WO2015004266A1

WO2015004266A1 - Personalized nutrient compositions and methods for producing these

Info

Publication number: WO2015004266A1
Application number: PCT/EP2014/064912
Authority: WO
Inventors: Daniel WALLERSTORFER
Original assignee: Novogenia Gmbh
Priority date: 2013-07-12
Filing date: 2014-07-11
Publication date: 2015-01-15

Abstract

The present invention relates to a genomic method for producing a personalized nutrient composition for one individual, wherein the nutrient composition is optimized for the individual's genomic risk profile for having or developing one or more pathological conditions. Furthermore, the present invention refers to an orally ingestible nutrient composition obtained from the method of the present invention and to said composition for use as a medicament, in particular for preventing or treating one or more of the pathologic conditions the individual is at risk of.

Description

Personalized Nutrient Compositions and Methods for Producing These The present invention relates to a genomic method for producing a personalized nutrient composition for one individual, wherein the nutrient composition is optimized for the individual's genomic risk profile for having or developing one or more pathological conditions. Furthermore, the present invention refers to an orally ingestible nutrient composition obtained from the method of the present invention and to said composition for use as a medicament, in particular for preventing or treating one or more of the pathologic conditions the individual is at risk of.

Numerous environmental factors are known that may increase one individual's risk of developing a pathological condition. One of the most important environmental factors in an individual's health is nutrition. For several pathological conditions, single nutrients have been identified that may decrease the risk of developing such pathological condition or even to treat one.

Today, most individuals bearing an elevated genetically predisposition for developing a particular pathological condition do not even know about it and, therefore, often do not behave in a way preventing the development of such pathological condition. Upon incidence of symptoms, the individual is frequently administered with a single nutrient known to be statistically of benefit when treating the pathological condition. Even in case the particular risk of one individual of developing a particular pathological condition is known, today, the individual will typically be administered with a single nutrient known to be statistically of benefit for preventing the pathological condition only. When, two or more nutrients that are each known to be of benefit to treat or prevent a particular pathological condition are administered concomitantly, a standard premixed nutrient mixture is administered.

In fact, it is a severe drawback that today only nutrient compositions that either comprise a single nutrient or a premixed standard nutrient mixture are administered to individuals. Herein, the personalized risk profile is entirely ignored. The administration of such a standard nutrient mixture to one individual may indeed be beneficial for preventing or treating one of the pathological conditions the individual is at risk of, but often also has a negative influence on one or more other pathological conditions the individual is at risk of or even suffering from. Then, the nutrient mixture may even have severe side effects. Exemplarily, the administration of iron may, on the one hand, be beneficial for one individual having certain types of heavy metal poisoning but may be avoided when the individual simultaneously is at risk of developing or even has an iron overload disorder. Therefore, in this case the administration of a standard nutritional supplement has severe side effects.

Optimizing the nutrient composition is today performed by long-lasting, laborious and expensive optimization processes mostly performed by alternative practitioners who merely test different nutrient compositions and possess a wide range of personal experience. It will be noted that no quality standards are applicable for such course of actions. So far, one individual rarely, (if ever) receives an optimal personalized composition of nutrients.

A standardized method, however, would be considerably more time and cost-efficient and would prevent the risk of medical malpractice such as harmful over- or under-dosage. So far no standardized method has been known in the art. Accordingly, there is still a strong need for improved personalized nutrient compositions optimized for one particular individual that are producible with a comparable low cost and work effort and that are usable in a standardized manner.

Surprisingly, we found a genomic method that enables the efficient production of a personalized nutrient composition for one individual.

In a first aspect, the present invention refers to a genomic method for producing a personalized nutrient composition for one individual, said method comprising the following steps:

(i) determining said individual's genetic predisposition for the risk of developing or having one or more of a set of pathological conditions associated with a set of alleles identified in said individual's genome,

(ii) determining the amounts and ratios of nutrients selected of a set of nutrients suitable for preventing or treating the one or more pathological condition(s) identified as being of risk, and

(iii) producing a nutrient composition comprising the determined amounts and ratios of nutrients. As used herein, the term "genomic method" may be understood in the broadest sense as any method that is based on the individual's genome, i.e., one or more sequence(s) identified in the genetic material of the individual's origin. As well-known by the person skilled in the art, the genome refers to the complete genetic information of one individual. In humans, a genome consists of roughly 3.2 billion genetic code letters and approximately 25.000 different genes. Particularly, in the context of the present invention, fractions of genomic material may be analyzed for their sequence or it is determined whether the whole genome comprises particular sequences.

The term "producing" as used herein may be understood in the broadest sense as any action of generating or preparing a particular compound or composition, i.e., in the context of the first aspect of the present invention, any action of generating a nutrient composition. Therefore, the terms "producing", "generating", "manufacturing", "preparing", "making", "establishing" and the like may be understood interchangeably.

A "nutrient composition" may be any mixture of one or more nutrient(s) with one or more further compounds. Herein, the terms "composition", "preparation", "composite", "mixture", "mix", "blend" and "intermixture" may be understood interchangeably. Preferably, a nutrient composition as used herein comprises more than one nutrient, more preferably even more than two different nutrients.

As used herein, the terms "nutrient" and "supplement" may be understood interchangeably in the broadest sense as any chemical substance that is present in at least one kind of foodstuff consumable by a mammalian, in particular humans, that may be beneficial for an individual to live, grow and/or maintain health. The nutrient may be an organic or inorganic chemical substance. Organic nutrients exemplarily include but are not limited to carbohydrates, fats, polypeptides, secondary plant metabolites, fibers, building blocks of one of the aforementioned (e.g., amino acid moieties, fatty acids, monosaccharides, disaccharides, polysaccharides), amino acids or vitamins, any precursors, salts or racemates of one of the aforementioned or any conjugates of two or more of the aforementioned. Inorganic chemical compounds exemplarily include but are not limited to dietary minerals. Preferably, a nutrient as used herein cannot be produced by the individual it is administered to in the context of the present invention in sufficient amounts by said individual. Then, the nutrient is an essential nutrient. Preferably, a nutrient is any compound designated as such by official agencies such as, e.g., the National Institute of Health (NIH) (9000 Rockville Pike, Bethesda, Maryland 20892, U.S.A.) and/or the U.S. Food and Drug Administration (FDA) (10903 New Hampshire Avenue, Silver Spring, MD 20993), in particular designated by the NIH as such at the filing date of the present invention.

In contrast to most medicinal agents, typically, also a healthy individual requires a certain amount of a nutrient to maintain health. Few nutrients, such as, e.g., some vitamins, may be produced to some extent by intestinal bacteria. A nutrient may be of organic and/or of inorganic origin. Organic nutrients are preferably of plant and/or bacterial origin. Inorganic nutrients are preferably of mineral origin. In the context of the present invention, a nutrient is preferably a micronutrient, therefore, a nutrient that is required in a low dose, i.e., typically at a dose of not more than 10 g per day, more preferably not more than 1 g, as exemplarily defined by the recommended daily allowance (RDA) in accordance with the recommendation of the NIH. Many nutrients are also known as nutritional supplements.

In a preferred embodiment, the nutrient composition may comprise amounts of the one or more nutrient(s) comprised in said nutrient composition for daily intake are not lower than the RDA as recommended by the official institutes such as the NIH and/or the FDA, in particular the NIH, in particular as recommended by the NIH at the filing date of the present invention, and not higher than the maximal recommended daily intake recommended by one or more of said institute(s), in particular by the NIH at the filing date of the present invention, wherein the increase in amount correlates with the determined risk of developing or having one or more particular pathologic condition(s). Preferably, the used amounts for daily intake of the following exemplified nutrients as far as comprised in the nutrient composition are:

alpha lipoic acid: between 200 mg and about 600 mg;

omega 3 fatty acids: between 250 mg and 2500 mg;

vitamin A: between about 1 .6 mg and about 8,4 mg, in particular between the RDA as recommended by the NIH and/or the FDA and the threefold of the RDA;

vitamin B2: between about 0.3 mg and 10 mg, in particular between the RDA as recommended by the NIH and/or the FDA and 10 mg;

vitamin B6: between about 0.1 mg and 10 mg, in particular between the RDA as recommended by the NIH and/or the FDA and the fivefold of the RDA;

vitamin B12: between about 0.0004 mg and 0.0072 mg, in particular between the RDA as recommended by the NIH and/or the FDA and the threefold of the RDA;

vitamin C: between about 15 mg and about 1500 mg, in particular between the RDA as recommended by the NIH and/or the FDA and 1500 mg; vitamin D3: between about 0.01 mg and 0.025 mg, in particular between the RDA as recommended by the NIH and/or the FDA and 0.025 mg;

vitamin E: between about 4 mg and about 200 mg, in particular between the RDA as recommended by the NIH and/or the FDA and 200 mg;

folic acid: between about 0,0325 mg and about 0,8 mg, in particular between the RDA as recommended by the NIH and/or the FDA and the fourfold of the RDA;

calcium: between about 200 mg and about 2500 mg, in particular between the RDA as recommended by the NIH and/or the FDA and 2500 mg;

magnesium: between about 65 mg and about 350 mg, in particular between the half of the RDA as recommended by the NIH and/or the FDA and 350 mg;

iron: between about 0.27 mg and 30 mg, in particular between the RDA as recommended by the NIH and/or the FDA and 30 mg;

selenium: between about 0.015 mg and about 0.3 mg, in particular between the RDA as recommended by the NIH and/or the FDA and 0.3 mg;

zinc: between about 2 mg and about 30 mg, in particular between the RDA as recommended by the NIH and/or the FDA and 30 mg;

manganese: between about 0.3 mg and about 3 mg, in particular between the RDA as recommended by the NIH and/or the FDA and the threefold of the RDA;

copper: between about 0.2 mg and about 3 mg, in particular between the RDA as recommended by the NIH and/or the FDA and 3 mg;

beta carotene: between about 1 .6 mg and about 7.5 mg, in particular between the RDA as recommended by the NIH and/or the FDA and the threefold of the RDA;

retinol: between about 0.8 mg and about 3.5 mg, in particular between the RDA as recommended by the NIH and/or the FDA and the threefold of the RDA;

lutein: between about 10 mg and about 30 mg;

lycopene: between about 10 mg and about 30 mg;

coenzyme Q10: between about 50 mg and about 300 mg;

ubiquinol: between about 50 mg and about 150 mg;

phytosterols: between about 500 mg and about 2500 mg; and/or

MSM: between about 300 mg and about 2500 mg.

The amounts as referenced in this context throughout the invention refer to the active ingredient. The RDA values herein are most preferably those recommended by the NIH at the filing date of the present application. Nevertheless, the person skilled in the art will notice that it may alternatively also be beneficial to use such amounts recommended at the time the method of the present invention is used. It will be noticed that the RDA and maximal amounts to be taken up per day may depend on age, sex and body weight as well as on environmental factors such as, e.g., physical activity, health state, pharmaceutical treatments, xenobiotic s' uptake etc.

Exemplarily, for most nutrients children require lower daily amounts of nutrients. Pregnant and breastfeeding women may be administered with higher amounts of many nutrients. Elderly people often may be administered with lower amounts of many nutrients than younger people. Under severe blood loss (e.g., by accident, surgical intervention and/or regularly strong menorrhea) higher amounts of iron may be administered. For excessive athletes, higher amounts of magnesium may be administered. Under malnourishment (e.g., anorexia and/or bulimia) higher amounts of most or even all nutrients may be administered to compensate the nutrient deficit. With respect to most vitamins, it is known that a large collective in the population is typically under-supplied by at least one vitamin. Exemplarily, approximately 15 % of the male population and approximately 10 % of the female population bear a deficiency for vitamin A. Even more severe, approximately 32 % of males and approximately 29 % of females are deficient for vitamin C. nearly half of the entire population, i.e., approximately 49 % of males and females take up too low amounts of vitamin E. The majority of men (approx. 82 %) and women (approx. 91 %) are deficient for vitamin D. Likewise, also folic acid (males: approx. 79 %, females: approx. 85 %) and calcium (males: approx. 44 %, females: approx. 54 %) deficiency is widely distributed throughout population. Zinc deficiency occurs approximately in 32 % of the male population and in approximately 21 % in the female population, whereas vitamin B deficiencies occur more often in women (vitamin B2: men: approx. 20 %, women: approx.. 26 %; vitamin B6: men: approx. 12 %, women: approx. 13 %; vitamin B12: men: approx. 8 %, women: approx. 26 %). Therefore, and with respect to the comparably broad range between the RDA and the upper safe limits, it may be valuable to administer vitamins at the RDA level or slightly below to most individuals throughout the population. When a risk for one or more pathologic condition(s) is recognized in one individual, said individual may be administered with other amounts such as, e.g., most typically increased amounts of said vitamin(s). The same holds true for the other nutrients, wherein in particular for the metal ions, also iron storage diseases (e.g., iron overload disorder) occur that may require the administration of a reduced amount of a particular metal (e.g., iron).

Exemplarily, an adult who is severely bulimic and/or anorectic may be administered with 600 mg alpha lipoic acid, 2.5 g omega 3 fatty acids, 7.5 mg vitamin A, 10 mg vitamin B2, 10 mg vitamin B6, 75 μg vitamin B12, 1 .5 g vitamin C, 25 μg vitamin D3, 30 mg vitamin E, 200 mg folic acid, 2.5 g calcium, 350 mg magnesium, 30 mg iron, 300 μg selenium, 30 mg zinc, 8 mg manganese, 10 mg copper, 7.5 mg beta carotene, 3.5 mg retinol, 30 mg lutein, 300 mg coenzyme Q10, 150 mg ubiquinol, 2.5 g phytosterols and 2.5 g MSM per day. Additionally, higher amounts of potassium and sugar may be administered to this individual in order to maintain cardiovascular activity.

An adult individual suffering from an iron overload disorder and of an excess of calcium may exemplarily be administered with 200 mg alpha lipoic acid, 250 mg omega 3 fatty acids, 1 .6 mg vitamin A, 1 .3 mg vitamin B2, 1.1 mg vitamin B6, 4 μg vitamin B12, 40 mg vitamin C, 10 μg vitamin D3, 10 mg vitamin E, 200 mg folic acid, 130 mg magnesium, 15 μg selenium, 2 mg zinc, 0.3 mg manganese, 0.2 mg copper, 1 .6 mg beta carotene, 0.8 mg retinol, 10 mg lutein, 10 mg lycopene, 50 mg coenzyme Q10, 50 mg ubiquinol, 500 mg phytosterols and 300 mg MSM, if not food covers sufficient amounts.

With respect to several nutrients, age- and sex-dependent recommended daily allowance (RDA) and upper safe limits are provided. Examples for those are:

Table 1. Examples for Age- and Sex-Dependencies of Nutrients

Without increased risk, the individual may preferably take up the RDA amount of the respective nutrient. Therefore, the nutrient composition may also comprise these nutrients in correspondingly lower amounts not higher than the maximal RDA.

In a preferred embodiment, the amount to be taken up per day, i.e., the "genetically recommended amount" ("GRA") may be directly proportional to the sum of all odd ratios

(ORs). Herein, an "odds ratio" (abbreviation: "OR") refers to the likelihood of developing a certain disorder or condition as defined by the known increase of disease risk caused by the presence of a genetic variant. An odds ratio of 1 demonstrates the average population risk, while an odds ratio of 2 indicates twice the lifetime risk of the average population. The genetic risk odds ratio converted to percent (%) (OR %) is defined as 0% for the lowest possible OR and 100% for the highest possible OR. Specific determination examples of the OR % are enlisted in detail in the example section.

As the amount may preferably not exceed above the maximum to be taken up, i.e., the "upper genetic limit" 'UGL"), the ORs may preferably be multiplied by the therapeutic index, i.e., the amount interval between the UGL and the recommended daily allowance (RDA) recommended by the NIH and/or the FDA and/or FDA for a comparable healthy individual. The GRA may preferably be directly proportional to (UGL - RDA) ^* ORs %). Highly preferably, the amount to be taken up per day, i.e., the GRA is determined by the following formula:

GRA = (RDA + ((UGL - RDA) ^* ORs %) with the provision that when GRA > UGL, then GRA = UGL

Legend

GRA = Genetically recommended amount meaning the amount of nutrient to be taken per day

RDA = Recommended daily allowance as determined by NIH and/or FDA (see examples below)

UGL = Upper genetic limit of nutrient amount to be taken per day based on scientific studies and recommendations from the NIH and/or FDA (see examples below) OR % = Determined odds ratio for the pathological condition based on genetic testing expressed as percentage (see examples in the example section below) The RDA and UGL values herein are most preferably those recommended by the NIH at the filing date of the present application. Nevertheless, the person skilled in the art will notice that it may alternatively also be beneficial to use such amounts recommended at the time the method of the present invention is used. Exemplarily, the amount recommended for calcium, when the set of pathological conditions tested comprises three pathological conditions (i.e., osteoporosis, heavy metal poisoning and calcium homeostasis disease) may optionally be determined by the formula:

⁺ ((L'GZ-(calcium)— ^* (OR % (osteoporosis) ⁺ OR % (heavy metal poisoning) ^"*~ OR />(calcium uptake)) with the provision that when GRA > UGL, then GRA = UGL Herein, the mentioned pathological conditions (i.e., osteoporosis, heavy metal poisoning and calcium uptake) mentioned in the context of odds ratios (OR %) mean the odds ratios for developing one or more of said pathological condition(s). The detailed values for OR % are exemplified in the example section below. For a healthy individual of between 19 and 50 years with medium risk for developing one of the pathological conditions of 50 % and negligible risks for the others, the

may exemplarily be determined as = (1000 mg + (2500 mg - 1000 mg) ^* (medium risk = approx. 50 %)) = (1000 mg + 1500 mg ^* 0.5)

= 1750 mg

For other nutrients and/or further pathological condition(s), the respective GRA may be determined correspondingly.

Table of the formulas to determine the GRA for each nutrient:

As mentioned above, in the context of the present invention, the nutrient composition is personalized. Herein, "personalized" means that the nutrient composition is optimized for one particular individual. It may be optimized with respect to the combination of particular types of nutrients and/or with respect to the amount of certain nutrient(s) to be administered per day. The amount to be administered per day may be, preferably, defined by an instruction leaflet accompanying the obtained nutrient mixture.

Exemplarily, in a highly preferred embodiment, a patient suffering of Alzheimer's disease and simultaneously being at high risk of developing osteoporosis may receive a nutrient composition comprising: calcium, in particular wherein the amount intended for daily administration is in the range of approximately 2500 mg,

vitamin D3, in particular wherein the amount intended for daily administration is in the range of approximately 0.025 mg,

magnesium, in particular wherein the amount intended for daily administration is in the range of approximately 350 mg,

iron, in particular wherein the amount intended for daily administration is in the range of approximately 30 mg,

vitamin A, in particular wherein the amount intended for daily administration is in the range of approximately 7.5 mg,

vitamin C, in particular wherein the amount intended for daily administration is in the range of approximately 1500 mg,

vitamin E, in particular wherein the amount intended for daily administration is in the range of approximately 200 mg,

zinc, in particular wherein the amount intended for daily administration is in the range of approximately 30 mg,

selenium, in particular wherein the amount intended for daily administration is in the range of approximately 0.3 mg,

manganese, in particular wherein the amount intended for daily administration is in the range of approximately 8 mg,

lycopene, in particular wherein the amount intended for daily administration is in the range of approximately 30 mg,

lutein, in particular wherein the amount intended for daily administration is in the range of approximately 30 mg, and

alpha lipoic acid, in particular wherein the amount intended for daily administration is in the range of approximately 600 mg,

Then, the nutrient composition sufficient for a period of 100 days may exemplarily comprise approximately: 250 g calcium, 2.5 mg vitamin D3, 35 g magnesium, 3 g iron, 750 mg vitamin A, 150 g vitamin C, 20 g vitamin E, 3 g zinc, 300 mg selenium, 800 mg manganese, 3 g lycopene, 3 g lutein and 60 g alpha lipoic acid and approximately 550 g filler.

According to this example, the individual to be administered will receive approximately 1 kg of nutrient composition and will be advised to swallow 1/100 thereof, i.e., an amount of 10 g, per day. Additionally, the composition may optionally further comprise one or more other nutrients in lower amount, in particular in an amount recommended as RDA by the FDA and/or NIH such as, e.g., omega 3 fatty acids, vitamin B2, vitamin B6, vitamin B12, folic acid, copper, beta carotene, retinol, coenzyme Q10, ubiquinol, phytosterols and/or MSM. Most preferably, the composition further comprises essentially all of these nutrients particular in an amount recommended as RDA by the FDA and/or NIH. Amounts intended for daily administration are further exemplified in the example section.

The term "individual" as used throughout the present invention may be understood in the broadest sense as any subject that may be administered with the nutrient composition according the present invention. Preferably, one individual is a multicellular animal, in particular a human or an animal of human use (e.g., a bovine, a swine, a sheep, a goat, a cat, a dog, a chicken, a duck, a turkey). Most preferably, the individual is a human. In case the individual is in a pathological condition it may also be designated as a "patient", most preferably wherein the patient is a human patient.

As used in the context of the present invention the term "pathological condition" may be understood in the broadest sense as any state of health that distinguishes from the healthy state. This may also refer to a metabolic abnormality that is in itself no disease, but shows a difference in metabolism when compared to the norm. In a more severe case, it may be a disease. A pathological condition may bear symptoms or may be free of any symptoms. Exemplarily, lactose intolerance is typically free of any symptoms as long as no milk products are ingested. A pathological condition may also include the pre-state of developing a disease as well as the rehabilitation phase after a disease.

As laid out above, the individual is tested for its predisposition for the risk of developing or having one or more of a set of pathological conditions. Herein, a "set of pathological conditions" is a plurality of defined kinds of pathological conditions. Preferably, a set of pathological conditions comprises at least two pathological conditions, more preferably at least three pathological conditions, even more preferably at least four pathological conditions, even more preferably at least five pathological conditions, most preferably more than five pathological conditions that are tested.

The risk of developing a pathological condition is the disposition for the pathological condition is, i.e., the statistical likelihood of bearing the pathological condition in the future. The alleles are thus over-represented in frequency in individuals bearing a particular pathological condition as compared to healthy individuals. Thus, these alleles can be used to predict pathological condition even in pre-symptomatic or pre-diseased individuals. This does evidently not mean that the pathological condition indeed appears in every case. The disposition in the sense of the present invention is the individual's genetic predisposition. Therefore, due to its genome, the patient has a certain risk of developing a particular pathological condition. The person skilled in the art will notice that the risk also depends on environmental influences.

According to the present invention, the risk of developing a pathological condition is determined by any means known in the art. Herein, the term "determining" may be understood interchangeably with "identifying", "detecting" and "defining". Should the determination be performed in vivo, also the term "diagnosing" may be understood interchangeably. Preferably, the step of determining the risk is performed in vitro.

Any pathological condition in which predisposition depends on the individual's genome will typically be associated with one or more particular allele(s) of one or more gene(s).

As well-known by the person skilled in the art, a gene is, in the broadest sense, a molecular string of genetic code letters (bases) containing instructions for the body how to construct a protein. Simplified, a gene is an instruction for the body to carry out one or more functions.

The person skilled in the art will immediately understand the meaning of an allele. In the sense of the present invention, an allele is one particular of a number of alternative forms of the same gene, i.e., a genetic variation. As used herein, a genetic variant refers to the coexistence of more than one form of a gene or portion (e.g., allelic variant) thereof. A portion of a gene of which there are at least two different forms, i.e., two different nucleotide sequences, is referred to as a "polymorphic region of a gene". The presence of an allele may or may not result in a characteristic observable phenotypic trait, i.e., exemplarily the incidence of one or more particular pathological condition(s). The wild- type allele is usually the most common version of the gene in the population and the low risk version/allele. Mutant allele may typically be the rarer allele of the allele that may carry the higher disease risk. The person skilled in the art will further be aware of the fact that most multicellular organisms have two sets of chromosomes, i.e., that they are diploid, and that the individual, therefore, may be homozygote (i.e., both genes represent the same allele) or heterozygote (i.e., both genes represent different alleles). An individual carrying two copies of the mutant allele is a homozygote mutant. This genetic combination is usually detrimental to the individual's health. In many cases, the individual in which the predisposition for a certain pathological condition is encoded by both genes, the risk for developing the pathological condition may be higher than in a heterozygote individual. Herein, an increased risk describes a statistically higher risk or frequency of the development of a disease or metabolic abnormality in a subject carrying a certain genetic variant. In many cases the risk of developing of a particular pathological condition is associated with a particular allele present in the individual's genome. Then, the correlation between the genetic background, i.e., the presence of a certain allele, and the risk is particularly easy to detect. In other cases, a particular pathological condition is associated with a particular pattern of a plurality of alleles present in the individual's genome. In yet other cases, a plurality of pathological conditions (a certain disease pattern) is associated with one or more particular allele(s) present in the individual's genome. In the latter cases, the correlation between the genetic background and the risk is more difficult to detect. However, the person skilled in the art will be aware of numerous pathological conditions and their genetic profile and the respective risks.

In order to enable determining the risk, a set of alleles is identified. These alleles represent the forms of a plurality of genes, i.e., a set of genes. Herein, a "set of genes" is a plurality of defined kinds of genes. Preferably, as a set of genes comprises at least two genes, more preferably at least three genes, even more preferably at least four genes, even more preferably at least five genes, most preferably more than five genes that are tested. In this context, the alleles of interest are identified in the individual's genome. This may be performed by any means for identifying alleles in the art.

Exemplarily, the alleles of interest may be identified in the individual's genome by means of performing a set of polymerase chain reaction (PCRs) each using a pair of primers specific for one particular allele. The results may optionally be visualized by electrophoresis (e.g., gel electrophoresis, capillary electrophoresis etc.) This may preferably be performed by real-time PCR. Alternatively or additionally, the fraction of the genome that is of interest is isolated and sequenced. The isolation may be optionally performed by PCR. Then the step of isolation also includes amplification of the fraction of interest. Alternatively or additionally, the fraction of the genome that is of interest is contacted with a set of specific probes each specific for one particular allele. Herein, an isolated fraction of interest or the whole genome or parts thereof may be use. Alternatively or additionally, the alleles of interest may be identified in the individual's genome by determining selective binding to one microarray spot bearing complementary structures selectively binding to one particular allele, to beads (e.g., by co-precipitating) or to a selective affinity column. Alternatively or additionally, the alleles of interest may be identified as part of a whole genome sequencing approach, whereby the entire genetic code of an individual (-3.2 billion genetic bases) is determined through either millions of parallel sequencing reactions or nanopore technology, whereby DNA is pulled through a microscopic pore and analyzed in the process.

From the step as laid out above, the user of the method of the present invention will obtain information on the presence of a particular pattern of alleles and is, based on the information on the association of certain pathological conditions with these alleles obtainable from literature, able to determine at which risk the individual is to develop a certain pathological condition or even more than one pathological conditions or whether the individual even has already developed one or more particular pathological condition(s). Based on the individual's genetic predisposition for the risk of developing or having one or more of a set of pathological conditions, the person skilled in the art using the method of the present invention will be able to determine the amounts and ratios of nutrients selected of a set of nutrients suitable for preventing or treating the one or more pathological condition(s) identified as being of risk. In this context, the person skilled in the art will preferably use amounts as recommended by official institutes such as the NIH and/or the FDA, in particular when the individual of interest is a human. The recommended amounts herein are most preferably those recommended by the NIH at the filing date of the present application. Nevertheless, the person skilled in the art will notice that it may alternatively also be beneficial to use such amounts recommended at the time the method of the present invention is used.

Should it be found out that a particular nutrient is determined as beneficial (and not detrimental) for the individual, typically an amount not lower than the recommended daily allowance (RDA) will be intended to be administered per day. The ratio between different ratios depends on the risk profile of the individual. The "risk profile" or "genetic risk profile" is the compilation of all risks for the set of pathological conditions the individual is tested for. Often, some nutrients may be particularly beneficial in combination with another as they bear a synergistic effect. In other cases, the use of a certain nutrient may be beneficial for preventing or treating one pathological condition, but is contraindicated when said individual is at risk of or even has another pathological condition. Then, as far as possible, the contraindicated nutrient is replaced by another nutrient beneficial for the first pathological condition. When the amounts and ratios of the nutrients in the nutrient composition are determined, the nutrient composition comprising the determined amounts and ratios of nutrients is actually produced. This may be performed by any means. Preferably, the nutrient composition is obtained from mixing defined amounts from nutrient stocks with another. These nutrient stocks may be solid stocks or liquid stocks and may optionally comprise one or more carrier(s) such as, e.g., fillers. The amounts obtained from the stocks may be mixed by any means such as, e.g., by means of a mixer and/or a blender, by shaking, by stirring and/or by dissolving the nutrient(s) in a liquid carrier.

Finally, the individual at risk of or having one or more of a set of pathological condition(s) may be administered with the nutrient composition obtained from the method of the present invention.

In the context of the present invention, the set of pathological conditions that is tested for may comprise any pathological condition associated with the presence of one or more particular allele(s) in the genome known in the art. Preferably, the contested pathological conditions are those being dependent on the genetic profile of the patient.

In a preferred embodiment, the set of pathological conditions comprises at least one pathological condition selected from the group consisting of:

(a) a neurogenerative disease, in particular Alzheimer's disease;

(b) a cardiovascular disease, preferably Atherosclerosis, hyperlipidemia, hypercholesterolemia, coronary artery disease or homocysteinemia;

(c) a calcium uptake modification, in particular likely daily uptake of calcium;

(d) a metabolic disorder, in particular hyperlipidemia, hypercholesterolemia, or increased homocysteine levels;

(e) metal poisoning, preferably iron overload disease and/or heavy metal poisoning, in particular quicksilver intoxication, cadmium intoxication or lead intoxication;

(f) iron overload disorders, in particular hemochromatosis;

(g) macular degeneration, in particular age-related macular degeneration;

(h) an inflammatory disorder, preferably arthritis, in particular rheumatoid arthritis, Bechterew's disease or periodontitis;

(i) neoplasia, preferably cancer, in particular prostate cancer or breast cancer, or prostatic hyperplasia;

(j) a reduced protection against oxidative stress; and

(k) a food intolerance, in particular lactose intolerance,

preferably wherein said method comprises determining the risk of developing at least two, at least three, at least four, at least five or even all of said pathologic conditions. For each determined risk or pathological condition, there may be a standard nutrient composition, i.e., a standard nutrient composition for individuals at risk of developing or having a particular pathological condition (e.g., for individuals at risk of developing osteoporosis). When there are standard nutrient compositions for each pathological condition, there may be at least two, at least five, at least ten, at least 15, at least 20 or even more different nutrient compositions each associated with the risk or presence of a particular pathological condition. In particular these nutrient compositions are multi-vitamin compositions. When an individual is determined to be at risk thereof or even already has such pathological condition(s), then the respective nutrient composition is administered.

Alternatively and particularly preferably, for each individual an entirely personalized nutrient composition is prepared. This requires the determination of the individuals alleles associated with the set of pathological conditions.

Accordingly, for each pathological condition, one or more alleles of one or more genes may indicate a certain risk. Today, it is estimated that every individual carries around 2000 genetic variants that negatively influence one individual's health and contribute to the likelihood of development of pathological conditions. Therefore, the method may be used to determine the presence of all of these 2000 alleles and even more or a selected set thereof. The determined alleles may be any alleles known or estimated as having an association with one or more pathological condition(s).

In a preferred embodiment, the set of alleles comprises alleles of at least one of the genes selected from the group consisting of:

(a) an apolipoprotein (APO) gene, in particular an apolipoprotein A1 (APOA1 ) gene, an apolipoprotein A5 (APOA5) gene and/or an apolipoprotein E (APOE) gene;

(b) a cadherin 13 (CDH13) gene;

(c) a coronary heart disease susceptibility to 8 (CHDS8) gene;

(d) a paraoxonase 1 (PON1 ) gene;

(e) a methylenetetrahydrofolate reductase (MTHFR) gene;

(f) a methionine synthase reductase (MTRR) gene;

(g) a collagen gene, preferably a collagen type 1 (Coll ) gene, in particular a collagen type 1 alpha 1 (Col1A1 ) gene;

(h) a vitamin D receptor (VDR) gene;

(i) a lactase (LCT) gene;

0 a heredity hemochromatosis protein (HFE) gene;

(k) a complement factor H (CFH) gene; (I) a high-temperature requirement A serine peptidase 1 (HTRA1 ) gene;

(m) an age-related maculopathy susceptibility 2 (LOC2) gene;

(n) a glutathion S-transferase (GST) gene, in particular a glutathion S-transferase M1 (GSTM1 ) gene, a glutathion S-transferase T1 (GSTT1 ) gene, a glutathion S- transferase P1 (GSTP1 ) gene, GSTP1 ;

(o) a tumor necrosis factor alpha (TNF-alpha) gene;

(p) a histocompatibility antigen B27 (HLA-b27) gene;

(q) a glutathione peroxidase 1 (GPX1 ) gene;

(r) a superoxide dismutase 2 (SOD2) gene; and

(s) a quinone acceptor oxidoreductase 1 (NQ01 ) gene,

preferably wherein the set of alleles comprises alleles of at least two, at least three, at least four, at least five or at least ten of said genes.

In the context of the present invention, an allele may be any variation of a gene. Exemplarily, different alleles may be single nucleotide polymorphisms (SNPs), frameshift mutations, the lack of a gene or of a part of a gene (excision, when the entire gene is absent from the persons genome also designated as "null allele") and/or the multiplication of a gene (duplicate, triplicate etc.).

It will be understood that genetic variants can be displayed in two orientations, one focusing on the so-called "sense" strand of the double stranded DNA molecule and the other focusing on the antisense strand. For the purpose of this invention, exemplarily, a genetic variant describing the genetic base letter "A" (i.e., nucleotide adenine) also describes the reverse of view of the same genetic variant corresponding to the letter "T" (i.e., nucleotide thymidine). High density lipoprotein, for example is the so called good cholesterol. High levels HDL are known to be beneficial for cardiovascular health.

Exemplarily, the following correlations between the presence of certain alleles and pathological conditions may be of use according to the present invention: a) APOA1 rs670 (A/A & A/G) causing Omega 3 to increase HDL cholesterol levels while the APOA1 rs670 (G/G) genotypes decrease HDL cholesterol;

b) CDH 13 rs8055236 (A/G & G/G), CHDS8 rs1333049 (C/G & C/C), APOA5 rs662799 (C/T & C/C), APOE (E2/E3, E3/E3, E2/E4, E3/E4, E4/E4), PON 1 rs662 (A/G & G/G) and rs854560 (A/T & A/A) increasing the risk of cardiovascular disease and atherosclerosis;

c) MTHFR rs1801 133 (T/T) giving the micronutrient Vitamin B2 homocysteine lowering properties; d) MTRR rs1801394 (A/G & G/G) and MTHFR rs1801 133 (C/T & T/T) increasing homocysteine levels,

e) APOE (E2/E2, E2/E3) lowering the Alzheimer's disease risk and APOE (E2/E4, E3/E4, E4/E4) increasing Alzheimer's disease risk;

f) Col1A1 rs1800012 (G/T & T/T) and VDR rs1544410 (A/G & A/A) increasing the risk of osteoporosis;

g) LCT rs4988235 (C/C) decreasing the average calcium intake;

h) HFE rs1799945 (C/G & G/G), HFE rs1800730 (C/G & G/G) and HFE rs1800562 (A/G & A/A) increasing iron absorption and the risk of iron overload disorder;

i) CFH rs1061 170 (C/T & C/C), HTRA1 rs1 1200638 (A/G & A/A) and LOC387715 rs10490924 (G/T & T/T) increasing the risk of age related macular degeneration; j) GSTM1 Null Allele, GSTT1 Null Allele and GSTP1 rs1695 (A/G & G/G) decreasing the detoxification capacity of the heavy metals lead, mercury and cadmium;

k) TNF-alpha rs1800629 (A/G & G/G) and HLA B27 increasing the risk of inflammation mediated joint damage;

I) GPX1 rs1050450 (C/T & T/T), SOD2 rs4880 (C/T & T/T), GSTM1 Null Allele, GSTT1 Null Allele and GSTP1 rs1695 (A/G & G/G) decreasing protection from oxidative stress; and

m) NQ01 rs1800566 (C/T & T/T) reducing the conversion of Coenzyme Q10 to the active form ubiquinol.

As used herein, the "rs"-numbers refer to the accession numbers used by the open excess data bank of the National Center for Biotechnology Information (NCBI) (U.S. National Library of Medicine 8600 Rockville Pike, Bethesda MD, 20894 U.S.A.) describing the respective genetic variant in detail.

Exemplarily, in an individual subjected to the method of the present invention the genotype of the APOA1 gene may be determined. Then, the determining of the genotype may preferably also include the determining the APOA1 rs670 alleles present in the individual's genome, in particular whether the individual has an APOA1 rs670 (A/A) homozygous genotype, an APOA1 rs670 (A/G) heterozygous genotype or an APOA1 rs670 (G/G) homozygous genotype. It is known that APOA1 rs670 (A/A) and APOA1 rs670 (A/G) typically cause an increase of HDL cholesterol levels when omega 3 fatty acids are ingested, while the APOA1 rs670 (G/G) genotype typically causes a decrease of HDL cholesterol levels. Accordingly, an individual having the APOA1 rs670 (A/A) or the APOA1 rs670 (A/G) genotype will typically experience a beneficial health effect from the administration of polyunsaturated fatty acids (PUFAs) (e.g., omega 3 fatty acids) and may, therefore, preferably be administered with PUFAs. In contrast, an individual having the APOA1 rs670 (G/G) genotype will typically experience no positive effect of the administration of PUFAs and may, therefore, preferably not be administered with PUFAs, more preferably PUFAs may even be avoided is the nutrition of said individual. Exemplarily, the amount recommended for omega 3 fatty acid, when the set of pathological conditions tested comprises the pathological condition cardiovascular disease may optionally be determined by the formula:

GRA_(omega 3) = {RDA_(omega 3) + {{UGL_{(omega 3)} - RDA_{(omega 3)}) ^* {OR %(cardiovascular disease))) with the provision that when GRA > UGL, then GRA = UGL

The values, in particular the OR % conversion is shown in detail in the example section below (cf., in particular table 6). Therefore, for an individual of between 19 and 50 years having an APOA1 rs670 (A/A) homozygous genotype, the GRA_{(omega 3)} may be defined as:

GRA_{(omega 3}) = (250 mg + (2500 mg - 250 mg) ^* 100%) = 2500 mq For an individual of between 19 and 50 years having the highest-risk combination of CDH 13 rs8055236 (G/G), CHDS8 rs1333049 (C/C), APOA5 rs662799 (C/C), APOE (E4/E4), PON 1 rs662 (G/G) and rs854560 (A/A), the risk of developing cardiovascular disease is highest. Then, the amount of omega 3 to be administered daily may be the highest on the scale, namely 2.5 g per day.

Optionally, phytosterols may be used instead of Omega 3 in carriers of the APOA1 rs670 (G/G) genotype that do not respond well to OMEGA 3 in order to lower cholesterol. Additionally or alternatively, in an individual subjected to the method, the genotype of the NQ01 rs1800566 alleles present in the individual's genome may be determined; In particular whether the individual is an NQ01 rs1800566 (C/C) homozygote, an NQ01 rs1800566 (C/T) heterozygote or an NQ01 rs1800566 (T/T) homozygote. When the individual is an NQ01 rs1800566 (C/C) genotype, the individual is able to convert Coenzyme Q10 effectively to Ubiquinol and thus only requires the RDA of Coenzmye Q10. When the individual is an NQ01 rs1800566 (C/T) genotype, the individual is not as effective in converting Coenzyme Q10 to Ubiquinol and may thus require 50% of the RDA of Coenzyme Q10 and 50% RDA of the already activated form Ubiquinol. When the individual is an NQ01 rs1800566 (T/T) genotype, the individual is unable to convert Coenzyme Q10 to the active form Ubiquinol and thus requires 100% RDA of the active form Ubiquinol and 0% RDA of Coenzyme Q10.

27 of the most prominent genetic variants are exemplarily depicted in table 2. Exemplarily, ten different genetic markers are provided that had been selected on the basis of their effect on the risk of cardiovascular diseases such as atherosclerosis, hyperlipidaemia, hypercholesterolemia, coronary artery disease, general heart disease, homocysteine regulation and high density lipoprotein cholesterol regulation.

Table 2. Genetic Markers and Risks of Developing Pa hological Conditions

These alleles and their applicability is further shown in more detail in the example section. The various alleles of APO-E are depicted in detail in table 3. Table 3. Genetic Determination of APO-E Type:

Herein, the risk for hyperlipoproteinemia type III, cardiovascular disease and Alzheimer's disease is: low for genotypes: E2/E2, E2/E3, E3/E3, whereas it is comparably high for genotypes: E2/E4, E3/E4, E4/E4. Many further correlations are well-known by those skilled in the art and published in literature.

Optionally, phytosterols may be used instead of Omega 3 in carriers of the APOA1 rs670 (G/G) genotype to lower cholesterol. Vitamin B2 may be increased above the RDA in carriers of the MTHFR rs1801 133 (T/T) genotype, but preferably only when homocysteine is lowered by vitamin B12. The amount of daily calcium may be increased in genotypes of LCT rs4988235 (C/C), likely to be, or become lactose intolerant and ingest less calcium per day. Iron may preferably only be given to an individual not genetically predisposed to iron overload disorder. Coenzyme Q10 may preferably only be given to an individual with the NQ01 rs1800566 (C/C & C/T) genotypes as only they are able to convert Coenzyme Q10 to the active form ubiquinol. Ubiquinol may preferably only given to NQ01 rs1800566 (C/T & T/T) genotypes as they have little or no conversion capacity from coenzyme Q10 to ubiquinol.

In a preferred embodiment, at least one of the identified alleles is tested for comprising a single nucleotide polymorphism (SNP) discriminating different alleles of a gene from another, preferably wherein at least two, at least three, at least four, at least five, at least ten or even all of the identified alleles are tested for comprising an SNP.

As laid out above, when a certain risk pattern for the individual has been established, the amounts and ratios of nutrients in the nutrient composition are determined and the nutrients are mixed accordingly. A nutrient as used herein may be any nutrient known in the art.

In a preferred embodiment, the set of nutrients comprises at least one nutrient selected from the group consisting of a fatty acid, a vitamin, a trace element, a secondary plant compound a coenzyme or a sulfur supplement,

preferably wherein

(a) a fatty acid is an essential fatty acid, preferably a poly unsaturated fatty acid, in particular an omega 3 fatty acid;

(b) alpha lipoic acid;

(c) a vitamin is folic acid, vitamin A, vitamin B2, vitamin B6, vitamin B12, vitamin C, vitamin D3 and/or vitamin E;

(d) a trace element is calcium, zinc, selenium, magnesium, iron, copper and/or manganese;

(e) a secondary plant compound is a carotenoid, in particular lycopene, beta-carotene, lutein and/or a phytosterol; (f) a coenzyme, in particular coenzyme Q10 and/or ubiquinol; and/or

(g) a sulfur supplement is methylsulfonylmethane (MSM),

in particular wherein the nutrient composition comprises at least two, at least three, at least four, at least five or even all of said nutrients.

Poly unsaturated fatty acids (PUFAs), for instance are a certain form of fat that is considered to be more healthy than other types of fat and commonly ingested in form of fish oil capsules (Omega 3) for their typical cholesterol-lowering effect. Preferably, the nutrients suitable for preventing or treating an individual being at risk of developing or having a particular pathological condition are orally administered. Exemplarily, a nutrient composition for preventing or treating an individual being at risk of developing or having a cardiovascular disease (including the risk factor of an elevated homocysteine level) may preferably comprise omega 3 fatty acid, one or more phytosterol(s), folic acid, vitamin B6, vitamin B12 and/or vitamin B2. More preferably, such composition comprises at least two of the aforementioned nutrients, even more preferably at least three of the aforementioned nutrients and even more preferably at least four of the aforementioned nutrients. In a particularly preferred embodiment, such composition comprises all of the aforementioned nutrients. Herein, the amounts of the particular nutrients sufficient for preventing or treating a cardiovascular disease are preferably calculated as shown above and exemplified in the examples section below.

Exemplarily, a nutrient composition for preventing or treating an individual being at risk of developing or having Alzheimer's disease may preferably comprise vitamin C, vitamin E, zinc, selenium, manganese, vitamin A, lycopene, lutein and/or alpha lipoic acid. More preferably, such composition comprises at least two of the aforementioned nutrients, even more preferably at least three of the aforementioned nutrients and even more preferably at least four of the aforementioned nutrients. In a particularly preferred embodiment, such composition comprises all of the aforementioned nutrients. Herein, the amounts of the particular nutrients sufficient for preventing or treating Alzheimer's disease are preferably calculated as shown above and exemplified in the examples section below.

Exemplarily, the amounts for a high risk individual may preferably be in the range of approximately:

vitamin C, in particular wherein the amount intended for daily administration is in the range of approximately 1500 mg, vitamin E, in particular wherein the amount intended for daily administration is in the range of approximately 200 mg,

alpha lipoic acid, in particular wherein the amount intended for daily administration is in the range of approximately 600 mg.

Exemplarily, a nutrient composition for preventing or treating an individual being at risk of developing or having osteoporosis may preferably comprise calcium, vitamin D3 and/or magnesium. More preferably, such composition comprises at least two of the aforementioned nutrients. In a particularly preferred embodiment, such composition comprises all of the aforementioned nutrients. Herein, the amounts of the particular nutrients sufficient for preventing or treating osteoporosis are preferably calculated as shown above and exemplified in the examples section below.

calcium, in particular wherein the amount intended for daily administration is in the range of approximately 2500 mg,

magnesium, in particular wherein the amount intended for daily administration is in the range of approximately 350 mg.

Exemplarily, a nutrient composition for preventing or treating an individual being at risk of developing or having a macular degeneration may preferably comprise vitamin C, vitamin E, zinc, vitamin A, lycopene and/or copper. More preferably, such composition comprises at least two of the aforementioned nutrients, even more preferably at least three of the aforementioned nutrients and even more preferably at least four of the aforementioned nutrients. In a particularly preferred embodiment, such composition comprises all of the aforementioned nutrients. Herein, the amounts of the particular nutrients sufficient for preventing or treating a macular degeneration are preferably calculated as shown above and exemplified in the examples section below. Exemplarily, a nutrient composition for preventing or treating an individual being at risk of developing or having a heavy metal poisoning may preferably comprise calcium, iron, vitamin C, vitamin E, zinc, selenium and/or alpha lipoic acid. More preferably, such composition comprises at least two of the aforementioned nutrients, even more preferably at least three of the aforementioned nutrients and even more preferably at least four of the aforementioned nutrients. In a particularly preferred embodiment, such composition comprises all of the aforementioned nutrients. Herein, the amounts of the particular nutrients sufficient for preventing or treating a heavy metal poisoning are preferably calculated as shown above and exemplified in the examples section below. Exemplarily, a nutrient composition for preventing or treating an individual being at risk of developing or having an inflammatory disease such as, e.g., arthritis may preferably comprise omega 3 fatty acids, vitamin C, vitamin E, zinc, selenium, manganese, copper and/or MSM. More preferably, such composition comprises at least two of the aforementioned nutrients, even more preferably at least three of the aforementioned nutrients and even more preferably at least four of the aforementioned nutrients. In a particularly preferred embodiment, such composition comprises all of the aforementioned nutrients. Herein, the amounts of the particular nutrients sufficient for preventing or treating an inflammatory disease are preferably calculated as shown above and exemplified in the examples section below.

Exemplarily, a nutrient composition for preventing or treating an individual being at increased oxidative stress may preferably comprise vitamin C, vitamin E, zinc, selenium, manganese, vitamin A, lycopene, lutein and/or alpha Lipoic acid. More preferably, such composition comprises at least two of the aforementioned nutrients, even more preferably at least three of the aforementioned nutrients and even more preferably at least four of the aforementioned nutrients. In a particularly preferred embodiment, such composition comprises all of the aforementioned nutrients. Herein, the amounts of the particular nutrients sufficient for preventing or treating a pathological condition associated with oxidative stress are preferably calculated as shown above and exemplified in the examples section below.

As laid out above, when a risks for developing or even the presence of more than one pathological condition is determined in a patient, the amounts of the single nutrients are preferably summed up until the level of the highest safe level. When it is calculated that the amount would be higher than the upper safe level, just the maximum amount thereof considered as safe is administered daily. When the individual is recognized as being of a particular risk for developing or even has a pathological condition that contraindicates the administration of a particular of these nutrients, then this nutrient may be preferably reduced in amount or - upon a severe increase of risk - omitted completely. Particularly preferably, then, this contraindicated nutrient is replaced by one or more other nutrient(s) considered useful to prevent or treat the pathological condition the individual is at risk of or even has, wherein said nutrient(s) is/are contraindicated for the individual.

The person skilled in the art will notice that the nutrients may be well-mixed in the nutrient composition. This may be achieved by any means known in the art. The person skilled in the art will further notice that the nutrient composition in the context of the present invention may also comprise further material.

In a preferred embodiment, producing a nutrient composition comprises mixing defined amounts of separate stocks each comprising one or more nutrient(s) and optionally further comprising an orally ingestible carrier, in particular wherein each stock comprises not more than a single nutrient and optionally an orally ingestible carrier.

As used herein, the term "orally ingestible carrier" may refer to any substance that is (nearly) not toxic when taken up orally and that is preferably accredited for oral uptake. Preferably accreditation is accreditation by the NIH and/or the FDA, in particular accreditation by the NIH at the filing date of the present application. Nevertheless, the person skilled in the art will notice that it may alternatively also be beneficial to refer to the current state of accreditation when employing the present invention. Accordingly, an orally ingestible carrier may be exemplarily any food or beverage.

The nutrient composition may be prepared as a dry form (e.g., as a powder, a tablet, a pill, a capsule, a chewable capsule, etc.) or a liquid (e.g., a spray, a syrup, a juice, a gel, a liquid, a paste, an injection solution, etc.) An acceptable carrier may be a solvent with no or low toxicity such as, e.g., water, dimethyl sulfoxide (DMSO), ethanol, vegetable oil, paraffin oil or combinations thereof. Furthermore, the carrier may optionally contain one or more detergents, one or more foaming agents (e.g., sodium lauryl sulfate (SLS)/ sodium doceyl sulfate (SDS)), one or more coloring agents (e.g., Ti0₂, food coloring), one or more salts (e.g., sodium or potassium salts), one or more humectants (e.g., sorbitol, glycerol, mannitol, propylenglycol, polydextrose), one or more enzymes, one or more preserving agents (e.g., benzoic acid, methylparabene), one or more texturing agents (e.g., carboxymethyl cellulose (CMC), polyethylene glycol (PEG), sorbitol), one or more emulsifiers, one or more fillers or bulking agents, one or more glacing agents, one or more separating agents, one or more antioxidants, one or more herbal and plant extracts, one or more stabilizing agents, one or more non-toxic polymers (e.g., hydroxypropyl methacrylamide (HPMA), polyethylene imine (PEI), carboxymethyl cellulose (CMC), polyethylene glycol (PEG)), one or more uptake mediators (e.g., polyethylene imine (PEI), dimethyl sulfoxide (DMSO), a cell-penetrating peptide (CPP), a protein transduction domain (PTD), an antimicrobial peptide, etc.) one or more antibodies, one or more sweeteners (e.g., sucrose, acesulfam K, saccharin Na), one or more dyes (e.g., fluorescein, fluorescein derivatives, Cy dyes, an Alexa Fluor dyes, S dyes, rhodamine, quantum dots, etc.), one or more homeopathic ingredients one or more gustatory substances and/or one or more fragrances.

A stock may be any storage form of which preferably the amount of nutrient per weight (weight/weight (w/w) or per volume (weight/volume (w/v)) of the stock material is known. This then enables the person skilled in the art to determine the amount and ratios mixed into the nutrient composition. Each stock may comprise one or more nutrient(s). Preferably, each stock comprises one nutrient. The stock may be solid or liquid. In a preferred embodiment, the stocks are stocks of solid material and/or liquid stock solutions, preferably stocks of solid material of spherical or ellipsoid pellets, in particular wherein the pellets have an essentially homogenous size.

As used herein, a spherical pellet is a ball-shaped globular particle. Preferably, a spherical or ellipsoid pellet in the sense of the present invention has a diameter between about 1 μηη and about 5 mm, more preferably between about 10 μηη and about 5 mm, even more preferably between about 0.1 mm and about 4 mm, even more preferably between about 0.5 mm and about 3 mm, in particular between about 1 mm and about 3 mm. Then, mixing the nutrients is particularly comfortable and less laborious. Preferably, the pellets of a nutrient stock are of essentially homogenous size. That mean that particle-size distribution (PSD), also designated as grain size distribution, has a comparably low polydispersity.

As mentioned above, the method of the present invention may, in a preferred embodiment, further comprise the step of identifying the alleles of a gene comprised in said individual's genome in vitro. As laid out above, this may be performed by any means known in the art. Exemplarily, the presence of certain alleles may be identified by means of polymerase chain reaction (PCR). Then a pair primers specific for a particular allele may be used. PCR may optionally also be performed as real time PCR. Alternatively or additionally, a set of alleles may also be tested on a DNA or RNA chip that is also commercially available from various suppliers. Alternatively or additionally, a set of alleles may also be tested by means of labeled probes, in particular fluorescently labeled probes. Herein methods such as, e.g., whole genome sequencing, fluorescence resonance energy transfer (FRET), fluorescence quenching, fluorescence correlation spectroscopy (FCS), fluorescence cross-correlation spectroscopy (FCCS) and/or fluorescence depolarization assays may be used. Such method may be based and whole genome sequencing on a crude sample or on isolated deoxyribonucleic acid (DNA). In the context of isolated DNA, the term isolated in reference to DNA refers to the separation of the DNA molecule from other cell components in preparation for further genetic analysis, but may also refer to any other technique to prepare a sample of cells for genetic analysis.

In general, the steps of determining said individual's genetic predisposition according to the step (i) and for determining the amounts and ratios of nutrients according to step (ii) of the method of the present invention may be determined by any means. The determination may be performed manually or may be performed by a computer-implemented method.

Preferably, the method is a computer-implemented method wherein steps (i) and (ii) are carried out on an electronic equipment suitable for processing pattern of identified alleles, in particular wherein further also step (iii) is performed in an automated manner based on the amounts and ratio of nutrients determined in step (ii).

Therefore, a further aspect of the present invention relates to a computer program directly loadable into the internal memory of a digital computer, comprising software code portions for implementing for determining said individual's genetic predisposition according to the step (i) and/or for determining the amounts and ratios of nutrients according to step (ii) of the method of the present invention.

All definitions laid out in the context of the method according to the present as laid out above, also apply to the computer program according to the present invention.

According to the invention, a computer program product is provided for performing the previously explained method, when the product is run on a computer. The computer program product is preferred to be directly loadable into the internal memory of a digital computer and comprises software code portions for implementing the calculation of the risk score. The computer program product may be a computer program preferably stored on a machine readable storage medium like RAM, ROM, or on a removable CD-ROM, flash memory, DVD or USB-stick. The computer program may be provided on a server to be downloaded via for example a data network such as the internet or another transfer system such as a phone line or a wireless transfer connection. Additionally, or alternatively, the computer program product may be a network of computer implemented computer programs such as a client/server system or a cloud computing system, an embedded system with a computer program or an electronic device like a smart phone or a personal computer (PC) on which a computer program is stored, loaded, running, exercised, or developed.

The outcome of the method according to the present invention, independent on how it is performed, is a nutrient composition.

Therefore, in a further aspect, the present invention also refers to a nutrient composition obtained from the method of the present invention, wherein said composition is personalized and orally ingestible, in particular wherein said composition further comprises an orally ingestible carrier.

All definitions laid out in the context of the method and/or the computer program according to the present as laid out above, also apply to the nutrient composition according to the present invention. The amounts of a nutrient intended to be administered per day may preferably be not higher than the minimal toxic dose. This minimal toxic dose is the upper genetic limit (UGL) of nutrient amount to be taken per day based on scientific studies. The UGL is reduced to the highest legal daily dosage in this market. This typically refers to the amounts accredited by the NIH and/or the FDA, but possibly is also subject to country specific regulations. The UGL values herein are most preferably those recommended by the NIH at the filing date of the present application. Nevertheless, the person skilled in the art will notice that it may alternatively also be beneficial to use such amounts recommended at the time the method of the present invention is used. That the composition is personalized means that it is optimized for one particular individual. This distinguishes the nutrient composition according to the present invention from standard nutrient compositions and comestibles. In a preferred embodiment, comprising amounts of the one or more nutrient(s) comprised in said nutrient composition for daily intake are not lower than the recommended daily allowance (RDA) as recommended by the National Institute of Health (NIH) and not higher than the maximal recommended daily intake of the NIH, wherein the increase in amount correlates with the determined risk of developing or having one or more particular pathologic condition(s). Herein, the RDA and amounts recommended maximally for daily intake are most preferably those recommended by the NIH at the filing date of the present application. Nevertheless, the person skilled in the art will notice that it may alternatively also be beneficial to use such amounts recommended at the time the method of the present invention is used.

The preferred amount of a nutrient intended for oral uptake in the sense of the present invention is the genetically recommended amount (GRA). The maximum amount recommended for an individual.

Preferably, the amounts for daily intake of the following nutrients as far as comprised in the nutrient composition are:

alpha lipoic acid: between 200 mg and about 600 mg;

omega 3 fatty acids: between 250 mg and 2500 mg;

vitamin A: between about 1 .6 mg and about 10.8 mg, in particular between the RDA as recommended by the NIH and/or the FDA and the threefold of the RDA;

vitamin B6: between about 0.1 mg and 8,5 mg, in particular between the RDA as recommended by the NIH and/or the FDA and the fivefold of the RDA;

vitamin B12: between about 0.004 mg and 0.072 mg, in particular between the RDA as recommended by the NIH and/or the FDA and the threefold of the RDA;

vitamin C: between about 15 mg and about 1500 mg, in particular between the RDA as recommended by the NIH and/or the FDA and 1500 mg;

vitamin D3: between about 0.01 mg and 0.025 mg, in particular between the RDA as recommended by the NIH and/or the FDA and 0.025 mg;

calcium: between about 200 mg and about 2500 mg, in particular between the RDA as recommended by the NIH and/or the FDA and 2500 mg; magnesium: between about 130 mg and about 350 mg, in particular between the half of the RDA as recommended by the NIH and/or the FDA and 350 mg;

manganese: between about 0.3 mg and about 7.8 mg, in particular between the RDA as recommended by the NIH and/or the FDA and the threefold of the RDA;

lutein: between about 10 mg and about 30 mg;

lycopene: between about 10 mg and about 30 mg;

coenzyme Q10: between about 50 mg and about 300 mg;

ubiquinol: between about 50 mg and about 150 mg;

phytosterols: between about 500 mg and about 2500 mg; and/or

MSM: between about 300 mg and about 2500 mg.

As mentioned above the RDA is most preferably that amount recommended by the NIH at the filing date of the present application. Nevertheless, the person skilled in the art will notice that it may alternatively also be beneficial to use such amounts recommended at the time the method of the present invention is used.

In order to enable the administration of the correct amount to the individual in need thereof, the nutrient composition may form part of a kit comprising:

a) the nutrient composition;

b) a volume measuring device, such as, e.g., a spoon or cup; and

c) a personal dosage instruction. The nutrient composition may be any form. It may be solid or liquid. In a preferred embodiment, the composition forms a plurality of pellets, a powder, a pill, a dragee, a capsule, a gel, a syrup or a juice, preferably a plurality of pellets or a powder, in particular a plurality of essentially spherical pellets. As mentioned above, the nutrient composition according to the present invention may be used for medicinal, in particular a preventive or curative context. Therefore, a further aspect of the present invention refers to the nutrient composition according to the present invention for use as a medicament.

All definitions laid out in the context of the method, the computer program and, particularly, the nutrient composition according to the present as laid out above, also apply to the nutrient composition for use as a medicament as well as for the specific use laid out in detail in the following.

Alternatively, the use may also be used in a cosmetic method. Therefore, the composition according to the present invention may be used as a cosmetic product and/or as a beauty product.

In a still further aspect, the present invention relates to the nutrient composition according to the present invention for use in a method for preventing or treating at least one pathologic condition selected from the group consisting of:

(a) a neurogenerative disease, in particular Alzheimer's disease;

(d) a metabolic disorder, in particular hyperlipidemia, hypercholesterolemia, or increased homocysteine levels

(f) iron overload disorders, in particular hemochromatosis;

(g) macular degeneration, in particular age-related macular degeneration;

0 a reduced protection against oxidative stress; and

(k) a food intolerance, in particular lactose intolerance. Further, upon malnourishment (anorexia and/or bulimia), nutrition according to the present invention may be useful.

The nutrient composition according to the present invention may be administered by any means known in the art. In a preferred embodiment, the nutrient composition is administered orally, in particular administered once, twice or three times a day. The person skilled in the art may be informed about the exact amount for daily administration from dosing instructions accompanying the nutrient composition. Such dosing instruction may preferably be a personalized dosing instruction for one particular individual. Alternatively, it may be a generalized dosing instruction and the amount of each nutrient per weight of the entire nutrient composition (w/w) is adjusted in a way that each individual is instructed to take up the same amount of the nutrient composition per day. If he or she requires a lower amount of nutrients, the nutrient composition may then comprise accordingly more carriers (e.g., fillers).

The person skilled in the art will understand that the present invention therefore also refers to a method of preventing or treating at least one pathologic condition selected from the group consisting of:

(a) a neurogenerative disease, in particular Alzheimer's disease;

(f) iron overload disorders, in particular hemochromatosis;

(g) macular degeneration, in particular age-related macular degeneration;

(j) a reduced protection against oxidative stress; and

(k) a food intolerance, in particular lactose intolerance,

wherein the individual in use thereof is administered with sufficient amounts of the nutrient composition according to the present invention, in particular wherein the nutrient composition is administered orally, in particular administered once, twice or three times a day. The following figures and example are intended to illustrate the invention but not to limit the scope of protection conferred by the claims.

Figures

Figure 1 depicts the dosage finding strategies of polyunsaturated fatty acids (omega 3) and polysterols (A) and of vitamin B2 (B). Whereas an individual of the homozygous genotype APOA1 rs670 (A A which corresponds to T/T) or the heterozygous genotype APOA1 rs670 (A/G which corresponds to C/T) is recommended a daily dose of omega 3, homozygous genotype APOA1 rs670 (G/G, which corresponds to C/C)) is recommended not to ingest additional polyunsaturated fatty acids such as omega 3, but instead should ingest a daily dose of phytosterols.

Figure 2 depicts an example of producing a personalized nutrient composition. Different stocks of nutrients are provided (here, exemplarily, vitamin C, vitamin A and zinc). These stocks also comprise orally ingestible carriers (here, exemplarily, fillers). Due to the determined genetic risk profile of the individual, particular amounts of the three exemplified nutrients from the stocks are mixed and a particular amount of the obtained mixture (here, exemplarily. 8 g/day) is intended to be swallowed by the individual.

Examples

1 . Calculating the Genetic Risk

1 .1 . General Implications Based on the genetic polymorphisms described within this document, a number of genetic risks or metabolic abnormalities can be determined. As various polymorphisms may modify the likelihood of development of the same pathological condition, a method of evaluating the overall risk must be employed. To this end the multiplicative approach is commonly used in human genetic studies. In this approach, the odds ratio of a polymorphism is multiplied with the odds ratio of any other polymorphism predisposing to the same pathological condition. The resulting odds ratio is the total risk or likelihood of that person developing the pathological condition. 1 .2. Formula for Daily Dosage

GRA = (RDA + {{UGL - RDA) ^* (sum of pathological condition(s) ORs %)) with the provision that when GRA > UGL, then GRA = UGL Legend:

RDA = Recommended daily allowance as determined by NIH and/or FDA

(examples see below)

UGL = Upper genetic limit of nutrient amount to be taken per day based on scientific studies and recommendations from the NIH and/or FDA (examples see below)

OR % = Determined odds ratio for the pathological condition based on genetic testing (examples see below) expressed as a percentage

As mentioned above, the RDA and UGL are most preferably those amounts recommended by the NIH at the filing date of the present application. Nevertheless, the person skilled in the art will notice that it may alternatively also be beneficial to use such amounts recommended at the time the method of the present invention is used.

Herein the "OR" and "odds ratio", respectively, demonstrates the likelihood of developing a certain disorder or condition. An odds ratio of 1 demonstrates the average population risk, while an odds ratio of 2 indicates twice the lifetime risk of the average population. The genetic risk odds ratio converted to % (OR %): The determined odds ratio for the disease or genetic abnormality based on genetic testing converted to %. This is further exemplified below.

RDA+ ( (UGL-RDA) x (ALZ OR % + HEAV OR % + OXIDOR

Lutein GRA = %) )

RDA+ ( (UGL-RDA) x (ALZ OR % + HEAV OR % + OXIDOR

Lycopene GRA = %) )

Magnesium GRA = 50% RDA + ( (UGL - RDA) x OSTEO OR % )

RDA + ( (UGL - RDA) x (ALZ OR % + OXID OR % + ARTH OR

Manganese GRA = % ) )

MSM GRA = RDA + ( (UGL - RDA) x ARTH OR % )

( RDA + ( (UGL - RDA) x (CARD OR % + ARTH OR %) ) x PUFA

Omega 3 GRA = OR%

( RDA + ( (UGL-RDA) x (CARD OR %) x ((PUFA OR % -1) x -

Phytosterols GRA = 1)

RDA + ( (UGL-RDA) x (ALZ OR % + HEAV OR % + OXIDOR

Selenium GRA = % + ARTH OR % ) )

Ubiquinol GRA = RDA x (Q10OR% - 100%) x -1)

RDA + ( (UGL-RDA) x (ALZ OR % + HEAV OR % + OXIDOR

Vitamin A GRA = %) )

Vitamin B12 GRA = ( RDA + ( (UGL - RDA) x (HOMO OR %) )

Vitamin B2 GRA = RDA + ( ( (UGL - RDA) x (HOMO OR %) ) x B2 HOM OR % )

Vitamin B6 GRA = ( RDA + ( (UGL - RDA) x (HOMO OR %) )

RDA + ( (UGL-RDA) x (ALZ OR % + AMD OR % + HEAV OR

Vitamin C GRA = % + OXID OR % + ARTH OR % ) )

Vitamin D3 GRA = RDA + ( (UGL - RDA) x (OSTEO OR % + CALC OR %) )

RDA + ( (UGL-RDA) x (ALZ OR % + AMD OR % + HEAV OR

Vitamin E GRA = % + OXID OR % + ARTH OR % ) )

RDA + ( (UGL-RDA) x (ALZ OR % + AMD OR % + HEAV OR

Zink GRA = % + OXID OR % + ARTH OR % ) )

Example Determination

Polymorphism 1 C/G OR: 1.85

Polymorphism 2 G/G OR: 1

Polymorphism 3 A/T OR: 2.65

Polymorphism 4 C/A OR: 2.2 Combined risk under the multiplicative model: 1.85 x 1 x 2.65 x 2.2 = OR 10.7855

This means the person with this genotype is 10.7855 times more likely to develop a given disease than an individual with the optimal genotype (1 x1 x1 x1 = OR 1).

It should be noted that for some polymorphisms, no odds ratios have been determined to date. In this case, the influences of these polymorphisms on risk are assumed to be equal in strength. 2. Determining Risks 2.1. Determining the Risk of Cardiovascular Disease

The likelihood of developing atherosclerosis, hyperlipidaemia, hypercholesterolaemia, heart disease and coronary artery disease (abbreviated as cardiovascular disease (CD)) is influenced by seven genetic polymorphisms in this program. While other genetic polymorphisms exist, that also modify the risk of developing these disorders, scientific studies have shown that the selected genetic polymorphisms have the greatest effect on the risk of developing the disorder.

Table 4. The Risk of Cardiovascular Disease

Example minimum risk:

(rs8055236 A/A) 1 x (rs 1333049 G/G) 1 x (rs662799 T/T) 1 x (E2 type) 1 x (rs662 A/A) 1 x (rs854560 T/T) 1 = OR 1 Example maximum risk:

(rs8055236 G/G) 2.23 x (rs1333049 C/C) 1 .9 x (rs662799 C/C) 1 .98 x ( E4 type) 2 x (rs662 G/G) 2 x (rs854560 A/A) 2 = OR 67 According to the current embodiment, the genetic profile demonstrating the highest genetic risk is approximately 67 times more likely to develop cardiovascular disease than the optimum (lowest genetic risk) profile. This can be displayed on a scale from 0% to 100% additional disease risk.

2.2. Determining the Risk of Alzheimer's Disease

The likelihood of developing Alzheimer's disease is strongly influenced by the genetic variant of the APOE gene. The combinations of two different genetic polymorphisms in this gene determine which genotype the person carries for the APOE gene according to the following table:

Table 5. The Risk of Alzheimer's Disease

According to the current embodiment, the genetic profile demonstrating the highest genetic risk is approximately 21.4 times more likely to develop Alzheimer's disease than the optimum (lowest genetic risk) profile. This can be displayed on a scale from 0% to 100% additional disease risk.

2.3. Determining the Effect of PUFAs

As described previously, they effects of polyunsaturated fatty acids (PUFA ES) may vary depending on the APOA1 genetic polymorphism. Carriers of the A/A or A/G genotype generally benefit from HDL cholesterol raising effects while carriers of the G/G genotype generally experience the opposite and negative HDL cholesterol lowering effect. The effect of polyunsaturated fatty acids on HDL cholesterol is determined as follows:

According to the current embodiment, persons carrying the A/A or A/G genotype experience a beneficial health effect from PUFA consumption while carriers of the G/G genotype experience the opposite and negative effect. This can be displayed on a scale from 0% to 100% additional disease risk.

2.4. Determining the Effect of Vitamin B2 on Homocysteine

As described previously, the effects of vitamin B-2 on homocysteine levels may vary depending on the MTHFR genetic polymorphism. Carriers of the rs1801 133 T/T alleles benefit from the homocysteine lowering properties of vitamin B-2 while carriers of the alternate alleles do not.

Table 7. The Effect of Vitamin B2 on Homocysteine Levels

According to the current embodiment, persons carrying the T/T genotype experience a beneficial homocysteine lowering health effect from vitamin B-2 supplementation while carriers of the C/T or C/C genotype experience no beneficial effect. This can be displayed on a scale from 0% to 100% additional requirement.

2.5. Determining the Risk of Elevated Homocysteine Levels

Two genetic polymorphisms have a significant impact on the levels of harmful homocysteine in blood serum. The total likelihood of developing elevated homocysteine levels is determined according to the following table:

Table 8. The Risk of Elevated Homocysteine Levels

Example minimum risk:

(rs 180139 A/A) 1 x (rs1801 133 C/C) 1 = OR 1

Example maximum risk:

(rs180139 G/G) 2 x (rs1801 133 T/T) 2 = OR 4

According to the current embodiment, the genetic profile demonstrating the highest genetic risk is approximately 4 times more likely to develop cardiovascular disease than the optimum (lowest genetic risk) profile. This can be displayed on a scale from 0% to 100% additional disease risk.

2.6. Determining the Risk of Osteoporosis Two genetic polymorphisms significantly modify the risk of developing osteoporosis. The total likelihood of developing osteoporosis is determined according to the following table: Table 9. The Risk of Develo ping Osteoporosis

RS

OSTEOPOROSIS GENE GENOTYPE ODDS RATIO NUMB.

G/G 1

Col1A1 rs1800012 G/T 1 .26

T/T 1 .78

Osteoporosis

G/G 1

VDR _rs 1544410 A/G 1 .14

A/A 1 .63

Calculation: OR to % risk conversion

Lowest OR: 1 1 .9 OR = 100%

Highest OR: 2.9 1 OR = 52.6% per 1 OR above 1

Example minimum risk:

(rs1800012 G/G) 1 x (rs1544410 G/G) 1 = OR 1

Example maximum risk:

(rs1800012 T/T) 1.78 x (rs1544410 A/A) 1.63 = OR 2.9

According to the current embodiment, the genetic profile demonstrating the highest genetic risk is approximately 2.9 times more likely to develop osteoporosis than the optimum (lowest genetic risk) profile. This can be displayed on a scale from 0% to 100% additional disease risk.

2.7. Determining the Likely Calcium Intake A genetic polymorphism in the promoter region of the LCT gene causes primary lactose intolerance and has been shown to be associated with lower calcium intake. The resulting estimated intake of calcium is determined according to the following table:

Table 10. The Likely Calcium Intake

According to the current embodiment, the genetic profile T/T or C/T is estimated to have a higher calcium intake than the genetic profile C/C. This can be displayed on a scale from 0% to 100%.

2.8. Determining the Risk of Hemochromatosis

Three genetic polymorphisms in the HFE gene predispose to iron overload disorder or hemochromatosis, whereby too much iron is absorbed from the intestine. Being a heterozygote for one risk allele leaves the person with one "defective" and one "functional" copy of the gene. While carriers of a heterozygous risk allele typically do not develop hemochromatosis, 10% of carriers show abnormally elevated levels of iron in the blood. Any person carrying two risk alleles would have two "defective" forms of the gene and would be at an increased risk of developing hemochromatosis. Two defective copies of the gene can also arise through a compound heterozygote, meaning that two different risk alleles are present, one on each of the two HFE genes of the person. Therefore one must employ an additive model in this case, whereby the genetic risk of the three different genetic polymorphisms is simply added together. The resulting estimated risk of hemochromatosis is determined according to the following table:

Table 11. The Risk of Developing Iron Overload D lisorder

RS

HEMOCHROMATOSIS GENE GENOTYPE VALUE NUMB.

C/C Low

0 risk

G/C part,

HFE rs1799945 1

risk

G/G high

2 risk

C/C Low

0 risk

Hemochromatosis, iron G/C part,

HFE rs1800730 1 overload disorder risk

G/G high

2 risk

G/G Low

0 risk

G/A part,

HFE rs1800562 1

risk

A/A high

2 risk

Calculation: OR to % risk conversion

Lowest OR: 1 7 OR = 100%

Highest OR: 8 1 OR = 14% per 1 OR above 1 According to the current embodiment, an individual with the genetic profile where the values add up to 0 is considered to be at lower risk of developing hemochromatosis.

According to the current embodiment, an individual with the genetic profile where the values add up to 1 is considered to be at a low risk of developing hemochromatosis, but at an intermediate risk of developing elevated iron levels in the blood.

According to the current embodiment, an individual with the genetic profile where the values add up to or are greater than 2 is considered to be at a high risk of developing hemochromatosis.

This can be displayed on a scale from 0% to 100% additional disease risk.

2.9. Determining the Risk of Age- Related Macular Degeneration (AMD)

Three different genetic polymorphisms modify the risk of developing age-related macular degeneration. The specific risk (odds ratio) is combined under the multiplicative model according to the following table: Table 12. Risk of Developing AMD

Example minimum risk:

(rs1061 170 T/T) 1 x (rs1 1200638 G/G) 1 x (rs10490924 G/G) 1 = OR 1 Example maximum risk:

(rs1061 170 C/C) 12 x (rs1 1200638 A/A) 8.7 x (rs10490924 T/T) 8.21 = OR 857.124

According to the current embodiment, the genetic profile demonstrating the highest genetic risk is approximately 857 times more likely to develop AMD than the optimum (lowest genetic risk) profile. This can be displayed on a scale from 0% to 100% additional disease risk.

2.10. Detoxification of Heavy Metals and Free Radicals

Three specific genes (GSTM1 , GSTT1 , and GSTP1 ) play an important role in the detoxification of the heavy metals lead, cadmium and mercury as well as in the neutralization of harmful free radicals. Should some of these genes be completely missing (called a null allele) or should an activity inhibiting polymorphism be present, the detoxification of these heavy metals and free radicals is severely reduced. The detoxification capacity for these harmful substances is determined according to the following table: Table 13. The Detoxification Capacity for Heavy Metals

According to the current embodiment, an individual with the genetic profile where the values add up to 0 is considered to have the full detoxification capacity. According to the current embodiment, an individual with the genetic profile where the values add up to between 1 and 5 is considered to have a reduced detoxification capacity. According to the current embodiment, an individual with the genetic profile where the values add up to 6 is considered to have the lowest detoxification capacity. This can be displayed on a scale from 0% to 100% additional disease risk.

2.1 1 . Determining the Risk of Arthritis or Inflammation Mediated Disorders

The TNF-alpha polymorphism modifies the risk of developing arthritis and the risk of one individual is determined according to the following table:

Table 14. Risk of Arthritis

According to the current embodiment, the genetic profile demonstrating the highest genetic risk is approximately 7.29 times more likely to develop arthritis than the optimum (lowest genetic risk) profile.

This can be displayed on a scale from 0% to 100% additional disease risk.

2.12. Determining Oxidative Stress Protection

Free radicals, which are one of the reasons for biological ageing, are largely neutralized by the action of five different genes. The antioxidant capacity of one individual is determined according to the following table: Table 15. The Oxidative Stress Protection

According to the current embodiment, an individual with the genetic profile where the values add up to 0 is considered to have the full anti-oxidative capacity.

According to the current embodiment, an individual with the genetic profile where the values add up to between 1 and 9 is considered to have a reduced antioxidative capacity. According to the current embodiment, an individual with the genetic profile where the values add up to 10 is considered to have the lowest antioxidative capacity. This can be displayed on a scale from 0% to 100% additional disease risk.

2.13. Determining the Conversion Rate of Coenzyme Q10 While coenzyme Q 10 has various functions in the body, it needs to be converted to ubiquinol in order to show its antioxidative capacity in cells. The conversion from coenzyme Q 10 to ubiquinol is mediated by the NQ01 gene and certain polymorphisms reduced the activity of this enzyme. The conversion efficiency of coenzyme Q 10 is determined according to the following table: Table 16. Conversion Efficiency of Coenzyme Q10

According to the current embodiment, persons carrying the C/C genotype have a normal and rapid conversion of coenzyme Q 10 to ubiquinol.

According to the current embodiment, persons carrying the C/T genotype have a medium conversion of coenzyme Q 10 to ubiquinol and therefore lack some oxidative stress protection.

According to the current embodiment, persons carrying the T/T genotype have virtually no conversion of coenzyme Q 10 to ubiquinol and therefore lack some oxidative stress protection.

This can be displayed on a scale from 0% to 100% Coenzyme Q10 requirement.

3. Summary of Scales of Risks for Pathological Conditions

Combining the information described above, a personal genetic profile always lies within the boundaries of the following scales:

Table 17. Summary of Risk Scales for Pathological Conditions

SCALE

DISEASE OR METABOLIC Short

GENES MIN TO MAX ABNORMALITY description

Cardiovascular disease risk CARD OR 5 0% >> 100%

Alzheimer's disease risk ALZ OR 1 0% >> 100%

Effect of PUFAS on HDL cholesterol PUFA OR 1 0% >> 100%

Risk of elevated homocysteine levels HOMO OR 2 0% >> 100%

Effect of vitamin B2 on homocysteine levels B2HOM OR 1 0% >> 100%

Risk of osteoporosis OSTEO OR 2 0% >> 100%

Likely calcium intake CALC OR 1 0% >> 100%

Risk of iron overload IRON OR 1 0% >> 100%

Risk of macular degeneration AMD OR 3 0% >> 100%

Risk of heavy metal poisoning HEAV OR 3 0% >> 100%

Risk of arthritis ARTH OR 1 0% >> 100%

Oxidative stress OXID OR 5 0% >> 100%

Coenzyme Q10 conversion Q10 OR 1 0% >> 100% 4. Methods of Creating a Personalized Nutrient Composition Based on a Genetic Risk Profile

Through analyzing the relevant genes, a personalized recipe stating the individual micronutnent requirements can be created. The next challenge is to create and mix a personalized nutritional supplement according to this recipe in a fast and cost-effective manner. This may be achieved by first creating separate "micronutrient mixes" including only one or a number of micronutrients plus any given filler (a substance not biologically active and only added to increase the volume of the mix). The next step is to calculate the required amounts of any micronutrient for a given period of time (e.g., 1 month) and to mix the appropriate amounts of all individual micronutrient mixes together, so that a daily dose of the homogenized final mixture results in the correct daily dosage for this individual. The daily volume or weight of the mixture is then given to the customer in form of dosage instructions to be followed.

Liquids

A micronutrient mix may be in the form of a liquid containing a certain percentage (weight/weight) of the active ingredient. Varying amounts of different micronutrient mix- liquids may then be mixed together in different rations and the customer instructed to ingest a certain volume of the mixed liquid per day.

Pellets

Pellets of 0.1 -3 mm in size that contain a certain percentage (weight/weight) of one or more active ingredients may be produced to form a micronutrient mix. These different types of pellets could then be added to a container in different amounts, thoroughly mixed and the mixture ingested with a measuring spoon. These pellets may be made of gelatin, cellulose, calcium alginate or similar substances modulating slow and fast release of the active ingredient. The pellet production technologies may be microencapsulation, extrusion, pan coating, air-suspension coating, centrifugal extrusion, vibration nozzle, spray drying or similar.

Powders

A micronutrient mixture may be produced in form of a powder that that contains filler and a certain percentage (weight/weight) of the active ingredient. Different volumes of each of the powder micronutrient mix may then be mixed with each other to create the personalized mixture. The right amount could then be measured using a measuring spoon before ingestion. Jellies

A micronutrient mixture may be produced in form of a jelly that contains gelatinous filler and a certain percentage (weight/weight) of the active ingredient. Different volumes of each of the jelly micronutrient mixes may then be mixed with each other to create the personalized mixture. The right amount could then be measured using a measuring spoon or measuring cup before ingestion.

Example calculations

The following steps show the example calculation for a low risk genetic profile:

Example genetic profile: LOW RISK PROFILE

Ste 1 determinin the enetic risk of cardiovascular disease

Step 2) determining the risk of Alzheimer's c isease

Step 3) determining the effect of PUFAs on HDL cholestero

Step 4) determining the effect of Vit B2 on homocystein

Step 6) determining the risk of osl teoporosis

RS ODDS

OSTEOPOROSIS GENE GENOTYPE VALUE NUMB. RATIO

rs 180001

Col1A1 G/G 1 1

2

Osteoporosis

r_s 154441

VDR G/G 1 1

0

Total

1 x 1 = 1 OR:

52.6% per 1 OR (above OR 1) = 0 %

OSTEO OR (%) = 0 % Step 7) determining the likely additional requirement of nutritional calcium

Step 8) determining the risk of iron overload disorder

Step 9) determining the risk of macular degeneration

AGE RELATED

RS ODDS MACULAR GENE GENOTYPE VALUE NUMB. RATIO

DEGENERATION (AMD)

Rs1061 1

CFH T/T 1 1

70

Age-related macular rs1 12006

HTRA1 A/G 2.2 2.2 degeneration (AMD) 38

LOC38 rs104909

G/G 1 1 7715 24

Total

1 x 2.2 x 1 = 2.2 OR:

0.12% per 1 OR (above OR 1 ) = 0.144 %

AMD OR (%) = 0.144 %

Step 10) determining the detoxification capacity of heavy metals

DETOXIFICATION OF RS

GENE GENOTYPE VALUE VALUE HEAVY METALS NUMB.

Phase 1 detoxification of GSTM1 Null Allele POS 0 0 the heavy metals lead,

GSTT1 Null Allele POS 0 0 mercury and cadmium as

well as free radicals GSTP1 rs1695 A/A 0 0

Total

0 + 0 + 0 = 0 OR:

Step 11 ) determining the risk of arthritis

ARTHRITIS AND

RS ODDS

INFLAMMATORY GENE GENOTYPE VALUE NUMB. RATIO

RESPONSE

rs180062

TNFa A/A 1 1

Arthritis (inflammatory 9

response) HLA

N/A NEG 1 1 B27

Total

1 x 1 = 1 OR:

1.74% per 1 OR (above OR 1) = 0 %

ARTH OR (%) = 0 %

Step 12) determining the risk of oxidative stress

RS

OXIDATIVE STRESS GENE GENOTYPE VALUE VALUE NUMB.

Oxidative stress through rs 105045

GPX1

(hydrogen peroxide) 0 c/c 0 0

Oxid. Str. (superoxide) SOD2 rs4880 c/c 0 0

GSTM1 Null Allele POS 0 0

Phase 1 detoxification

GSTT1 Null Allele POS 0 0 free radicals

GSTP1 rs1695 A/A 0 0

Total

0 + 0 + 0 + 0 + 0 = 0 OR:

10% per 1 OR 0 %

OXID OR (%) = 0 %

Step 13) determining the conversion capacity for Coenzyme Q10

COENZYME Q10 RS

GENE GENOTYPE CONVERS. VALUE CONVERSION NUMB.

Activity of CoEnzyme rs180056

NQ01 C/C 100% 100% Q10 conversion 6

Q10 OR (%) = 100%

Step 14) Summarizing genetic risks as percentages

2.9294

CARD OR (%) =

%

ALZ OR (%) = 2.058 %

PUFA OR (%) = 0 %

B2HOM OR (%) = 0 %

HOMO OR (%) = 33 % OSTEO OR (%) = 0%

CALC OR (%) = 0%

IRON OR (%) = 0%

AMD OR (%) = 0.144%

HEAV OR (%) = 0%

ARTH OR (%) = 0%

OXID OR (%) = 0%

Q10OR (%) = 100%

Step 15) determining the RDAfor the individual (Age 45, Female)

Step 16) Calculating the optimal dose of OM EGA 3

RDA UGL UGL-RDA

Omega 3 250 mg 2500 2250

( RDA + ( (UGL - RDA) x (CARD OR % + ARTH OR %) ) x

PUFA OR % = GRA

( 250 + ( 2250 x ( 2.92% + 0% ) ) ) x 0% 0

Recommended daily dose (mg) 0

Step 17) Calculating the optimal dose of Phytosterols

RDA UGL UGL-RDA

Phytosterols 500 mg 2500 2000

Step 18) Calculating the optimal dose of Vitamin B6

RDA UGL UGL-RDA

Vitamin B6 1 .7 mg 8.5 6.8

Step 19) Calculating the optimal dose of folic acid

RDA UGL UGL-RDA

Folic Acid 0.2 mg 0.8 0.6

Step 20) Calculating the optimal dose of Vitamin B12

RDA UGL UGL-RDA

Vitamin B12 0.0024 mg 0.0072 0.0048

( RDA + ( (UGL - RDA) x (HOMO OR %) ) = GRA

0.0024 + ( 0.0048 x 33% ) 0.00398

Recommended daily dose (mg) 0.00398 Step 21) Calculating the optimal dose of Vitamin

Step 22) Calculating the optimal dose of Magnesium

Step 23) Calculating the optimal dose of Vitamin D3

RDA UGL UGL-RDA

Vitamin D3 0.015 mg 0.025 0.01

RDA + ( (UGL - RDA) x (OSTEO OR % + CALC OR %) ) = GRA

0.015 + ( 0.01 x ( 0% + 0% ) ) 0.015

Recommended daily dose (mg) 0.015

Step 24) Calculating the optimal dose of Calcium

RDA UGL UGL-RDA

Calcium 1000 mg 2500 1500

Step 25) Calculating the optimal dose of Iron

RDA UGL UGL-RDA

Iron 18 mg 30 12

Step 26) Calculating the optimal dose of Vitamin C

Step 27) Calculating the optimal dose of Vitamin

Step 28) Calculating the optimal dose of Zink

Step 29) Calculating the optimal dose of Seleni

RDA + ( (UGL - RDA) x (ALZ OR % + HEAV OR % +

OXID OR % + ARTH OR % ) ) GRA

0.055 + ( 0.245 x (2.058% + 0% + 0% + 0%)) 0.06

Recommended daily dose (mg) 0.06 Step 30) Calculating the optimal dose of Manganese

Step 31 ) Calculating the optimal dose of Vitamin

Step 32) Calculating the optimal dose of Lycopene

Step 33) Calculating the optimal dose of Lutein

Step 34) Calculating the optimal dose of Copper

RDA + ( (UGL - RDA) x (AMD OR % + ARTH OR % ) ) GRA

0.9 + ( 2.1 x (0.144% + 0%)) 0.903

Recommended daily dose (mg) 0.903 Step 35) Calculating the optimal dose of Alp ia Lipoic Acid

RDA UGL UGL-RDA

Alpha Lipoic Acid 200 mg 600 400

Step 36) Calculating the optimal dose of MSM

RDA UGL UGL-RDA

MSM 300 mg 2500 2200

Step 37) Calculating the optimal dose of Coenzyme Q10

RDA UGL UGL-RDA

Coenzyme Q10 50 mg 300 250

RDA x Q10 OR % GRA

50 x 100% 50

Recommended daily dose (mg) 50

Step 38) Calculating the optimal dose of Ubiquinol

RDA UGL UGL-RDA

Ubiquinol 50 mg 150 100

Step 39) Checking that no values exceed UGL

Step 40) Calculating daily amount of each nutrient stock

Copper 1 % 0.903 90 8127

Alpha Lipoic Acid 60% 200 333 30000

MSM 70% 300 429 38571

Coenzyme Q10 80% 50 63 5625

Ubiquinol 60% 0 0 0

5462 492

mg mix/d g mix/90d

Step 42) Mix the defined amounts of stock for 90 days thoroughly

Step 41) Defining ingestion instructions

Ingest 5.5g of nutrient mixture daily

Example calculation

The following steps show the example calculation for a high risk genetic profile

Example genetic profile: HIGH RISK PROFILE

Step 1) determining the genetic risk of cardiovascular disease in %

CARDIOVASCULAR RS

GENE GENOTYPE ODDS RATIO VALUE DISEASE NUMB.

CDH1 rs805523

G/G 2.23 2.23 3 6

CHDS rs133304

C/G 1 .47 1 .47

Atherosclerosis, 8 9

hyperlipidemia, APOA

hypercholesterolemia, rs662799 T/C 1 .98 1 .98

5

coronary artery disease APOE E4/E4 2 2 rs662 A/G 2 2

PON1

rs854560 A/A 2 2

2.23 x 1.47 x 1 .98 x 2 x 2 x 2

Total OR: 51.93

1.51% per 1 OR (above OR 1 )= 76.9 %

CARD OR (%) = 76.9 %

Step 2) determining the risk of Alzheimer's c isease

Step 3) determining the effect of PUFAs on HDL cholestero

CARDIOVASCULAR RS

GENE GENOTYPE EFFECT VALUE DISEASE NUMB.

PUFA consumption effect APOA

rs670 G/G lower HDL 10 on HDL Choi. 1

Total OR: 10 = 10

11.1% per 1 OR (above OR 1 )= 100 %

PUFA OR (%) = 100 %

Step 4) determining the effect of Vit B2 on homocystein

Step 6) determining the risk of osteoporosis

RS

OSTEOPOROSIS GENE GENOTYPE ODDS RATIO VALUE NUMB.

coHA rs 180001

T/T 1 .78 1 .78

1 2

Osteoporosis

r_s 154441

VDR G/G 1 1

0

Total OR: 1.78 x 1 = 1.78

41.028

52.6% per 1 OR (above OR 1 ) =

%

41.028

OSTEO OR (%) =

% Step 7) determining the likely additional requirement of nutritional calcium

Step 9) determining the risk of macular degeneration

AGE RELATED

RS MACULAR GENE GENOTYPE ODDS RATIO VALUE NUMB.

DEGENERATION (AMD)

Rs1061 1

CFH T/T 1 1

70

Age-related macular HTRA rs1 12006

G/G 1 1 degeneration (AMD) 1 38

LOC38 rs104909

G/G 1 1 7715 24

Total OR: 1 x 1 x 1 = 1

0.12% per 1 OR (above OR 1) = 0 %

AMD OR (%) = 0 %

Step 10) determining the detoxification capacity of heavy metals

DETOXIFICATION OF RS

GENE GENOTYPE VALUE VALUE HEAVY METALS NUMB.

GSTM

Phase 1 detoxification of Null Allele POS 0 0

1

the heavy metals lead,

GSTT1 Null Allele NEG 2 2 mercury and cadmium as

well as free radicals GSTP

rs1695 A/A 0 0 1

Total OR: 0 + 2 + 0 = 2

13% per l OR = 26 %

HEAV OR (%) = 26 % Step 11 ) determining the risk of arthritis

ARTHRITIS AND

RS

INFLAMMATORY GENE GENOTYPE ODDS RATIO VALUE NUMB.

RESPONSE

rs180062

TNFa G/G 7.29 7.29

Arthritis (inflammatory 9

response) HLA

N/A NEG 1 1 B27

Total OR: 1 x 7.29 = 7.29

1.74% per 1 OR (above OR 1) = 11 %

ARTH OR (%) = 11 %

Step 12) determining the risk of oxidative stress

RS

OXIDATIVE STRESS GENE GENOTYPE VALUE VALUE NUMB.

Oxidative stress through rs 105045

GPX1 T/T 2 2 (hydrogen peroxide) 0

Oxid. Str. (superoxide) SOD2 rs4880 c/c 0 0

GSTM

Null Allele POS 0 0 1

Phase 1 detoxification

GSTT1 Null Allele NEG 2 2 free radicals

GSTP

rs1695 A/A 0 0 1

Total OR: 2 + 0 + 0 + 2 + 0 = 4

10% per 1 OR = 40 %

OXID OR (%) = 40 %

Step 13) determining the conversion capacit y for Coenzyme Q10

COENZYME Q10 RS

GENE GENOTYPE CONVERS. VALUE CONVERSION NUMB.

Activity of CoEnzyme rs180056

NQ01 C/T 50% 50% Q10 conversion 6

Q10 OR (%) = 50%

Step 14) Summarizing genetic risks as percentages

CARD OR (%) = 76.9 %

ALZ OR (%) = 100 %

PUFA OR (%) = 100 %

B2HOM OR (%) = 100 %

HOMO OR (%) = 0 %

41.028

OSTEO OR (%) =

%

CALC OR (%) = 100 %

IRON OR (%) = 28 % AMD OR (%) = 0%

HEAV OR (%) = 26%

ARTH OR (%) = 11 %

OXID OR (%) = 40%

Q10OR (%) = 50%

Step 16) Calculating the optimal dose of OMEGA 3

( RDA + ( (UGL - RDA) x (CARD OR % + ARTH OR %) ) x

PUFAOR% = GRA

( 250 + ( 2250 x ( 76.9% + 11%))) x 100% 2228

Recommended daily dose 2228 Step 17) Calculating the optimal dose of Phytosterols

RDA UGL UGL-RDA

Phytosterols 500 mg 2500 2000

Step 18) Calculating the optimal dose of Vitamin B6

RDA UGL UGL-RDA

Vitamin B6 1 .7 mg 8.5 6.8

ecommen e a y ose .

Step 19) Calculating the optimal dose of folic acid

RDA UGL UGL-RDA

Folic Acid 0.2 mg 0.8 0.6

Step 20) Calculating the optimal dose of Vitamin B12

RDA UGL UGL-RDA

Vitamin B12 0.0024 mg 0.0072 0.0048

( RDA + ( (UGL - RDA) x (HOMO OR %) ) = GRA

0.0024 + ( 0.0048 x 0% ) 0.0024

Recommended daily dose 0.0024

Step 21) Calculating the optimal dose of Vitamin B2

RDA UGL UGL-RDA

Vitamin B2 1 .1 mg 10 8.9

Ste 22 Calculatin the o timal dose of Ma nesium

Step 23) Calculating the optimal dose of Vitamin D3

RDA UGL UGL-RDA

Vitamin D3 0.015 mg 0.025 0.01

RDA + ( (UGL - RDA) x (OSTEO OR % + CALC OR %) ) = GRA

0.015 + ( 0.01 x ( 41.028% + 100% ) ) 0.0291028

Recommended daily dose 0.0291028

Step 24) Calculating the optimal dose of Calcium

RDA UGL UGL-RDA

Calcium 1000 mg 2500 1500

Step 25) Calculating the optimal dose of Iron

RDA UGL UGL-RDA

Iron 18 mg 30 12

Step 26) Calculating the optimal dose of Vitamin C

RDA UGL UGL-RDA

Vitamin C 75 mg 500 425

RDA + ( (UGL - RDA) x (ALZ OR % + AMD OR % +

HEAV OR % + OXID OR % + ARTH OR % ) ) GRA

75 + ( 425 x ( 100% + 0% + 26% + 40% + 1 1 % )) 827.25

Recommended daily dose 827.25 Step 27) Calculating the optimal dose of Vitamin

Step 28) Calculating the optimal dose of Zink

RDA + ( (UGL - RDA) x (ALZ OR % + AMD OR % +

HEAV OR % + OXID OR % + ARTH OR % ) )

GRA

8 + ( 22 x (100% + 0% + 26% + 40%)) 44.52

Recommended daily dose 44.52

Step 29) Calculating the optimal dose of Selenium

RDA UGL UGL-RDA

Selenium 0.055 mg 0.3 0.245

RDA + ( (UGL - RDA) x (ALZ OR % + HEAV OR % +

OXID OR % + ARTH OR % ) ) GRA

0.055 + ( 0.245 x (100% + 26% + 40% + 1 1 %)) 0.48865

Recommended daily dose 0.48865

Step 30) Calculating the optimal dose of Manganese

RDA UGL UGL-RDA

Manganese 1 .8 mg 5.4 3.6

Step 31) Calculating the optimal dose of Vitamin A

RDA UGL UGL-RDA

Vitamin A (as Retinol) 1 .4 mg 4.2 2.8

Step 32) Calculating the optimal dose of Lycopene

RDA UGL UGL-RDA

Lycopene 10 mg 30 20

RDA+ ( (UGL-RDA) x (ALZ OR % + HEAV OR % +

OXIDOR%) ) GRA

10 + ( 20 x (100% + 26% + 40%)) 43.2

Recommended daily dose 43.2

Step 33) Calculating the optimal dose of Lutein

RDA UGL UGL-RDA

Lutein 10 mg 30 20

RDA+ ( (UGL-RDA) x (ALZ OR % + HEAV OR % +

OXIDOR%) ) GRA

10 + ( 20 x (100% + 26% + 40%)) 43.2

Recommended daily dose 43.2

Step 34) Calculating the optimal dose of Copper

RDA UGL UGL-RDA

Copper 0.9 mg 3 2.1

RDA+ ( (UGL-RDA) x (AMD OR % + ARTH OR % ) ) GRA

0.9 + (2.1 x(0% + 11%)) 1.131

Recommended daily dose 1.131

Step 35) Calculating the optimal dose of Alp ia Lipoic Acid

RDA UGL UGL-RDA

Alpha Lipoic Acid 200 mg 600 400

Step 36) Calculating the optimal dose of MSM

Step 37) Calculating the optimal dose of Coenzyme Q10

RDA x Q10 OR % GRA

50 x 50% 25

Recommended daily dose 25

Step 38) Calculating the optimal dose of Ubiquinol

RDA UGL UGL-RDA

Ubiquinol 50 mg 150 100

Step 39) Checking that no values exceed UGL

MSM 542 2500 >>> 542

Coenzyme Q10 25 300 >>> 25

Ubiquinol 25 150 >>> 25

Step 40) Calculating daily amoun t of each nutrient stock

Step 42) Mix the defined amounts of stock for 90 days thoroughly

Step 41) Defining ingestion instructions

Ingest 14.3g of nutrient mixture

daily

Claims

1 . A genomic method for producing a personalized nutrient composition for one individual, said method comprising the following steps:

(iii) producing a nutrient composition comprising the determined amounts and ratios of nutrients.

2. The method according to claims 1 , wherein the set of pathological conditions comprises at least one pathological condition selected from the group consisting of:

(a) a neurogenerative disease, in particular Alzheimer's disease;

(f) iron overload disorders, in particular hemochromatosis;

(g) macular degeneration, in particular age-related macular degeneration;

(j) a reduced protection against oxidative stress; and

(k) a food intolerance, in particular lactose intolerance,

preferably wherein said method comprises determining the risk of developing at least two, at least three, at least four, at least five or even all of said pathologic conditions.

3. The method according to claim 1 or 2, wherein the set of alleles comprises alleles of at least one of the genes selected from the group consisting of:

(b) a cadherin 13 (CDH13) gene;

(c) a coronary heart disease susceptibility to 8 (CHDS8) gene;

(d) a paraoxonase 1 (PON1 ) gene;

(e) a methylenetetrahydrofolate reductase (MTHFR) gene;

(f) a methionine synthase reductase (MTRR) gene;

(h) a vitamin D receptor (VDR) gene;

(i) a lactase (LCT) gene;

(j) a heredity hemochromatosis protein (HFE) gene;

(k) a complement factor H (CFH) gene;

(I) a high-temperature requirement A serine peptidase 1 (HTRA1 ) gene;

(m) an age-related maculopathy susceptibility 2 (LOC2) gene;

(o) a tumor necrosis factor alpha (TNF-alpha) gene;

(p) a histocompatibility antigen B27 (HLA-b27) gene;

(q) a glutathione peroxidase 1 (GPX1 ) gene;

(r) a superoxide dismutase 2 (SOD2) gene; and

(s) a quinone acceptor oxidoreductase 1 (NQ01 ) gene,

4. The method according to any one of claims 1 to 3, wherein at least one of the identified alleles is tested for comprising a single nucleotide polymorphism (SNP) discriminating different alleles of a gene from another, preferably wherein at least two, at least three, at least four, at least five, at least ten or even all of the identified alleles are tested for comprising an SNP.

5. The method according to any one of claims 1 to 4, wherein the set of nutrients comprises at least one nutrient selected from the group consisting of a fatty acid, a vitamin, a trace element, a secondary plant compound a coenzyme and a sulfur supplement, preferably wherein (a) a fatty acid is an essential fatty acid, preferably a poly unsaturated fatty acid, in particular an omega 3 fatty acid;

(b) alpha lipoic acid;

(e) a secondary plant compound is a carotenoid, in particular lycopene, beta- carotene, lutein and/or a phytosterol;

(f) a coenzyme, in particular coenzyme Q10 and/or ubiquinol; and/or

(g) a sulfur supplement is methylsulfonylmethane (MSM),

in particular wherein the nutrient composition comprises at least two, at least three, at least four, at least five or even all of said nutrients. 6. The method according to any one of claims 1 to 5, wherein producing a nutrient composition comprises mixing defined amounts of separate stocks each comprising one or more nutrient(s) and optionally further comprising an orally ingestible carrier, in particular wherein each stock comprises not more than a single nutrient and optionally an orally ingestible carrier.

7. The method according to claim 6, wherein said stocks are stocks of solid material and/or liquid stock solutions, preferably stocks of solid material of spherical or ellipsoid pellets, in particular wherein the pellets have an essentially homogenous size.

8. The method according to any one of claims 1 to 7, wherein said method further comprises the step of identifying the alleles of a gene comprised in said individual's genome in vitro. 9. A computer program directly loadable into the internal memory of a digital computer, comprising software code portions for implementing for determining said individual's genetic predisposition according to the step (i) and/or for determining the amounts and ratios of nutrients according to step (ii) of any of the preceding claims.

10. A nutrient composition obtained from a method of any one of the preceding claims, wherein said composition is personalized and orally ingestible, in particular wherein said composition further comprises an orally ingestible carrier. The nutrient composition according to claim 10, comprising amounts of the one or more nutrient(s) comprised in said nutrient composition for daily intake not lower than the recommended daily allowance (RDA) recommended by the National Institute of Health (NIH) and not higher than the maximal recommended daily intake of the NIH, wherein the increase in amount correlates with the determined risk of developing or having one or more particular pathologic condition(s),

preferably wherein the amounts for daily intake of the following nutrients as far as comprised in the nutrient composition are:

alpha lipoic acid: between 200 mg and about 600 mg;

omega 3 fatty acids: between 250 mg and 2500 mg;

vitamin A: between about 1 .6 mg and about 10.8 mg;

vitamin B2: between about 0.3 mg and 10 mg;

vitamin B6: between about 0.1 mg and 8,5 mg;

vitamin B12: between about 0.004 mg and 0.072 mg,

vitamin C: between about 15 mg and about 1500 mg;

vitamin D3: between about 0.01 mg and 0.025 mg;

vitamin E: between about 4 mg and about 200 mg;

folic acid: between about 0,0325 mg and about 0,8 mg;

calcium: between about 200 mg and about 2500 mg;

magnesium: between about 130 mg and about 350 mg;

iron: between about 0.27 mg and 30 mg;

selenium: between about 0.015 mg and about 0.3 mg;

zinc: between about 2 mg and about 30 mg;

manganese: between about 0.3 mg and about 7.8 mg;

copper: between about 0.2 mg and about 3 mg;

beta carotene: between about 1 .6 mg and about 7.5 mg;

retinol: between about 0.8 mg and about 3.5 mg;

lutein: between about 10 mg and about 30 mg;

lycopene: between about 10 mg and about 30 mg;

coenzyme Q10: between about 50 mg and about 300 mg;

ubiquinol: between about 50 mg and about 150 mg;

phytosterols: between about 500 mg and about 2500 mg; and/or

MSM: between about 300 mg and about 2500 mg.

The nutrient composition according to claim 10 or 1 1 , wherein said composition forms a plurality of pellets, a powder, a pill, a dragee, a capsule, a gel, a syrup or a juice, preferably a plurality of pellets or a powder, in particular a plurality of essentially spherical pellets.

13. The nutrient composition according to any one of claims 10 to 12 for use as a medicament.

14. The nutrient composition according to any one of claims 10 to 13 for use in a method for preventing or treating at least one pathologic condition selected from the group consisting of:

(a) a neurogenerative disease, in particular Alzheimer's disease;

(f) iron overload disorders, in particular hemochromatosis;

(g) macular degeneration, in particular age-related macular degeneration;

(j) a reduced protection against oxidative stress; and

(k) a food intolerance, in particular lactose intolerance.

15. The nutrient composition for use according to claim 13 or 14, wherein the nutrient composition is administered orally, in particular administered once, twice or three times a day.