A GENETIC APPROACH TO WEIGHTLOSS
VITAMINS DEFICIENCY RISK:
There is no such thing as absolute good nutrition or healthy foods. These days, there is a high pressure to look young and to have that pleasant body. When it comes to developing new and healthy eating habits to get the body shape you are looking for, sometimes you lack time or willpower, or may be traditional diets simply do not work for you.
The key to an effective weight management -
a diet that really works - may be found in your genes.
Your genetic makeup determines which nutrients are used, how toxins are removed, and the effectiveness of your body's key processes. Adjusting your lifestyle can impact how your genes function, and compensate for genesfunctioning at an altered level.
Experts agree that a personalized approach to nutrition could transform the way people lose weight. It's not a lack of willpower; it is due to a persons individual make-up - their genes, hormones and psychology.
The latest weight loss science-based approach is that instead of reaching for a one-size-fits-all diet, people should follow one that is tailored to their individual needs.
(Halal, Hindu, Buddhist, Kosher)
Exclude food responsible for:
between dietary approaches scientifically proven to delay aging at a cellular level and according to your individual genetics and your salt, caffeine, lactose and gluten sensitivity.
adapting your food plan and your food environment to your healthy eating needs.
For all time.
Each time you select a food,
The anti-aging nutrition plan made to measure from your DNA can be further upgraded - the same moment, or whenever you want during your lifetime - to one of those special regimens:
Scientific studies document the benefit of a personalized nutrition plan rather than generic diets. Subjects who received DNA-based dietary advice showed improvements after three months, and the changes became even more apparent after 12 months - managing to achieve their objectives in terms of weight loss and ideal weight maintenance over time. In addition, blood tests showed that their sugar levels had improved significantly.
Popular diets may work in the short term, but even the best ones don't keep most people slim over time. Researchers report that just about everyone starts gaining back weight after a year or so. Dr. Mark Eisenberg of Jewish General Hospital/McGill University in Montreal, Canada and colleagues reviewed major studies looking at four of the most popular and medical lauded diets: Atkins, South Beach, Weight Watchers and the Zone (Eisenberg et al., American Heart Association journal Circulation: Cardiovascular Quality).
The FTO gene encodes the homonym enzyme, associated with the amount of body fat and with the risk of obesity in both children and adults. Its function is not yet completely clear, but it is thought that it may act as a switch for other genes: its regulatory action appears to be influenced by nutrition and fasting. Given that FTO is highly expressed in hypothalamic regions important for the increase of appetite, it influences the energy balance and consequently the eating behavior. FTO could highlight if you are prone to develop fat mass in excess, and it could also be due to a lower sense of satiety, which the presence of this variant entails.
The ACE gene encodes a protein that acts on the system that regulates blood pressure and the phenomena of vasodilatation and vasoconstriction. It has been shown that in the musculature an increase of blood supply increases the amount of nutrients and oxygen required for muscles to function. The ACE gene allows the muscle to sustain the physical effort required by the body, determining the right type of exercise for each of us. The test could highlight the presence of the II (insertion) variant that seems to be associated with physical exercise relative to strength rather than endurance.
Lipoprotein lipase (LPL) is an enzyme present in the endothelial cells of blood capillaries. Its function is to hydrolyze triglycerides contained in lipoproteins (chylomicrons and VLDL), releasing fatty acids which then diffuse into cells. Freed fatty acids may be metabolized in skeletal muscle and in the heart or, in periods of over-nutrition (energy surplus), may be used as substrates for the resynthesis of triglycerides, which will be accumulated as an energy reserve in the form of fat. Variations in this gene may cause an increased level of triglycerides in the blood, increasing the risk of cardiovascular diseases.
The BDNF protein plays several roles in the brain and nervous system and, at high levels, the protein can stimulate the feeling of fullness. After analyzing brain tissue samples, the researchers identified an area of the gene where a single change reduced BDNF levels in the hypothalamus, a key area that controls eating and body weight. The genetic change is not a rare mutation, but rather a variation that occurs in the general population. Every person has two copies, or alleles, of each gene, inheriting one copy from each parent. Alleles can vary at any location across the gene. The C allele of the BDNF gene may be linked to obesity in people. The area of interest interacts with a protein called hnRNP D0B. In laboratory experiments it was found that hnRNP D0B had trouble interacting with the C allele, resulting in less BDNF production. Lower BDNF levels may contribute to obesity in people with the C allele.
Two general population studies of European women strongly indicated an association between the Met–Met genotype in BDNF and lower BMI (Gunstad et al, 2006, Shufart et al, 2009).
Apolipoprotein C3 is a lipoprotein capable of binding lipids and is responsible for transporting cholesterol and triglycerides to various tissues and organs through blood circulation. It plays a key role in lipids metabolism; in particular, it inhibits the enzyme lipoprotein lipase (LPL), which blocks the metabolism of triacilglycerol. This may cause an increase in the levels of triglycerides (hypertriglyceridemia) often associated with cardiovascular risk.
PPARG is a cellular receptor linked to the metabolism of sugars which controls the levels of glucose and insulin in the blood. Variations of the gene may alter the amino acid sequence of the protein, rendering it less efficient and effective in the regulatory processes, with an increase of adipose tissue and reduction of insulin sensitivity. The presence of the CC variant renders one more susceptible to alterations in the levels of insulin in the blood, increasing the risk of development of Type 2 diabetes.
TCF7L2 is a transcription factor, a protein that when bound to DNA is capable of influencing the activity of nearby genes, which plays an important role in glucose homeostasis. The presence of an unfavorable variant may adversely affect the balance of insulin and glucose, especially in diets rich in fat. This variant may cause a moderately increased sensitivity to carbohydrates.
The MTHFR gene encodes an enzyme involved in the metabolism and utilization of folic acid, vitamins B6, and B12. Its role is to transform the 5-10 methylene-tetrahydrofolate (THF) into 5 methyl-THF, the most abundant circulating form of folic acid, which serves as a methyl donor for the remethylation of homocysteine into methionine. This reaction helps to regulate homocysteine levels and requires vitamin B12. Mutations in this gene may lead to reduced enzymatic activity, often associated with increased levels of homocysteine in plasma.
The VDR gene encodes the Vitamin D receptor whose role is to regulate calcium transport and homeostasis. It is also critical for the proper process of bone mineralization. Scientific studies have shown that interactions with the Vitamin D receptor may influence the effect of caffeine in bone mineral density. The presence of the AA variant combined with large caffeine intake may be linked to a weakening of bone mass due to an alteration of the absorption of calcium in the bones.
The SOD2 gene encodes manganese superoxide dismutase (MnSOD), an enzyme localized in the mitochondrial matrix, which is the first line of defense of cells against free radicals. MnSOD catalyzes the dismutation of superoxide (a dangerous reactive oxygen species) into oxygen and hydrogen peroxide. Its role is to protect cells from oxidative stress caused by free radical damage. These are in fact the basis for many degenerative diseases, and are among the most important factors responsible for skin aging.
The genes GSTM1 and GSTT1 encode for the glutathione S-transferase proteins, a family of detoxifying isoenzymes that catalyze the conjugation of various toxic molecules with glutathione, rendering them less reactive and more easily to eliminate from the body. Their role is therefore to protect us from harmful substances, preventing their accumulation. The specific task of these enzymes consists in the detoxification of carcinogens, such as those contained in cigarette smoke; harmful substances such as benzopyrene, polycyclic aromatic hydrocarbons, solvents, medicines; and heavy metal ions such as cadmium, gold, copper, nickel, mercury and zinc.
The IL10 gene encodes the homonym anti-inflammatory cytokine (IL-10). Its role is to inhibit the release of pro-inflammatory cytokines during the development of inflammatory responses. This molecule, mainly produced by monocytes, T lymphocytes, and macrophages, plays an immunosuppressive role in the regulation of inflammatory responses. The polymorphisms in this gene may influence the amount of cytokines produced. The presence of this variant entails an increased production of these cytokines, with a greater risk of developing cardiovascular and inflammatory diseases compared to non-carriers. In these cases it is important to take action to reduce the overall inflammatory state of the organism by consuming foods with anti-inflammatory action.
The TNF-alpha is a pro-inflammatory cytokine involved in systemic inflammation and it induces both acute and chronic responses. It has been shown that TNF plays an important role in the various processes of cell proliferation. TNF is produced in a controlled manner by many types of cells in response to both endogenous and exogenous stimuli, such as bacterial toxins and viral infections.
The CYP1A2 gene encodes the enzyme cytochrome P450 involved in the removal of toxins (such as food and smoke cancer causing agents). In addition, this gene seems to be the most responsible for the regulation of the metabolism of caffeine. It has been shown that people who present the slow variant of this enzyme will be predisposed to metabolize caffeine more slowly, and will thus have a higher concentration of caffeine in the blood, resulting in an increase in its stimulating action. The presence of the AC variant entails the activity of two enzymes, one that works quickly and one that works slowly. This activity may render the metabolism of xanthine bases (such as caffeine) more difficult, thus we recommend you limit the consumption.
ACE (Angiotensin Converting Enzyme) is an enzyme that has the task of catalyzing the conversion of angiotensin I (inactive form) into angiotensin II (active form), which is a powerful vasoconstrictor. Its involvement in the RAS system (renin-angiotensin) controls blood pressure and electrolyte balance. Furthermore, ACE is able to inactivate the vasodilator bradykinin. Its role is therefore to maintain cardiovascular homeostasis, since it regulates both vasoconstriction and vasodilation. The gene may carry an insertion/deletion polymorphism (I allele = insertion, D allele = deletion) that influences the enzyme activity, increasing the risk of vascular disease. Certain studies have also shown an association between this type of variation and sensitivity to salt in diets. The presence of the II (insertion) variant entails an increase in plasma levels of ACE, thus increasing the risk of cardiovascular disease. It is also a risk factor for myocardial stroke and hypertension, as it is related to an excessive use of salt in the diet. Therefore, it is advisable to limit as much as possible the use of salt.
Approximately 90% of the cases with reference to lactose intolerance resides in a polymorphism in the regulatory region of lactase gene, which may lead to a deficiency of lactase in the microvilli of the small intestine. The inheritance of this polymorphism is autosomal recessive, which means that only those who have both copies of the mutated gene (homozygous) suffer from this type of intolerance. In Europe, approximately 15% of the population is homozygous for the mutated form of lactase, while 45% carry only one copy of the gene with the defect, and therefore do not suffer lactose intolerance. This genetic analysis allows us to identify those with both of the normal copies of the gene (TT), those who have only one healthy copy and anyway do not present the intolerance (CT), and those who have both copies mutated (CC). The presence of the CC variant signifies that one does not have sufficient amounts of the lactase enzyme needed to digest lactose, leading to clinical manifestations such as colic, cramps, bloating and diarrhea.
The association between Coeliac disease and the genes that code Class II HLA is evidence of the importance of genetic factors. Over 90% of Coeliac patients present the HLA DQ2 molecule. Those who don’t express the DQ2 molecule, express, in most of the cases, the DQ8 molecule. It should however be kept in mind that the analysis of HLA may not be used to confirm a diagnosis of Coeliac disease because the genes encoding these molecules are present in 30% of the general population. On the other hand, however, the negativity for these haplotypes may exclude, or at least render extremely unlikely, a diagnosis of gluten intolerance. DQ2 and DQ8 negative Coeliac patients are in fact very rare.
The glycemic load (GL) of food is a number that estimates how much the food will raise a person's blood glucose level after eating it. A diet focused on foods with a low glycemic load can:
But a low glycemic index is not enough; we need carbs in our diet, and we have to learn which ones are good and which are bad. The Insulinemic Index of a food represents how much it elevates the concentration of insulin in the blood in the two-hour period after the food is ingested.
Potential Renal Acid Load (PRAL) is a calculated value of certain nutrients in food that have the most significant indication of changing the acidity or alkalinity of the body.
The absolute foundation of sound nutrition is to maintain the correct acid/alkali balance in the body. The ideal diet should consist of 75%-80% alkali-forming foods, i.e., foods that have an alkali residue after metabolism. The proper alkaline pH of the blood is critical for the overall health of the body.
Oxygen radical absorbance capacity (ORAC) is a method of measuring antioxidant capacities in biological samples in vitro.
FODMAPs are carbohydrates (sugars) that are found in foods. FODMAPs are osmotic (means they pull water into the intestinal tract), may not be digested or absorbed well and could be fermented upon by bacteria in the intestinal tract when eaten in excess. The low FODMAP diet is often used in those with irritable bowel syndrome (IBS). This approach is used in those with similar symptoms arising from other digestive disorders to accelerate a flat stomach (flat-belly).
Satiety value is the degree to which food gives a human the sense of food gratification, the exact contrast feeling of hunger. The highest satiety value is expected when the food that remains in the stomach for a longer period produces greatest functional activity of the organ. Limiting food intake after reaching the satiety value helps reduce obesity problems.
Circadian clocks that comprise clock genes exist throughout the body and control daily physiological events. The central clock that dominates activity rhythms is entrained by light/dark cycles, whereas peripheral clocks regulating local metabolic rhythms are determined by feeding/fasting cycles. Nutrients reset peripheral circadian clocks and the local clock genes control downstream metabolic processes. Metabolic states also affect the clockworks in feedback manners. Because the circadian system organizes whole energy homeostasis, including food intake, fat accumulation, and caloric expenditure, the disruption of circadian clocks leads to metabolic disorders. Time-restricted feeding or a balanced breakfast can powerfully entrain and thus amplify circadian clocks in peripheral tissues, whereas feeding at unusual times or with a high-fat diet attenuates these clocks.
Telomere length has been shown to be positively associated with nutritional status in human and animal studies.
Various nutrients influence telomere length potentially through mechanisms that reflect their role in cellular functions including inflammation, oxidative stress, DNA integrity, DNA methylation and activity of telomerase, the enzyme that adds the telomeric repeats to the ends of the newly synthesized DNA (Paul L., J Nutr Biochem, 2011).
An appropriate food selection can support our healthy hormonal response: adjusting growth and sex hormones, improving the receptor response to these hormones.
Studies indicate that the Mediterranean diet is linked with improved health and longevity.
The Mediterranean dietary pattern centers upon fruits, vegetables, whole grains, legumes, monounsaturated fats (MUFA; like those found in olive oil), and a healthy ratio of Omega-3 to Omega-6 polyunsaturated fatty acids (PUFAs). An impressive amount of epidemiological data link the Mediterranean diet with improved cardiovascular, cognitive, and metabolic health (Episoto 2010, 2011; Galland 2010; Nordaman 2011; Kastorini 2011).
Following a Mediterranean style diet may be associated with greater telomere length - a finding that further supports the diet’s links to health and longevity, say researchers. The data, published in the BMJ, shows that greater adherence to the Mediterranean diet was associated with longer telomeres (Crous-Bou et al., BMJ, 2014, Nilsson, BMJ, 2014).
The nutrient range of Nordic diets is associated with better physical performance and a decrease in disability risk later in life, a study confirms. Along with the Mediterranean diet, the Nordic approach to food has long been held up as a blueprint for healthy eating and nutrition. The diet is rich in apples and berries, roots and cabbages, rye, oats and barley, low-fat milk products, rapeseed oil and fish.
The Nordic Diet improves: Blood lipid profile, Insulin sensitivity, Inflammation, Lowers blood pressure, Reduced waist circumference.
A healthy Nordic diet reduces inflammatory gene expression in subcutaneous adipose tissue compared with a control diet independently of body weight change in individuals with features of the metabolic syndrome.
Ailments like asthma, migraines, mood disorders or skin problems can be result of a difficult-to-detect moderate food sensitivity with: Poor nutrients absorption, Damaged gut cells, Increased inflammation.
Problems in the GI tract can ultimately disturb hormonal, metabolic and immune functions. Cutting away some foods can help you detect moderate food sensitivities you were unaware of.
Want to lose abdominal fat, get smarter and live longer?
New research led by USC Stem Cell principal investigator Valter Longo shows that periodically adopting a diet that mimics the effects of fasting may yield a wide range of health benefits.
In a new study, Longo and his colleagues show that cycles of a four-day low-calorie diet that mimics fasting (FMD) cut visceral belly fat and elevated the number of progenitor and stem cells in several organs of old mice — including the brain, where it boosted neural regeneration and improved learning and memory.
The iDDNA® Anti-Aging Diet adopts state-of-the-art research and development; pre-clinical and clinical trials were conducted at the University of Southern California's Longevity Institute, sponsored by the National Cancer Institutes (NCI) and National Institute on Aging (NIA) of the National Institute of Health (NIH). The results of this research were published in top scientific peer-reviewed journals.
Prolonged fasting (PF) promotes stress resistance; alternating PF and nutrient-rich medium extended yeast lifespan independently of established pro-longevity genes.
iDDNA® is designed to achieve the beneficial effects of fasting while providing micronutrient nourishment (vitamins, minerals and others) from which the body is deprived during fasting and minimizing the psychological burden of pure fasting.
Harvard performed a recent study that showed an 80% decrease in infertility with lifestyle changes made by switching to a fertility diet. Women who followed a combination of five or more lifestyle factors, including changing specific aspects of their diets, experienced more than 80% less relative risk of infertility due to ovulatory disorders compared to women who engaged in none of the factors, according to a paper published in Obstetrics & Gynecology.
The women with the highest fertility diet scores ate less trans fats and sugar from carbohydrates, consumed more protein from vegetables than from animals, ate more fiber and iron, took more multivitamins, had a lower body mass index (BMI), exercised for longer periods of time each day, and, surprisingly, consumed more high-fat dairy products and less low-fat dairy products. The relationship between a higher “fertility diet” score and lesser risk for infertility was similar for different subgroups of women, regardless of age and whether or not they had been pregnant in the past.