Obesity is a disease that brings several complications and increases the risk of other diseases like metabolic syndrome, diabetes mellitus type 2, and cardio vascular diseases. A quarter of the population of Pakistan would be classified as overweight or obese with the use of Indo-Asian-specific BMI cutoff values. The growing prevalence of type 2 diabetes, hypertension and cardiovascular disease, is tied to excess weight (Afridi and Khan, 2004). The heterogeneity of different ethnic population is always plays important role and should be considered in autoimmune disease or have sedentary life style (Gul et al; 2010). Obesity develops as a result of complex interactions between a person’s genes and the environment characterized by long term energy balance due to excessive calorie
consumption, insufficient energy output. Diet and lifestyle play a significant role both in
development and control of obesity (Greenspan and Gardner, 1997)
Changing lifestyle over the last century, including increased calorie consumption and
reduced physical activity have played a key role in obesity development. Many molecular
mechanisms reported to be involved in development of obesity. Obesity has strong
endocrinological and neurological basis (Sowers et al, 1992).
Thyroid hormones are a major regulator of energy metabolism in vertebrates and defects
in thyroid status are frequently associated with changes in body weight. Thyroid hormones
regulate in vivo and in vitro the tub gene, which when mutated in tubby mice causes
obesity, insulin resistance and sensory defects. These changes could be attributed to
thyroid hormone deficiency since T3 or T4 treatment restored normal tub expression
(Koritschoner et al, 2001). Reinehr and Andler (2002) reported that T3 and T4
concentration was significantly higher in obese children compared to those of normal
weight. Rosenbaum et al, (2001) suggested that changes in body weight were associated
with changes in catecholamine excretion and thyroid hormones, which might by virtue of
the effects on energy expenditure, have favored a return to usual body weight.
Overweight women with a family history of obesity may have lower levels of the thyroid
hormone triiodothyronine (T3) in their blood. Treatment to raise T3 levels may help reduce
some metabolic risk factors associated with abdominal obesity in some overweight
women (Yokoyama et al, 2000). Sari et al,(2003) in his study stated that thyroid volume
and function may vary in obese and non-obese women.
Knudsen et al, (2005) found a positive correlation between BMI and serum TSH (P <
0.001) and a negative association between BMI and category of serum T4 (P < 0.001). No
association was found between BMI and serum free T3 levels. Even slightly elevated
serum TSH levels are associated with increase in the occurrence of obesity.
As main regulators of the body rate of metabolism, thyroid hormones have a profound
impact on weight. By increasing enzyme levels in the cell, mitochondria, which produce
energy, thyroid hormones control how the body burns up carbohydrates and fats. (Astrup
et al, 1996).
Hypothyroidism occurs when the thyroid gland does not produce enough energy
generating thyroid hormones. Weight gain is a classic symptom of this dysfunction. In
such cases levels of thyroid stimulating hormone (TSH) may rise in an attempt to spur
more production and secretion of thyroid hormones from thyroid gland (Kotkiewskiet al,.
1997).The aim of the present study is to assess the thyroid hormone levels in obese
women and to find the correlation of thyroid with obesity.
MATERIALS AND METHODS
The study was carried out in Pakistan on female population of Allama Iqbal Town,
Lahore, Alshafa Clinical Laboratory, Samanabad Lahore and Lahore College for Women
University Lahore. Study constitutes 180 female subjects of age group 20 – 45 years.
Subjects were divided into three categories 60 obese, 60 overweight and 60 controls
Waist was measured horizontally at the level just above the uppermost border of the iliac
crest. The measurement was made at a normal minimal respiration. Hip was measured as
the maximum circumference over the buttocks (Molarius et al., 1999). Central obesity was
calculated by dividing the waist measurement over the hip measurement and defined as
Height was taken using standard apparatus with the subjects wearing light clothing and
without shoes. Weight was measured in the upright position with a weighting scale to the
nearest 0.01 kilogram (kg). Height was measured to the nearest 0.1 cm by using a nonstretching
tape. Obesity index or Body mass index (BMI) was calculated as weight (kg)
divided by height squared (m2) to estimate overall body fat distribution (Greenspan and
Gardner, 2004). Overweight and obesity was defined according to Asian criteria (Dhiman
et al., 2005) and BMI greater than 23 was considered as overweight and BMI greater than
25 was considered obese. Participants who reported smoking at least 3 cigarettes per day
during the previous year were classified as current smokers. Physical activity was defined
as (i) sedentary, no extra physical activity apart from activities of daily living, (ii) or
physical active if they do brisk walking at least half an hour for three days in a week.
T3, T4 and TSH were measured by Enzyme immunoassay (EIA). T3 was estimated using
Medicorp HRP EIA Kit (Cet No. KTSP-21651). T4 and TSH were measured by using
Medicorp HRP EIA Kit (Cat No. KISP-22551) and Biocheck EIA Kit respectively.
The study was approved by the ethical committee of the university .A written consent was
taken from all the participants of the study. They cooperated throughout the period of
Statistical analysis was performed using the SPSS (version 13.0) software. All results are
expressed as Mean ±SD. Spearman correlation was used to find the correlation and
ANOVA was applied to find the significance between the studied groups.Data was
analyzed statistically applying ANOVA to find significance of results.
Serum T3, T4 and TSH concentrations were clinically in the normal range in all the studied
groups (Normal weight, overweight and obese)
TABLE 1: T3, T4 and TSH Levels in Normal weight, Overweight and Obese Subjects.
Serum T3 concentration was 1.16 ± 0.17 ng/ml in normal weight, 2.00 ± 0.33 ng/ml in
over weight subjects and 2.07 ± 0.93 ng/ml in obese subjects. Statistical analysis showed
that T3 concentration in over-weight subjects was significantly higher than that of normal
weight subjects (P = 0.05). Serum T3 concentrations in obese subjects were significantly
low than that of normal weight subjects (P = 0.05). Serum T3concentrations in obese
subjects were significantly lowers than that of overweight (p = 0.05).
Serum T4 concentration were 9.99 ± 1.96µg/dl in normal weight subjects, 10.28 ± 0.97
µg/dl in over weight subjects and 11.89 ± 2.43 µg/dl in obese subjects. Statistical analysis
showed that serum T4 concentration was significantly lower in overweight subjects than
that of normal weight subjects (P < 0.05). Serum T4 concentration was significantly lower
in obese subjects than that of normal weights subjects (P = 0.05). Serum T4 concentration
was non -significantly lower in obese than that of overweight subjects (P <0.05).
Serum TSH concentration was 1.66 ± 0.26 µIU/ml in normal weight subjects, 1.92 ± 0.14
µIU/ml in overweight subjects, 2.82 ± 0.67 µIU/ml in obese subjects. Statistical analysis
showed that serum TSH concentration was non-significantly higher in overweight subjects
than that of normal weight subjects (P = 0.05). Serum TSH concentration was
significantly higher in obese than that of normal weight subjects (P = 0.05). Serum TSH
concentration was non-significantly higher in obese than that of overweight subjects (P =
0.05).Serum T3 and TSH concentration had a positive significant correlation with BMI (r=
0.361, r=0.413, P<0.05) respectively.
It is observed that thyroid and its regulatory hormone levels are altered in obesity. Thyroid
hormones are potent modulators of adaptive thermo genesis and can potentially contribute
to the development of obesity (Krotkiewski, 2002).Serum T3 concentration was found
significantly lower in over weight and obese subjects as compared to normal weight
subject.conflicting reports from the literature are available. Stichel et al, (2000) studied
thyroid function and obesity in children and adolescent .They concluded that in childhood
obesity TSH and T3 levels are significantly increased.Serum T4 concentration was found
non-significantly higher in obese subjects than that of overweight subjects. Sari et al,
(2003) reported that thyroid volume and TSH concentration were higher; free T3 (P <
0.001) and free T4 concentration (P = 0.045) were lower in obese women; however all
were still in the normal range.
This study shows that serum TSH concentration was found significantly higher in over
weight and obese subjects as compared to normal weight subjects Serum TSH
concentration was found non-significantly higher in obese subjects as compared to
overweight subjects. A significant and positive correlation was observed between serum
concentration of TSH and BMI in the control group only. Contradictory reports from the
literature are available in this regard. Lacobellis et al. (2005) and Bastemir et al. (2007)
observed higher TSH levels in obese subjects with normal thyroid function, while some
other studies showed no relationship between TSH and obesity (Wesche et al., 1998; Ritz
et al., 2002). Chang et al. (1994) in his studies reported no relationship of TSH with
obesity. Lacobellis et al, (2005) studied possible relationship of thyroid function with BMI
in euthyroid obese women. TSH was positively correlated with BMI. TSH could represent
a marker of attenuated energy balance in severe, but uncomplicated obese women.
It is concluded that thyroid hormones level was in normal range in all the subjects but
serum T3 concentration was significantly lower in obese subjects, T4 concentration and
serum TSH concentration were higher in obese subjects as compared to normal weight
subjects and these difference were significant.
1. Afridi, K.A. and Khan, A. 2004. Prevalence and etiology of obesity- An overview. Pak.
J. Nutr. 3 (1): 14-25.
2. Astrup, A., Buemann, B., Toubro, S., Rannereies, C. and Raben, A. 1996. Low resting
metabolic rate in subjects predisposed to obesity: a role for thyroid status. Am. J. Clin.
Nutr. 63 (6): 873-879.
3. Gul Afshan, Nadeem Afzal, Sadia Qureshi, 2010. Establishment of cd4+ cd25hi t
cells reference intervals in healthy adult pakistani males versus females. Journal of
Applied Pharmacy, J App. Phram. 4 (2) : 104-111 (2010)
4. Filer, J. S. and Foster, D. W. 1998. Eating disorder: Obesity, Anorexia Nervosa and
Bulimia Nervosa. In: Williams Textbook of Endocrinology (Wilson, J. D., Foster, D. W.,
Kronenberg, H. M. AND Larsen, P. R.), 9th Edition. W.B. Saunders Company,
Philadelphia. Pp 1061 –
5. Greenspan, F. S. and Gardner, D.G., 1997. Basic and Clinical Endocrinology. 6th Ed. Lange
Medical books McGraw Hill., 633-637.
6. Guyton, M. D. and Hall, J. E. 2000. Texibook of Medical Physiology. 10th Edition. W.B.
Saunders Company, Philadelphia.
7. Knudsen, N., Lauberg, P., Rasmussen, L., Billow, I., Perrid, L., Ovenson, L. and
Jorgenson, T. 2005. Small differences in thyroid function may be important for Body
Mass Index and occurrence of obesity in the population. J. Clin. Endocrinol, Metab. 90
8. Koritschoner, P. N., Alvarez-Dolado, M., Kurz, M.S., Heiaenwaldr, F. M. Hacker, C.m
Vogel, F., Munoz, A. andZenke, M. 2001. Thyroid hormone regulates the obesity gene
tub. Euro. Mole. Bio. Org. 2 (6): 499-504.
9. Korthiewski, M. 2002. Thyroid hormones in the pathogenesis and treatment of obesity.
Eur.J. Phrmacol. 440 (2-3): 85-98.
10. Krothiewski, M., Holm, G. and Shono, N. 1997. Small dosage of triiodothyronine can
change some risk factors associated with abdominal obesity. Int. J. Obes. Relat. Metab.
Disord. 21 (10): 922-9.
11. Lacobellis, G., Ribaudo, M.C., Zappaterrreno, A., lannucci, C.V. and Leoetti, F. 2005.
Relationship of thyroid function with body mass index, leptin, insulin sensitivity and
adiponectin in euthyroid obese women. J. Clin. Endocrinol (Oxf). 64 (4): 487-9
12. Reinehr, T. D. and Andler, W. 2002. Thyrooid hormones before and after weight loss in
obesity. Arch. Dis. Child. 84 (4): 320.
13. Sari, R., J.C. 2000. Obesity, insulin resistance and diabetes- a worldwideepidemic.Br. J.
Nutre. 83: 5-8.
14. Sowers, J.R., Whitfield, A. and Beck, B. W., 1982. role of enhanced sympathetic nervous
system activity and reduce Na+, K+ dependent adenosine triphosphatase activity in maintenance
elevated blood pressure in obesity: effects of weight loss. Clin. Sci. 63: 121-
15. Stichel, H., Allemand, D. and Gruters, A. 2000. Thyroid function and obesity in children
and adolescents. Pediatrics. 51(1): 14-9.
16. Wlodek, D. and Gonzales, M. 2003. Decreased energy levels can cause and sustain
obesity. J. Theo. Biol. 225 (1): 33-44.
17. World Health Organization. 1998. Obesity: Preventing and Managing. Geneva. World Health
18. Bastemir, M., Akin, F., Alkis, E. and Kaptanoglu, B., 2007. Obesity is associated with
increased serum TSH level, independent of thyroid function. Swiss Med. Wkly, 137: 431-434.
19. Dhiman, R.K., Duseja, A. and Chawla, Y., 2005. Asians need different criteria for
defining overweight and obesity. Arch. Intern. Med., 165: 1069-1070