You are a collection of cells (literally trillions of them), each with a specific design and function. However, with a few exceptions, your cells all have a basic architectural design. Most of the time they are depicted as looking like a fried egg cooked sunny side up, but in reality they are three dimensional beings, more akin to a golf ball that you’ve cut across its midline. The “white” of our cell model is the body of the cell, and here are found many specialized areas called organelles that do particular jobs, much like our own internal organs have specific jobs as well. The “yolk” of our cell model is called the nucleus, and in this compartment there lies the object of our affections, the chromosomes.

Chromosomes were first discovered at the end of the 19th century by a German biologist named Walther Flemming. Flemming was looking at cells under a microscope and got the idea to use colors to dye the cell to make it easier to see things. The idea must have worked better than anticipated since he at once began to see spaghetti looking things in the nucleus that dyed a very deep color. As is the fashion, he named these entities chromosomes which is Greek for “colored bodies”.

Chromosomes are one of the more dynamic faces of Nature; they have to be, since they are responsible for the passing on of the 'Baton of Life' that we call reproduction. The number of chromosome in the cell nucleus differs somewhat from species to species. We humans have 46 chromosomes; dogs have 78; alligators 32; cabbage plants 18.

Your chromosomes are both the governess and chauffeur of the most important molecule in your body: DNA --which is actually two molecules wrapped around each other. Like any blueprint, DNA needs to be read in order for the work order to be constructed. Now, DNA is a long, long molecule. If it were completely unraveled it would be about six feet long, yet so thin that it would be invisible, since you can easily fit one million cells on the head of a pin. If the entire DNA, in every cell of your body, was stretched out and laid end-to-end in a straight line, it would reach to the sun and back over one thousand times.

Heavy.

I think an effective way of describing the dynamic qualities of the chromosome is to use a few metaphors. My older daughter likes to knit, so we often visit the knitting supply shop in town for fresh yarn. Yarn usually comes wrapped in skeins, a length of yarn wound around a reel. Most yarn comes in lengths of 80-150 yards. One of the nice things about buying yarn this way, rather than just as one long unwound string, is that you can put it under your arm and walk to the car. This is certainly better than tying a knot to the rear bumper and pulled the unwound string all the way home. Thus, the first important lesion of chromosome dynamics; if you’re going to reproduce you’ve got to stuff that entire DNA into a very small, tight package. Chromosomes are just that: tight packages of DNA.

On the other hand, it is very difficult, if not downright impossible to knit anything if the skein of yarn still has the paper label wrapped around it. In order to use the yarn, you have to unwind it. That’s the formula: when the cell needs to use DNA to get information about how to make a protein, it has to unwind it. When it needs to reproduce, or turn off the DNA information flow, it needs to concentrate and condense it.

How this occurs is rather wondrous, and will be the subject of much discussion later on when we talk about how you can modify your genetic destiny, but for now we’ll just stick to the basics. DNA is packaged and concentrated by special proteins termed histones. This concentrated DNA is called chromatin, which is the DNA plus the histones that package DNA within the cell nucleus. Chromatin structure is also relevant to DNA replication and DNA repair.

Histones are very cool bead-like proteins that spool the DNA in a way that makes it either tighter or looser, sort of like the cardboard around which our skein of yarn is wrapped. Histones respond to changes in their structure by tightening the DNA wrap or loosening it. Whenever a cell needs to access the genetic information encoded in its DNA, the histones on the section of the DNA that is needed undergo a chemical reaction called acetylation by which a molecule called an acetyl group is stuck on the histones, causing them to relax and unravel. When business is concluded for the day, special enzymes come along and chomp off the acetyl group cause the histones to become de-acetylated, which makes them tighten up again, sending the DNA in the region back to its resting state. Think of it like this; when your DNA needs to work its histones chow down on acetyl groups for breakfast and they do yoga; when it needs to reproduce or shut down, the histones lift weights --the strain of which causes the acetyl group to pop out of their mouths.

Make sure that you’ve mastered the last paragraph, because much of the very cool stuff dealing with how you can modify gene functions pretty much requires that you know this stuff. By the way, this is very, very cutting edge material; only until recent times have we understood this mechanism, and of supremely paramount importance, that it is used by the environment to influence gene function and that influence, for either good or bad, can be passed on as inheritance.

Scientists have given each human chromosome a number, according to its size; thus chromosome number 1 is the largest, then number 2, etc. Chromosomes come in pairs, one from each parent. So there are 23 pairs, for a total of 46 in us humans. Numbers 1-22 are non-sex chromosomes called autosomes, and pair 23 contains the X and Y sex chromosomes.

In the few minutes it has taken to read up to here, this, around 400 million of your red blood cells were depleted and replaced, consistent with the set of genetic instructions contained in your DNA.

I received an interesting question from my Facebook Page.

Thanks for providing an awesome guide in the Genotype Diet. Been practicing it as best I can for about 7 months and feel powerful. (I'm also doing good vitamins which is definitely part of the reason I feel really good.)

When I talk to people about the Genotype Diet and the benefits I've achieved from it, the main question I get is: Exactly what research has determined the genotypes, and the superfoods/toxic foods in the book? I can't begin to answer that question as I don't recall seeing it addressed in the book or on the website.

I'd love to learn more about the types of tests that you did to determine which people are in what genotypes as well as which foods are in which categories, per type.

This is a great question, but given that the best 'scientific answer' would be to show you the data tables and computer source code I can only try to explain a bit of the process. The problem with mass-market books is that you can only provide the upper-most level of information and a simplified version of that to boot, so I understand.

What I term the 'genotypes' (really 'epigenotypes' or 'morphotypes' but try to get a publisher to agree to use these words) are semi-synthetic constructs involving a stepwise statistical analysis of variation. They stem from the phenotypic (real world) characterizations reported for the ABO groups, Rh, secretor and additional biometric markers (D2-D4, fingerprints, etc). The idea was to look for pleiotropic (sympathetic) relationships between the multi-dimensional genotype/ phenotype data, especially if they are known to exert their effects through transgenerational actions. Using multivariate analysis we then look to see how the data separates or groups together. Since, with the exception of secretor, taster, Rh and ABO, we're looking at phenotype, I felt very comfortable including data from other, traditional typing systems (Ayurveda, TCM) which were also based of physical traits.

The base data includes virtually all published scientific tabular data on variations in physiology and pathology associated with these parameters, in addition to our own profiles of roughly 3,000+ additional people. At that point the data was filtered according to degrees of three basic metabolic 'biases': 'thriftiness' (metabolic compromise), 'receptorism' (immune tolerance) and 'reactance' (auto-immunity).

The genotypes are not 'perfect' typologies (every Explorer does not look or act exactly as every other Explorer) because we cannot possibly encapsulate all variation in everybody. Two families using the same set of blueprints will most likely build two different houses, due to differing financial constraints, choice of land plot, etc. Most of the time and given the tools we might encapsulate 30-50 percent of the data variation (principal components) in any one person and what we encapsulate in one might be slightly different than what we get for another. In statistical terms this is called 'multiple inclusion criteria' and it is a keynote of factor analysis or 'fuzzy logic.'

What results are six basic 'types' that with considerable tweaking encapsulate an acceptable amount of variation. Crunching the system into six types and cramming them into a hard-coded 'book' is much less effective than dynamically generating one-to-one diets in software, but it is still a pretty good approximation of some basic phenotypic variation and is more helpful than not.

Once we get here, the next step was to match the expected physical manifestations to a large database of foods that I've been collecting for the last two decades. For each food, this database contains about 300 individual values (gluten content, vitamin A, known allergen, etc.) At this point a second set of algorithms takes over and each food is evaluated constituent-wise based on a weighed value system much like a lawyer might argue a case in court. For example, evidence of developmental instability or constrained growth (differences between left/right sides of body, certain fingerprints, short leg length) might result in limiting foods that cause excess glycation.

If no negative attributes (for example, if the food contains a lectin or is known to encourage bacteria overgrowth, etc) is recorded, then the next step is to see if a case can be built for the food having any specialized benefit (for example, sardines might become a superfood if increasing the amount of RNA nucleotides is desirable; artichokes because they encourage probiotic growth in a strain of bacteria known to be good for a certain blood type). Lacking either of these elements, the food is simply labeled 'food' and considered more or less neutral.

In the simple case of rice versus rice milk it is most likely additional gums in the milk that are the issue. Certain gums amplify the effects of problematic proteins in other foods.

http://www.drpeterjdadamo.com/wiki/wiki.pl/Lectins

People also ask a lot about peanut oil versus peanuts or cherries versus cherry juice. Usually it is a difference between one form that contains some sort of problematic protein versus the other that doesn't. Also, occasionally in the Genotype diet (unlike the BTD) with complex foods, sometimes one nutrient influences the value of another which alters the value of the food.

Here are blogs of mine tagged as 'genotype diet.' You will see some elements of the process discussed in detail in many of these entries.

http://www.dadamo.com/B2blogs/blogs/index.php/genotype-diet/?blog=24

Growing up in Brooklyn I remember many exciting and fun filled trips to Manhattan --or as anyone from Brooklyn calls it, “The City.” One of the features I always looked forward to seeing was a huge advertisement for a paint company that featured a can of paint pouring itself over a globe of the world, its byline proclaiming “We Cover the Earth with Our Paints.”

Excepting the obvious question as to why anyone would ever want to cover the world in it, paint is not a bad metaphor for how most scientists viewed inheritance before Mendel, it being a sort of “blended essence” --a mix of the features of both mom and dad, much like how we might combine white and black paints to make gray. In the late 1800s Charles Darwin proposed a mechanism of inheritance by means of gemmules, imaginary granules or atoms which are continually being thrown off from every cell or unit, and circulate freely throughout the system. Yet Mendel’s research showed that it was nothing of the sort; being in fact much more digital, like how a computer makes all sorts of interesting stuff out of what are essentially zeros and ones. Mendel’s theory nixed that notion completely, although after a while things started to be observed that appeared to indicate that genetics wasn’t all that black and white, on and off after all, but I’ll save that for a later story.

I’ve married a blue eyed woman, and have two daughters. The first daughter has brown eyes just like me. Simple enough: My brown-eyed alleles squash my wife's blue-eyed ones. However, my second daughter has greenish-hazel eyes, much lighter than mine or her sister, but certainly not bright blue like those of my wife, so it would seem like a little blending is going on over there after all. Eye color is not a simple dominant-recessive trait, although knuckle hair and tongue rolling are. The eye color trait is what geneticists call polygenic, which simply means that it is not decided by one single gene. In order to account for my younger child’s green-hazel eyes, we have to add other factors to the mix.

My wife is pure Irish on her mother’s side and a mix of Slovakian and Hungarian on her father’s. Hungarians have the highest percentage of green eyes of any population, close to 20%, so something in my wife’s blue-eyed world (the blue-eyed allele of her Hungarian father) produced a variant that refused to role over and die, but instead made alliances with other genes --including a recently discovered one that may go back to the Neanderthals--- that slips green eyes and red hair in between things, ultimately producing my younger daughter’s wonderful green eyes. Given that, you'd think I'd get the tongue rolling gene and she the knuckle hair, but alas, the results are quite opposite.

Many traits are polygenic, and when when added to the tremendously under-appreciated epigenetic effects on gene expression, explain why we have never found a single gene for diabetes, or cancer or Alzheimer’s disease. If it were that simple, we’d have had the answers to these questions already.

Another type of inheritance is very close to my heart. The allele (the set of alternate genes for any trait) for type O blood is recessive to the alleles for type B and type A. Again using my family as an example, biologically I am type A blood and my wife is type O. My daughters are both type A blood, so we know that they must have received a type O allele from mom and a type A allele from me. Their genotype for ABO blood type is A/o (recessive alleles are usually depicted in lower case, dominant in capitals, and genetic things are usually rendered in italics).

If I was instead type B blood and had provided a type B allele, the children would have type B, as type B is dominant to type O as well.

But here is where things get interesting. What happens if you were to receive one type A allele and one type B allele? Why, you would be blood type AB! The reason behind this is that although both B and A clobber O, they strike a tentative truce between themselves and split the kingdom and declare a dual monarchy. This is called co-dominance. There are not many instances of co-dominance in genetics, and ABO inheritance is almost always given as the example.

You may well ask why, if type O is recessive to types A and B, why hasn’t it disappeared, leaving only A and B to slug it out, and eventually producing a world of only type AB people? The reasons and proofs for this are mathematical, so I won’t bore you with them, but suffice it to say that if a population is large enough, and the individuals in that population tend to mate randomly, and there are no other major influences (such as one type being more resistant to an infectious disease), after one generation the gene pool will stabilize and reach a sort of equilibrium.

Since there is such a huge amount of o allele in the human population (so much so, in fact, that even though it is the recessive allele, individuals with type O blood constitute the majority of most populations around the world) it will keep propagating itself, whereas the type you’d have though would be replacing everyone else by now, AB, comprises at best about 2% of the population.

Most people probably have a negative concept of mutation, spawned by a slew of admittedly great science fiction. However, it might surprise you to learn that that vast majority of mutations, at least the ones that get incorporated into our genetic heritage, are not lethal and often don’t do very much at all. For example, let’s again turn to our trusty blood types. As we will explore in more later on in this book, genes are chunks of DNA that do things, like code for specific proteins. Although DNA is an incredibly long molecule (if all the DNA in all your cells was unwound and placed end to end it would produce a string capable of reaching to the sun and back several times) it is composed of a simple string of four repeating nucleotides abbreviated A,T,C and G. The sequence of these four repeating nucleotides is what contains the instructions for the protein.

The difference between having the gene for type A blood or type B blood is a variation of a mere seven letters out of the total of 1,062 that make up the entire gene. We even know exactly where they differ: letters number 523, 700, 793 and 800. If you are type A blood, you have C,G,C,G in these locations, whereas if you are type B blood you have G,A,A,C there instead. Yet however slight this difference is, it is enough to cause a major problem if you were to receive the wrong blood in a transfusion. These are called point mutations because they are a simple one-letter misspelling in a gene, unless as in the case of blood type it is a consistent variation that is inheritable, in which case it is called a polymorphism.

The type O gene mutation is even more interesting. It derives from a frame shift mutation. If you are type O you may be surprised to discover that rather than having a difference of letters, like A and B, you're just missing one letter, number 258, entirely.

So hopefully by now you are comfortable with the notion that mutations are just part of life, unless of course you are unfortunate enough to have gotten a lethal one (and there are many) which probably would never have allowed you to get so far in life as to be able to read this blog. Many, if not most, of these mutations are spontaneously terminated while the sufferer is still an embryo in utero. Virtually all of the well-known genetic disorders are semi-lethal.

There are may causes of mutations, including viruses and radiation, but the most common cause is the simple fact that when our cells reproduce, they must make a complete copy of there DNA, and sometimes the copies don’t turn out so great. Think about the photocopy of that great joke that circulated around the office cubicle the other day. If it was barely legible, with bloated letters that ran one into the other, it was probably because someone made a photocopy of the original, which was quite likely a photocopy of the previous copy. Each time a copy was made of a copy, the writing was degraded a bit more.

Genes are like that. Often as we get older, we tend to get more and more of this “photocopy effect”. Perhaps what was once a word string of CAG became CAA. Even if it is copied correctly, it will be CAA from there on. Perhaps not unexpectedly these mutations are called “copying errors” and given the enormous amount of cell division that goes on over the course of a lifetime it is the real surprise is just how good of a job we do at it.

Fascinating presidential election; certainly a very unique and historic outcome. It will be interesting to see --given the perilous state of affairs we find ourselves in-- whether 2008 is also the first presidential election in which (come January) it is the winner rather than the loser who demands a recount.

You are a collection of cells, literally trillions of them, each with a specific design and function. With a few exceptions, cells have a basic architectural design, most of the time being depicted as looking like a fried egg cooked sunny side up. However, in reality they are three dimensional beings, so it might be better to think of the average cell as a golf ball that you’ve cut across its midline. The “white” of our cell model is the body of the cell, and here are found many specialized areas called organelles that do particular jobs, much like our own internal organs have specific jobs as well. The “yolk” of our cell model is called the nucleus, and in this compartment there lies the object of our affections, the chromosomes.

Chromosomes were first discovered at the end of the 19th century by a German biologist named Walther Flemming. Flemming was looking at cells under a microscope and got the idea to use colors to dye the cell to make it easier to see things. The idea must have worked better than anticipated since he at once began to see spaghetti looking things in the nucleus that dyed a very deep color. As is the fashion, he named these entities chromosomes which is Greek for “colored bodies”.

Chromosomes are one of the more dynamic faces of Nature; they have to be, since they are responsible for the passing on of the Baton of Life that we call reproduction. The number of chromosome in the cell nucleus differs somewhat from species to species. We human have 46 chromosomes; dogs have 78; alligators 32; cabbage plants 18.

Your chromosomes are both the governess and chauffeur of the most important molecules in your body; DNA. Like any blueprint, DNA needs to read in order for the work order to be constructed. Now, DNA is a long, long molecule. If it were completely unraveled it would be about six feet long, yet so thin that it would be invisible. If the entire DNA, in every cell of your body, was stretched out and laid end-to-end in a straight line, it would reach to the sun and back over one thousand times.

I think an effective way of describing the dynamic qualities of the chromosome is to use a few metaphors. My older daughter likes to knit, so we often visit the knitting supply shop in town for fresh yarn. Yarn usually comes wrapped in skeins, a length of yarn wound around a reel. Most yarn comes in lengths of 80-150 yards. One of the nice things about buying yarn this way, rather than just as one long unwound string, is that you can put it under your arm and walk to the car. This is certainly better than tying a knot to the rear bumper and pulled the unwound string all the way home. Thus, the first important lesion of chromosome dynamics; if you’re going to reproduce you’ve got to stuff that entire DNA into a very small, tight package. Chromosomes are just that: tight packages of DNA.

On the other hand, it is very difficult, if not downright impossible to knit anything if the skein of yarn still has the paper label wrapped around it. In order to use the yarn, you have to unwind it. That’s the formula: when the cell needs to use DNA to get information about how to make a protein, it has to unwind it. When it needs to reproduce, or turn off the DNA information flow, it needs to concentrate and condense it.

DNA is packaged and concentrated by special proteins termed histones. This concentrated DNA is called chromatin, which is the DNA plus the histones that package DNA within the cell nucleus. Chromatin structure is also relevant to DNA replication and DNA repair.

Histones are very cool bead-like proteins that spool the DNA in a way that makes it either tighter or looser, sort of like the cardboard around which our skein of yarn is wrapped. Histones respond to changes in their structure by tightening the DNA wrap or loosening it. Whenever a cell needs to access the genetic information encoded in its DNA, the histones on the section of the DNA that is needed undergo a chemical reaction called acetylation by which a molecule called an acetyl group is stuck on the histones, causing them to relax and unravel. When business is concluded for the day, special enzymes come along and chomp off the acetyl group cause the histones to become de-acetylated, which makes them tighten up again, sending the DNA in the region back to its resting state. Think of it like this; when your DNA needs to work its histones chow down on acetyl groups for breakfast and they do yoga; when it needs to reproduce or shut down, the histones lift weights --the strain of which causes the acetyl group to pop out of their mouths.

Only until recent times have we understood this mechanism, and of its supremely paramount importance: That it is used by the environment to influence gene function and that influence, for either good or bad, can be passed on as inheritance. Amazingly, we not only inherit the genes from our parents, but state of histone acetylation of the genes as well. Thus, the histone acetylation patterns of the genome are a prime mechanism of epigenetic inheritance, along with DNA methylation.

Scientists have given each human chromosome a number, according to its size; thus chromosome number 1 is the largest, then number 2, etc. Chromosomes come in pairs, one from each parent. So there are 23 pairs, for a total of 46 in us humans. Numbers 1-22 are non-sex chromosomes called autosomes, and pair 23 contains the X and Y sex chromosomes.

In the few minutes it has taken to read up to here, this, around 400 million of your red blood cells were depleted and replaced, consistent with the set of genetic instructions contained in your DNA. This is where the genetic code comes in.

I'm just back from a site visit to the Dolce Conference Center, scene-to-be of the upcoming IFHI 2009 Conference and Certification. What a facility! If you've been to the Buttes for 2005 or 2007 prepared to get gob-smacked! The premises (a former monastery) are just gorgeous this time of year. The intimacy of the lecture halls combined with the terrific AV capabilities of the facility already have my mind running in overdrive. I think it was very smart to top the attendance at 125. This will insure that everyone feels that they are a real part of the event.

Unfortunately, despite the fact that the conference is three weeks away, I'm told that all available rooms at the Dolce Conference Center have been taken. We have a few seats still available for the day sessions, and if anyone plans to register from this point on, we can book them at the nearby Double Tree Inn and the Dolce will bus these folks back and forth.

Anyway, if you want to attend IFHI, even at this late point in the process, contact IFHI Conference Services and maybe they can work something out for you.