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4. BMI ≥30 kg/m2 is considered as obesity. Above picture shows rising trends in obesity .
According to WHO statistics in 2008, 12% of adults aged 20 and over were obese globally.
Medical cost for obesity in United States is alarming, it is $147 billion dollars in
2008(Finkelstein, 2008) . Diet, Physical activity, Pharmacotherapy, Bariatric surgery are
major classes of obesity treatment. It is believed that 93 billion dollars were spent by US
citizens alone for practicing various diets for weight loss. Even then the obesity epidemics is
rising. Obesity epidemics considered as prime task for health care professionals because it
leads to other comorbidities like diabetes, hypertension, cardiovascular diseases etc. So,
research is focusing on finding route cause for obesity. We all know obesity is multifactorial
disease. Genes are one among them. Genes interact with obesogenic environment to cause
obesity. A new science is emerging to treat obesity by tailoring personalized diet basing on
gene diet interactions that is “NUTRIGENETICS”.
It is a science that “Examines the effect of genetic variation on the interaction between diet
and disease. This includes identification and characterization gene variations associated
with, or responsible for, differential responses to nutrients.” (J. Robitaille, 2009).
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5. As mentioned previously. Various genes for obesity are being identified. It is believed that
genes from different areas cause obesity. The up regulation and down regulation of genes
in hypothalamus is believed to cause obesity. Hypothalamus is region for energy balance.
Digestive enzymes secreted in stomach signals hypothalamus, which in turn gives appetite
and satiety cues to person. Any variation in genes that signals hypothalamus might increase
or decrease food intake depending on appetite and satiety cues. As of Jan 1 2008 total 27
genes were identified from hypothalamus to cause obesity, recently 6 new genes were also
identified. These include. FTO,GHSR,MCHR2,NMU,PSK1 and TUB. (van Vliet-Ostaptchouk, J.
V.; Hofker, M. H.; van der Schouw et.al)
Liver is also other major site for digestive enzymes. Genes that are responsible for this
enzymes were also thought to cause obesity. An animal study by Eun Jung Kim, Eun-Young
Kwon, Hyun-Seo Jang et.al , (2009) show that up on consumption of High Fat Diet(HFD),
genes that regulate lipid metabolism, fatty acid synthesis, and carbohydrate metabolism
were up regulated and genes that regulate sterol synthesis, insulin signaling and oxidative
stress defensive system were down regulated. This imbalance in signaling causes obesity.
Genes present in other areas like adipose tissue, skeletal muscle, abdominal fat tissue,
genes that involve in energy metabolism are also though to cause obesity.
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6. The above picture shows that though two people eat alike their gene interaction with diet
is not same. This makes one look thin and one look fat. It clearly indicates that there is
need for personalized diet. There comes Nutrigenetics.
In Nutrigenetic testing studies various gene diet interactions are needed to know how a
person responds to particular diet. For example Simopoulos in his review mentioned that
on low fat/high cholesterol diet people with Apo lipoprotein E4/4 genotype respond with
increased serum cholesterol. Whereas Apo lipoprotein E2/2, E3/2 genotypes do not show
any increase. Present research is focusing on identifying gene diet interactions for all major
macronutrients that are thought to cause obesity. Kalioet al. in his study found that
replacing simple carbohydrate with complex carbohydrates modulates gene expression.
Similarly genotype variation has its effect on individual’s salt intake and hypertension. So,
identifying various gene diet interactions is major task in implementing Nutrigenetics for
personalized diet.
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7. The details of above study are as follows:
A study by Arkadianos et al.(2007)conducted on patients, who have history of failure in
following weight loss programs were given Nutrigenetics test screening, for 24 variants in
19 genes, related to metabolism. Fifty patients were given Nutrigenetics test and 43
people were attending same test as previous weight loss therapy. BMI reduction and
fasting blood glucose testing were observed for both groups at 100 and >300 days. After
300 days weight loss was sustained in Nutrigenetics group than other group and BMI
reduction was 1.93kg/m2 that is 5.6% loss vs. gain of 0.51kg/m2 that is 2.2% gain was
observed for other group. Initially patients have fasting blood glucose levels >100mg/dl.
Whereas after 57% of Nutrigenetically tested patients have reduced fasting glucose levels
to <100mg/dl, but it is only 25%of non tested patients have reduced fasting blood glucose
level. Thus this study show Nutrigenetically tailored diet show good BMI reduction, good
levels of fasting glucose levels and good compliance.
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8. This slide clearly indicates pros and cons of implementing Nutrigenetics in clinical settings.
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