This 2-year study compared the effects of a ketogenic diet versus a nutrigenetic diet on weight loss and clinical parameters in 114 obese subjects. The nutrigenetic diet was personalized based on each subject's genetic test results. After 2 years, the nutrigenetic group had greater BMI loss (25.03% vs 17.62%), larger decreases in total cholesterol and blood glucose, and higher HDL levels compared to the ketogenic group. The study concludes that a nutrigenetically matched diet may be more effective than a standard ketogenic diet for long-term weight management and improvement of metabolic health markers.

1. IMPROVEMENTS IN LONG TERM WEIGHT-LOSS
AND CLINICAL PARAMETERS WITH THE USE
OF NUTRIGENETICS IN A 2-YEARS
PROSPECTIVE STUDY
Maria Vranceanu
Nutritionist, expert
nutrigenomics and antiaging

2. Can obesity really
be ‘in our
genes’?

3. Last 40
years
Our genes
have not
changed
Explosion
of obesity
Is genetics the first
driver of obesity?

4. Genetic variations contributes
to the development of obesity

5. Obesity is a disease with genetic
predisposition
The expression of obesity varies with social,
cultural, environmental, economic and
psychological influences

6. Obesity
metabolic syndrome
hypertension, cardiovascular
diseases, arthritis,various
cancers, diabetes
Increasing health care
cost

7. Google research:
diet and Angelina Jolie
Google research:
Diet
Angelina Jolie

8. A significant number of health
interventions have been trialled in an
attempt to reduce obesity

9. Emerging research suggests that the ability
to place weight loss subjects on a diet that
is matched to their genotype may increase
both adherence and health outcomes.

10. OBJECTIVES
This study investigated whether the inclusion of genetic
information to personalize a patient's diet (nutrigenetics)
could improve long term weight management.

11. METHODS
Subjects
• A convenience sample of 114 obese subjects
(M = 55, F = 59, age 24-56y) who were
patients at a weight management clinic
volunteered to take part in this study.
• Following explanation of procedures and
risks, subjects gave written informed consent
to participate in the study.
• All patient data was handled according to the
Romanian Code of Medical Deontology and in
accordance with the Helsinki Agreement.

12. 53
PATIENTS
KD plan
1600
kcal/day
61
PATIENTS
Nutrigenomi
cs
1600
Kcal/day
Upon recruitment to the study, the
subjects were presented with a
choice of either a ketogenic diet or a
nutrigenetic diet.

13. Subjects in a nutrigenetics
group underwent DNA testing
for 30 gene variants in 24 genes
involved in metabolism.
Steril bucal swab

14. Table 1: Gene and polymorphisms tested in the
nutrigenetic patients group
Gene Polymorphism Reference
ACE Ins/Del (rs4646994) Bienatrova-Vascu; Muthumala
ADRB2 Arg16Gly (rs1042713)
Gln27Glu (rs1042714)
Prior; Martinez
APOC3 C3175G (rs5128) Arai; Song
APOA2 -265T>C (rs5082) Corella (2011a); Smith
CAT C-262T (rs1001179) Bastaki; Ahn
CYP1A2 -163A>C (rs762551) Pavanello; Cornelius
EPHX1 Tyr113His (rs1051740)
FABP2 Ala54Thr (rs1799883) Zhao; Tavridou
FTO A/T (rs9939609) Sonnestedt; Corella (2011b)
GPX1 Pro198Leu (rs1050450) Jablonska; Zhou
GSTT1/GSTM1 Ins/Del Palli; Steinbrecher
HLA-DQ rs2187668_DQ25 rs2395182_DQA1201 rs4639334_DQ7
rs4713586_DQ4 rs7454108_DQ8 rs7775228_DQB1202
Kaukinen; Sollid
IL6 G-174C (rs1800795) Razquin; Jones
LCT -13910-CT (rs4988235) Enattah; Jarvela
LPL C1595G (rs328)
MTHFR C677T (rs1801133) Ashfield-Watt; Tsang
PPARG PRO12ALA (rs1801282) Memsioglu; Ruchat
SOD2 C-28T (rs4880) Li; Ambrosone
TCF7L2 C/T (rs7903146) Hindy; Bo
TNF G-308A (rs1800629) Grimble; Fontaine-Bisson
VDR C>T(taq1) (rs1544410) Rapuri; Stathopoulu

15. • Fasting venous blood samples
were taken at baseline, 24-weeks
and 104-weeks to determine total
cholesterol (TC), high density
lipoprotein (HDL) cholesterol, and
fasting blood glucose (BG).
• TC and HDL-c concentrations were
measured using an enzymatic
colorimetric method (CHOL-CHOD-
PAP, HDL Homogenic Enzymatic
reaction, Roche Diagnostic,
Germany).
• BG was determined using an
enzymatic kit (Glucose GOD-PAP,
Roche Diagnostic, Germany).

16. • Weight and height were also
measured, and body mass
index (BMI) was calculated

17. Table 3: Baseline Characteristics of Subjects. Data is
reported as mean ± SD
Parameter Ketogenic Diet Nutrigenetic Diet p-value
Participants (n) 53 61
Age (years) 43.0 ± 7.2 42.0 ± 6.7 0.424
Female (%) 47.2% 55.7% 0.361
Baseline body weight (kg) 113.0 ± 13.0 108.5 ± 16.0 0.106
BMI (kg/m2
) 37.2 ± 3.1 37.0 ± 4.6 0.789
Normal weight (19-24.9) [n (%)] 0 0
Overweight (25-29.9) [n (%)] 0 1 (0.6%)
Obesity level I (30-34.9) [n (%)] 12 (22.6%) 21 (34.4%)
Obesity level II (35-39.9) [n (%)] 32 (60.4%) 29 (47.5%)
Obesity level III (≥40) [n (%)] 9 (17%) 10 (16.3%)
Total Cholesterol (mg/dl) 245.6 ± 39.3 242.0 ± 27.3 0.567
Desirable (<200) [n (%)] 10 (18.9%) 3 (5%)
Borderline-high (200-239) [n (%)] 18 (34%) 29 (47.5%)
High (≥240) [n (%)] 26 (49%) 29 (47.5%)
HDL Cholesterol (mg/dl) 45.1 ± 6.1 47.6 ± 4.8 0.016
Too low (<40) [n (%)] 10 (18.9%) 3 (5%)
Borderline (40-59) [n (%)] 41 (77.4%) 58 (95.1%)
Protective against heart disease (≥60) [n (%)] 2 (3.8%) 0
Fasting blood glucose (mg/dl) 120.5 ± 3.8 105.7 ± 8.8 <0.0001
Normal (60-99) [n (%)] 0 21 (34.4%)
Impaired (100-125) [n (%)] 48 (90.5%) 39 (64%)
Risk (≥126) 5 (9.4%) 1 (0.6%)

18. Both diets were followed for 24
weeks and contained 1600kcal
per day.
KD
≤35g of carbs/day
≤10% of total calories from
saturated fats.
Protein intake:
1.2g/kg bodyweight for
females
1.5g/kg bodyweight for males.
NG
individualised
dietary
instructions based
on their genetic
results

19. Table 2: Personalized recommendations given to the
patients in Nutrigenetic group in addition to base diet
Personalized recommendations based on DNA profile alongside base diet
Variation in ACE, PPARG Low glycemic load (GL) diet in addition to extra exercise, specifically power-based exercise such as step
aerobics, spinning, at high intensity weight training.
Variation in LPL, FTO, APOA2, APOC3 Restriction of saturated fats to no more then 16 g/day with concurrent increase in unsaturated fat
consumption, such as olive oil. Supplementation with niacin.
Variation in GSTM1 and GSTT1 Ensure consumption of an adequate intake of cruciferous vegetables - 200 g five times per week. If both
null genotypes were present, supplementation with broccoli extract and allium was recommended.
Variation in GPX Consume foods rich in selenium such as Brazil nuts, fresh fish, meat, wheat germs, brown rice, oats, and
onion. In case of low plasma selenium, supplementation of 200mcg/day was recommended.
Variation in TNF and IL 6 Increased consumption of omega-3 rich foods. Green tea, turmeric, ginger, rosemary, oregano were also
recommended, along with supplementary omega 3 (1-2g/day)
Variation in MTHFR Increase consumption of folate-rich foods(dark leafy greens, asparagus, bean, peas, lentils, avocado,
okra). Supplementation with 400mcg folate, 3 mg B6, 5mg B12, 2.5 md B2, 12mg Zn, 250 mg
TMG/betain
Variation in CYP1A2 and EPHX1 Increase consumption of antioxidants, such as grapes, blueberries, sweet potatoes and orange
vegetables. Also recommended to increase consumption of dark green veggies, whole grain, and
tea, along with a decreasein caffeine consumption to 200mg/day. Decrease consumption of grilled
meat and fish to 1-2 servings per week.
Variation in SOD2 and CAT Increase antioxidant consumption through diet, and add supplements containing vitamin A(5,000 IU)
vitamin C (250 mg) and vitamin E (200IU)
Variation in LCT-lactose intolerance Elimination of dairy, followed by a rotation diet.
Variation in VDR Keep caffeine below 2 cups coffee/day. Increase dairy component of diet (yoghurt, cheese and low fat
milk). If required add supplement containing 800 IU vitamin D and 1,300 mg Calcium.
Variation in TCF7L2 Follow a very low GL diet(<70/day)
Variation in HLA-DQ Eliminate gluten for 3 month followed by a rotation diet. Total elimination of gluten in absence of celiac
disease is not recommended.

20. RESULTS
At baseline there were no significant differences in age,
sex, BMI, lipids and blood glucose levels.
After 24 weeks the BMI loss were again similar but this
time the loss in the ketogeneic group was significantly
greater.
After 2 years there was a much larger BMI loss in the
nutrigenetic group (25.03% vs 17.62%, p=0.00001), in fact
the nutrigenetic group had continued to lose weight while
the control had regained some of the weight lost.
Figure 1: BMI loss

21. Table 4: Weight and BMI loss/gain between
groups.
(* = One-Way ANOVA for weight loss between
groups)
Ketogenic group Nutrigenetic group P (Effect
Size) *
Time Point Weight as
% of
baseline
∆ kg vs
baseline
∆ BMI
(kg/m2
)
Weight as
% of
baseline
∆ kg vs
baseline
∆ BMI (kg/m2
)
Baseline 100% 100%
6 weeks 93.7 -7.2 -2.40 93.3 -7.2 -2.59 1 (0 – no
effect)
12 weeks 87.9 -13.7 -4.59 85.8 -15.5 -5.33 0.0029
(0.6 –
Medium)
24 weeks 76.8 -26.2 -8.71 78.4 -23.5 -8.14 0.0024
(0.6 –
Medium)
2 years 82.8 -19.4 -6.53 74.7 -27.5 -9.45 <0.0001
(0.8 –
Large)

22. • At 2-years follow up, the
nutrigenetic group have increased
their HDL significantly (p<0.0001)
more than the ketogenic group.
• Similarly, the nutrigenetic group
had significantly greater
(p<0.0001) decreases in both
total cholesterol and fasting blood
glucose when compared to the
ketogenic diet.

23. • In the nutrigenetic group, all
subjects had BG values <100,
compared to 34.4% at baseline.
• In the ketogenic group, 16
subjects (26.2%) had BD values of
<100, compared to 0% at baseline.
• For TC, 95% of nutrigenetic
subjects had a value of <200 mg/dl
(compared to 5% at baseline),
whereas 17% of ketogenic
subjects were below this group,

24. • For HDL, a value of ≥60 mg/dl
is determined to be
protective against heart
disease
• at 2-year follow up, 62.3% of
nutrigenetic and 1.9% of
ketogenic subjects had
scores within this category,
compared to a baseline score
of 0% and 3.8% for the

25. Figure 2: 2-year follow up Total Cholesterol (TC), High
Density Lipoprotein (HDL) and Blood Glucose (BG)
measurements as a percentage of baseline for both groups

26. DISCUSSION
The main finding of this study is that a
nutrigenetically matched diet is better
than a ketogenic diet for improvements
in weight, total cholesterol, HDL and
blood glucose over two years.

27. CONCLUSIONS
• Genetically matched diets and dietary
advice may be useful in the treatment of
obesity and altered haematological
markers of metabolic health.
• Genetically tailored diets may reduce the
risk of developing obesity or type-II
diabetes in non-obese individuals,
although research in this area is required
to confirm this.
• The results of this study suggest that the use of
nutrigenetics could be an effective aid in long
term lifestyle changes leading to sustained
weight loss and health improvements.