Alzheimer’s disease (AD) is an irreversible neurodegenerative disorder. Being the most common type of dementia, 35.6 million people worldwide were affected in 2010 and the number is estimated to double every 20 years. It affects primarily people above the age of 65, with a low rate of the patients being younger.  The condition is characterized by loss of neurons and synapses in the brain, caused by development of amyloid plaques and neurofibrillary tangles.

Currently there is no cure for Alzheimer’s disease, and management of patients is significantly costly, especially in Europe and the United States. Moreover due to the nature of the disease, psychological burden for people close to patients is a serious effect. Thus scientist’s efforts have been for years focused on understanding the roots of the condition that could lead to an effective treatment and/or even prevention ^(1,2).

Genetics research has enlightened over the past few years the role of genes in manifestation of the condition. Early onset of the condition (hereditary-familial form) is caused by rare, fully penetrant mutations in three different genes. However for the vast majority of cases (90%), the exact cause of the disease on a molecular level remains unclear ⁽³⁾.

The most recent research evidence leads scientists to list Alzheimer’s disease among the multi-factorial conditions, where both genetic and environmental factors playing a crucial role. Genome-wide association studies (GWAS) of late-onset Alzheimer disease have consistently observed strong association with polymorphisms (SNPs) in gene APOE ^(4,5,6). Specifically it has been shown that carriers of the allele e4 (resulting from a haplotype of two SNPs in APOE), deal with significantly increased risk for Alzheimer’s. APOE is the major cholesterol carrier in brain and the presence of the allele e4 is shown to disrupt cholesterol regulation and β-amyloid degradation. This results to β-amyloid accumulation in brain supporting the most established theory for β-amyloid deposits being the main cause of the condition.  However this gene variant seems to explain approximately 50% of the cases. Strong association was also found for a SNP in APOC1, which modulates the function of the APOE gene ^(7,8). Such evidence suggested a strong link between cholesterol regulatory pathway and Alzheimer’s condition. Other genetic variants have been also implicated in Alzheimer’s disease, which act rather in a more synergistic way, conferring a risk that could be considered important when combined with the presence of APOE4 allele.

Moreover increased plasma homocysteine levels are implicated in the disorder. MTHFD1L encodes an enzyme in one of the steps for homocysteine conversion to methionine. A gene variant in MTHFD1L has been associated with increased risk for Alzheimer’s disease, indicating that an additional molecular pathway involved in Alzheimer’s disease is homocysteine metabolism ⁽⁹⁾.

Assessing an individual’s genetic profile by testing for the polymorphisms known to affect risk for AD, could have a key role in prevention of the disorder. An estimated increased genetic risk -compared to the general population- will motivate individuals to get advice from health professionals for appropriate and effective guidelines. Based on the DNA results, certain nutritional recommendations that focus mainly on low saturated fat diet and low sugar intake can be importantly beneficial for brain function. Regular check up of cholesterol and homocysteine levels will help individuals at risk for better and efficient monitoring of those substances which are implicated in AD manifestation. Moreover regular physical exercise has shown tremendous benefits in AD prevention. The most stunning results however can be achieved with brain gymnastics (reading, crossword puzzles, board games, etc.) according to Neurologists, since mental practice can reduce up to 70% the risk for AD ⁽¹⁰⁾. The future of preventive rather than invasive medicine is very promising; identifying the personalized risk of individuals allows the implement of early and effective adjustments that address to personal genetic needs.

Aging is a normal process of the cells and the human body in general. As we get older our natural defenses are reduced, free radicals are less deactivated, resulting to internal damages. Cells’ proliferation rate is reduced, and cells’ death increases, something obvious in our skin appearance. A similar process occurs inside our body, and several conditions threat our health.

In many cases aging begins to show its signs earlier in life than expected. This is observed primarily in our skin condition, as this outer layer of epidermis is the most exposed to several environmental pollutants. Other factors, like unhealthy nutrition poor in vitamins, smoking, sunlight, and air pollution contribute significantly to premature forming of wrinkles and skin slacking.

However we often come across people who -in contrast to their old age- show a very good skin health, maintaining a youthful appearance. This can be -to an extent- the result of the cosmetic products available nowadays, which contain important ingredients for the skin protection and rejuvenation. But this alone is not sufficient to lead to a youthful skin looking, as genes play also a significant role.

The human body has numerous of mechanisms to ensure its survival. Anti-oxidation and Detoxification systems are of the most important, protecting our cells from free radicals. These reactive oxygen species are produced either as natural by-products from several functions in the cells, or come from toxins that the body, like environmental pollutants and drugs’ compounds. Free radicals can cause a condition known as oxidative stress, when their production exceeds their deactivation. This harms seriously the cells, causing significant damage to its genetic material, DNA. And as DNA contains the necessary information for all the normal functions of the body, such harmful effects are responsible for many diseases, from cancer to neurological disorders ^(1,2).

Genetic research over the past years has revealed several gene mutations which can cause defects in processes of anti-oxidation and detoxification, like GSTT1, GPX1, CAT and several others ^(3,4,5,6). People carrying such mutations are less protected to skin cells’ damages and more susceptible to premature skin aging.

Moreover genes like MTHFR, MTR and MTRR are involved in folic acid metabolism. Mutations in such genes can results to serious defects in DNA synthesis and repair, causing earlier cells’ death and again earlier development of skin aging (7,8).

Collagen is a structural protein of the skin that gives the smoothness and youth to this layer of epidermis. As we grow older, collagen production is importantly reduced in contrast to collagen breakdown which is increased. Genetic background is also very important for the age of skin aging onset, as gene mutations involved in collagen synthesis and/or breakdown may lead to early skin slacking and other signs of skin aging ^(9,10).

Increased exposure to sunlight can also harm seriously the health of skin cells. UV irradiation causes DNA damages that lead to early formation of skin wrinkles, freckles and even skin cancer. Some people however are more vulnerable to such harmful effects of the sun than the general population due to their genetic profile.

Nowadays that we can be aware -at some important extent- of the roots of the aging process, people can be more properly guided to avoid early symptoms of aging. One aspect is the use of the appropriate cosmetic products (creams that purify the skin and clean from toxins, and sunscreens with increased SPF) that address to their personal needs as indicated by their genetic profile.

Furthermore individuals can follow what is called a personal Nutritional Plan based on their genetic needs. Based on their genetic profile they can be provided with appropriate nutritional recommendations (e.g. for increased intake of fresh fruits and vegetables) or guidance for supplements with certain bioactive compounds. Thus they can enhance the battle against aging, from the inside out, targeting to internal systems of the body.

Diabetes Mellitus belongs to the most common medical conditions worldwide, showing importantly increasing rates. Data from the WHO (World Health Organization) are far from being pessimistic for the future as more than 400 millions of people around the world are expected to suffer from the condition in the next 2 decades ⁽¹⁾.

When we eat, glucose (commonly known as sugar) coming from food metabolism is released in blood circulation and is ready to be used from the body, as it is the most important energy source for the cells. Insulin – a hormone produced in pancreas and released in blood circulation- is responsible for the absorption of glucose from fat, muscle and liver cells. Diabetes occurs when either insulin production from pancreas is not sufficient or insulin is not effectively used by the body. Consequently glucose levels in blood are excessively increased with serious health implications. Cardiovascular disease, nephropathy, foot damage are some of the complications of diabetes, which lead to death millions of people annually.

There are two types of diabetes mellitus. Type 1 is due to defective insulin production and requires daily administration of insulin. The cause has not been yet clear, but genes play a dominant role. Usually symptoms begin from childhood and prevention measures seem to have only limited effects.

Type 2 Diabetes is the most common form of diabetes, with 90% of cases being characterized as such. It occurs either because cells become resistant to insulin signaling (insulin resistance) resulting to a not properly absorption of the glucose, or because pancreas stops to produce/release adequate insulin. Environmental factors, like nutritional habits, being overweight and following a sedentary lifestyle play a significant role in development of the condition. However genetic background of an individual can also increase his/her risk to Type 2 Diabetes ^(1,2).

DNA is our genetic blueprint and despite 99.9% of it is identical among people, the remaining 0.1% defines our individuality: from physical characteristics to disease susceptibility. These tiny variants are called polymorphisms/mutations and scientists in the fields of Medical Genetics and Predictive Genomics have focused to identify their effects primarily in health. Knowing the roots of the problem leads to a better understanding of the causing mechanisms and thus to more efficient preventive measures.

Genetic composition is a strong factor for predicting an individual’s risk to Type 2 Diabetes. Scientists have over the past years identified several polymorphisms in genes associated with higher risk for Type 2 diabetes. Mutations in genes known to affect the sensitivity / response of cells to insulin (like PPAR-γ, CDKAL1, HHEX, IGF2BP2, SLC630A8) have been found to increase the risk for a person who carries them ^(3,4,5,6,7).  Moreover – and a bit unexpected- genes involved to inflammatory conditions seem to have a strong effect on blood glucose levels. Certain variants in genes like TNF-a, IL-6 ^(8,9,10,11) have shown to affect the risk for this metabolic disorder. More data will be definitely available in the future, contributing even more to the efforts of scientists involved in Medical Genetics.

The ultimate purpose of Predictive Genomics is to pave the way for the appropriate, early, and as much as possible individualized and personalized actions to help individuals to reduce disease risks. This also applies to the case of Type 2 Diabetes test, since – as stated before – environmental factors can importantly alter a person’s risk. In case an individual is assessed with a higher risk compared to the general population appropriate Medical, Pharmacological, Nutritional and Environmental pre-symptomatic measures –addressing to the personal genetic risk of the individual- and therapies can be implemented for prevention or delay of disease onset.

Bones have crucial and multiple roles: support and protect the organs of the body, produce red and white blood cells, store minerals. Therefore bone health is very important to ensure the general normal function of the body. However as we get older, bones tissue begins to lose some of its abilities to support sufficiently the body, resulting to health problems.

Osteoporosis is a common condition, characterized by low bone mineral density-BMD.  The bones resorption exceeds bone formation, resulting to progressive loss of bone mass. Bone tissue structure deteriorates and individuals deal with increased risk for fractures. This condition is observed more often in women, especially after menopause, due to estrogen deficiency. Also it can result from other exogenous reasons, like under-nutrition and use of corticosteroids.

Fracture rates depend importantly on lifestyle factors. Sufficient intake of Calcium and Vitamin D can protect significantly from acceleration of osteoporosis and reduce the risk for serious fracture. In fact, such dietary factors play a crucial role from the very early time in a person’s life. Especially for girls, who acquire most of their skeletal mass by their 20’s, it is crucial to supply their bodies with sufficient nutrients even from childhood.

Moreover physical activity has been proved to be very beneficial in preventing osteoporosis. Regular exercise that includes weight bearing activities (like walking, basketball, jogging, dancing and weight lifting) improves muscles and bones structure and better body support.  A proper plan for physical activity should be again -like the nutritional one- followed from early in life, to ensure optimal bone health in adulthood ^(1,2).

However the risk for osteoporosis is not only a matter of lifestyle. Genetic research has shown that some people deal with increased risk compared to the general population, due to their genetic background. Despite we all share approximately 99.9% of common genetic material, there are DNA variants in the genes, which can affect importantly the susceptibility to health conditions.

VDR is a protein involved in Vitamin D and calcium absorption, having an important role in proper bones structure and function. However certain DNA changes in the gene encoding for this protein have been associated with defects in the normal function of VDR and thus increased risk for bones problems ^(3,4,5,6).

CTR which binds to calcitonin, also functions to ensure calcium homeostasis, particularly with regard to bone metabolism. During the normal process of bone turnover, a microscopic amount of bone is removed (bone resorption) and then replaced by new tissue. Scientists have found that when CTR variants are present in the gene an individual may deal with problems in calcium homeostasis and thus increased risk for osteoporosis ^(7,8,9).

In skeletal homeostastis LPR5 protein has also an important role. Several disorders related to bone density (like osteoporosis) are caused by mutations in the gene that encodes this protein ^(10,11,12).

With all the major steps made the past few years in Genetics field, people are able to know their genetic profile (regarding the mentioned and other mutations) and if their genes increase their susceptibility to osteoporosis.

Such knowledge can have tremendous results in prevention of the condition. Personalized nutritional and general lifestyle consultation is nowadays more feasible than ever, since it is based not only to clinical and biochemical data (“what we see”) but also on the precious (“hidden”) information that genes provide. Thus the effectiveness of prophylactic measures can increase substantially.  Moreover appropriate medical and nutritional advice can be implemented as earlier as possible, without waiting for the first clinical symptoms. But even in cases the conditions develops, knowing the genetic background will provide health professionals with important information regarding the roots of the problem, giving the option for therapies with more effective results.

Obesity has increased dramatically over the past years -mostly in industrialized but also in developing countries- and is classified by the WHO (World Health Organization) as epidemic. With major consequences in health, public health, economy and society, an important effort has been made by scientists to discover the cause for this phenomenon ^(1).

In order to classify individuals as overweight or obese, a measurement called BMI (Body Mass Index) is used. BMI is the individual’s body weight (kg) divided by the square of the height (m). A person with a BMI between 25 and 30 is considered as overweight, whereas one who has exceeded 30 is considered as obese. There are also other markers taken into account, like fat accumulation versus muscle mass, but BMI is the most commonly and well accepted measurement to distinguish people who exceed the normal weight.

Being overweight or obese does not only affect the self-esteem of an individual, but has serious implications for the health. Importantly increased risk for cardiovascular disease, diabetes, hypertension, obstructive sleep apnea, even certain types of cancer.

Contrary to conventional wisdom, being overweight or obese is not just because of overeating. It is the result of many factors, as obesity is nowadays characterized as a multi-factorial, polygenic disorder. What and how we eat is determined by a numerous of factors, not all of them being obvious. Scientific research has revealed that apart from environmental factors, genetic background plays also an important role, as certain gene mutations can make some people more susceptible to obesity.

A group of such mutations are found in genes that are involved in appetite regulation, feeding behavior and metabolism. It is not surprising that most of these genes produce proteins in hypothalamous, the portion of brain that regulates hanger and others that are produced in adipose (fat) tissue.

FTO ^(2,3,4) is an example of such genes, as mutations can cause defects in energy intake regulation and satiety. In simple words a person who carries such mutations, may be unable to control his/her appetite, and know when he/she had enough of food.

ACDC ^(5,6) gene produces a hormone in adipose tissue involved in fatty acid breakdown and glucose regulation. Mutations in this gene have shown to cause increased fat storage. This results to reduced insulin levels and increased glucose levels in plasma, leading individuals to easier weight gain and higher BMI.

LEPR ^(7,8,9) is also involved in regulation of adipose (fat) tissue mass. Its functions in hypothalamus influence the feeling of satiety and energy balance. The type of the gene affects the feeding behavior and the susceptibility of individuals to weight gain and obesity. Mutations in LEPR result to higher circulating levels of leptin. Despite Leptin levels within normal rates are beneficial as they reduce appetite, high levels lead to Leptin resistance and consequently appetite is not properly regulated.

MC4R ^(10,11) produces a protein that binds to the hormone melanocortin, involved in regulation of appetite and metabolism. Certain mutations have been associated with increased susceptibility to weight gain and obesity.

The group of genes taking part in feeding behavior and the mutations found in such genes creates a panel of genetic variants, like the ones mentioned above, for which nowadays an individual can be tested to know whether his/her genetic profile increase the risk to be obese. It is of outmost importance that for the majority of the genes, the effect of such mutations is modifiable with the appropriate corrective actions. Next step for a person found to have a genetic profile of increased risk, will be to imply the appropriate recommendations in everyday life which can prevent excessive gain weight.

Numerous guidelines by health organizations are available in order to prevent obesity, and worldwide campaigns are trying to motivate people, and especially children, to follow a healthy diet combined with physical exercise. But one could wonder if such strategies have the shown expected results or there is a deeper root for this condition. Undoubtedly following such recommendations for a healthy lifestyle, can cause no harm. But these apply to the general population, taking into account only one aspect of the problem. Nowadays an individual can be provided with a personalized approach, which takes into account not only the person’s lifestyle habits, but also his/her genetic makeup. Nutritional consultation and suggestions on certain supplementation (like appetite suppressants) that will address to an individual’s genetic needs can have far more effective and long-standing results in prevention of obesity and maintenance of normal weight.

In recent years the concept of Predictive Genomics has attracted increasingly the interest not only of health professionals but most importantly of the general population. The numerous developments in the field of medical genetics have offered the chance to individuals to have an access to their genetic makeup and understand what kind of information is “hidden” in their genes. A very simple –in procedural way- DNA test can reveal whether a person has increased genetic risk for common conditions compared to the risk of the general population. Identifying genetic changes (mutations) which are involved in certain diseases and thus access a person’s risk based on the genetic profile can provide health professionals with crucial information on prevention and more effective treatments.

The leading causes of death worldwide are diseases which are multi-factorial, for which genetic background as well as environmental factors has a crucial role. Cardiovascular disease is an outstanding example of such conditions.

Cardiovascular disease refers to a defective function of heart and/or vessels. The major cause is atherosclerosis, a condition in which the arteries are thickened, due to accumulation of fatty acids on their walls forming atheromatous plaques. This is very dangerous as progressively the plaque can rupture and block the blood supply to heart or brain and lead to heart attack or stroke respectively. During the past years cardiovascular system problems have increased dramatically –mostly in Western communities- and in some countries have led to death more people than cancer.

Despite the medical community has provided the past years with lifestyle guidelines to prevent cardiovascular risk, these measures apply to the general population, without taking into account the personal genetic profile of individuals. However scientific research has revealed specific DNA alterations that increase importantly the risk for cardiovascular disease, making a person who carries them more susceptible and increasing the need for personalized corrective actions that can modify this higher risk.

A group of such DNA changes are in genes involved in lipids metabolism, like APOA1, APOE, PON1, and CETP ^(1,2,3,4). Such mutations increase the risk for reduced levels of HDL (good cholesterol) and increased levels of LDL and triglycerides, resulting to higher risk for atheromatosis. Of course we cannot change our genes; however it is of outmost importance that the effect of such mutations can be modified if we apply the appropriate guidelines (like specific dietary habits, exercise and certain clinical screening tests), addressing to our personal genetic background. Limitation of saturated fatty acids and increased intake of ω-3 fatty acids has been proved to be one of the most efficient ways to reduce the cardiovascular risk, even if the genes do not function properly.

Another example is the group of genes involved in homocysteine metabolism, like MTHFR, MTR and CBS ^(5,6,7,8). DNA changes in such genes are associated with higher homocysteine blood levels, another risk factor for cardiovascular disease.  Again certain personalized guidelines apply to an individual who has a genetic profile indicative of possible defects in homocysteine metabolism. Regular test of folic acid and homocysteine levels, and increase intake of folic acid through diet along with other measures could help individuals overcome such genetic defects.

The list of newly added polymorphisms involved in certain diseases is daily increasing, making the personalized genomic medicine more promising than ever. Nutritional guidelines that address to the specific genetic needs of an individual can undoubtedly be a much more efficient approach in prevention of cardiovascular risk compared to measures for the general population. Nutritional consultation based on an individual’s genetic makeup will be targeted to the roots of the risk and can be implied even from early youth years importantly earlier before atherosclerosis develops. Moreover nutritional supplementation can be proposed to enhance the cardiovascular health, providing the individuals with increased intake of certain vitamins and substances that the person tested needs, instead of overloading the body with excessive compounds.

Talent is a term frequently used to describe a natural ability for which some people are distinguished, referring to an innate component to perform at higher than the median level of population at a certain work/task. The question whether an elite athlete is born with a natural talent or is “made” through adaptation to training has for many years concerned scientists and professionals involved in sports. Nowadays it is well accepted that there are many factors determining elite athletes; genetic makeup and environment (training, social environment, nutrition) playing both a crucial role. These factors determine also the type of sport where an individual shows a better level of competence, either a sport requiring increased endurance capacity and/or muscle performance.

Focusing on endurance, there are many factors that affect a person’s performance. VO2 max is the most often mentioned when analyzing endurance performance. It refers to maximal oxygen uptake (or aerobic capacity) and is defined as the maximum capacity of the body to transport and use oxygen during exercise. Athletes of endurance sports (e.g. long distance running, swimming, cycling, etc.) performing at high levels of competition have been genetically “gifted”, carrying often specific DNA variants (polymorphisms) in genes involved in metabolism, energy production and muscles formation. Such DNA variations can provide a person with an increased innate ability to have a higher VO2 max, increased exercise economy, and increased aerobic energy production.

Regarding VO2max related genes, VEGF is an example. This gene is involved in angiogenesis. The cells of vascular system, in which blood flows, receive a signal to grow and multiply. This is crucial before and after intensive exercise when blood flow needs to provide the muscle tissues with more oxygen. The type of the gene is associated with the oxygen supplies in muscles and affects the endurance capacity of individuals.

ACE is a well examined gene in relation to endurance capacity, due to its role in cardiovascular system. ACE encodes an enzyme that converts Angiotensin I to Angiotensin II and is involved in the function of cardiovascular system and muscle performance. The levels of the enzyme affect the regulation of blood pressure and are associated with the levels of lipids, glucose and total cholesterol in blood. One of the polymorphisms extensively studied is the I/D, referring to an insertion (I) in the gene. Individuals who carry the variant I, are shown to have increased rate of energy production during incremental exercise, which permits the muscles to perform better in activities with longer duration.

Another polymorphism in gene HIF-1 is associated with a significant advantage of endurance capacity, affecting the oxygen and energy supplies in muscles. This variant results to increased activation of other genes involved in energy metabolism and transport of oxygen to muscles. Athletes seem also to respond very good to high altitude training.

Moreover polymorphisms in genes involved energy production and expenditure energy either from carbohydrates and/or, like PPARD and ADRB2, can affect importantly the genetic tendency of an individual regarding endurance performance levels.

The panel of polymorphisms affecting endurance constantly is constantly enriched with new research data. However for a number of DNA variants the scientific data are quite strong. DNA tests available in the market worldwide offer the chance for individuals to discover their personal genetic advantages or barriers regarding performance in endurance sports. Such tests do not only address to professional athletes but also to amateurs, who just wish to make the right choice of sport or enhance their performance in the sport they are already involved in.

What needs to be emphasized when analyzing the effect of such DNA variants, is that despite the fact that our genetic makeup is something we carry for a lifetime and cannot be altered, it is possible to modify to an important extent the effect of certain polymorphisms. Individualized consultation regarding endurance training strategies based on the genetic profile is now feasible. With the appropriate guidance even people who carry disadvantageous polymorphisms can increase importantly their VO2 max and exercise economy. Adaptation to endurance training will be significantly more effective when sports professionals are aware of the genetic limits of their athlete.

Moreover knowing the genetic needs of an athlete, makes it much easier to choose the appropriate supplementation that will address to the personal needs for certain nutrients.

Undoubtedly sports’ training is moving towards a much more personalized approach of the athlete, taking advantage of the genetic “insight” that science nowadays offers.

All human characteristics – from the colour of our hair and even our personality to our physical condition and vulnerability to disease – are to a significant degree defined by the genetic information hidden in our DNA! Genes ­ which are particular segments of the DNA – control traits, characteristics and overall health. Although more than 99% of human DNA is identical among all people, it is the remaining 1% that makes us each unique. These tiny differences are called mutations.

Predictive Genomics is the field of medicine that deals with the detection of such mutations which are associated with certain traits, characteristics or common polygenic – multifactorial diseases.

The Predictive Genomics DNA Testing aims to reveal important information on the genetic profile of an individual regarding health risks and general physical condition. Such testing mainly focus on mutations which are relevant to certain biological systems and can – to a significant degree – be modifiable by appliance of Medical, Nutritional and general lifestyle guidelines. These measurers based on an individual’s genetic profile have the major advantage of being personalized and thus have are significantly more efficient compared to guidelines addressing to the general population.

Genetic risks and Nutrition

Over the past few years the scientific research in genetics has revealed several variants in the genome which can increase risks for certain health conditions, increase sensitivity to weight gain and predispose to problems in feeding behavior. These mutations are not proven to be causative, but they rather act accumulatively, increasing the risk for disease. In such cases the role of dietary habits becomes crucial, as they can trigger or prevent the manifestation of certain conditions.

For example a person may be found with an increased risk for cardiovascular disease due to accumulation of mutations in genes regulating lipid levels, like APOA1, APOE, PON1, and CETP ^(1,2,3,4). The dietary habits should be adjusted properly in order to reduce the risk indicated by the genetic profile. Increase intake of ω-3 fatty acids, found in fish, is proved to be a significant ally in prevention of a heart attack or stroke, as they can modify the expression of genes involved in atherosclerosis. On the other hand the increased consumption of saturated fats, found in red meat and full-fat dairy products, affects negatively the function of the cardiovascular system.

Another example is a woman’s genetic profile that is associated with increased risk for osteoporosis. In this case the studies have shown that increased intake of Calcium and Vitamin D confers importantly in prevention of the disease, or even if osteoporosis develops it could prevent severe symptoms, like frequent and serious bone fractures ^(5,6,7).

Genetic needs & Nutrition

Apart from reducing the risks for certain conditions, the genetic profile can indicate increased needs of an individual for specific nutrients.

There are specific genes with a crucial role in detoxification and anti-oxidation. These are very important functions for cells in order to deactivate toxic substances, which are either by-products of metabolism or came into the body from the environment. Such substances if not removed can cause serious damages in the DNA with harmful consequences to the health, like development of cancer. In case a genetic profile is indicative of risk for defects in anti-oxidation and detoxifications (with several mutations in genes like GSTT1, GSTM1, CAT), then the individual has increased needs for foods rich in antioxidants, like Vitamins A, C, E, found in fresh fruits and vegetables, nuts, etc. ^(8,9,10).

Scientific research in human genome has shown already significant evidence regarding the ways that genes interact with nutrition. Therefore it is becoming crucial for Nutritionists and other health professionals to use this knowledge when address to an individual, offering advice that serves certain and personalized needs.