyperglycemia, which "can produce noticeable organ damage over time," it seems clear that the body treats glucose as a more toxic substance than saturated fat, to be controlled and eliminated as rapidly as possible.

Based on these basic biochemistry facts, it would appear that the most scientific, rational approach to diet would regulate glucose intake to keep it at the very minimum required to support one's typical type and level of physical activity, liberalize intake of fats having a fatty acid profile similar to our own body fat, and stay near or in ketosis to provide the heart with its preferred fuels on an ongoing basis.


1.  Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman; 2002. Section 30.2, Each Organ Has a Unique Metabolic Profile. Available from:
2. Mayo Clinic, "Hyperglycemica in diabetes."
3.  Bettelheim FA, Brown WH, March J. Introduction to General, Organic, & Biochemistry, sixth edition. Brooks/Cole, 2001:482.
4.  Enig M. Know Your Fats. Silver Spring, MD: Bethesda Press, 2000:270.
5.  IBID., 60.
6.  Whitney and Rolfes, Understanding Nutrition 11th Edition (Cengage Learning, Apr 30, 2007), p. 156.