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 ( http://www.jadenutra.com/aminoacids.html); the composition of human myoglobin (http://www.aw-bc.com/mathews/ch07/c07emhp.htm, http://www.aw-bc.com/mathews/ch05/fi5p14.htm, the molecular weight of the various proteins that compose human myoglobin (http://www.webqc.org/aminoacids.php).

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 (http://davidvirgil.blogspot.com/2009/06/myoglobin-used-by-body-during-prolonged.html) 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 " (http://books.google.com/books?id=lIsrAAAAYAAJ&pg=PA131&lpg=PA131&dq=%22there+is+no+evidence+that+histidine%22+histidine+humans&source=bl&ots=rDVyISBP8q&sig=wB1uRjbZjbrgjf2MR-dIjFnH0mQ&hl=en&ei=JO41SpWPO6K_twe455j5Dg&sa=X&oi=book_result&ct=result&resnum=3). Wikipedia now says, "After reaching several years of age, humans begin to synthesize it (histidine) and it thus becomes a non-essential amino acid" (http://en.wikipedia.org/wiki/Histidine).

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" (http://whqlibdoc.who.int/trs/WHO_TRS_935_eng.pdf), "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" (http://en.wikipedia.org/wiki/Amino_acid#In_human_nutrition).
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 (http://www.nutrientfinder.com/nfsearch.php)

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 (http://davidvirgil.blogspot.com/2009/06/myoglobin-used-by-body-during-prolonged.html), 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" (http://davidvirgil.blogspot.com/2009/06/heart-health-and-aerobic-exercise.html).

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

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 http://davidvirgil.blogspot.com/2009/06/jogging-is-bad-for-you-new-theory-of-dr.html 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, http://www.accessmylibrary.com/coms2/summary_0286-22651044_ITM ). 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, http://books.google.com/books?id=AbmXeprR82sC ).

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" ( http://66.102.1.104/scholar?num=100&hl=en&lr=&scoring=r&q=cache:AGMt7CIFhzUJ:ajcp.ascpjournals.org/content/126/2/185.full.pdf+Siegel++%22changes+in+cardiac+markers%22++cardiac+markers
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' ( https://www.health.harvard.edu/fhg/updates/BNP-An-important-new-cardiac-test.shtml). 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, http://66.102.1.104/scholar?num=100&hl=en&lr=&scoring=r&q=cache:AGMt7CIFhzUJ:ajcp.ascpjournals.org/content/126/2/185.full.pdf+Siegel++%22changes+in+cardiac+markers%22++cardiac+markers).

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 ( https://www.health.harvard.edu/fhg/updates/BNP-An-important-new-cardiac-test.shtml) 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