Wednesday, December 15, 2010

Weekly Strength Training Provides Long-Term Cognitive and Economic Benefits

Joyce Mar works on her strength training at the Langara Family YMCA in Vancouver on Tuesday.

Photograph by: Steve Bosch, Vancouver Sun, Vancouver Sun

Today the Archives of Internal Medicine published results of a study that found that women aged 65 to 75 years who engaged in progressive strength training once or twice weekly over 12 months had improved executive cognitive functions and lower medical care costs than control women when evaluated again one year later.

Today's publication provides a follow-up on the Brain Power study which the Archives of Internal Medicine published inpublished in its January 2010 issue.  The original study demonstrated that 12 months of once-weekly or twice-weekly progressive strength training improved executive cognitive function in women aged 65- to 75- years- old.  

 One report of the the study results released today states:

Both studies were led by Teresa Liu-Ambrose, principal investigator at the Centre for Hip Health and Mobility and Brain Research Centre at Vancouver Coastal Health and UBC, and assistant professor in the Department of Physical Therapy at UBC's Faculty of Medicine. The one year follow-up study found the cognitive benefits of strength training persisted, and with two critical findings.

"We were very surprised to discover the group that sustained cognitive benefits was the once-weekly strength training group rather than the twice-weekly training group," says Liu-Ambrose, who's also a Michael Smith Foundation for Health Research scholar. "What we realized was that this group was more successful at being able to maintain the same level of physical activity achieved in the original study."

In this study, one group did once-weekly strength training, another did twice-weekly strength training, and a third group "control" group did something the authors refer to as "balance and tone" which according to a Vancouver Sun article featured "stretching, range of motion, core strength, balance and relaxation exercises." 

According to the report, only the once-weekly group maintained the cognitive benefits at the follow-up.  Strength training may keep you smarter than doing "balance and tone" training.

 Regarding economic benefits:

The second important finding relates to the economic benefits of once-weekly strength training. Using the data from the Brain Power Study and the one-year follow-up study, health economists Jennifer Davis and Carlo Marra, research scientists with the Collaboration for Outcomes Research and Evaluation at St. Paul's Hospital and UBC Faculty of Medicine, were able to show that the economic benefits of once-weekly strength training were sustained 12 months after its formal cessation. Specifically, the researchers found the once-weekly strength group incurred fewer health care resource utilization costs and had fewer falls than the twice-weekly balance and tone group.

"This suggests that once-weekly resistance training is cost saving, and the right type of exercise for seniors to achieve maximum economic and health benefits," says Davis.

The study found that the once-weekly strength training group had the fewest fall and lowest medical care utilization costs. 

Thus,  this study shows that standard strength training helps seniors maintain balance more effectively than exercises supposedly dedicated to "core" strength, balance, and range of motion.  That's partly because maintaining balance requires muscular strength.  If your inner ear detects that you are off balance, but you lack the strength required to correct the movement, you will fall.  Moreover, a properly designed strength training routine will itself provide so-called "core" strength, balance training, and movement through full ranges of motion.  

In other words, strength training does it all in just one session per week.

Stay strong, stay smart, stay healthy.

The Blood Type Diet: A Critical Perspective

01/20/14 UPDATE:   On January 15, 2014 Wang et al published an empirical test of the central claim of the blood type diet hypothesis, i.e. that each blood type benefit more from one particular diet than others.  Confirming what I wrote in this post in 2010, Wang et al concluded: "Adherence to certain ‘Blood-Type’ diets is associated with favorable effects on some cardiometabolic risk factors, but these associations were independent of an individual's ABO genotype, so the findings do not support the ‘Blood-Type’ diet hypothesis." Read the full text in PLOS One.  Read my blog about the study here.

Thanks to Peter J. D’Adamo, N.D. , author of the book Eat Right 4 Your Type, many people believe that blood type determines your dietary requirements and that only people with O-type blood should eat a paleo/primal diet.  

In this post I will discuss all the errors in this blood type hypothesis. 
The Blood Type Diet Hypothesis

D’Adamo’s hypothesis can be distilled down to four main claims and a conclusion drawn from these claims.

Claim A: Evolutionary adaptation to diet patterns resulted in the ABO blood groups, so each of the four types is adapted to a different type of diet and set of foods.
Claim B: People of different blood types have different antibodies in their blood and each blood type has a different susceptibility to diseases.
Claim C: Foods contain lectins that mimic blood group antigens and selectively cause blood agglutination (i.e. each food affects each blood group differently), and this causes diseases.
Claim D: Exposure to foods containing lectins incompatible with your blood type will cause agglutination of your blood which will cause diseases. As D’Adamo puts it, the lectins “target  an organ or bodily system and begin to agglutinate blood cells in that area.”

Conclusion: Therefore, people require diets tailored to their blood types, eliminating foods that have harmful lectins for their blood type.

The Four Diets

Blood type O

According to D’Adamo,  O-type blood is the “Original” blood type which evolved when humans lived by hunting supplemented by gathering.  He says these people should base their diets on lean meat and fish, supplemented with a selection of fruits and vegetables he deems suitable for this blood type.  O-types should avoid or greatly minimize dairy products and minimize or avoid grains and beans, particularly wheat.  According to D’Adamo, people with O-type don’t tolerate wheat “at all” yet he also says that they can eat sprouted wheat products (?).

Blood type A

D’Adamo claims that A-type blood arose as an adaptation to agriculture; conveniently, A is for agriculture.  He claims that this type can eat grains (except wheat), beans, most seafoods, many vegetables and  fruits, but should avoid dairy, meat, wheat, kidney beans, and lima beans.  He states that only people with A-type blood can and should eat a vegetarian diet.
Blood type B

D’Adamo refers to B-type as  “The Nomad.”  He implies that this type arose as an adaptation to pastoral lifestyles based on use of dairy products and meat from domesticated animals.  He states that B-types are adapted to a “balanced omnivore” diet that meat (but no chicken), eggs, dairy, beans, fruits, vegetables.  He advises people having the B blood type to avoid chicken, corn, lentils, peanuts, sesame, buckwheat, and wheat.

Blood type AB

D’Adamo calls type AB blood “The Enigma” and states that people having this blood type are adapted to a “mixed diet in moderation.   He advises that they can safely eat lamb, mutton, rabbit, turkey, pheasant, most seafood, dairy, beans, grains,             fruits,             and vegetables, but should avoid beef, chicken, kidney beans, lima beans, seeds, corn, buckwheat.

Basic Errors

As someone basing his whole approach to diet on blood types, D’Adamo appears disturbingly ignorant of basic facts about the evolution of the ABO types.

First, he claims that the O-type is the original blood type. He published his book in 1994, but by 1990 molecular biologists had determined that A-type is the original blood type.   In “Evolution of Primate ABO Blood Type Genes and Their Homologous Genes [full text available free],” Saitou and Yamamoto state [p. 405]:

“..the common ancestral gene for the hominoid and Old World monkey ABO blood
group is A type, and three B alleles evolved independently on the human, gorilla, and baboon lineages.”

The fact that both A-type and B-type antedate O-type seems predictable from the fact that O-type blood carries antibodies to A-type and B-type blood; for this to happen, O-type blood had to have emerged in an environment in which A-type and B-type antigens (the markers on A- and B- type blood cells) already existed. 

D’Adamo suggests that the blood types arose in humans as adaptations to dietary variations, implying that they are unique to humans.  In fact, ABO blood types occur not only in humans, but also in other primates.  Again, according to Table 5 in Saitou and Yamamoto, which presents data dating to 1964, more than 30 years before D’Adamo published his books:
·      The A phenotype occurs in chimps, orangutans, gibbons, baboons, Java macaques, sulawesi crested macaques, and squirrel monkeys (7 speicies).
·      The B phenotype occurs in gorillas, orangutans, gibbons, baboons, Rehsus macaques, pigtailed macaques, Java macaques, sulawesi crested macaques, and cebus monkeys (9 species).
·      The AB phenotype occurs in oragutans, gibbons, baboons, and Java macaques (4 species).
·      The O phenotype occurs in chimps, Java macaques, squirrel monkeys, and cebus monkeys (4 species).

Since none of these primates have ever practiced agriculture or domesticated dairy animals, it is clear that the A allele did not evolve as an adaptation to agriculture nor did the B allele emerge as an adaptation to consumption of dairy products. 

As noted above, the B-type has been found in the largest selection of species (9), followed by the A-type (7), and both O- and AB- type occur in the smallest selections (4 species each).  According to Saitou and Yamamoto, among this list of primates checked for ABO blood type, A phenotype occurred in 191 individuals, B in 75 individuals, AB in 44 individuals, and O in 20 individuals. 

According to Saitou and Yamamoto “It seems that the time of gene dupulication producing ABO and GAL genes may be around the emergence of vertebrates (ca. 500 MYA).”  [p.408]  In other words, these blood types have a much longer history than human dietary variations. 

Human Data

Its possible that D’Adamo did not mean to imply that the blood types arose only in humans.  Perhaps he meant that human adoption of hunting lifestyle selected for O-type, agriculture for A-type, and pastoralism for B-type.  In this case, we should find a predominance of O-type among all ethnic groups with a long history of living by hunting, especially those eating little plant food; a predominance of A-type among  ethnic groups having the longest histories of practicing agriculture; and a predominance of B-type among ethnic groups with long histories of pastoralism.

Unfortunately, the available data does not support this either.  So far as we know, Eskimos have never practiced agriculture or animal husbandry, and have long lived primarily by hunting, a diet enforced by their environment.  D’Adamo’s hypothesis would predict that Eskimos would have predominantly O-type blood.  According to, this is true of Greenland Eskimos (54% O, 36% A), but not of Alaskan Eskimos (38% O, 44% A), who have more A-type than O-type individuals, contradicting D'Adamo's hypothesis.

According to Wikipedia and, people of the Blackfoot or Niitsítapi tribe traditionally lived primarily on buffalo meat; classic hunters.  From Wikipedia:

“While the Niitsitapi were in the Great Plains, they came to depend on the buffalo (American bison) as their main source of food. The bison are the largest mammals in North America and stand about 6 ½ feet tall and weigh up to 2,200 pounds.[6] Before the introduction of horses, the Niitsitapi had to devise ways of sneaking up close to the buffalo without the animals' noticing so they could get in range for a good shot. The first and most common way for them to hunt the buffalo was using the buffalo jump. The hunters would round up the buffalo into V-shaped pens and drive them over a cliff (they hunted prong-horned antelopes in the same way). After the buffalo went over the cliff, the Indians would go to the bottom and take as much meat as they needed and could carry back to camp. They also used camouflage for hunting.[6] The hunters would take buffalo skins from previous hunting trips and drape them over their bodies to blend in and mask their scent. By subtle moves, the hunters could get close to the herd. When close enough, the hunters would shoot the bison with arrows, or use lances and spears to bring them down.

They used virtually all parts of the body and skin. They prepared the meat for food: by boiling, roasting and drying for jerky. This prepared it to last a long time without spoiling, and they depended on bison meat to get through the winters.[7] The winters were long, harsh, and cold due to the lack of trees in the Plains, so the people stockpiled the meat when they had the chance.[8] The hunters often ate the bison heart minutes after the kill, as part of their hunting ritual. The skins were prepared and used to cover the tepee. The tepee was made of log poles with the skin draped over it. It remained warm in the winter and cool in the summer, and a great shield against the wind.[9] With further preparation of tanning and softening, the women made special clothing from the skins: robes and moccasins. They rendered bison fat to make soap. Both men and women made utensils, sewing needles and tools from the bones, using tendon for fastening and binding. The stomach and bladder were cleaned and prepared for use as containers for storing liquids. Dried bison dung was fuel for fires. the fires. The Niitsitapi used almost every part of the buffalo and considered it a sacred animal, integral to their lives.[10]”

From this D’Adamo would predict that they had primarily O-type blood.  Wrong again. states that 82% of Blackfoot people have A-type blood, and only 17% have O-type. 

Looking from the other side, D’Adamo’s hypothesis would predict that Cantonese Chinese would have a higher incidence of A-type and lower incidence of O-type because they have lived for millennia on a rice-based agricultural diet. states that Cantonese Chinese have 46% O- and 23% A- types, the reverse of the D’Adamo prediction. 

Meanwhile, the northern Chinese (Peking) have 29% O, 27% A, and 32% B, a distribution which according to D’Adamo’s hypothesis would predict that the population has a long history of living on dairy products.  Unfortunately for D’Adamo, the pastoral lifestyle is not common in China at all, only practiced by Chinese in the western, mountainous provinces.

Just as one black swan is sufficient to disprove the claim that all swans are white, these few counter examples are sufficient to disprove the claims that hunting-based subsistence favors the O-type blood, while an agricultural subsistence favors the A type blood.  D’Adamo is just wrong when he asserts that dietary differences drive differences in distribution of blood types among humans. 

No Anatomical Evidence

All humans, regardless of blood type, cultural background, or  diet histories have the same basic gut design, dentition (number and type of teeth, type of enamel), type of saliva and digestive enzymes.  This is why we call them humans.  

For example, scientists have found no nutritionally relevant anatomical, physiological, or biochemical differences between Chinese and Eskimos. 

Nor are there any such differences between people with A-type and O-type blood.  

Medical Evidence?

D’Adamo claims that O-type people get ulcers more frequently than people with A-type because O-type individuals, according to him, produce more stomach acid than people with A-type blood.  He says that O-types produce this greater amount of acid as an adaptation to a high meat diet; A-types have less acid because they are adapted to a low protein, low meat diet. 

Apparently he missed the memo when research discovered that gastric ulcers arise from infection with H. pylori bacteria, not excessive stomach acid production.  While it is true that group O individuals have approximately 35% greater risk of gastrointestinal ulcer when compared to group A individuals, this is not because O-types produce more acid that A-types.   The ulcer-causing bacterium, H. pylori, can more easily attach to the G.I. lining of Group O, because it has a protein structure that mimics the Group O host (which confuses the host’s immune system).  In contrast, the immune system of A-type individuals more easily recognizes the bacterium as a foreign invader, making them more resistant to this infection.

D’Adamo correctly states that group A individuals have a higher risk of cancer than group O individuals.  Relative to Group O individuals, Group A individuals have higher risks of cancers of stomach , colon, ovary, uterus, cervix, and salivary glands (relative risks 1.2, 1.11, 1.28, 1.15, 1.33, and 1.64).  D’Adamo implies that this difference arises due to influence of dietary lectins. Presumably, the more vegetarian diet  he prescribes for A-types will protect them from cancer by reducing their exposure to harmful lectins.

First of all, if dietary lectins are the cause of cancers in anyone, it is very hard to understand how a vegetarian diet based on grains and beans will help prevent cancer.  Lectins are carbohydrate-binding proteins found in the highest concentrations in carbohydrate-rich foods like gains, legumes, and potatoes, not meat.  From Wikipedia entry on lectins:

“The toxicity of lectins has been identified by consumption of food with high content of lectins, which can lead to diarrhoea, nausea, bloating, vomiting, even death (as from ricin). Many legume seeds have been proven to contain high lectin activity, termed as hemagglutinating activity. Soybean is the most important grain legume crop, the seeds of which contain high activity of soybean lectins (soybean agglutinin or SBA). SBA is able to disrupt small intestinal metabolism and damage small intestinal villi via the ability of lectins to bind with brush border surfaces in the distal part of small intestine. Heat processing can reduce the toxicity of lectins, but low temperature or insufficient cooking may not completely eliminate their toxicity, as some plant lectins are resistant to heat.”

Therefore, the diet he apparently prescibes to A-types to reduce their risk of cancer actually provides MORE potentially hazardous dietary lectins than the diet he prescribes to O-types.

Secondly, D’Adamo doesn’t appear to know that the reason for increased risk of cancers in individuals with A-type blood is similar to the reason for the increased risk of ulcers in individuals with O-type blood.  Tumors often express an A-like antigen that the immune system of an A group individual will accept as “self” while the immune system of an O or B group individual will attack any cell with an A antigen. 

Note also that group O- and B- individuals still get these tumors. For example, the relative risk of stomach cancer is only 20% greater among A-type individuals compared to O-type.  This means that if 5 of 100 individuals having blood type O get stomach cancer, 6 of 100 individuals having blood type A get the same cancer; if 50 type Os get the cancer, 60 type As will get it.  In absolute numbers, the difference between these groups is not significant. 

Do Lectins Cause Selective Agglutination?

A lynch pin of D’Adamo’s hypothesis is the claim that lectins selectively cause agglutination in different blood types.  For example, according to D’Adamo, people with B-type blood should avoid chicken because it contains lectins that will agglutinate blood in these individuals, but not in people with other blood types.

We don’t have any evidence for this.  In fact, published data indicates that any individual lectin will affect all blood types in essentially the same way. 

Wikipedia discusses this topic:

“D'Adamo claims there are many ABO specific lectins in foods.[14] This claim is unsubstantiated by established biochemical research, which has not found differences in how the lectins react with a given human ABO type. In fact, research shows that lectins which are specific for a particular ABO type are not found in foods (except for one or two rare exceptions, e.g. lima bean), and that lectins with ABO specificity are more frequently found in non-food plants or animals.[15][16]

The Nachbar Study[17] has been cited in support of D'Adamo's theories, because it reports that the edible parts of 29 of 88 foods tested, including common salad ingredients, fresh fruits, roasted nuts, and processed cereals were found to possess significant lectin-like activity (as assessed by hemagglutination and bacterial agglutination assays). However, almost all of the 29 foods agglutinated all ABO blood types, and were not ABO blood type specific. Since D'Adamo's theory has to do with lectins in food that are "specific for a certain ABO blood type", this study does not support his claim that there are many ABO specific lectins in foods.”

Reference 15 in this excerpt refers to The Handbook of Plant Lectins

So Why Do People Feel Better?
D’Adamo advises the avoidance of wheat to O, A, and B blood types. Collectively, these comprise 96% of all people in the U.S..  Therefore, most people who read the book will get advice to avoid wheat, and they may try it.  This alone will improve health for some people who are wheat sensitive. 

Besides this, most people adopting the blood type diet will simply make general improvements to their diets, like reducing sugar intake, eating less processed and more unprocessed foods. D’Adamo suggests these steps to all blood types.  The general steps will help most people feel significantly better and perhaps lose some body fat. 

Bottom Line

The blood type diet does not have a solid leg on which to stand.  The hypothesis is riddled with errors. 

Addendum 10/28/11

Michael Klaper, M.D.: Challenges to the Blood Type Diet

Tuesday, September 14, 2010

4000 IU Vitamin D Daily Cuts Preterm Birth Risk in Half

A new study by researchers from Medical University of South Carolina has found that women taking 4000 IU of vitamin D daily during pregnancy cut their chances of a preterm birth in half compared to women taking only 200-400 IU.  The women taking 4000 IU of vitamin D also has a reduced risk of infections.  There were no adverse effects found for this level of supplementation.  

If you think you live in a sunny environment and don't need vitamin D, consider this:
"All the women taking part in the study were living in Charleston — in sunny South Carolina. Overall, 85 per cent were either insufficient, or "frankly deficient" in vitamin D when the study began."

This adds to the list of studies indicating that the vast majority of urbanites are deficient even if they live in sunny places.  

Canada's Health Care System in Financial Crisis

Just as the U.S. has started moving toward a Canada-esque health care system, the Canadian
Organisation for Economic Cooperation and Development has announced that Canada's health-care system is in a financial crisis, and needs significant -- if controversial -- reform to survive.

Read more:
Some bits from the report:
"Canada should end its status as the only OECD country -- other than the United Kingdom -- that mandates solely government funding of medical care, and allow co-payments and deductibles. Having to pay a modest fee to visit a doctor would limit government spending, likely reduce demand on the system and possibly encourage healthier lifestyles."

"The report notes that, with governments funding the entire cost of medical service and user charges outlawed, cost pressures and rising demand have forced healthcare rationing: long queues for some services and a shortage of physicians. "

Contracts for health services, especially hospital services, should be opened up to both private and public facilities. As with any government contracting process, this could "stimulate public-sector accountability."

People should be allowed to buy private health insurance and opt out of the public system for some basic medical services "at the margins" of the system, spurring on private health providers and generating competition to the public sector. To make the idea work well, doctors should be able to serve both publicly and privately funded patients."

Read more:

Friday, August 20, 2010

Fructose Feeds Cancer Follow-up: Is all fructose metabolized in the liver?

In response to my posting entitled Fructose Feeds Cancer, which referred to the Reuters story entitled Cancer Cells Slurp Up Fructose, some commenters on my blog and other bloggers have stated that fructose gets metabolized by the liver so doesn't make it into the blood stream and couldn't promote cancer anywhere but in the liver. 

I dissented and today took a moment to search for studies measuring fructose concentrations in the blood.  My first find was Increased Fructose Concentrations in Blood and Urine in Patients With Diabetes published in Diabetes Care.  From the abstract:

"Serum fructose concentrations in patients with diabetes (12.0 ± 3.8 μmol/l) were significantly higher than those in healthy subjects (8.1 ± 1.0 μmol/l, P < 0.001) and nondiabetic patients (7.7 ± 1.6 μmol/l, P < 0.001), and daily urinary fructose excretion was significantly greater in patients with diabetes (127.8 ± 106.7 μmol/day) than in nondiabetic patients (37.7 ± 23.0 μmol/day, P < 0.001)."

So there you have it.  Non-diabetics, healthy subjects, and diabetics all have fructose in serum, with the diabetics carrying an average of about 50% more fructose in serum than healthy subjects. 

If you read the full text, you will learn that inadequate technology once made detection of fructose in serum difficult, and the authors of this study overcame that limitation.  You will also see this discussion of several mechanisms which might explain increased fructose in serum of diabetics:

"First, impaired fructose metabolism in the liver might play an important role, given that several studies have shown that the liver metabolizes at least half of all fructose (11,13). Second, the transport system for fructose might be disrupted. Fructose is transported into the liver, at least in part, by the same system as glucose and galactose (14,15). In adipocytes, fructose can enter by at least two different carriers. Hajduch et al. (16) reported that GLUT5 was responsible for mediating ∼80% of the total cellular fructose uptake, whereas the remaining 20% was cytochalasin B-sensitive, which most likely reflects transport via GLUT1 and/or GLUT4. Third, the polyol pathway might play a role in the increment of serum and urinary fructose concentrations. This pathway reportedly contributes to increased fructose concentrations in many tissues of patients with diabetes (17) and diabetic animals (1820)."

Notice that the authors say "the liver metabolizes at least half of all fructose,"  not "the liver metabolizes all of ingested fructose."  Also, they cite four studies that found increased fructose concentrations in "many tissues" of diabetic humans and animals.  To get to those tissues it had to go through the blood from the gut.  These findings clearly indicate that the development of diabetes involves a rise in serum and tissue levels of fructose, providing fuel for cancer proliferation in affected tissues.  And we don't have to eat an diet of 100% fructose to get this result.  

Some might scoff at the micromolar concentrations but the authors also point out that fructose is so much more reactive than glucose that it has comparable pathological effects even at these very low concentrations:

"Although glucose circulates in millimole concentrations, only ∼1/1,000 molecules circulates as a free aldehyde and can therefore participate in glycation reactions. Fructose, although circulating in micromole concentrations, is much more reactive in this regard and, therefore, may be comparable to glucose in terms of mediating pathology through nonenzymatic reactions and downstream processes."

Thursday, May 27, 2010

Exercise and Fitness Buffer the Life-Shortening Effects of Psychological Stress

A new article published in the on-line Public Library of Science journal reports on a study which compared the effects of chronic psychological stress on either sedentary or physically active people.

The study involved looking at telomere length in 63 healthy post-menopausal women. The researchers measured telomere length in the women, then had the women complete the Perceived Stress Scale. After this, for three days the women reported their daily investment of time (in minutes) in vigorous physical activity. The researchers then calculated the likelihood of having long or short telomeres relative to age, body mass index, education, perceived stress, and activity level.

Among the sedentary women, each unit of increase in perceived stress (on the Perceived Stress Scale) was associated with a 15-fold greater odds of having short telomeres, a marker of biological aging. However, among those who got an average of at least 14 minutes daily of vigorous exercise, the researchers found no increase in odds of short telomeres regardless of perceived stress.

In other words, it appears that people who engage in sufficient, but not excessive, physical activity have greater resistance to the aging effects of psychological stress.

The authors propose several explanations for the beneficial effects of activity:

1. Moderate physical activity appears to increase endogenous antioxidant production, which may buffer the pro-oxidative effects of stress.
2. Physical fitness and activity appear to blunt neuroendocrine responses to stress, particularly reducing sympathetic nervous system responses and cortisol production.
3. Physical activity appears to reduce cognitive rumination (i.e. it quiets the mind), which results in less sympathetic nervous system activity and lower cortisol production under stress.

In short, this study suggests that by engaging in regular physical activity we protect ourselves from both the immediate and the aging effects of stress. We would expect this from a species that evolved by route of a lifestyle that required physical activity in the pursuit of food. Proper exercise is essential to not only physical but also mental health.

Wednesday, April 21, 2010

Practically Paleo Perspective: Rice

A commenter asked me for my opinion on rice, so here you have it.

[Updated 4/20/12:  The original version of this post illustrates some of the poor reasoning I fell into as a result of reading books and blogs by people advocating paleo diet, while ignoring the bulk of research on diet and health.  My critiques and corrections of the original appear in brackets.]

Botany and Antinutrients

Rice is the seed of a monocotyledonous plant known to botanists as Oryza sativa. 

Like other seeds, whole (brown) rice contains chemical defenses against predation, primarily present in the hull and bran of the seed.  They include phytin (phytate), trypsin inhibitor, oryzacystatin and haemagglutinin-lectin.

Phytate binds minerals including calcium, zinc and iron; it also binds with protein.  Heat (cooking) does not denature phytate.  Studies have found that subjects fed brown rice diets have poorer mineral balance when compared to subjects fed milled rice diets.  On the other hand, phytate protects against dental caries, so white rice promotes dental decay more than brown rice.

[4/20/12:   Phytate fears are not founded on good science.  Science does not support claims that dietary phytate causes harm to humans.  Humans adapt to phytate ingestion, dietary vitamin C cancels the negative effect of phytate on mineral absorption, phytate adversely affects mineral balance only if the diet is deficient in minerals, and research has shown that dietary phytate has a strong health benefits for prevention and treatment of cardiovascular disease and cancer; it even inhibits the growth of malignant tumors.]

Trypsin inhibitor occurs in rice bran.  Steaming rice bran at 100 degrees C (212 F) inactivates trypsin inhibitor.  [4/20/12:  This means that boiled brown rice has no active trypsin inhibitor.] Polishing rice eliminates trypsin inhibitor.

Haemagglutinins  or lectins consist of globulins that agglutinate mammalian red blood cells and precipitate glycoconjugates or polysaccharides. Lectins bind to specific carbohydrate receptor sites on the intestinal mucosal cells and thus interfere with the absorption of nutrients across the intestinal wall.  Rice lectin agglutinates human A, B and O group erythrocytesAccording to the FAO, rice lectin sharply loses activity when heated to 100 degrees C. [4/20/12: Hence, since we boil rice at 100 degrees C before eating it, we don't have to worry about this lectin.]

Oryzacystatin is an inhibitor of protein-digesting enzymes.  Oryzacystatin remains 100% active after at least 30 minutes of boiling.

Rice also contains an allergenic protein that occurs primarily in the milled rice, not the bran, and remains stable (60%) even after boiling for 60 minutes at 100 C (212 F).

[4/20/12: Rice allergies occur in only 10% of atopic patients in Japan and less in Europeans and Americans.  Compare this to beef allergy:

"The prevalence of beef allergy is between 3% and 6.5% among children with atopic dermatitis and can be up to 20% in cow's milk allergic children. Several studies reported an incidence of 1-2% of food-induced anaphylactic reactions caused by ingestion of beef. In another study an even higher figure of 9% of anaphylactic events from foods were induced by beef."
These data appear to indicate a much greater incidence of anaphylactic events triggered by beef than by rice.]
Nutritional value

Rice has a very high carbohydrate content and low levels of micronutrients compared to vegetables or fruits.  The following table compares the levels of selected vitamins and minerals in 50-kcal portions of brown rice and a selection of vegetables and fruits.  Red numbers indicate items with the highest levels among the foods compared. Click on image to see larger version.

Notice that brown rice does not have the highest level of any of the nutrients listed.  White potatoes have twice as much riboflavin (B2), 2.5 times as much folate, vitamin C not present in rice, 10 times more potassium, more than 3 times as much iron, and 25% more calcium than brown rice.    Sweet potatoes supply carotenes (provitamin A) and vitamin C not present in brown rice, three times as much B2, 5.5 times as much folate, 9 times as much potassium, slightly more iron, and more than 3 times as much calcium.  Winter squash also makes brown rice pale in comparison.

Strawberries have 10 times as much B2, 12.5 times as much potassium, nearly 3 times as much iron, and more than 5 times as much calcium.

No matter which vegetable or fruit you compare to brown rice, you find the vegetable or fruit makes brown rice pale in comparison.

Then if you compare brown to white rice:

Brown Rice vs. White Rice

Brown Rice (1 cup)
White Rice (1 cup)
Energy (kcal)
Protein (g)
Carbohydrate (g)
Fat (g)
Fiber (g)
Thiamin (mg)
0.3 (synthetic)
Riboflavin (mg)
0.03 (synthetic)
Niacin (mg)
2.8 (synthetic)
Pyridoxine (mg)
Folacin (mcg)
109.8 (synthetic)
Calcium (mg)
2.7 (fortified)

Laying aside the synthetic fortification, brown rice supplies nearly 3 times as much pyridoxine, 10 times as much calcium, almost 6 times as much magnesium, more than 3 times as much phosphorus, more than 3 times as much potassium, and almost twice as much zinc.  Therefore, white rice doesn't hold a candle to brown rice, and brown rice doesn't hold a candle to white potatoes.

[4/20/12:  Turn this around, and judge by energy, protein, and carbohydrate delivery per unit volume, and you find that brown rice surpasses non-starchy vegetables and fruits.  We need some foods for energy and macronutrients, and some foods for micronutrients.  Brown rice is a nutrient-dense starch and energy source compared to white rice.]

White or brown, rice is basically filler with little nutritional value compared to vegetables and fruits.  If you eat rice, you crowd out more nutrient-dense sources of carbohydrate. 

[4/20/12:  Wow, what a ridiculous argument!  Both brown and white rice are much more nutrient-dense than fats like butter, lard, and olive oil, so I would have been more correct to state that fats are fillers compared to brown rice.  When I compared the micronutrient content of two equicaloric diets, one high in meat and supplying most of its energy from fat, and the other low in meat and supplying most of its energy from starches like brown rice, the starch-based diet won hands down.]


Environmentalist vegetarians like to blame livestock for global warming, but according to Wikipedia:

In many countries where rice is the main cereal crop, rice cultivation is responsible for most of the methane emissions....Methane is twenty times more effective as a greenhouse gas than carbon dioxide.
[4/20/12:  This is an example of the half-truths used to support paleo perspectives.  How about taking a look at relative contributions of rice compared to animal products?  A study published in the American Journal of Clinical Nutrition calculated the amounts of greenhouse gases (carbon dioxide, nitrous oxide, and methane) emitted in the production of 22 different commonly consumed foods, in kg of CO2 equivalents per kg of final product:   Rice, 1.3;  eggs, 2.5; rapeseed oil, 3.0; chicken, 4.3; cod, 8.5; pork, 9.3; cheese, 11; beef, 30.  So the favored foods of low carb and paleo diets produce 2 to 23 times as much greenhouse gas emissions as rice.]

Further, rice fields are the principal breeding grounds for mosquitos that carry malaria.

So there you have my perspective on rice.   I do not recommend regular consumption of either brown or white rice. [Line through added on 4/20/12.]

[4/20/12:  I now highly recommend eating rice and other grains as staple foods, and I no longer recommend eating eggs, poultry, fish, pork, or beef or beef products.  Grains are far superior to meats and fats as human energy sources and for health support, and have much less deleterious effect on the environment.  Science has shown us that meat- and fat-based paleo dieting is not beneficial to human health, animal welfare, or for ecosystem preservation.]

Wednesday, March 31, 2010

Paleo Basics: How Much Sugar in Wild Fruits?

I frequently see the claim that wild fruits have less sugar than cultivated varieties.  It must sound reasonable to those who state it, but what does the evidence show?

In "Australian Aboriginal plant foods: a consideration of their nutritional composition and health implications" Brand-Miller and Holt discuss the carbohydrate contents of wild fruits consumed by Australian Aborigines and report:
"The average nutrient analysis of all the dried AA [Australian Aborigine] fruits in Table 1 (n = 7) shows that they are high in carbohydrate (59 %, v. 65 % in cultivated sultanas and raisins), and contain moderate amounts of protein (8 %) and fat (4 %) depending on the state of desiccation."

They also report:
"The average nutrient composition of all the fruit samples analysed (n = 334) is shown in Table 1 (macronutrients) and Table 2 (micronutrients). On first inspection they appear to be a little higher in protein (2 v. 1 %) and fat (1 v. 0 %) compared with the average of 17 types of cultivated western fruits. These small differences could be explained in large part by the lower water content of the wild foods (72 v. 85 % in cultivated foods). 
"Native fruits also appear to be twice as high in both carbohydrate (21 v. 9 %) and fibre (8 v. 3 %). However, because the methods used are not ideal (see above), the carbohydrate is probably an overestimate and the fibre an underestimate."

So analyses show that wild fruits have, in the first comparison, about the same sugar content as cultivated varieties, and in the second comparison, at least as much sugar, probably more, and up to twice as much, as cultivated.  Neither analysis showed them to have significantly less carbohydrate.

Paleo Basics: Fructose Fact Vs. Fiction

In response to my post on the Kitavan diet, which includes plenty of fruit and likely 36g of fructose daily, "gn" asked me if I think it plausible to suppose that human ethnic groups differ in ability to deal with fructose loads, so that daily fruit won't harm dark-skinned Kitavans living in tropical climate (constant summer) for hundreds of generations, but will harm people of European descent whose ancestors had fructose supply only in late summer and fall seasons.

From this question, which I will address below,  I get the impression that the Lustig lecture embedded above has led many to believe that daily ingestion of fructose in any quantity has toxic effects, such as non-alcoholic-fatty-liver-syndrome (NAFLS), particularly to people of European descent.

Unfortunately, Lustig's lecture contains misleading hyperbole or exaggeration (e.g. within the first five minutes he says "The Japanese diet is all carbs and no fat, and the Atkins diet is all fat and no carbs" and later he claims that Japanese eat no sugar, a falsehood) and doesn't give important details about research on fructose metabolism. The main problem lies in a failure to define the dose of fructose required to produce the adverse effects. Let's take a look at some of the research to see what people have missed.

Fructose Research

Le et al investigated the effect of fructose overconsumption on blood lipids and ectopic lipid deposition in healthy subjects with and without a family history of type 2 diabetes.   In this study they found that fructose overconsumption  "increased ectopic lipid deposition in liver and muscle and fasting VLDL-triacylglycerols and decreased hepatic insulin sensitivity" and the effect appeared greater in offspring of parents who had type 2 diabetes.

To get this effect, they used a hypercaloric high-fructose diet supplying 3.5g fructose per kg of fat free mass, amounting to more than 35% of energy intake.  For a lean individual like myself, that would require putting down more than 222g/888kcal of fructose daily while also consuming more calories than I expend.   This is an unrealistic intake of fructose for a person eating a whole foods diet.  It would require consuming more than 444g of table sugar, 12 non-diet sodas, or about 18 medium size apples or bananas.

For another example, Ackerman et al studied fructose-induced fatty liver disease in rats.  To induce FLD in the rats, they used a diet consisting of 60% fructose by weight, which supplied all the carbohydrate in the diet.  Humans do not typically consume diets in which fructose is the sole carbohydrate and the major macronutrient by weight.

Brown et al looked at the effect of fructose on blood pressure in young healthy people.  They had 15 volunteers drink a 500ml  beverage containing a single dose of 60g fructose or glucose.  Both sugars produced an increase in heart rate, and the fructose dose produced an elevation in blood pressure that persisted for at least 2 hours.  To get a single dose of 60g fructose from sucrose (table sugar) would required ingesting about 120g sugar in one sitting--or, 157g of high-fructose corn syrup, or more than 4 apples or 4 bananas.  This says nothing about the effects of consuming the more typical 15g fructose per serving found in a serving of soda, let alone eating whole fruits, which contain other components (e.g. potassium) that tend to reduce blood pressure.  For my n=1 experiment, I have routinely eaten 3-4 pieces or servings (cups) of fruit in a day for more than 10 years in a row and my blood pressure remains at 110/60.

Swarbrick et al claimed to show that consumption of fructose-sweetened beverages increases postprandial triglycerides and fasting apoB concentrations, and suggest that long-term consumption of diets high in fructose could lead to an increased risk of CVD.  To produce their results, they fed study subjects diets providing 25% of total energy as fructose.  For a 2000 kcalorie diet, that is 500 kcalories or 125g of fructose.  Again, this would require consuming a total of 250g of sugar from sucrose or high-fructose corn syrup, i.e. more than 6 non-diet sodas, or at least 10 pieces or cups of fruit in a day. 

As John White noted in the American Journal of Clinical Nutrition, in the typical U.S. diet, fructose contributes about 200–250 kcal/d, which amounts to about 7–8% of the current 2700-kcal/d per capita total calorie intake, a much smaller intake than used in these experiments, so they provide no evidence that typical intakes of fructose induce fatty liver disease.  He added:

"Although examples of pure fructose causing metabolic upset at high concentrations abound, especially when fed as the sole carbohydrate source, there is no evidence that the common fructose-glucose sweeteners do the same. Thus, studies using extreme carbohydrate diets may be useful for probing biochemical pathways, but they have no relevance to the human diet or to current consumption."
I could go on but instead I will refer you to an excellent critical review of Lustig's lecture by Alan Aragon:  The bitter truth about fructose alarmism.  After reviewing 19 papers on the effects of dietary fructose disputing some of the anti-fructose claims made by Lustig, and finding Lustig's presentation lacking, Alan comments:

"So, what’s the upper safe limit of fructose per day (all sources considered)? Again, this depends on a number of variables, not the least of which are an individual’s physical activity level and lean body mass.Currently in the literature is a liberal camp reporting that fructose intakes up to 90 grams per day have a beneficial effect on HbA(1c), and  no significant effects are seen for fasting triacylglycerol or body weight with intakes up to 100 grams per day in adults [15]. The conservative camp suggests that the safe range is much less than this; roughly 25-40 grams per day [19].  Figuring that both sides are biased, the middle figure between the two camps is roughly 50 grams for active adults."  
Back To The Original Question

As I noted above, "gn" asked me if I find it plausible that Europeans have less tolerance for fructose than Kitavans.  Short answer: No.  Long answer:  All of the above studies were done on people of European descent, illustrating that Europeans have a quite high tolerance for fructose.  Further, fructose tolerance developed millions of years ago in the African primate lineage from which we all hale, due to primate consumption of fruit as a dietary staple.  When humans moved out of Africa about 50 thousand years ago, they would have lost fructose tolerance only if maintaining it proved a disadvantage in northern climates.  In other words, they would have lost fructose tolerance only if maintaining it resulted in death before reproduction.

I can't imagine a scenario in which the environment would select against fructose tolerance, i.e. in which maintenance of fructose tolerance despite a fructose-poor environment, would cause a person to lose fertility or die before having a chance to reproduce.  I also can't imagine a scenario in which the environment (seasonal variations in supply of fructose) would select for fructose-intolerance, i.e. favor the reproduction of fructose-intolerant individuals.  On the contrary, seasonal supply of fructose would continue to select for those who could eat naturally large amounts of fructose (i.e. fruits) when seasonally available, because those people maintaining the deeply ingrained primate ability to metabolize fructose would even in the north have a greater total available food supply than fructose-intolerant individuals.

I routinely eat three to five servings of fruits daily, i.e. 30 to 50g of fructose, and have done so most days for the past 10 years that I have eaten a practically paleo diet.  My ethnic background consists of Hungarian, French, and German.   My last blood profile showed my total lipoproteins at 231 mg/dL, my HDL at 85, and my triglycerides at 47.  Using the Friedewald equation they calculated the LDL at 138, but since I have very low triglycerides, using the Iranian formula calculator I calculate my LDL equals 104.  Since I have nearly twice as much HDL as triglycerides, and low fasting glucose, I have extremely low heart disease risk.  My liver enzyme levels and bilirubin all fell in low normal values, indicating no liver dysfunction.


Tuesday, March 30, 2010

Paleo Diet Analysis: Kitavan Analogue Diet

This weekend I spent some time reading Stephan Guyenet's excellent series of posts on the Kitavans, along with parts of Staffan Lindeberg's website and book Food and Western Disease: An Evolutionary Perspective, which also contain information on the Kitavans.

The Kitavans display exceptional health and live well into their 90s without heart disease, cancer, diabetes, obesity, high blood pressure, or other diseases of civilization. They eat eat a diet composed primarily of tubers (sweet potatoes, cassava, yam, taro), coconut, fruit (bananas, guava, watermelon, pineapple), vegetables, and fish. Far from a low carbohydrate or high animal protein diet, this supplies 69% carb, 21% fat, 10% protein. They maintain immunity to modern diseases and have low insulin levels (almost half those of Swedes).

I decided to create a Kitavan diet analogue for analysis. They have an average caloric intake of 2200 kcal per day, so I aimed for that figure and incorporated the foods Lindeberg lists as their staples (above). The food list looks like this (click on images to enlarge for ease of reading):

The diet supplies 376g carbohydrate, 63g fat, and 64g protein.  The macronutrient analysis looks like this:

By energy, 66% carbohydrate, 24% fat, 10% protein, close enough to Lindeberg's reported 69:21:10 to serve as a valid measure.  It contains 52g saturated fat and supplies 20% of calories as saturated fat, again not significantly different from Lindeberg's reported 17% of calories from saturated fat.  Polyunsaturates and monounsaturates each contribute only 1% of calories.

Kitavans, photo source:  Staffan Lindeberg

The four fruits (one serving of each) supply about 72g of the total carbohydrate, which would mean an intake of about 36g of fructose.  Since the Kitavans have low insulin levels and don't have heart disease, cancer, diabetes, dementia, or any other disorder, they seem to provide evidence against the claim that more than 15g/d of fructose causes insulin resistance, etc.

The micronutrient analysis looks like this in tabular then graphic display:

The menu shows shortages in vitamin D and calcium.  Kitavans get plenty of sunshine so don't need dietary vitamin D.  My analysis assumed that they don't consume soft fish bones or make broth from fish bones, probably an incorrect assumption, and also does not account calcium they may get from drinking water (mineral waters can supply up to 500mg per liter), so their calcium intake probably exceeds the level in this menu.

 Kitavan fisherman, photo source:  Staffan Lindeberg 

One note about zinc:  Two thirds of the zinc supplied by this menu comes from one single oyster. Oysters supply 150mg of zinc per 100g serving, so a Kitavan needs only one oyster daily to bring the zinc level to well above recommended levels. 

In short, the Kitavan diet easily supplies all the essential nutrients at recommended levels, and affords a high immunity to modern diseases along with excellent longevity, without a high protein or low carbohydrate intake.

Paleo Diet pH: Does It Matter, part VII

Some people appear to believe that Stefansson's 12 month trial of an all meat diet published in JAMA proved that an all meat diet provides adequate skeletal nutrition for prevention of osteoporosis.

According to the JAMA report on the all meat experiment, Stefansson consumed ends of bones supplying about 100mg calcium daily (less than by Inuit). The report on the experiment states:

"The increased amount of tartar on Stefansson's teeth and the lack of evidence of lowered blood calcium offers an interesting field for speculation. There was no decreased density in roentgenograms of the hands at the end of the experiment when compared with the hand of a man on a general diet."

Testing only the hands with X-ray does not tell us whether he lost vertebral or trochanter bone; and X-rays don't have the ability to detect the small amount of bone density lost in one year.

In fact, the National Institute of Arthritis, Musculoskeletal, and Skin Diseases (NIAMS) has this to say about X-ray tests for bone density:

"X-Ray Tests

If you have back pain, your doctor may order an x ray of your spine to determine whether you have had a fracture. An x ray also may be appropriate if you have experienced a loss of height or a change in posture. However, because an x ray can detect bone loss only after 30 percent of the skeleton has been depleted, the presence of osteoporosis may be missed."

So the test used to evaluate effects of an all meat diet on Stefansson's bone density would only have detected loss of bone if he had lost 30 percent of his bone mass. Simply put, at the time of the experiment, they did not have a technology capable of detecting smaller yet significant changes in his bone mass.

Further, they don't report before and after X-rays of Stefansson, they report comparing Stefansson's hands to those of a man "on a general diet." Which can't tell us whether the diet had any impact on Stefansson's bones.

The failure of Stefansson's blood calcium to decline is not surprising, since body can prevent drops in blood calcium by extracting calcium from the bones and tissues. Low calcium in blood causes PTH release, which extracts calcium from bone to raise blood calcium to normal levels. Thus, on a calcium deficient diet, blood calcium will not go below normal until bone stores of calcium have been exhausted.

Stefansson reportedly had increased dental tartar, which indicates increased salivary calcium and phosphorus. What makes this happen?

This study showed that administration of PTH increases calcium and phosphorus in saliva:

Thus, we can surmise that Stefansson probably had increased PTH, which was probably resorbing bone to maintain normal blood calcium, simultaneously raising the calcium content of his saliva, producing increase in tartar. The calcium and phosphorus should stay in bones, not be deposited on the outside of teeth.

I also want to note that Stefansson consumed organ meats that supply vitamin C (brains, liver, etc). To that extent Stefansson did replicate an Inuit diet. He in fact made it very clear that to live on an all-meat diet requires replicating the Inuit diet in several important respects, including eating far more fat than protein, eating organs, etc.

As an experiment, I ate an all meat diet for more than one month. I ate ends of bones, but not every day, and liver once weekly. Within a few weeks, I developed severe muscle cramps indicative of mineral (primarily potassium) deficiencies. When I added vegetables and fruits back to my diet, the cramps diminished. This tells me that an all meat diet does not adequately provide me with potassium, for which I have to eat plants.