Monday, June 15, 2009

Histidine consumption prior to prolonged aerobic exercise as a method to increase myoglobin production potential

I was able to, with difficulty, find information regarding: the molecular weight of specicic amino acids in the human body as a percent of the total molecular weight of amino acids in the human body (; the composition of human myoglobin (,, the molecular weight of the various proteins that compose human myoglobin (

Thus I was by extrapolation able to estimate the difference between an amino acid's percent of total molecular weight in the human body in general compared to an amino acid's percent of total molecular weight in myoglobin. The idea being that the more the latter exceeds the former, the more the amino acids should be emphasized for consumption prior to prolonged aerobic exercise.

I found that certain amino acids comprise a higher percentage of the total molecular weight of myoglobin, compared to their percentage of the total molecular weight of amino acids in the human body.

My estimates (% of molecular weight of myoglobin, % of molecular weight of amino acids in body in general, the first stat divided by the second to produce a ratio for the third stat, the third ratio stat multiplied times the first stat to produce the fourth stat):

Table 1:

glutamate 10.4, 6.2, 1.7, 17.7; histidine 7.2, 2.1, 3.4, 24.5; tryptophan, 2.0, 1.1, 1.8, 3.6; lysine 14.9, 7.0, 2.1, 31.3.

The fourth stat in table 1 is an attempt to measure an amino acid's importance at a time when the intent is to increase myoglobin production potential in the body (at such a time amino acids that are especially important for myoglobin production should be prioritized).

The fourth stat in Table 1 is the highest for lysine (31.3), and the second highest for histidine (24.5).

Using the method used in the previous post of comparing ('essential' amino acids only) an amino acid's percentage of total pieces of amino acids in myoglobin, to percent of total mg per kg body weight requirements, the figures for histidine are 12% and 6% a ratio of 2.0 (third stat in table 1). The 2.0 ratio figure times 12% = 24 (fourth stat in table 1) as an indicator of importance for timely production of myoglobin specifically, which is almost the same as the 24.5 figure for 'the fourth stat' for histidine derived from the method used today.

In the previous post ( I reported that since lysine's mg per kg estimated requirement is 17% of the total mg per kg estimated requirements for "essential" amino acids in the human body, whereas 29% of the pieces of amino acid in myoglobin are lysine, my estimate was that lysine should be emphasized when attempting to increase the body's myoglobin production potential.

The ratio of 29/17 = 1.7 for number of lysine amino acids in myoglobin as a fraction of total number of amino acids in myoglobin compared to kg per mg requirement for lysine as a fraction of total essential amino acids kg per mg requirements, is similar to the ratio I report in this post in table 1 for lysine's molecular weight as a fraction of total molecular weight in myoglobin compared to lysine molecular weight as a fraction of total molecular weight of amino acids in the human body in general.

The idea has been: improvement in terms of the amount of energy expended prior to the onset of fatigue lead to improvements in cardio health; such improvements can be facilitated by providing the body with precursors for creatine and myoglobin (which rise to high levels in the blood of marathoners during and after the marathon) prior to the body engaging in prolonged aerobic exercise.

Lysine's pre-eminent position in myoglobin, and dietary sources of lysine were discussed in the previous post; dietary sources of precursors of creatine was the subject of the post before that. In this post I discuss the importance of histidine, an important ingredient in myoglobin, and dietary sources of histidine.

The US National Rsearch Council stated in 1973, "there is no evidence that histidine is synthesized by mammals " ( Wikipedia now says, "After reaching several years of age, humans begin to synthesize it (histidine) and it thus becomes a non-essential amino acid" (

The popular and scientific literature has divided the amino acids such as those that are used to form myoglobin molecules into "essential", "conditionally essential" (or "semi-essential"), and "non-essential" groups. Histidine depending on the information source and the time at which the info source provided the info, has been classified sometimes as non-essential, sometimes as conditionally essential, and sometimes as essential.

Histidine originally was classified as non-essential, because the body is able to maintain the nitrogen balance without consuming histidine.

Then concerns began to develop, that there arise circumstances during which, due to lack of histidine in the diet and/or the body's inability to produce sufficient quantities, the body's supply of histidine becomes insufficient.

According to the 2007 WHO technical report "PROTEIN AND AMINO ACID REQUIREMENTS IN HUMAN NUTRITION" (, "Histidine is considered to be an indispensable amino acid because of the detrimental effects on haemoglobin concentrations that have been observed when individuals are fed histidine-free diets"...Histidine was accepted in the 1985 report as an indispensable amino acid in human adults, despite controversy regarding its essentiality...Kopple & Swendseid found that nitrogen balance was negative in healthy adults and uraemic patients when diets were devoid of histidine for 25–36 days...A recent study confirmed many of these findings and showed that histidine depletion over 48 days resulted in a fall in albumin and transferrin, as well as a 24–28% decline in whole-body protein turnover. Because of the extended period of time (>56 days)".

The WHO report describes how the body deals with histidine shortages: "When a histidine-deficient diet was consumed for a prolonged period, a decrease in haemoglobin, in conjunction with a rise in serum iron,was observed...histidine pools may be maintained through the release of histidine from the degradation of haemoglobin (75), or through the reduction in haemoglobinsynthesis (82)".

Histidine is probably under-emphasized in the popular and scientific literature due to its history of being considered a "non-essential", or "conditionally essential" amino acid. Even today, the venerable Wikipedia classifies histidine as "nonessential" (
Hemoglobin and myoglobin are both involved in binding and transporting inhaled oxygen so as to make the oxygen available to muscles utilizing oxygen (aerobic means, 'requiring air'). The WHO report's finding indicates histidine shortage could result in degradation or reduction of synthesis of myoglobin, which is produced in large quantities by marathoners during the running of the marathon.

Dietary sources of histidine (

egg white dried flakes 1 lb 8 g

canned tuna fish 1 lb 6g

beef round 1 lb raw or braised, 5g,

pork loin chops raw 1 lb 5g,

swiss cheese 2c 5g

pork loin cooked 1 lb 4g

roasted soybean seeds, 2c 4g

pumpkin and squash seeds roasted 2c 4g

lupin seeds 2c 4gcottonseed kernels roasted 2c 3g

pheasant 1 lb 3g,

nonfat dry milk 2c 2g,

turkey roast meat raw or cooked, 1 lb, 2g

turkey pastrami 1 lb 2g

almond butter 2c 2g

dried pumpkin squash seeds 2c 2g

almond 2c 2g

roasted sunflower seeds 2c 2g

Note: dried pumpkin seeds provide half the histidine value of roasted pumpkin seeds (most 'authorities' ignore such important distinctions).

In the previous blog-post (, I wrote that my first and second choices for providing the body with lysine, an important ingredient in the body's production of myoglobin, are soybean seeds and pistachios.

In the post before that, I listed my top choices for providing the body with the ingredients for creatine (the creatine level in marathoners rises during their run): "Pumpkin seeds (excellent source of methionine and arginine); dried egg white (excellent source of methionine and arginine); dry gelatin powder (excellent source of glycine); milk (good source of glycine); tangerine juice" (

Several foods are good at providing precursors for all the biochemicals thus far of interest: creatine (glycine, arginine, and methionine), and for myoglobin (lysine, and histidine). A few foods have already been picked out as sources for creatine and lysine. What foods that have not already been picked out, should be added to the list of pre-prolonged-aerobic-exercise foods?

Yet again I make my choice with an eye towards avoiding troubles with animal foods such as cooking and cleanliness (at a later time I'll list the cooked foods that are useful for producing creatine lysine histidine etc).

Two cups of lupin seeds provide as much histidine as one pound of cooked pork loin; however, lupin seeds are difficult to find; even 'Whole Foods' does not carry lupin seeds or cottonseed kernels.

As of now, my first choice to add to my ingredient list with an eye on providing histidine in my diet, is almonds/almond-butter, which are available at Whole Foods.

My second choice would be (preferably roasted not dried) sunflower seeds.

Thus so far, my ingredients list is:

pumpkin seeds (excellent for glycine methionine & arginine for creatine; excellent for lysine and histidine for myoglobin)

Dried egg white flakes (excellent for glycine, methionine & arginine for creatine; excellent for lysine and histidine for myoglobin)

Dry gelatin powder (conventional jello mix, health-conscious whole foods jello mixes lack gelatin) (excellent source of glycine, arginine, and lysine; good source of histidine, not a good source of methionine);

Tangerine juice (facilitates absorption of methionine and glycine used to build creatine).

Milk (good source of glycine, methionine, arginine, lycine, and histidine)

Pistachios (very good source of lysine, good source of methionine, glycine, histidine, & arginine) (could not find the preferred soybean seeds at Whole Foods)

Almonds (very good source of arginine, glycine, lysine, & histidine, good source of methionine) (preferred lupin seeds unavailable at store),

Off the bat I would award points to each of these foods based on how good a source they are for the nutrients of interest and how many nutrients of interest they are a good source for; this provides me with a basis for determining how much of each substance should be used. On this basis my estimate is that the concoction should use:

1 unit milk, 1 unit tangerine juice, 1 unit pistachios, 2 units almonds, 2 units gelatin, 3 units egg white flakes, and 3 units pumpkin seeds (adjusted to provide desired consistency with flavorings added for palatibility) (unit can be tablespoon, half-cup, whatever).

The idea is to combine this (unsavory?) nutrient-rich concoction with an undisciplined consumption of whatever it is that I feel like eating.

Interesting how the stars of the show that have been discovered so far, are eggs and seeds. An egg is like a seed of a chicken.

@2009 David Virgil Hobbs

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Saturday, June 13, 2009

Myoglobin, used by the body during prolonged aerobic exercise--providing the body with natural precursors

In the previous blog-post ( I discussed the foods that would provide the body with myoglobin and precursors to creatine. Seems whale-sushi would be the best source of myoglobin. I wanted to look for cleaner, simpler, sources of myoglobin precursors.

Looking at essential amino acids, an amino acid as a percentage of total essential amino acids in myoglobin, is one statistic (,,

The same amino acid's mg per kg body weight as a percentage of the total mg per kg body weight requirements for essential amino acids in total, is a second statistic (

The second statistic divided by the first gives you a third statistic. This third statistic shows the importance of the given amino acid in myoglobin, compared to its general importance in the body.

I find that lysine is the amino acid with the greatest score on this third statistic. Lysine also is the amino acid that is, compared to other amino acids, most present in myoglobin. Lysine is more present in myoglobin than any other protein/amino-acid.

Lysine's mg per kg body weight requirement is 17% of all the amino acid mg per kg body weight requirements combined; whereas, 29% of the 153 different proteins in myoglobin are lysine proteins. 29/17 = 1.7.

Thus I estimate that a good starting point for providing the body with precursors for myoglobin prior to prolonged aerobic activity would be substances that naturally provide high levels of lysine to the body.

Consumption of one substance, leaves less digestive power and stomach room available for another substance. All persons have limited digestive power, limited stomach space, and limited appetite. As a matter of timing, the substances that are especially required during prolonged aerobic activity should be consumed prior to prolonged aerobic activity and other substances that are not especially in demand during prolonged aerobic activity should be consumed at other times. Often, a food substance that rates especially high in terms of the presence of a given nutrient per ounce of the food-substance, also rates high with regards to certain other nutrients of interest also. The body is able to convert certain of the basic 20 amino acids into other of the basic 20 amino acids. A nutrient can be a precursor for more than one substance in the blood. All these facts add up to the conclusion that concentrating on a nutrient, lysine, that scores high when measured by the third statistic (described above) is a reasonable approach.

Leading sources of lysine (

1 lb egg white flakes 22 g
1 lb beef bottom round 13 g
2 cup pumpkin and squash seeds 12 g
1 lb canned tuna 12 g
2 cup egg white powder sifted 10 g
2 c soybean seeds 10 g
1 lb raw beaver meat 10 g
1 lb boneless pork loin 9 g
1.0 lb turkey pastrami 8 g
1 lb lamb foreshank 8 g
1 lb chicken roasting meat 8 g
1 12" pizza cheese meat veggies 8 g
2 c dry reg nonfat milk, 6 g
2 c egg yolk raw fresh 6 g
2 c egg whole dried 6 g
2 c cottonseed kernals 5 g
2 cup raw green soybeans 4 g
2 cup egg white raw fresh 4 g
2 c egg yolk dried 4 g
2 c scrambled eggs 4 g
2 c pistachio nuts 3 g
1 lb parmesan cheese 3 g
2 c hard boiled eggs 2 g

Notice how there are foods that are superior in terms of providing the body with what it needs to produce creatine, which are also superior for providing the body with what it needs to produce myoglobin. Looking at the above list my first instinct, is that the food that I would use to provide a basis for internal myoglobin production would be soybean seeds (my second choice would be pistachios). It's nice to be able to skip the fuss of dealing with meat poultry fish etc.

Egg white flakes (concise informative page at, pumpkin/squash seeds, and milk have already been selected as precursors for the amino acids used by the body to synthesize creatine. It is reasonable to suspect that the diversity produced by combining soybean seeds with pumpkin seeds would be advantageous. .

The authoritative Wikipedia's blythe list of "good sources of lysine" is unintentionally deceptive as are most such lists. According to the venerable Wikipedia, "good sources of lysine are foods rich in protein including meat (specifically red meat, lamb, pork, and poultry), cheese (particularly Parmesan), certain fish (such as cod and sardines), and eggs" (

The wiki article lists lamb as if it was equal to egg whites for lysine content. Actually, dried egg-white flakes (can be eaten raw because pasteurized) give you three times as much lysine per pound as lamb; plus, dried egg whites do not require cooking and mix easily with other foods into one drink or dish.

Even with regards to eggs themselves, we would be missing out on some important facts if we simply took Wiki's word for it that eggs are a good source of Lysine.
As it turns out, the lysine value in eggs ranges enormously from 2 grams lysine in two cups chopped hard boiled eggs to 22 grams lysine in one pound of dried egg white flakes.

The general idea is to provide the body with precursors for substances that marathon runners start out with at a normal level in their blood, which then increase to a high level in their blood through production/release of such substances in the bodies of the marathoners during and after the running of the marathon. This should increase the amount of effort that the body is able to expend, prior to the onset of fatigue. This increase in fitness in turn should result in improved cardio-vascular health.

@2009 David Virgil Hobbs

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Friday, June 12, 2009

Heart health and aerobic exercise performance enhancing super-foods

Building on the work of the previous two nights (, (, I decided to take a stab at estimating what would be a good pre-game meal or snack for someone about to run 26 miles in a marathon or say 7 miles in a soccer game.

My theory was that the body should prior to the prolonged act of aerobic exertion, be loaded with the precursors to the substances that are at normal levels in the blood of marathoners prior to the start of the marathon, but end up at a high level in their blood during and after the marathon.

My idea was not that marathoners are an example of disease, but rather that they are an example of health. Most people: lack the energy to run a marathon; or, develop pains and injuries that interfere with the ability to run the marathon.

In support of my contradiction of the theory that elevated levels of creatine found in the blood of marathoners during and after a race indicate that running a marathon is an unhealthy activity,I discovered a dramatic and poetic example in nature:

"(1847) a German scientist named Justus von Liebig proposed that creatine is necessary to support muscular activity when he observed that wild (active) foxes contain more intramuscular creatine than foxes kept in captivity" (

Humans synthesize creatine within the body by using three ingredients: arginine, glycine, and methionine (

I finally found an online database that ranks various foods by how much of a particular type of protein they contain, at

Based on a cursory examination of the results from this database, I concluded that the best snack for providing the body with what it needs in order to produce creatines such as ck-mb, would contain the following:

Pumpkin seeds (excellent source of methionine and arginine); dried egg white (excellent source of methionine and arginine); dry gelatin powder (excellent source of glycine); milk (good source of glycine); tangerine juice (facilitates body's absorption of methionine and glycine,(see

Personally I'd mix these all up in a blender combined with some ingredients added for the sake of flavor and palatibility.

Another substance that increases in the blood level of marathoners when they are running the marathon, is myoglobin.

Along the lines that the events during the marathon in the bodies of the marathoners illustrate processes in bodies that are unusually healthy to the point of being able to run a marathon at a fast pace, my idea was that before engaging in some form of prolonged aerobic exercise, one should consume substances that provide the body with what it needs in order to produce myoglobin.

Yet again, I found poetic slash dramatic confirmation of my idea in nature:

"The richest source of myoglobin is the muscle of aquatic diving mammals, such as seals or whales, since these tissues need a very rich store of oxygen to see them through long anoxic periods during a dive" (

"The role of myoglobin as an oxygen storage protein in the muscles of diving birds and mammals is well-established"(

"Mammals such as whales and seals are capable of diving to incredible ocean depths...The sperm whale is able to dive down 3,000 meters (9,900 feet). That's *eight times* the height of the Empire State Building! Other deep-diving mammals include the bottlenose whale (2,000 m), the killer whale (1,000 m) and the elephant seal (700 m)" (

I estimate as of now that superior sources of myoglobin to be (in approximate order of quality as a source of myoglobin):

(the pinker when eaten the better for these foods so long as the pinkness does not introduce risks of infection)

whale sushi; tuna sushi; steak cooked to rare; heart meat; cooked whale; cooked tuna; poultry dark meat; chicken legs; chicken thighs.

I base my estimate that such are the best sources of myoglobin on the following sources:

"Myoglobin: The pigment in muscle that carries oxygen" --

As of now my opinion is that these foods that contain the precursors to creatine and myoglobin combined with prolonged aerobic exercise will improve heart health.

My estimate is that the foods will promote the body's ability to exert itself during prolonged aerobic exercise, which in turn will lead to improvement in cardiovascular health.

@2009 David Virgil Hobbs

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Thursday, June 11, 2009

Jogging is bad for you 'cause it elevates blood-levels of heart disease markers theory of Dr Al Sears debunked part II

Dr. Al Sears bases his 'revolutionary insight' that prolonged aerobic exercise damages the health, on two pillars. Beyond these two pillars of Hercules (Hercules, musclebound and heavy avoider of prolonged merely aerobic exercise) lies his lost Atlantis filled with a deep respect for couch potatoes who avoid prolonged aerobic exercise, combined with just abhorrence of those who dare to engage in prolonged aerobic exercise.

One, he alleges based on a 1995 study by Queseda-Sanchez, that the increase in blood level of LDL and TG, and the increase in oxidization of such that occurs as a result of running the Marathon, proves that prolonged aerobic exercise is unhealthy. I demolish this argument at in the post I put up yesterday June 10, 2009.

His second pillar:

"Worse yet, a report in the American Journal of Cardiology found distance running disrupted the balance of blood thinners and thickeners elevating clotting levels and inflammatory factors (footnote 5, referring to Siegel A, Lewandrowski EL, Chun KY, et al. Changes in cardiac markers including B-natriuretic peptide in runners after the Boston Marathon. American Journal of Cardiology, 2001 Oct 15; 88(8):920-23, ). These changes are signs of heart distress, not a heart that's becoming stronger after exercise" (page 18, 'the Doctor's Heart Cure: Beyond the Modern Myths of Diet and Exercise', 2004, ).

Now I proceed to demolish the second pillar.

None of the substances for which Siegal tested the Boston Marathoners, are known as "blood thinners", or "blood thickeners".

Siegal tested for five different substances that have been used as markers for heart disease (their level of the blood in persons sick with heart disease is elevated). He tested for levels of myoglobin, ck-mb, cntI, cntT, and BNP in the blood of marathoners before and after they ran the Boston Marathon.

Siegal found evidence that supposedly 'condemns' the Marathoners. He found that myoglobin and ck-mb levels are at elevated levels in Marathoners both 4 hours after the end of the Marathon and 24 hours after the end of the Marathon.

He also found evidence to exonerate the Marathoners:

Levels of substances in the blood can be looked upon in relation to the upper level for what is considered normal. This can be expressed as a percentage--the level in the blood as a percent of the upper limit for what is considered normal. Here are these percentages for Marathoners prior to starting to run the Boston Marathon, as reported by Siegal:

Myoglobin, 43% 1998-99, 89% 2001; CK-MB 42% 1998-2000, 53% 2001; ctnI <1% 1998-2000, 5% 2001; ctnT <10% 2001; BNP 17% 2001.

Similarly the level of a substance in the blood compared to the upper limit of the normal range for that substance can be expressed as a percentage for substance levels found 4 hours and 24 hours after the Marathon by Siegal. These percentages as reported by Siegal:

4 hours after end of Marathon: ctnI 10% 1998-2000, 14% 2001; ctnT 41% 2001; BNP, 18% 2001.

24 hours after Marathon: ctnI 9% 1998-2000, 1% 2001; ctnT <10% 2001; BNP, 49% 2001.

Thus it is clear that:

With all substances tested for (myoglobin, ck-mb, cntI, cntT, and BNP), the marathoners were at a normal (myoglobin, ck-mb) or very low (cntI, cntT, BNP) level prior to starting the Marathon race

With all substances tested for except myoglobin and ck-mb, the marathoners were at a normal (ctnT) or low (ctnI, BNP) level 4 hours after the race

With all substances tested for except myoglobin and ck-mb, the marathoners were at a normal (BNP) or low (ctnI, ctnT) level 24 hours after the race

To look at these results and declare that they prove that running the Marathon is bad for the health because it throws the 'blood-thinner' vs 'blood thickener' balance dangerously out of balance, is ridiculous.

Myoglobin is the earliest and most primitive marker used to detect heart disease (the higher the myoglobin the more likely heart disease exists supposedly). Myoglobin levels rise when muscles are suffering temporary mild injuries as they do during long distance running. Myoglobin is used by the muscle cells to store oxygen so it is natural that it's level would rise during exercise.

CK-MB succeeded Myoglobin as the prince of the markers detecting heart disease (supposedly the higher the ck-mb level, the more likely the existence of heart disease). It helps skeletal muscle to utilize ATP so it is natural that it would rise in level during exercise. Elevated levels of CK-MB are commonly known to accompany extreme physical exercise, muscle weakness, and mild levels of dehydration such as one would expect during the running of a Marathon.

A paper co-authored by Siegal himself that came out in 2006, after Dr. Siegal's report of 2001 and after Dr. Sears' book came out in 2004, says: "Given their rich abundance in skeletal muscle and owingto the expected muscle injury related to prolonged running,elevations in myoglobin, CK, and the isoenzyme CK-MB more likely reflect acute skeletal muscle injury due to exer-tional rhabdomyolysis (5) with a cardiac signal somewhat obscured" (
Saenz, Adam, " Measurement of a Plasma Stroke Biomarker Panel", Amer J Clin Pathol, 2006).

Cardiac-specific Troponins such as ctnI and ctnT seized the throne as markers detecting heart disease, replacing CK-MB. Cardiac-specific Troponins are preferred to ck-mb because they are found only in the heart whereas ck-mb composes 1% of the skeletal muscle CK. Cardiac-specific Troponin levels in the blood are not affected by acute or chronic muscle injury of the type experienced by marathoners during marathone, whereas CK-MB levels are. The Cardiac-specific Troponins can be detected in blood in which the CK-MB cannot be detected. Even microscopic myocardial necrosis can be detected by measuring cardiac-specific Troponin levels.

Therefore the Al Sears' interpretation of the Siegal 2001 study of Boston Marathoners (that the study proves that prolonged aerobic exercise is bad for you), relies on outmoded markers of heart disease and ignores the currently favored markers used for identifying the presence of heart disease.

Sears' interpretation favors as markers substances which the body uses to facilitate physical exertion and which are commonly known to rise in terms of level in the blood during intense physical exertion. The cardiac-specific Troponin markers are apparently much less effected by simple non-diseased states of physical exertion compared to CK-MB and Myoglobin.

BNP is a peptide hormone does nice things like 'promote urine excretion, relax blood vessels, lower blood pressure, and reduce the heart’s workload' ( High BNP blood levels are also associated with heart disease and used as markers to detect heart disease. It is like a new rookie marker who suddenly rises to stardom amongst markers. At the time of its rise to stardom, the world had begun to shed its ignorant notion that high levels of substances that are at high levels in the blood of sick persons, are evil things.

The BNP level in the Marathoners was low compared to the upper limit of that considered normal both before and 4 hours after the Marathon. Then it went up to a normal level 24 hours after the Marathon. Therefore even those (such as Dr. Sears) who inflexibly associate elevated BNP levels with heart disease cannot say the BNP levels indicate the Marathon caused heart disease.

My estimate as of now is that the measurements taken by Siegal show, not prolonged aerobic exercise inducting disease into the body, bur, rather, changes that the healthy body goes through during and after exercise.

A healthy body running a marathon:

Starts out at a normal myoglobin level, goes up to a myoglobin level about sixteen times greater than normal four hours after the Marathon, then gradually declines to a myoglobin level about three times greater than normal 24 hours after the Marathon has ended.

Starts out at a normal CK-MB level, goes up to a CK-MB level about three times normal 4 hours after the Marathon has been ended, continues up to a CK-MB level that is eight times greater than normal 24 hours after the Marathon has ended.

Starts out at a ctnI level that is extremely low (in marathoners 3% of the upper limit of the normal range), goes up to low (in marathoners 12% of the upper limit of the normal range) level 4 hours after the marathon has ended, and then declines to a very low (in marathoners 5% of the upper limit of the normal range) level 24 hours after the marathon has ended.

Starts out at a ctnT level that is very low (in m arathoners <10% of the upper limit of the normal range), goes up to normal (in marathoners 41% of the upper limit of the normal range) level 4 hours after the marathon has ended, and then declines to a very low (in marathoners <10% of the upper limit of the normal range) level 24 hours after the marathon has ended.

Starts out at a BNP level that is low (in marathoners 17% of the upper limit of the normal range), stays at a low (in marathoners 18% of the upper limit of the normal range) level 4 hours after the marathon has ended, and then rises to a normal (in marathoners 49% of the upper limit of the normal range) level 24 hours after the Marathon has ended.

Note that these admirable marathoners, do not start out with an abnormal level of myoglobin or CK-MB. They start out with these at normal levels, and then during or after the run their bodies increase the level of myoglobin and CK-MB in the blood to abnormally high levels.

Thus it would appear to be an error to produce a sports drink that contains myoglobin and ck-mb that one is supposed to consume in order to achieve athletic conquest during prolonged aerobic endeavors.

Rather, the intelligent option would seem to be a meat, fish, protein and organic-acid based sports food that contains natural substances (minerals or derived from plants or animals) which enhance the body's ability to increase myoglobin and CK-MB levels in the blood without myoglobin and ck-mb being introduced into the body from the outside environment.

Siegal's data indicates that the bodies of the Marathoners produce and utilize myoglobin (a protein), ck-mb (an enzyme, an organic acid found in meat and fish), ctnI (a protein) and ctnT (a protein) during the marathon, and BNP (a protein peptide hormone) after the marathon. These substances are proteins and an acid, not fat.

By way of contrast, according to Sears, Marathoners 'burn fat' and this trains the body to store fat for use as a fuel.

Dr. Sears in basing his condemnation of prolonged aerobic exercise on the Siegal 2001 study, ignores the fact that the Siegal study ignores the possibility that certain of the substances tested might when at elevated levels in the blood, counteract the effects of high blood level elevations of other substances tested, or counteract the effects of biochemical changes produced by exertion which produce symptoms of such changes such as high blood levels for such substances.

Dr. Sears bases his persecution of prolonged aerobic exercise on a study which ignores blood levels of substances, high levels of which are, aside from exercise induced physiological states, associated with health as opposed to sickness. Such substances have been found to counteract the substances regarding which high blood levels are feared by Dr. Sears.

The 2001 Siegal study focused on substances that increase in terms of presence in the blood during exercise. It ignored substances that decrease in terms of presence in the blood during exercise.

There are substances which rise in terms of blood level in proportion to the level of fatigue; when a person is ill they fatigue easily. It is basically a leap of faith and poor logic to assume that if some substance is at an elevated level when sick, this means that elevations in levels of such generally indicate the presence of sickness.

In a nutshell to rephrase an important point, there are substances that increase in terms of level in the blood when the body is fatigued, and also during sickness. This is because during sickness, activities that are not usually tiring become tiring. The substances rise to elevated levels during sickness and also during health during and after physical exertion, because during sickness, being a couch-potato is as fatiguing as running the marathon is when healthy. The conclusion that since these substances are at elevated levels during sickness therefore an elevation of their levels signifies the presence of sickness, is a mere leap of faith.

Surprisingly, Siegal, who himself produced the 2001 report which Dr. Sears mininterpreted into something to base his 'prolonged aerobic exercise is bad for you' 'revolution' on, was still in 2006 co-authoring a report that declared:

"In our study, 70% of runners had a measurable level of troponin T after the race, and 23% had levels higher than the manufacturer’s recommended cutoff value. These results provide strong evidence of subclinical myocardial injury in middle-aged marathon runners...We report significant elevations in the levels of cardiacTnT, D dimer, MMP-9, and a multimarker stroke index innonprofessional middle-aged marathon runners before and after competition. The changes in troponin values in 70% of our subjects most likely reflect myocardial stunning and/or true ischemic cell injury" (Saez, 'Measurement of a Plasma Stroke Biomarker...', American Journal of Clinical Pathology, 2006,

Translation: Saez who co-authored the study with Siegal, is waving the alarm flag, because the marathoners had a Troponin T or ctnT level of 0.01 ng/ML pre-marathon, and this rose to 0.03 ng/ML after the marathon.

Absolutely un-frigging believable! the ctnT level of the runners starts out at 10% of the upper limit for the normal range before the marathon, and ends up at 30% of the upper limit for the normal range after the marathon, and Saez and his co-author Siegal darkly insinuate that this indicates that running the marathon inflicts myocardial injury on the marathoners!

Incredible. If Siegal has been so unable to learn from his 2001 study so as to be able to notice that the ctnT level in marathoners scrutinized in his own studies has consistently both before, 4 hours after, and 24 hours after the marathon been less than 50% of the upper limit of what has been considered normal, how do you expect him to master the more subtle points that I, a mere dabbling generalist, have made earlier in this post with regards to his 2001 study?

Siegal apparently after his 2001 study continued to plow ahead testing out ever more and new bad guy markers whose presence in increased levels is associated with sickness. This time the new bad guy markers are 'De dimer', 'MMP-9', and a 'multimarker stroke index'!

The details regarding the new 'bad-guy' markers are another matter, but it is apparent that Siegal amonst other conceptual failures has failed to understand what I was able to grasp after reading his 2001 report, and what even the be-knighted general consensus ( has recently begun to understand: the fact that some substance is elevated in the blood when people are sick does not mean that it is a bad guy substance.

Note: Siegal's attempt (in his 2001 report) to verbally express in plain text the contents of his data tables is confusing. The confusion is worsened due to: the non-html-table nature of his tables; the breaking up of the tables into several tables; the lack of use of 'percent as relative to upper-level-of-normal' and 'percent of total population' figures. What do you expect, html tables are beneath the dignity of Roxbury I mean Harvard University and it's disdain for the 'overqualified'. I estimate that Siegal would have understood his own results better if he had worked with HTML tables which can easily be annotated.

@2009 David Virgil Hobbs

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Wednesday, June 10, 2009

Jogging is bad for you -- the new theory of Dr. Al Sears debunked

Dr. Al Sears has set forth a revolutionary theory that aerobic exercise such as long distance running is bad for you (linked to at the George Noory Coast to Coast website This theory has apparently not yet been refuted by anyone or reconciled to and compared with the traditional theory adhered to by almost everyone even now, that aerobic exercise such as long distance running is good for you.

Dr. Sears in making his arguments combines: assertions not backed by evidence or citations of scientific literature; evidence that he says is backed by scientific literature without providing a footnote linking to the study; evidence supposedly backed by scientific literature that is footnoted and linked to a study.

Thus a mere assertion takes on the color of a hypothesis strongly supported by data.

His argument that long distance running is bad for you is combined with: arguments that long distance running does not improve the health and arguments that anaerobic type interval training boosts the health more than aerobic-type nonstop training like long distance running. These arguments are presented jumbled up together as if proving that long distance running is useless or not as good for you as intervals or wind-sprints, proves that long distance running is bad for you.

With regards to the idea that long distance running is bad for you, Sears presents two pieces of evidence:

A 1995 study by Sanchez-Queseda showing that long distance running increases the level of LdL (low density lipoprotein) and TG (triglyceride)in the blood and increases their oxidation (it is a commonly held belief that high levels of LDL and TG lead to blood clots and heart attacks)

A study showing that aerobic exercise disrupts blood thinner vs thickener level and elevates clotting level and inflammation

Also Dr. Sears asserts without providing any evidence that I can see, that: long distance type aerobic exercise shrinks the heart and the lungs; and, aerobic exercise results in the harm of the body producing fat for use as a fuel.

In this post I take up the argument re the long distance running type aerobic exercise increasing the LDL and TG levels and the level of their oxidization in the blood of the long distance runner during and after the long-distance aerobic exercise.

Sears' book that presents his theory that aerobic exercise is bad for you, was written in 2004; yet one of his main three evidential arguments against long distance running is based on a 1995 study.

Even an amateur such as myself could easily find in one evening, several studies that came out between 1995 and 2004 that contradict Dr. Sears' argument.

Several studies that have been done since 1995 have shown that persons who engage in aerobic long distance running type exercise have in their blood, both before they exercise and during and after the exercise relatively high (compared to less exercised individuals) levels of substances that counteract balance and neutralize increased levels of LDL and TG and increased oxidization of LDL and TG.

Even person who do not regularly exercise, produce during and after exercise elevated levels of substances that counteract balance and neutralize high levels of LDL and oxidization of LDL in the blood.

Dr. Randolph Howes has produced a lengthy and impressive pdf that challenges the whole taken for granted notion that high levels of LDL and high levels of LDL oxidization have anything to do with heart disease in the first place.

Although Dr. Sears enunciates the principle that wisdom is to realize that what is important is what happens to the body after exercise and that this is not the same thing as what happens to the body during exercise, Dr. Sears is focused on the elevated levels of LDL and TG in the blood during long distance exercise.

the consensus opinion as of 2009 as reflected by a review of the literature regarding the subject of elevated levels of oxidants caused by exercise: such elevated levels of oxidants may be healthy in that they trigger and promote reactions in the body which produce anti-oxidants or other beneficial chemicals. Meaning, these chemicals signal the body that the body has exercised, and prompt the body to react to the exercise by producing wonderful natural wholesome chemicals.

sears ignores that even the exercise that he adores and pushes, anaerobic exercise, releases into the body the same substances that he loathes, which are released into the body by the aerobic exercise that he despises.

Even Sanchez-Quesada himself, in a 1998 article coming out three years after the 1995 article Sears bases his argument on, argues that ascorbic acid as found in orange juice counteracts the increased susceptibility to oxidation of LDL that is caused by intense aerobic exercise.

I personally know from having studied training from the point of view of performance improvement, that it is a myth that interval training of the type enthused over by Dr. Sears, is 100% anaerobic and 0% aerobic.

Actually to some extent interval wind sprint type training is aerobic. Thus aerobic training of the type Dr. Sears despises, improves performance and results when it comes to the anaerobic training that Dr. Sears adores.

Anaerobic improvement promotes aerobic improvement and aerobic improvement promotes anaerobic improvement so one could say they are like two sides of a coin. I suspect that aerobics prepares the mind and the body for anaerobics.

Everybody know that if if you give a person a physical work level that outstrips his nutrient intake you can work him to death. Such a worker would be better off limiting his activities to correspond with his limited nutritional intake.

It is common sense that since healthy nutrients enhance athletic performance, this means that athletic performance uses up, depletes, the beneficial chemicals in the healthy nutrients.

Therefore with regards to point number one, the alleged harm caused to the body by long distance running type aerobic exercise due specifically to the increase in production and oxidization of LDL and TG, the logic and the evidence is overwhelmingly against Dr. Sears.

As of now I am convinced that the rest of Dr Sears' arguments alleging that aerobic exercise is harmful will likewise collapse.

My natural tendency is to sometimes feel like going out and running say 9 miles slowly non-stop. This is my way of recovering from the interval training of the type advocated by Dr. Sears.

Sometimes if the choice is between interval training and not doing anything, I will choose to not do anything whereas it would have been better if I had followed the alternative of doing slow nonstop long distance running.

Sometimes if I have not been exercising for a few days, long slow non-stop running comes naturally to me as the first thing to do when I start exercising again. The slow running loosens me up and prepares me mentally and physically for the challenge of the interval type running. Similarly the general consensus: increase in free radicals produced by exercise promotes healthy reactions that neutralize the supposedly harmful substances that instigate these reactions and also accomplish other beneficial effects.

Long distance nonstop running sometimes improves my sense of physical and mental well-being more than interval training. Quite possibly the optimal course of action for me is following my own natural inclinations, mixing wind-sprint interval type training with long distance non-stop runs.

I am an individual, different from all other individuals on earth. What is good for my mind might be different from what is good for the minds of others. What is good for my mind could be good for my body.

I've heard that successful men rest from one type of activity by performing another type of activity. Likewise, one could rest from aerobics through anaerobics and vice versa.

I say this all as someone who is not good at long distance running and would prefer to have to do it as little as necessary to maintain mental health.

I simply find that sometimes long distance running is the superior course of action; I and millions of others resent (or would resent if we knew about Dr. Sears) the implication that by going out and running a few miles nonstop slowly we are damaging our bodies.

We resent the idea of facing disrespect in society, unemployment and even high insurance payments simply because sometimes we like to go on long slow runs.


@2009 David Virgil Hobbs

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Tuesday, June 09, 2009

American Indian vs Whites Conflict Level of Intensity relative to population size c. 1835 AD estimated

Joseph Smith Jr (,_Jr. ), who lived from 1805 to 1844, was the author of the 'Book of Mormon' ( , this site has the best version of the Book of Mormon, lots of chapters on one page that you can use the hilite and word search on, the poor website needs money). The main topic of the Book of Mormon is roughly speaking, unrecorded history of war between whites and American Indians prior to the arrival of Columbus etc c. 1492.

So I wanted to be able to visualize in my mind, what the fighting between the American Indians and the US whites was like during the time of Joseph Smith, as I felt this would help me to better understand Mormonism. I wanted to understand the level of conflict from the perspective of a 21st century person.

As usual researching the subject took too much time and energy because of writers having left important information out of the picture in the process of spewing out little nuggets of information. I had to draw together several different sources of info to make several extrapolations in arriving at my estimates regarding what the intensity level of the fighting was like relative to population size of the whites and the American Indians.

I wanted a visual picture that I as a 21st century person could understand, meaning, relative to the modern population of 300 million in the US, what would the annual war casualties be, if the proportion of casualties relative to total US population were to be the same as it was in the days of Joseph Smith, around 1835 AD.

My estimate as of now:

The American Indian violence in the US on average, from 1775-1894, 119 years (estimated US population in 1835 15 million, US native population 1 million), was proportionally speaking in relation to a US population of 300 million something like: US: 300 million population, 3200 killed per year, 3200 wounded per year, 1350 captured per year; American Indians: 20 million population, 7600 killed per year, 7600 wounded per year, 2300 captured per year. Imagine this continuing, year after year for 100 years, and you have some idea regarding the intensity level of the conflict.

In the 20th century, the US did not have war in every year. The US had war in about 20 of those 100 years. If you imagine the 119 years of warfare with the American Indians from 1775 to 1894 as five wars each lasting four years, the casualties in the wars with the American Indians can be looked upon as five wars each lasting four years, with each war on average, involving casualties as follows: 76,000 whites killed; 76,000 whites injured; 32,000 whites captured. American Indians: 180,000 killed; 180,000 injured; 55,000 captured.

Thus one can see that during the 1800s when Joseph Smith lived, the conflict between whites and American Indians was more than a mosquito bite.

Comes a time when we have to give up the childish attitude that violence between American Indians and whites can be understood simply by the amount of persons seen shot during cowboy movies about American Indians on TV.

Proportionally speaking, the violence in the 1800s between Whites and American Indians, in and of itself and aside from the other conflicts of the US, was approximately equal relative to the size of the US society, to US combat deaths in 8 Vietnam wars, or US combat deaths in WW I and WW II combined.

Thus Joseph Smith produced his anti-American-Indian Mormon religion during times involving what must have seemed like unceasing, eternal large-scale warfare involving Whites against American Indians.

At the same time the stats indicate the majority of Whites and American Indians never engaged in violence between Whites and American Indians.

Seems any time there is war and violence, the majority forget about the non-violent majority. Two different groups living peacably side by side, does not make the headlines and get turned into movies as much as two groups fighting.

If a group of people of 20 million (the US population today is 300 million twenty times larger than the US population of 15 million in 1835; , in 1835 the native population in the US is estimated to have been 1 million) suffers 7600 killed in war every year, that means roughly speaking that a male from said group who lives to age 75 has over the course of his lifetime about a 6 percent chance of being killed in war. This would seem to leave plenty of room for persons from the group who are not involved in violence.

My estimate is that respected scholars like Russell Thornton (who wrote a book entitled 'American Indian Holocaust' and is supposed to be the leading authority on American Indian demographics) overestimate the extent to which the American Indian was destroyed by the Whites.

Today in the US population, about ten percent of the Y-dna chromosomes are haplogroup Q, the American Indian haplogroup. Compare that to the American Indian population of one million being 6 percent of the total US population of 15 million non-Indian plus 1 million American Indian in 1835. Despite the most famous and classical period of white vs American Indian conflict, the 'Indian Wars' from 1865 to 1898, the percentage representation of the American Indian population in the US population genetically speaking, seems to have increased.

Sources of Extrapolations

US population c. 1835 AD
Texas state census
US population in 1850 was 23.2 million, 1860 it was 31.4 million; based on this I estimate the US population was 17.2 million in 1840, 12.7 million in 1830, 14.9 million in 1835

US whites killed in conflicts vs American Indians,M1
'the Captured', by Zesch, 2005, p 235-6.
19,000 whites were killed due to conflict with American Indians during the 119 years from 1775-1894 according to US Dept of Interior report of 1894. That comes to 160 per year.

US whites wounded in conflicts vs American Indians
During the 1865-1898 Indian Wars US wounded was about equal to US killed

US whites captured,M1
'A Fate worse than death', by Michno, 2007, p 470
1000 Americans captured from 1860-1875, that is 67 per year.

American Indian population in US c. 1835 AD,M1.
'American Indian Holocaust', by Thornton, 1990, p 31-32
Russell Thornton's (supposed to be the leading scholar on this, I should get a nobel prize for wading through reams of his verbiage to extract this) estimate is that in 1492 when Columbus arrived, what is now the US contained 5 million natives or American Indians; and Canada 2 million; in 1900 the US contained 250,000 American Indians and Canada 100,000; the rate of change from 1492 to 1900 was linear. Thus I (not Thornton)) estimate that in 1835 the American Indian population in the US was 1 million, and the American Indian population of Canada was 400,000.

American Indian haplogroup representation in US population in 2006

American Indians killed,M1
'the Captured', by Zesch, 2005, p 235-6
45,000 American Indians were killed in the 119 years from 1775-1894 according to an 1894 US Dept of Interior report. That comes to 380 per year.

American Indians wounded
During the 1865-1898 Indian Wars US wounded was about equal to US killed; so for now I estimate the same ratio held for American Indians. However Michno reports that during the Snake War (see section below re American Indians captured), 985 American Indians were killed, 209 wounded, and 303 captured.

American Indians captured
'the Deadliest Indian War', by Michno, 2007, p 345
During the Snake War, the American Indians captured was 30% of the American Indians killed.

@2009 David Virgil Hobbs

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Saturday, June 06, 2009

Mormonism: it's insights, it's distortions, it's negative and postive influences

I met and shook hands with Danny Ainge at the Hannaford supermarket in Waltham MA during the month of May 2009.

Later I discovered that when I met him, he had just had a heart attack, a big thing for an athletic relatively young man. I sort of marvel at the coincidence of meeting him right after he had the heart attack.

I shook his hand, told him about the emails that I had sent the Boston Celtics. He twice told me that he gets "thousands of emails". I gave him a chance to volunteer a method by which I could communicate with him. He did not reject the idea of further emails being sent, or of paper letters being sent.

I told him about me shooting at rates of up to 40% from up to 27 feet from the basket with my eyes closed when shooting basketball shots; I told him about me sprinting 20 yards keeping the soccer ball off the ground but close to my body. I told him I realized that if everyone was as talkative as me, life would become unbearable for him. I felt as if it would be improper to take too much of his time talking.

After I met Danny Ainge, I read up about him on the internet, discovered that he was an active Mormon. So I read up on the Mormon religion on the internet.

My first reaction was that people who criticize Mormons develop tunnel vision as a result of which, they lose a sense of perspective proportion and relativity, failing to take into account how protestant christianity, Catholicism, and non-Christian religions can also be found to be defective and faulty.

Seems Mormons consider the Book of Mormon to be some kind of fictional novel inspired by God, similar to how Christians consider the text in the Bible to be inspired by God. Question becomes, what is the influence of people who ignore the fact(?) that the writer of their special fiction novel 'holy scripture', pretended to be transmitting words dictated by angels when in fact he was just creating a special work of fiction?

I do not claim to be an expert on Mormonism so you can forgive me if I spew out a little humor, exaggeration, and mistakes setting forth my understanding of Mormonism having spent a few hours tonight reading about it:

My Idea as of now re The Book of Mormon Story:

Long ago, (c. 600 BC) half of a group of white jewish immigrants to America turned black due to their wickedness and fought with the good white half; they went through a unified phase after Christ visited America; then there developed division between anti-christians and Christians and the anti-christs won and exterminated the Christians; goodness turns a person's skin white, and wickedness turns it black; the lighter-color a person's skin is the better a person he is; c. 1800 AD Mormons arrived and discovered this history of skin color in America, which according to them, contains the most profound lessons ever revealed to mankind.

Mormonism's Message to Mankind (most important message ever, they say):

1) Dark-skinned people like American Indians are genetically evil, white-skinned persons are genetically good;

Extrapolations based on Supremely Important Mormon message to mankind:

1) In modern times, whites are good and stay good whatever they do, and dark-skinned people are evil and stay evil whatever they do. This is because when whites become evil their skin color turns dark and when dark-skinned people become good their skin color turns white; at the same time there have been no reports of person's skin color changing. True some evil dark Lamanites joined the Nephilites and vice-versa, but when they changed sides there was a corresponding change in skin color.

2) In the old days things were different, good white people used to become evil and dark-skinned, and evil dark people used to become good and light-skinned. This we know from the inspired Book of Mormon.

3) The whiter a person's skin is, the better a person he is. This can be understood as follows: God cursed the Lamanites with dark skin because of their evil conduct; in the old days, people's skin would turn white when they were good and dark when they were bad;

4) Exposing oneself to sunlight is a sin because it turns the skin dark (recent word is a little sunlight can do wonders for disease prevention through the promotion of the production of natural vitamin D).

5) People with white skin are beautiful whereas people with dark skin are ugly. This based on the book of Mormon repeatedly associating white skin color with attractiveness and beauty but dark skin color with ugliness and repulsiveness.

Book of Mormon's Message from a more realistic, sympathetic, perspective:

The Book of Mormon sends the message that the white man, who is in a precarious position and has a tragic victimized past, has even more of a natural right to be in America than the American Indian, because: the white man's presence avenges historical wrongs perpetrated on more ancient white men, regarding which the white man feels a deep sense of loss and a justification for revenge; and because the white man is racially superior to the 'chosen people' the American Indians as evinced by his lighter skin color signifying moral superiority.

Ways in which Book of Mormon reflects current realities:

If any ethnic group is genetically special it is the group containing the descendants of the Jewish Christians who merged with the Gentile populations

There exists in America, the offspring of the Jews who rejected Christ, and the offspring of the Jews who accepted Christ (found amongst the Gentiles).

There exists friction between the two groups, the descendants of the Jews who rejected Christ (Lamanites(?)) and the descendants of the Jews who accepted Christ (Nephilites(?)).

The descendants of the Jews who followed Christ who are found amongst the Gentiles in America, are from the genetic/Christian perspective (I realize this perspective can be overemphasized): the true Israel, have the dignity of being the current chosen people second to none; through this dignity, are a natural and dignified presence in America; their dignity imparts dignity to the white Gentile peoples; they have had a tragic past and face a precarious future (Americans tend to overestimate the security of their own position).

Past migrations of caucasoid/white types to America are under-reported, seemingly due to a political correctness (PC) prejudice that results in 'scientists' acting like lawyers attempting to prove that the presence of white-man-types in the Americas prior to Columus was minimal. Conceivably, these white-man types were overpowered by East-Asian types in the struggle to survive in the Americas.

The PC-scientists would have us believe that all of the American Indian Y-Dna and MtDna is from haplogroups such as Y-dna haplogroup Q which are characteristic of the majority of the native-American population. However close inspection of the subject reveals that many different haplogroups are significantly represented in the American Indian population and that the haplogroup composition varies significantly from tribe to tribe.

Joseph Smith grew up in a time and place featuring speculation that the builders of the ancient mounds found in Smith's area, were white men not American Indians. The majority scientific PC-opinion is that these mound-builders were ancient ancestors of the American Indians.

However, there are reports that: male skeletons found in the mounds were around 7 feet in length and female skeletons around 6 feet in length at a time when the average American Indian was 5.5 feet tall (which translates to men being 7.5 feet tall compared to the 5'10" average of today); artifacts such as arrow-heads found in the mounds resemble early European artifacts; legends relate that the moundbuilders preceded the Indians and came from Mexico and prior to that from a land named 'Mu' that was submerged in a flood.

The de-glamorizing factoid is that several tall skeletons found in the mounds, had skulls containing two rows of teeth in both the upper and lower jaw.

Haplogroup Y-dna R is characteristic of whites of european ancestry and a large segment of the population in India. The recent advances in genetics-based history show that the Mormon instincts re whites and American Indians being closely related to each other, may not have been so far off the mark. the relative closeness of the American Indian Y-dna to white european Y-dna, tends somewhat to support the idea that white Americans are a natural part of the American landscape.

Symbolically speaking, haplogroup R (white europeans) is like:

A brother to haplogroup Q (American Indians); a cousin to haplogroups N (northern Asia) and 0 (E. Asia, China/Japan); a second cousin to L (India), and M (E. Indonesia/Papua-New Guinea; a third cousin to I (white Europe) and J (Arabs); a fourth cousin to G (Caucasus) and H (India); a fifth cousin to C (northeast Asia); a sixth cousin to D (Tibet/Japan) and E (Africa); a seventh cousin to B (Africa), and an eighth cousin to A (E. Africa).

Societies such as ancient Israel were able to maintain themselves as top-notch societies, despite suffering gigantic losses of men in wars and civil wars. This may have been due to the presence of polygamy, which allowed such societies to bounce back from the losses sustained. Ancient Israelite kings such as King David and his son King Solomon had so many wives and children that one suspects a deliberate plan to, so-to-speak improve the 'crops' by using the 'best seeds'.

Modern war could be said to damage the population even more than ancient wars, because in modern war it is so easy to kill off the best soldiers. In modern war, a significant percentage of the young men are excused from military service (about 30% of American youth in WWII). In modern war, the most competent men often receive the most dangerous assignments. Perhaps the societal insistence on monogamy is interfering with society's ability to bounce back from massive losses of males in wars.

Mormonism, sets forth the idea that persons of different skin colors can be genetically similar (the dark Lamanites and the white Nephites). Modern PC science may be correct in emphasizing genetic similarity of those who have different skin colors.

Mormonism's idea that the good and the evil are genetically similar would be applauded by the PC scientists and reflects current notions regarding the nature of reality.

Ways in which Mormon attitudes might promote psychological health in America

Looking at Danny Ainge's career one wonders whether Mormonism has effects like some kind of super-psychiatrist.

Seems that Mormonism may counteract ideas that can damage the psychological health of Americans such as: white people are bad guys; the white presence in America is unnatural; the white presence in America is not digified; white people are just somebody compared to the superior special race the Jews; a man having children with more than one woman is evil.

Mormonism forbids coffee, tea, tobacco and alcohol. Abstention from such can promote an individual's economic well-being hence his psychological health. Americans are well-known to consume excessive quantities of mind-altering substances. Persons are beginning to suspect that abstention from consuming substances often consumed in society, can result in improved ability to attain to supernatural states of mind.

Those who radically underestimate the dangers threatening them, could be said to be psychologically sick. The Mormon legend re the disaster that befell the good white Nephites, on the other hand, could be said to promote a reasonable sense of insecurity. One could say that the idea that white people and good people are never endangered is hubristic madness.

Ways in Which Mormonism may have damaged America

The Mormons for a long time have been associated with whiteness, repubicanism, conservativism.

The conservative republicans like to blame anybody but themselves for the nation's problems. They tend to excoriate groups other than themselves for allegedly causing the despised societal problems that actually they themselves have caused. The conservative republicans: agitated to remove tariffs; agitated for tax cuts giving themselves more spending money; and spent excessively on imports. Thus in a sense they single-handedly generated trade and budget deficits that threaten to collapse the US economy.

(Ron Paul would retort that the problem has been US govt borrowing of money. However, the money was borrowed because of pressures generated by tax cuts and trade deficits. The borrowing of money did not cause the tax cuts and the trade deficits; in reality, the tax cuts and the trade deficits led to the borrowing of money. Fact is, that it is obvious that individuals families and societies can financially ruin themselves without borrowing money).

The money that was borrowed from foreign nations as a result of tax cuts are what 'stimulated' the economy and made the tax cuts look as if they had improved the economy.

There seems to be in Mormonism undercurrents of: a lack of rigor in terms of demands for precision with regards to 'facts' and words presented by others; a lack of emphasis on precision with regards to one's own words and actions; a devaluation of important criteria as a result of a hyper-emphasis on skin color. I wonder if such influences through their effect on the political process have damaged the United States.

Note: To be fair to the conservatives, the most recent dream I had: I was running 220 yard runs at Stagg Field on the campus of the U of Chicago. I was doing really well, improving very fast, becoming one of the fastest 220 runners in my age group in the US, getting into the top dozen or so in my age group. Rush Limbaugh was sitting on a park bench right outside the fence that surrounded the field. He was wearing a colorful suit and tie. His face was pink, almost red as if was blushing. He was sitting on the bench facing away from the track, but the reason he was sitting there was that I was doing great things in track and he is a sports fan.

@2009 David Virgil Hobbs

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Thursday, June 04, 2009

Riddle--the decline and fall of Emerico Ribner

Mr. Qeronimo was an American Indian. He married Jaffa Rasputin, who was half Jewish and half-Russian. they had a daughter named Jane R Qeronimo. She was like a mix of American Indian and white.

Mr. Efrico Rebelez was half-black and half-Spanish. He married Ebonya, who was black. They had a son named Ed Rebelez, who was black.

Ed Rebelez married Jane Qeronimo, they had a daughter named Elaine Queronimo JR Rebelez.

Mr. Rabble was a British white man, he married a white Irish woman named Roberta. They had a daughter named Rory Rabble who was white.

Mr. Ribner was a German-ancestry white man, he married Ingrid who was a white lady from Sweden. They had a son named Ian Ribner.

Ian Ribner who was white, married Rory Rabble, who was white. They had a son named Inderson R.R. Ribner, who was white (boldface=two paras I accidentally left out even after proofreading several times).

Elaine Rebelez on her father's side was 3/8ths black and 1/8th Spanish, on her mother's side she was 2/8ths American Indian, 1/8th Russian, and 1/8th Jewish. Basically she was about half-black.

Elaine looked like the mix of black and American Indian and white that she was. She was a light-skinned black with American Indian features.

As for Mr. Inderson Ribner, his ancestry was simpler: white, a quarter British, a quarter Irish, a quarter German, and a quarter Swedish.

Mr Inderson Ribner was put in the awkward position of a blind date with Elaine Rebelez. He took comfort in knowing that at least her mother's grandfather was Mr. Rasputin who was white; and her father's grandfather was a white Spanish gentleman Mr. Rebelez.

Inderson Ribner married Elaine Rebelez, they had a son named Emerico Rebelez Ribner.

Emerico was 70% white, if you count Russian, Spanish, and Jewish as white; he was 20% black, and 10% American Indian.

Emerico looked like a light-skinned black, or a dark-skinned white; handsome, with caucasoid features influenced by his American Indian ancestry.

Emerico had a distinctively American look, he had the dignity of a natural American. He was a great basketball player who appeared on national TV in the college finals. He was a good musician, gifted with a great voice for singing. He was a likeable and popular young man.

But something went wrong. He did'nt make the pros in basketball. Studying and working both fatigued him. He wasn't a fast thinker, or good at memorizing things. His parents divorced. And Emerico began to fall apart.

Emerico's father Inderson Ribner began to have secret doubts about having married Elaine Rebelez, Emerico's mother. He secretly began having guilty thoughts such as: "my ancestors were great white men but my son is a negro; if we treat blacks as just like us as I have, soon we will all be black".

Emerico while using his father's computer stumbled across text in which his father had written out his secret thoughts. Emerico looked in the mirror and for the first time felt shame regarding his skin color and the texture of his hair.

Emerico and his father Inderson turned to drink. They spent the family savings. They borrowed and spent. They sold what they had and spent the proceeds. And now Emerico and his father Inderson Ribner, totter at the point of collapse.

Some say it is all because the two of them both think Emerico is black because Emerico is 20% black, and feel guilty about helping to turn the world's white people into blacks.

Explanation of Riddle:

Emerico = USA

First letters of names, sometimes second or third letters of names, initials in names = Y-dna haplogroups.

Original link re US Y-dna haplogroups:
The above link is now a broken link. Now to get the paper in question:

@2009 David Virgil Hobbs

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Reverse-genetic-drift and reverse-migration effects on estimates re ancient haplogroup percentages in local human populations

A principle of genetic history, is "genetic drift" ( ), meaning that in isolated populations, the y-haplogroups that are in a plurality or majority (supposedly) become more and more dominant in terms of percentage-wise representation in the population (soon perhaps I'll understand exactly how such occurs and be totally convinced of the validity of the concept).

So one could say that the opposite of genetic drift, would be haplogroups that dominate an area simply due to the area's isolaton, having been less dominant in terms of percentage representation in the given local population in the past.

At the same time it is reasonable to suspect that in the past, since localities were more isolated from each other, localities resembled each other less than they do now, in terms of percentage of persons in given localities possessing given haplogroup markers.

Extrapolating and projecting backwards in time accounting for such effects, even assuming very slight annual change in percentage representation of a haplogroups in localities over the past few thousands of years, the calculated level of change over the past few thousands of years from the distant past to the present, can be dramatic.

This compound-interest-type effect can be understood by toying with a compound interest calculator online.

Imagine two nations, land X, and land Y.
The following gives numbers and percentages for individuals carrying haplogroups A, B and C in 2000 AD for the two nations:

land X: A 20 (20%) B 10 (10%) C 70 (70%);

land Y: B 15 (15%) C 05 (5%) D 80 (80%);


Now imagine that it is 1500 years BP (before present), in the year 500 AD. 1500 years ago due to the reverse migration effect as we go back in time, the B group had not migrated from land Y to land X, and the C group had not migrated from land X to land Y. As a result, the situation was:

(10 B's moves to Y, 5 C's moved to X in formula)

500 AD

X: a 20 (21%) c75 (79%).

Y: b 25 (24%) d80 (76%).


Now imagine that it is 3000 BP, in the year 1000 BC. In the 1500 years transpiring between 1000 BC and 500 AD, genetic drift increased the percentage-wise dominance of the more common haplogroups in the localities. Therefore in 1000 BC the dominant groups were less dominant than they were in 500 AD. Thus in 1000 BC, the haplogroup percentage scores were closer to each other than they were in 500 AD:

1000 BC:

X: a 33 (35%) c 62 (65%)

Y: b 39 (37%) d 66 (63%)

In the end,

in land X, in terms of change in percentages from 2000 AD to 1000 BC, the change was: A 20->35; B, 10-> 0; C, 70-> 65;

And in land Y the change was: B, 15 -> 37; C, 5-> 0; D, 80->63.

Star of the show in terms of showing itself to have once been powerful in an area where it now just seems to be a small fry: haplogroup B, for whom the estimate of percentage representation in land Y using the formula is 40% for 1000 BC compared to 15% in 2000 AD.

Generally it seems possible that the effect of conceptual reverse-genetic-drift and reverse-migration when imaginatively going back in time, is that the estimate is that in the point back in time, the haplogroups that are weakly represented now in a locality were not represented at all, and the remaining haplogroups that are moderately represented now, were closer to other haplogroups in terms of percentage representation in the locality.

@2009 David Virgil Hobbs

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Tuesday, June 02, 2009

The two boys who were ethnically three-quarters the same, who crippled each other in a fight

Riddle: Who do the characters in the following story represent?

There were two half-brothers, Haridass Rasputin and Famerlaine Rasputin.

Their father was a Russian prince who had two wives.

Haridass' mother Hemavati was from central India, and Famerlaine's mother Fazakha was from Kazakhstan; these two women were both married to prince Rasputin.

So Haridass Rasputin was Russian and Indian, and Famerlaine Rasputin was Russian and Kazakh.

These two half-brothers, both married daughters of King Latif Jemal who was of mixed Pakistani and Turkish descent.
The two daughters they married were half-sisters because they had different mothers, both married to King Latif Jemal.

Hayana Latif Jemal, daughter of King Latif Jemal, had a mother from central India whose name was Hanjali, she was the sister of Haridass's mother Hemavati.

Rajani2 Latif Jamal, daughter of King Latif Jemal, had a mother from Bengal whose name was Radha2.

King Rasputin's 'Indian' son Haridass Rasputin married Rajani2 Latif Jemal, who was King Latif Jemal's 'Bengali' daughter by his wife Radha2; they had son named Sinharaj Haridass Rajani2 Latif Jemal Rasputin.

King Rasputin's 'Kazakh' son Famerlaine Rasputin married Hayana Latif Jemal, the 'central Indian' daughter of King Latif Jemal. They had a son named Tamilarasan Famerlaine Hayana Latif Jemal Rasputin.

Thus you had the boy Mr. Sinharaj H.R2.L.J Rasputin, and the boy Mr. Tamilarasan F.H.L.J Rasputin.

Their fathers were half-brothers. Their mothers were half-sisters. Mr. Sinharaj HR2LJ Rasputin's father's mother, and Mr. Tamilarasan FHLJ Rasputin's mother's mother, were sisters.

Thus they had in common three quarters of their ancestry, Russian, central Indian, and Pakistani. But they differed in the sense tht a quarter of Sinharaj Rasputin's ancestry was Bengali, whereas a quarter of Tamilarasan's ancestry was Kazakh.

People are still trying to figure out why Sinharaj Rasputin, the 'Bengali' one, and Tamilarasan Rasputin, the 'Kazakh' one, got into a gunfight and crippled each other so that they are now both wheeling themselves along in wheelchairs.

Both boys had the same ethnicity in their father's father, and in their mother's father. They had different ethnicities in their father's mother and in their mother's mother.

Thus from a confused point of view (which may have infected them) they were ethnically speaking more different from each other than it seemed--because Tamilarasan's mother's mother, and Sinharaj's father's father, had the same ethnicity, but in different positions relative to the grandson in question.

Answer to riddle:

The first letters of the names of the characters in the story represent Y-dna haplogroups (y-dna is inherited only from fathers, but to illustrate the ethnic situation some of the y-dna groups are represented as female ancestors. The names used resemble names found in areas considered to be the sources of the haplogroups. Tamilarasan represents the Sri Lankan Tamils, and Sinharaj represents the Sri Lankan Sinhalese.

Initial - haplogroup - haplogroup origin
H = haplogroup H, central India
L = haplogroup L, Karachi Pakistan area
R = haplogroup R1a1, Russia-central Asia-north India
R = haplogroup R2, Bengal
J = haplogroup J, Turkey
F = haplogroup F, Kazakhstan


@2009 David Virgil Hobbs

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