People Reviews on Genetic Testing for Weight Loss
Improved weight direction using genetic data to personalize a calorie controlled diet
Ioannis Arkadianos
iThe Dr Arkadianos Clinic, Messogion Av, Athens, Greece
Ana Thou Valdes
2Twin Research Unit of measurement, King'due south Higher London, U.k.
Efstathios Marinos
iiiBiomedical Engineering science Laboratory, National Technical University of Athens, Greece
Anna Florou
1The Dr Arkadianos Clinic, Messogion Av, Athens, Greece
Rosalynn D Gill
4Sciona Inc, Boulder, 80302, Colorado, The states
Keith A Grimaldi
4Sciona Inc, Boulder, 80302, Colorado, USA
Received 2007 May 23; Accepted 2007 Oct 18.
Abstract
Background
Gene-environment studies demonstrate variability in nutrient requirements depending upon private variations in genes affecting nutrient metabolism and transport. This study investigated whether the inclusion of genetic information to personalize a patient's diet (nutrigenetics) could improve long term weight management.
Methods
Patients with a history of failures at weight loss were offered a nutrigenetic test screening 24 variants in xix genes involved in metabolism. l patients were in the nutrigenetic group and 43 patients attending the aforementioned clinic were selected for comparison using algorithms to lucifer the characteristics: age, sex, frequency of clinical visits and BMI at initial dispensary visit. The 2d group of 43 patients did non receive a nutrigenetic test. BMI reduction at 100 and > 300 days and blood fasting glucose were measured.
Results
After 300 days of follow-up individuals in the nutrigenetic grouping were more than likely to have maintained some weight loss (73%) than those in the comparing group (32%), resulting in an age and gender adapted OR of v.74 (95% CI 1.74–22.52). Average BMI reduction in the nutrigenetic grouping was 1.93 kg/m2(five.six% loss) vs. an average BMI gain of 0.51 kg/mtwo(2.ii% gain) (p < 0.023). Among patients with a starting claret fasting glucose of > 100 mg/dL, 57% (17/30) of the nutrigenetic group but only 25% (4/xvi) of the non-tested group had levels reduced to < 100 mg/dL later on > ninety days of weight direction therapy (OR for lowering glucose to < 100 mg/dL due to diet = 1.98 95%CI 1.01, 3.87, p < 0.046).
Conclusion
Addition of nutrigenetically tailored diets resulted in better compliance, longer-term BMI reduction and improvements in blood glucose levels.
Background
Information technology has been thoroughly documented that the percentage of the population that is overweight and obese is rising to epidemic proportions all over the world with all the bellboy health, social and economical consequences [one-5]. While many reasons take been put forward equally causes of the epidemic [6] the most likely remain the increased calorie intake and reduced practice typical of the modern lifestyle. Certainly most people who eat more and practice less will increase their weight, but arriving at a land of overweight or obesity is a gradual process, taking place over many years of even simply slight backlog energy intake. For example, in the USA people gain an average of xv kg (30lb) body weight between the ages of 25 and 55 years sometime. This level of weight gain represents only ~0.5 kg (1lb) per yr, the equivalent of overeating by just a few calories per day [7].
Behavioral treatments can effect in a weight loss sufficient to ameliorate health for many patients, but frequently the weight is regained over fourth dimension [eight]. Although for many people a reduction in weight is difficult to achieve, maintaining the weight loss is even harder. Indeed, few non-surgical treatments for obesity event in sustained weight loss [9]. Long term maintenance of weight loss requires permanent lifestyle changes in exercise and eating habits. These changes need to exist significant just not necessarily radical or unachievable if planned over several years of gradual but sustainable weight loss. The National Institutes of Health recommend a x% weight loss target in the kickoff six months (at a rate of 0.25–0.50 kg/calendar week) followed by a weight maintenance program or further weight loss, at a lower rate, if required [x].
It has long been suspected that "one size does non fit all" in terms of determining the optimal diet for an private, and this has been demonstrated over the recent years in studies on cistron-nutrition interactions and the emergence of nutrigenetics [11-13]. The goal of nutrigenetics is to add a level of personalization to a prescribed diet, by adjusting information technology according to genetic variation. For example people carrying the MTHFR 677T allele require more folate and B vitamins in their diet in order to go on homocysteine levels low [14,15]. Nutrigenetic testing in clinical practice analyzes genes principally involved in the metabolism and transport of nutrients, removal of toxins and protection from oxidation. Co-ordinate to the particular pattern of genetic variation, personalized communication can be generated that contains recommendations on dietary and lifestyle modifications to reach genetically based, specific goals in nutrition and exercise.
The nutrigenetic nutrition utilized in this written report was not designed nor proposed to patients equally a weight loss diet; the aim was to optimize the food content of an private's daily food intake, based on electric current understanding of an individual'due south genetic profile. While an individual is achieving weight loss, food consumption is generally reduced and particular nutrients in the diet may not be in acceptable supply. Nutrigenetics may be a tool to help achieve optimum nutrient content on an individual footing. Furthermore, the use of nutrigenetics in designing personalized diet and lifestyle programs has the potential to increase motivation and compliance with long-term lifestyle changes.
The Dr Arkadianos clinic in Athens began exploring the use of nutrigenetic testing in weight management protocols in 2003 and initial observations suggested that tailoring the diet co-ordinate to genetics might improve weight loss and control of biomarkers, such as blood fasting glucose levels. In guild to examine these findings in more detail, a formal case history study was initiated. Case histories were followed for a grouping of 50 patients who took the test and received a personalized nutrition and compared to a grouping of 43 patients (matched for historic period, sex activity and frequency of dispensary visits) who were non tested and who received merely the standard clinical diet.
Methods
Patients with a history of unsuccessful attempts at weight loss (defined every bit at least 2 or more unsuccessful attempts) attention a weight management clinic in Athens, Hellenic republic were offered nutrigenetic testing. Nutrigenetic kits were used as part of the comprehensive weight management program. The report was constructed through the use of a computerized analysis of patient records. A computer program was written to query the patient clinical records database to select patients who had taken the nutrigenetic test who could be matched for age, sex, starting BMI and number of clinic visits with patients who had not taken the test. In this article, the investigators report the analysis of patient clinical records at a single bespeak in time, which ways that unlike patients were at different fourth dimension points in their weight direction treatment program. The case histories of fifty "nutrigenetic" patients (22 female, 28 male) were compared to those of 43 patients in the non-tested group (eighteen female and 25 male) which had a follow-up either betwixt 90–365 days (24 nutrigenetic 21 not-tested), a year or more (6 nutrigenetic, seven non-tested) or both (20 nutrigenetic, fifteen non-tested). 7.v % of study subjects (iv in the nutrigenetic group and 3 in the not tested group) were in the normal weight range (BMI < 25 kg/thousand2). Notwithstanding, they had tried to lose weight on repeated occasions and had failed which is why they attended the dispensary.
The written report procedure involved periodic analysis of patients' clinical records, which were anonymized and assigned identification numbers. The clinicians involved in the patient handling were not aware of which patients were included in the report.
All study participants' data was anonymous. Those conveying out the nutrigenetic examination signed a consent form and all patient data was handled according to the Greek Code of Medical Deontology and in accordance with the Helsinki Understanding.
Nutrition and Exercise
All patients followed a traditional weight management programme involving a depression glycemic index Mediterranean nutrition, recommended practice routines and regular follow-up visits in the dispensary (Table 1). The dietary programme of the patients in the nutrigenetic group was modified from the standard diet based on the genetic results of each patient. Other than the modifications to the standard diet and exercise program, the patients in both groups were treated in an identical fashion
Tabular array i
Sample low saturated fat and depression glycemic load Mediterranean diet
| Breakfast: |
| One cup of coffee or tea One thin slice of whole grain bread or rye beige with ane piece of cheese and a slice of turkey ham or with margarine (Becel) and picayune dearest Or One portion of cereal with low fat 1.5% milk |
| |
| Lunch-Dinner: |
| |
| Twenty-four hours 1: I salad of fresh or boiled vegetables, i slice of cheese, 1 piece of bread. Day ii: *Grilled fish + salad Day 3: *Grilled Chicken + salad Day 4: I portion of dark-green beans, cooked with tomato plant & olive oil. Ane slice of cheese and bread Day five: *Grilled fillet + salad Mean solar day 6: One portion of lentils, one slice of cheese, one slice of bread Twenty-four hour period 7: *Grilled fish + salad |
| |
| Notes : |
| |
| • Salads should be dressed with fresh extra virgin olive oil, up to 3 dessert spoons per day • * means that you tin can eat a lot – just do non overfill • Add together a little olive oil to the grilled meat, fish and chicken • You should have one fruit with breakfast, one after dinner and ane or two fruits between meals, you may have also one yogurt between meals. • Bread is whole grain or rye. • You may have if you similar one glass of wine every twenty-four hours • Program is changed weekly • If increased weight loss is required mainly salads are selected for the dinner meal |
Laboratory Measurements
BMI and claret test results were analyzed from patients' clinical records at regular intervals. A venous blood sample was taken in the early on morning time after an overnight fast. Serum samples were stored at -40°C until analysis. Fasting glucose was determined using an enzymatic kit (Glucose GOD-PAP, Roche Diagnostic, Deutschland). Serum total cholesterol and HDL cholesterol concentrations were measured using enzymatic colorimetric methods (CHOL CHOD-PAP, HDL Homegenic Enzymatic reaction, respectively, Roche Diagnostic, Frg).
For nutrigenetic testing, the Sciona MyCellf kit was used (Sciona Inc, Bedrock, CO). Cheek cell samples were taken in the dispensary using two buccal swabs and the patient completed a comprehensive diet and lifestyle questionnaire. The swabs and samples were sent by courier to Sciona and genetic testing was carried out using a Sequenom Mass Array organization. Variants of 19 genes were tested (Table 2).
Table 2
Genes and polymorphisms tested in the nutrigenetic patient group.
| Factor | Cistron symbol | Polymorphism | % homozygote wild type | % heterozygote | % homozygote variant | HWE p < |
| Angiotensin I converting enzyme | ACE | INS/DEL | 14.6% | 48.viii% | 36.6% | 0.99 |
| Apolipoprotein C-III | APOC3 | 3175C>G | 73.3% | twenty.0% | 6.seven% | 0.17 |
| Cystathionine-beta-synthase | CBS | 699C>T | 53.5% | 41.9% | 4.7% | 0.81 |
| Cholesteryl ester transfer protein | CETP | 279G>A | 48.8% | 39.5% | xi.half-dozen% | 0.86 |
| Collagen, type I, blastoff 1 | COL1A1 | M Sp1 T | 58.ane% | 34.9% | seven.0% | 0.94 |
| Glutathione S-transferase M1 | GSTM1 | Deletion (*) | 52.0% | 0.0% | 48.0% | N/A |
| Glutathione Due south-transferase pi | GSTP1 | 313A>G | 57.8% | 33.three% | 8.9% | 0.68 |
| 341C>T | 56.viii% | 34.ane% | 9.1% | 1.00 | ||
| Glutathione S-transferase theta 1 | GSTT1 | Deletion (*) | 86.0% | 0.0% | xiv.0% | N/A |
| Interleukin vi | IL6 | -174G>C | 66.7% | 33.3% | 0.0% | 0.37 |
| -634G>C | 86.0% | 14.0% | 0.0% | 0.89 | ||
| Lipoprotein lipase | LPL | 1595C>G | 69.viii% | 27.9% | 2.3% | 1.00 |
| 5-methyltetrahydrofolate-homocysteine methyltransferase reductase | MTRR | 66A>G | nineteen.0% | 45.2% | 35.7% | 0.90 |
| 5,10-methylenetetrahydrofolate reductase | MTHFR | 1298A>C | 34.0% | 48.9% | 17.0% | ane.00 |
| 677 C>T | 48.0% | 44.0% | 8.0% | 0.95 | ||
| v-methyltetrahydrofolate-homocysteine methyltransferase | MTR | 2756A>G | 59.five% | 33.3% | vii.1% | 0.86 |
| Nitric oxide synthase 3 (endothelial cell) | NOS3 | 894G>T | 44.ii% | 44.2% | eleven.6% | one.00 |
| Peroxisome proliferator-activated receptor gamma | PPARG | Pro12Ala | 75.6% | xv.6% | viii.9% | 0.02 |
| Superoxide dismutase 2, mitochondrial | SOD2 | -28C>T | 10.0% | 54.0% | 36.0% | 0.57 |
| Superoxide dismutase iii, extracellular | SOD3 | 760C>Grand | 100.0% | 0.0% | 0.0% | i.00 |
| Tumor necrosis factor | TNFα | -308G>A | 71.one% | 24.iv% | four.iv% | 0.72 |
| Vitamin D receptor | VDR | C Taq1 T | 23.3% | 46.v% | xxx.2% | 0.91 |
| T Bsm1 C | 23.three% | 46.5% | 30.2% | 0.91 | ||
| T Fok1 C | eleven.6% | 58.i% | 30.two% | 0.41 |
Genotype frequencies in the study grouping and p-values for Hardy Weinberg Equilibrium (HWE) are shown. (*) the assay just measured presence or absenteeism of the deletion so a HWE test is not applicable.
Statistical analysis
Baseline characteristics were compared using a one-mode assay of variance in the natural (age, weight, BMI kg/chiliad2) or logarithmic scales (glucose, insulin, lipids) or a Pearson'southward chi-squared test for binary traits. No significant (p > 0.05) deviation from normality was found for the baseline characteristics using a Kolmogorov-Smirnov test of composite normality. Because assumptions of normality are non violated a ane-way ANOVA, which is formally equivalent to a t-test, was carried out to test the null hypothesis of no deviation in the continuous baseline characteristics between the nutrigenetic and the non-tested grouping. Change in BMI or weight was compared using analyses of co-variance which included study group (nutrigenetic tested or non-tested) as the independent variable, age and sex equally covariates. Odds ratios were estimated using logistic regression models which included age and sex as covariates and belonging to the Nutrigenetic test group (1) or to the non-tested (0) group equally the predictor variable. All tests were carried out using South-Plus 6.0 (Insightful Corp, Seattle, WA).
Results
The genotype frequencies for the genes tested in the nutrigenetic written report population are presented in tabular array 2. 1 of the 24 variants tested deviated significantly from Hardy-Weinberg equilibrium, but given the large number of tests carried out nosotros aspect this observation to type I error. The proportion of patients given personalized advice according to the gene groupings for the individual intervention categories and the rationale for such communication are shown (Table three). All patients received nutrigenetic based communication in at to the lowest degree ane of the intervention categories, with the majority (85%) receiving communication in 4 or more of the 7 possible categories.
Table 3
Personalized recommendations given to the Nutrigenetic exam patient grouping in addition to base diet.
| Food intervention group | % Receiving modified communication |
| Variation in MTHFR, MTRR, MTR or CBS : | 98.vi |
| Rationale: Polymorphisms in genes involved in folic acid metabolism have been shown to influence this pathway affecting plasma homocysteine levels as well as the balance betwixt DNA methylation and synthesis of nucleotides [14, 15]. | |
| Recommendation: Add supplement containing 800 mcg folic acid, fifteen mg Vitamin B6 and twenty mcg B12 | |
| Variation in GSTM1, GSTT1 or GSTP1 : | 76.1 |
| Rationale: Patients with deletions in GSTM1 which touch on Phase II detoxification processes take been shown to have reduced levels of Deoxyribonucleic acid adducts [16], and increased levels of GSTA1 circulating activity [17], when adequate levels of cruciferous vegetables have been consumed. Risk for lung cancer drops by up to fourscore% in individuals defective GSTM1 and/or GSTT1 genes when consumption of cruciferous vegetables is high [18]. | |
| Recommendation: Ensure diet includes regular portions of cruciferous (5 times per calendar week) and allium (daily) vegetables (suggestions and recipes provided to patient). Add broccoli extract and allium supplement if required. | |
| Variation in SOD2, SOD3, NOS3 : | 48.6 |
| Rationale: superoxide dismutase enzymes are free radical scavengers that accept important antioxidant activity which can be afflicted by genetic polymorphism [19] | |
| Recommendation: Add supplements containing antioxidants, Vit A (v,000 IU), Vit C (250 mg) and Vit E (200 IU). | |
| Variation in VDR, COL1A1 : | 87.five |
| Rationale: Several studies accept shown that gene-nutrition interactions have a function to play in maintenance of bone condition. For example caffeine increased rate of bone loss just only in the presence of the VDR taq1 variant [20]. Others have shown gene-diet effects involving calcium [21, 22] and vitamin D [23]. | |
| Recommendation: Keep caffeine below ii cups coffee/day. Increase dairy component of nutrition (yoghurt, cheese and low fat milk). If required add supplement containing 800 IU vitamin D and 1,300 mg Calcium | |
| Variation in TNFα, IL6, NOS3 : | 65.3 |
| Rationale: Variations in inflammation pathway genes TNFα and IL6 have been shown to exist pro-inflammatory and the effect can be modulated by increased levels of fish oil in the nutrition [24] | |
| Recommendation: Add supplement Omega three (700 – 1,400 mg). Make certain weekly diet contains portions of oily fish | |
| Variation in CETP, LPL, APOC3 : | 79.2 |
| Rationale: Polymorphisms in genes involved in lipid metabolism and send, in combination with dietary fat intake, take been shown to bear upon plasma cholesterol levels [25] | |
| Recommendation: The base low fat is already within the limits recommended for these variations so no farther specific communication is given but current advice is reinforced and advice given to restrict consumption of dairy foods. | |
| Variation in ACE, PPARG : | fourscore.6 |
| Rationale: gene-diet and gene-practise interactions have been reported to bear upon blood glucose and insulin levels [26, 27] | |
| Recommendation: The base low glycemic diet is already within the limits recommended for these variations and then no further specific advice is given merely current advice is reinforced. Extra exercise advised for this group |
The two study groups selected were very similar at the beginning of the clinical plan; there were no significant differences in historic period, sex activity, BMI, lipids and glucose profiles (Table 4). The majority of the patients were classified equally obese with an average BMI of approximately 32 kg/chiliadii in both groups. No pregnant deviation in co-morbidities was constitute. In addition to the conditions listed (Table 4), two patients from the nutrigenetic grouping had had a history of ischemia, ii nutrigenetic patients had a history of hypothyroidism and two others had undergone surgical thyroid removal, versus none in the control group. None of these differences were statistically significant.
Table four
Descriptive characteristics of study subjects
| Non-tested | Nutrigenetic patients | p-value | |||||
| Sample size | 43 | fifty | |||||
| Gender % female person | 41.9% | 44% | 0.99 | ||||
| % obese (BMI = 30 kg/mii) | 62.8% | 70% | 0.61 | ||||
| % Hypertension | 13.nine% | 8.0% | 0.56 | ||||
| | |||||||
| mean | SD | Q1-Q3 | mean | SD | Q1-Q3 | ||
| | |||||||
| BMI kg/m2 | 33.1 | 6.6 | (29.3–35.8) | 33.ane | six.seven | (29.5–36.9) | 0.98 |
| Weight kg | 99.i | 24.9 | (83.6–110.viii) | 96.v | 23.three | (81.7–106.7) | 0.60 |
| Age years | 45.8 | 11.five | (37–54.5) | 46.0 | 12.1 | (36.five–54.7) | 0.92 |
| Glucose mg/dL | 94.four | eleven.5 | (87–99) | 91.8 | 22.three | (88–99) | 0.65* |
| Total cholesterol mg/dL | 205.viii | 45.eight | (179–235) | 214.1 | 53.0 | (191–246) | 0.37* |
| HDL mg/dL | 55.6 | 28.0 | (45–61) | 50.0 | 15.8 | (twoscore–57) | 0.33* |
| LDL mg/dL | 135.0 | 38.four | (114–157) | 137.nine | 50.one | (111–165) | 0.64* |
| Insulin (mU/L) | 11.4 | 8.0 | (v.5–fifteen.2) | 13.0 | 10.3 | (6.iv–14.three) | 0.54* |
* analysis of variance carried out on log-transformed variable.
During the starting time 180 days of weight management therapy, the clinical records demonstrated that the 2 groups were very similar. Both groups showed a comparable overall boilerplate weight loss and approximately 90% had maintained weight reduction (92.9% in the nutrigenetics tested group vs. 88.nine% in the non-tested comparison group. Tabular array 5). There was a trend for the nutrigenetic tested grouping to have greater BMI reduction, but there were no meaning differences up to the 100–300 day period. In the patients who had been followed upward for more than 300 days (26 in nutrigenetics tested group, 22 in comparing not-tested grouping), results were significantly ameliorate in the nutrigenetic tested group (p < 0.023). Individuals in the nutrigenetic test group were more than likely to have maintained some weight loss (19/26; 73%) than those in the comparing group (7/22; 32%) resulting in an age and gender adjusted odds ratio of 5.74 (95% CI ane.74–22.52 p < 0.005). Boilerplate BMI reduction in the nutrigenetic group was one.93 kg/10002 vs. an average BMI proceeds of 0.86 kg/m2 (p < 0.023). The difference was more than apparent when expressed as a percentage of BMI gain/loss, subjects in the nutrigenetic grouping had a 5.6% loss vs. a ii.2% gain in the not-tested group (p < 0.004). Moreover, from 100 days follow-upwardly onwards, individuals in the nutrigenetic group were significantly more likely to have maintained some weight loss than those in the comparison grouping (Figure 1). After the 300 days follow-upward this resulted in an age and gender adapted odd raio of 5.74 (95% CI 1.74–22.52).
Table five
Weight and BMI loss (or gain if negative) in the two groups.
| Non tested group | Nutrigenetic group | P < * | |||||||||
| | |||||||||||
| Time indicate | northward | weight as % of baseline | Δ kg | Δ BMI (kg/m2) | % lost weight | northward | weight as % of baseline | Δ kg | Δ BMI (kg/yard2) | % lost weight | |
| baseline | 43 | 100.0% | fifty | 100.0% | |||||||
| 30–45 | 35 | 95.four% | 4.77 | 1.59 | 94.3% | 40 | 96.3% | three.lxx | ii.10 | 92.5% | 0.50 |
| ninety–100 | 23 | 92.2% | eight.42 | 2.78 | 86.9% | 26 | 93.four% | 6.42 | iii.51 | 96.1% | 0.64 |
| 100–300 | 36 | 93.4% | vi.94 | 2.35 | 88.nine% | 44 | 92.9% | 6.88 | iii.nineteen | 96.4% | 0.29 |
| > 300 | 22 | 103.2% | -2.74 | -0.86 | 31.viii% | 26 | 95.vi% | iii.61 | 2.54 | 73.1% | 0.023 |
Odds ratio of losing weight (adjusted for age and gender) for individuals in the nutrigenetic examination grouping compared to the command groups. age and sex adjusted odds ratio for weight loss > 0 betwixt the nutrigenetic test grouping and the non-tested group.
Sufficient blood fasting glucose measurement records were available for comparison for a proportion of the patients in the two groups. Amid patients with a starting blood fasting glucose above the pre-diabetic level of 100 mg/dL, 57% (17/xxx) of the nutrigenetic tested group but only 25% (iv/16) of the non-tested comparing grouping had levels reduced to < 100 mg/dL afterward > 90 days of weight management therapy (odds ratio for lowering glucose to < 100 mg/dL due to diet = 1.98 95%CI 1.01, iii.87, p < 0.046), (Figure ii).
Plasma fasting glucose levels among pre-diabetic subjects at baseline and at or after ninety days follow-up.
Discussion
The addition of nutrigenetically tailored diets resulted in better long-term BMI reduction and improvements in blood fasting glucose. Interestingly, the performance of the 2 groups over the first few months was very like in terms of weight lost. However, after ane twelvemonth, the not-tested control groups showed a slight average weight gain while the nutrigenetic tested group continued to lose weight, although at a lower rate than during the starting time ninety days. This suggests that compliance to the weight management programs was better in the nutrigenetics tested group, achieving long term lifestyle changes and resulting in sustained weight loss and improved blood fasting glucose levels. The majority of "pre-diabetic" subjects returned to normal blood fasting glucose levels (< 100 mg/dL), which represents a significant wellness benefit. Nosotros note that the number of pre-diabetic subjects studied in the nutrigenetic group (n = 30) was considerably larger than in the control group (north = 16) which enabled usa to detect the improvement in glucose levels in the nutrigenetic grouping as statistically pregnant but not in the command group. Still, the overall drop in fasting glucose levels was over twenty% larger in the nutrigenetic group than in the command group (12.3 mg/dL vs. 10.1 mg/dL). The weight loss recorded in the nutrigenetically tested group after one twelvemonth was moderate, and it has been well established that even a small weight loss coupled with a healthier diet and lifestyle can lead to significant reduction in risks for diseases associated with excess weight such every bit diabetes, CVD and metabolic syndrome [four,5].
The nutrigenetic examination used in this study determines genetic variation in 19 genes in 7 nutrition intervention groups. The test was non developed specifically as a weight direction tool but as a means to optimize and provide a level of personalization to support full general salubrious eating practices. The factor variants were selected according to documented prove of gene-diet interactions where a nutrition or exercise intervention has been demonstrated to modify the effect of the variation (see refs cited in Tabular array 3). All patients in the nutrigenetic test grouping were prescribed a dietary modification in at least one nutrition intervention grouping with the bulk receiving specific advice in 4 or more groups. Overall, there was considerable variation in the sets of advice given to the individual patients in the nutrigenetic tested group. The differences in long term outcomes between the two written report groups suggest that the use of nutrigenetic testing to add personalization to private diets may be a useful new tool in the management of weight loss and weight control. The maintenance of weight loss is specially significant in this group of patients who attended the dispensary following previous unaided and unsuccessful attempts at weight control. Calculation a genetic, personalized component to a weight loss plan may improve motivation and compliance, but information technology is also possible that the personalized diet is meliorate suited by optimizing the content of macro- and micro-nutrients for an individual during a flow when overall nutrient consumption is reduced and free energy expenditure increased.
We annotation some limitations to the electric current study. Our data could be explained by a difference in compliance levels between groups. As there is no placebo arm in this study, it is not possible to evaluate any physiological improvements due to the specific nutritional communication targeted to the patient's genotype. Another limitation is that this study refers only to Caucasian individuals from Greece who had experienced issues losing weight in the past and therefore results may not be necessarily representative of other groups, either from dissimilar ethnic or cultural backgrounds, or with different clinical characteristics.
Finally, the sample size, particularly for the comparison of alter in glucose levels was fairly modest. Withal, the effect size seen in the nutrigenetic group was larger than in the non-tested group (0.81 vs 0.66 standard deviations) and a significantly college proportion of nutrigenetically tested than non-tested individuals lowered their glucose levels to < 100 mg/dL. Therefore, the lower sample size in the not-tested group alone does non explain the difference between the tested and non-tested groups.
The patients in this study group were given a platform nutrition which consisted of a low-glycemic index Mediterranean balanced nutrition, with modifications for the tested patients where appropriate. There are a plethora of different types of low calorie diets bachelor to patients who want to lose weight containing very dissimilar levels of diverse macronutrients. Although nutrigenetics is not yet a predictive tool to make up one's mind which blazon of diet will lead to greater weight loss for a particular individual, this is an active expanse of inquiry. The data from the electric current study advise that the use of nutrigenetics to improve and optimize a healthy balanced diet in a clinical setting could be an effective aid in long term lifestyle changes leading to sustained weight loss.
Competing interests
This work was funded in office past Sciona Inc., Boulder, CO, United states
Thou. Grimaldi and R. Gill are employees of Sciona Inc
I. Arkadianos is a distributor of Sciona products in Hellenic republic
Southward. Marinos, A.Chiliad. Valdes, and A. Florou declare no conflicts of interest.
Authors' contributions
AMV, who is contained of the sponsors of this project, had total access to all the information in the study and takes responsibility for the integrity of the information and the accuracy of the data assay.
All authors have read and approved the final manuscript.
Written report concept and design: IA, RDG, KAG
Acquisition of data: IA, EM, AF
Analysis and interpretation of information: AMV, KAG, RDG, EM, IA
Drafting of the manuscript: KAG, AMV, RDG, IA, AF, EM
Statistical analysis: AMV
Acknowledgements
The authors would similar to thank Prof. Jose Ordovas and Dr Gil Leveille for their critical reading of before versions of this manuscript. Thanks also to Alli Spence for conscientious proof reading.
The contribution of Sciona (KG, RDG) was partially supported by the European Commission nether the FP6-IST4-027333 projection "Micro2DNA: Integrated polymer-based micro fluidic micro organization for Deoxyribonucleic acid extraction, amplification, and silicon-based detection
Written consent for publication was obtained from the patient or their relative
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2151062/
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