Improved weight management using genetic information to personalize a calorie controlled diet
Abstract - Background
Gene-environment studies show variability in nutrient demand as a function of individual gene variations that influence nutrient metabolism and transport. This study examined whether incorporating genetic information to personalize a patient's diet (nutritional medicine) could improve long-term weight management.
Methods
Patients with a history of weight loss errors were offered a nutrigenetic test, which screened 24 variants in 19 genes involved in the metabolism. Fifty patients were in the nutrigenetic group and 43 patients are visiting the same clinic were selected for comparison with algorithms that matched the characteristics: age, sex, the frequency of clinical visits and BMI at the first clinic visit. The second group of 43 patients received no nutrigenetic test. The BMI reduction at 100 and> 300 days and blood fasting glucose were measured.
Results
After 300 days of follow-up, subjects in the nutrigenetic group were more likely to lose some weight (73%) than the control group (32%), resulting in an age- and gender-adjusted OR of 5.74 (95% CI) 1.74-22.52) , The average BMI reduction in the nutrigenetic group was 1.93 kg / m2 (5.6% loss) versus an average BMI increase of 0.51 kg / m2 (2.2% increase) (p <0.023). In patients with incipient blood fasting glucose> 100 mg / dl, 57% (17/30) of the nutrigenetic group but only 25% (4/16) of the non-tested group were reduced to <100 mg / dl after> 90 days of weight management therapy ( OR for lowering glucose to <100 mg / dL due to diet = 1.98 95% CI 1.01, 3.87, p <0.046).
Conclusion
The addition of genetically modified nutrients resulted in better compliance, longer-term BMI reduction and improvements in blood sugar levels. Genetic Healing weight management genetic test in Pune
Background
It has been well documented that the percentage of the population that is overweight and obese is reaching epidemic proportions around the world, with all the associated health, social and economic consequences [1-5]. Although many reasons have been cited as the cause of the epidemic [6], the increased calorie intake and reduced exercise typical of the modern lifestyle are most likely to remain.
Of course, most people who eat more and do less exercise will increase their weight, but achieving a state of overweight or obesity is a gradual process that over many years even represents a small excess of energy intake. For example, in the US, people between 25 and 55 years of age gain an average of 15 kg of body weight. This weight gain is only ~ 0.5 kg (1 lb) per year, which equates to overeating just a few calories per day [7].
Behavioral treatments can lead to weight loss in many patients, which is sufficient to improve health, but often the weight is regained over time [8]. Although losing weight is difficult for many people, maintaining weight loss is even more difficult. In fact, few non-surgical treatments for obesity lead to sustained weight loss [9]. Long-term maintenance of weight loss requires lasting lifestyle changes in exercise and eating habits. These changes must be significant, but not necessarily radical, or unattainable if they are gradual but sustained in weight loss over several years. The National Institutes of Health recommend a weight loss goal of 10% in the first six months (at a rate of 0.25-0.50 kg/week), followed by a weight-maintenance program or further weight loss, if necessary, at a lower cost [10 ].
It has long been suspected that "one size does not fit all" regarding determining the optimal diet for an individual, and this has been demonstrated in recent years in studies of gene-diet interactions and the emergence of nutrigenetics [11- 13]. The goal of nutrigenetics is to provide a prescribed diet with a level of personalization by adapting it to genetic variation. For example, people who carry the MTHFR 677T allele need more folate and B vitamins in their diet to keep homocysteine levels down [14,15]. Nutrigenetic tests in clinical practice analyze genes that are primarily involved in the metabolism and transport of nutrients, the removal of toxins and the protection against oxidation. Depending on the particular pattern of genetic variation, personalized advice may be provided that includes recommendations on dietary and lifestyle changes to achieve genetically-based, specific nutrition and exercise goals.
The nutrigenetic diet used in this study was not designed or suggested as a weight loss diet for patients; The goal was to optimize the nutrient content of an individual's daily food intake, based on the current understanding of the genetic profile of an individual. While a person achieves weight loss, food consumption is reduced, and certain nutrients in the diet may not be inadequate supply. Nutrigenetics can be a means of achieving optimal nutritional content on an individual basis. Also, using Nutrigenetics to create 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 using nutrigenetic tests in weight management protocols in 2003, and initial observations suggested that adapting diets to genetics could improve weight loss and control of biomarkers such as blood sugar levels. To further investigate these findings, a formal medical history survey was initiated. Case histories were followed for a group of 50 patients who took the test and received a personalized diet and compared to a group of 43 patients (matched to age, gender, and frequency of visits to the clinic) who were not tested and only the norm get clinical diet.
Methods
Patients with a history of unsuccessful weight loss attempts (defined as at least two or more unsuccessful attempts) visiting a weight management clinic in Athens, Greece were offered nutrigenetic tests. Nutrigenetic kits were used as part of the comprehensive weight management program. The study was created using a computer-aided analysis of patient records. A computer program was written to query the database of clinical patient records to select patients who had made the nutrigenetic test, which could be matched for age, gender, incipient BMI and number of clinic visits with patients who had not taken the test.
In this article, researchers report analyzing clinical patient records at a specific time, meaning that different patients were at different times in their weight management treatment program. The case histories of 50 "nutrigenetic" patients (22 female, 28 male) were compared with those of 43 patients in the non-tested group (18 female and 25 male) who had a follow-up of either 90-365 days (24) nutrigenetic 21 not tested), one year or more (6 nutrigenetic, 7 not tested) or both (20 nutrigenetic, 15 untested). 7.5% of the study participants (4 in the nutrigenetic group and 3 in the untested group) were in the normal weight range (BMI <25 kg / m2). However, they had tried several times to lose weight and therefore failed, which is why they had visited the clinic.
The study procedure included a regular analysis of the clinical records of patients who were anonymized and provided with identification numbers. Clinicians involved in patient care did not know which patients were included in the study.
The data of all study participants were anonymous. Those who performed the nutrigenetic test signed a consent form and all patient information was treated according to the Greek Code of Medical Deontology and the Helsinki Accord.
Diet and exercise
All patients followed a traditional weight management program with a Mediterranean diet with a low glycemic index, recommended exercise routines and regular follow-up visits to the clinic (Table 1) .1). The diet program of the patients in the nutrigenetic group was modified from the standard diet based on the genetic outcomes of each patient. Apart from changes to the standard diet and exercise program, patients in both groups were treated identically.
Laboratory Measurements
BMI and blood test results were analyzed periodically from patients' clinical records. A venous blood sample was taken in the early morning after a quick night attempt. Serum samples were stored at -40 ° C until analysis. Fasting glucose was determined using an enzymatic kit (Glucose GOD-PAP, Roche Diagnostic, Germany). Serum total cholesterol and HDL cholesterol concentrations were measured using enzymatic colorimetric methods (CHOL CHOD-PAP, HDL-homogeneous enzymatic reactions, and Roche Diagnostic, Germany, respectively).
For nutrigenetic testing, the Sciona MyCellf kit (Sciona Inc., Boulder, CO) was used. Cheek samples were taken at the clinic using two buccal swabs, and the patient completed a comprehensive diet and lifestyle questionnaire. The smears and samples were sent to Sciona by courier, and genetic tests were performed using a Sequenom Mass Array System. Variants of 19 genes were tested (Table (Table 22).
Statistical Analysis
Baseline characteristics were compared with a one-way analysis of the variance in natural (age, weight, BMI kg / m2) or logarithmic scales (glucose, insulin, lipids) or a Pearson Chi-square test for binary traits. No significant (p> 0.05) deviation from normality for baseline characteristics was found using a composite normality Kolmogorov-Smirnov test. Since no normality assumptions are violated, a one-way ANOVA formally equivalent to a t-test was performed to test the null hypothesis that there were no differences in the continuous baseline characteristics between the nutrigenetic and untested groups. The change in BMI or weight was compared using covariance analyzes that included a study group (nutri genetically tested or untested) as an independent variable, age, and gender as covariates. Odds ratios were estimated using logistic regression models that included age and sex as a covariate and were predicted to belong to the Nutrigenetic Test Group (1) or untested (0) group. All tests were performed using S-Plus 6.0 (Insightful Corp, Seattle, WA).
Results
The genotype frequencies for the genes tested in the nutrigenetic study population are shown in Table 2.2. One of the 24 variants tested differed significantly from the Hardy-Weinberg balance, but due to a large number of tests, we attribute this observation to the Type I error. The proportion of patients individually counseled by gene group for each intervention category and the justification for such consultation are shown (Table 3) .3). All patients received nutritional counseling in at least one of the intervention categories, with the majority (85%) providing advice in 4 or more of the seven possible categories.
The two selected study groups were very similar at the beginning of the clinical program; There were no significant differences in age, sex, BMI, lipids and glucose profiles (Table 4) .4). The majority of patients were classified as obese with an average BMI of approximately 32 kg / m2 in both groups. No significant difference in comorbidities was found. In addition to the conditions listed (Table 4, Table 4), two patients from the nutrigenetic group had a history of ischemia, two nutrigenetic patients had a history of hypothyroidism, and two others had undergone surgical removal of the thyroid gland, versus none in the control group, None of these differences was statistically significant.
During the first 180 days of weight management therapy, clinical records showed that the two groups were very similar. Both groups showed a comparable overall average weight loss and approximately 90% had retained weight reduction (92.9% in the Nutri genetically tested group vs. 88.9% in the untested control group, Table 5) .5). There was a tendency for the Nutri genetically tested group to have greater BMI reduction, but there were no significant differences until the 100-300 day period. In the patients who had been followed up for more than 300 days (26 in the Nutri genetically tested group, 22 compared to the non-tested group), the results were significantly better in the Nutri genetically tested group (p <0.023).
People in the nutrigenetic test group were more likely to have some weight loss (19/26, 73%) than in the comparison group (7/22, 32%), resulting in an age- and a gender-adjusted odds ratio of 5.74 (95%). CI 1.74-22.52 p <0.005). The average BMI reduction in the nutrigenetic group was 1.93 kg / m² compared to an average BMI increase of 0.86 kg / m² (p <0.023). The difference was more pronounced when expressed as a percentage of BMI increase/loss, persons in the nutrigenetic group had a 5.6% loss versus an increase of 2.2% in the untested group (p <0.004). Also, subjects from the nutrigenetic group showed a significantly greater weight loss from the 100-day follow-up compared to the control group (Figure 1) .1). After the 300-day follow-up, age and gender-matched the odds ratio of 5.74 (95% CI, 1.74-22.52).
Sufficient blood glucose measurements were available for some of the patients in the two groups. In patients with incipient blood fasting glucose above the pre-diabetic level of 100 mg/dl, 57% (17/30) of the Nutri genetically tested group, but only 25% (4/16) of the non-tested control group, had values <90 after 90 days of weight management therapy mg / dl reduced (odds ratio for lowering glucose to <100 mg / dl due to diet = 1.98 95% CI 1.01, 3.87, p <0.046), (Figure (Figure 22)).