2National Obesity Center, Yaoundé Central Hospital, Cameroon
3Department of Internal Medicine and specialties, Faculty of Medicine and Biomedical sciences, university of Yaoundé 1, Cameroon
Methods: This was a cross-sectional and analytical study over a period of 3 months at the National Obesity Center of Yaoundé. We included people who came to a dietetic consultation and had a BMI ≥ 30kg / m2. All patients with a known Cushing’s syndrome, or who taking corticosteroids, as well as any other drug that has an influence on the bioavailability of dexamethasone were excluded. We evaluated the corticotropic axis by quantitative determination of plasma cortisol before and after the overnight dexamethasone suppression test. After the clinical examination, the eating behavior was assessed using the Three-Factor Eating Questionnaire Test (TFEQ-R18).
Results: We included 25 patients (15 women and 10 men) aged 54 ± 10 years and with an average BMI of 37.8 kg / m2. There was an association between BMI hyperphagia of disinhibition, cognitive restriction and hunger (P <0.0001). There was a significant association between disinhibition hyperphagia, susceptibility to hunger, cognitive restriction, and the level of cortisol after the overnight dexamethasone suppression test (P <0.0001).
Conclusion: The strong association between eating disorders, body mass index, and cortisol levels suggests that the adrenocorticotropic axis would influence dietary behavior in obese subjects.
Keywords: Dietary disorders, Obesity, Serum cortisol.
The practician, faced with obesity, always has the idea that there is an association between eating disorders and obesity [6]. The impact of eating behavior on hormonal changes or the metabolic syndrome is known [6,7]. The relationship between obesity and eating disorder is two-way: in fact, an eating disorder predisposes to obesity, and obesity predisposes to eating disorders including compulsion [8]. The aim of this study was to establish the relationship between the serum cortisol and the eating behavior in obese patients in Cameroon.
It was a cross-sectional and descriptive study. The study took place over a period of 3 months at the National Obesity Center (NOC) of Yaoundé. The study population consisted of obese subjects aged 18 to 60 years. We included all non-diabetic obese patients with BMI ≥30kg / m2 who give an informed consent. We excluded any patient with a known Cushing’s syndrome, patients taking corticosteroids regardless of the route of administration, patients on estrogen / progestin and patients on drugs that can modify the bioavailability of dexamethasone. The study was proposed to the people coming in dietetic consultation.
We invited all people coming to routine dietetic consultation for obesity, to participate to the study. Capillary blood glucose was sampled in order to eliminate the presence of diabetes according diabetes diagnosis criteria.
b. Inclusion visit
Participants arrived at the NOC at 07A.M. The last meal must have been taken at 08P.M the day before the inclusion visit. In order to limit the stress induced by our interrogation which could have repercussions on the corticotropic axis, the patients were first sampled for biological work-up at laboratory. They observed a rest period of 30 minutes and after that, each participant was taken to the sampling room. All sampling started at 8:00 A.M.
Biological work-up include the lipid profile; basal cortisol levels and the overnight dexamethasone suppression test (ODST). Next step consisted in filling the TFEQ-R18 by the participant himself in the consultation box. Sometimes, investigator could help if there were any concerns in the questionnaire. After all, we completed the visit by a physical exam.
Exploration of the corticotropic axis: Overnight Dexamethasone Suppression Test (ODST):
We gave 2 tablets of dexamethasone dosed at 0.5 mg tablet. The participant had to take 1mg of dexamethasone at home between 11pm and midnight. He returned the next day from 7:30 for a 2nd blood sample at 8 am.
c. Dietary assessment
The Three-Factor Eating Questionnaire Test (TFEQ) The TFEQ is a standardized questionnaire with 51 questions. It assesses the eating habits of an individual in three main modes namely:
-The cognitive restriction capacity of food intake
-The susceptibility to hunger
- Disinhibition of hyperphagia.
In our study we used the revised 18-item test: TFEQ R- 18. A 10-15 minutes period was required to complete the questionnaire.
Each answer of the 18 items of the questionnaire is scored from 1 to 4; a score of 4 indicating a strong addiction to the behavior studied. Cognitive restriction, Disinhibition and Hunger were considered as low if the values were 0–10, 0–8 and 0–7, respectively. The values above 10, 8 and 7 of cognitive restriction, disinhibition and Hunger respectively, were high. The results are presented as mean scores. Each question in the test is related to a type of eating behavior, and each factor measured by the test has an alpha Cronbach coefficient of 0.83-restrictive cognition,0.77- dishinibition and 0.80-feeling hunger [9].
The table I below represents the questions related to each eating behavior.
Eating behavior |
Number of the question of the TFEQ related to a eating behaviour |
Total of points |
Cognitive Restriction |
4, 6, 10, 14, 15, 18 |
24 |
Susceptibility to Hunger |
3, 5, 8, 12, 17 |
20 |
Disinhibition of hyperphagia |
1, 2, 7, 9, 11, 13, 15, 16 |
32 |
1. Population distribution by gender and clinical characteristics of the population:
We recruited 25 people who agreed to participate in our study. The study population consisted of 40% (n=10) men and 60% (n=15) women. The mean age of our subjects was 54 ± 10 years.
The average body mass index was of 37.8 kg / m2. However, there was no elevation of blood pressure in these subjects (Table II)
Clinical Characteristics |
Median [II Q] |
Age (years) |
54[40.5-60.5] |
BMI(Kg/m2) |
37.8[32.8-44.9] |
Fat Mass(Kg) |
160[93-117.5] |
Systolic Blood pressure(mmHg) |
131[117.5-140.5] |
Diastolic Blood pressure(mmHg) |
81[73-89] |
Height(cm) |
164[160-172] |
Waist circumference(cm) |
114[107-121] |
Hip circumference(cm) |
120[111-134] |
No patient had a fasting glucose disorder. Regarding the lipid profile, our subjects had a high LDL-cholesterol level> 1g/l. The average basal 8AM cortisol was strictly normal at 162.7nmol/l. The determination of the basic 8 AM cortisol showed a maximun at 391nmol/l and the minimim at 9.7nmol/l. After the ODST, there was a suppression of cortisol with a maximum at 163nmol /l and a minimum of 9.18nmol /l (Figure 1). In addition, the ODST resulted in a suppression of > 50% of basal cortisol in 76% (n=19) participants and a significant absence of suppression in 25%(n= 6) participants.
Regarding disinhibition of hyperphagia the highest score was 25 and the lowest score was 10/32. Regarding the feeling of hunger, the maximum score was 17 with a minimum of 5/20. For cognitive restriction we had a maximum score at 18 and a minimum of 8/24. (Figure 2)
Measures of association
Tables III, IV and V showed a high association between disinhibition of hyperphagia and suppression of cortisol after ODST by more than 50% (Eta = 0.737), between feeling hungry and a suppression > 50% of cortisol post ODST (Eta = 0.591) and also between cognitive restriction and post ODST suppression of cortisol > 50% (Eta = 0.824). After calculating the percentage of cortisol suppressed after ODST, we performed multivariate analyzes between different eating behaviours and the difference in cortisol concentration. Our results show that there is a strong association between the difference in cortisol suppressed and each eating behaviour P <0.001. There was also a very strong association (p <0.0001) between body mass index, eating behaviour, and percentage of suppression of cortisol (table VI). The multivariate analysis of each parameter of the lipid profile has shown that there is a strong association between these different parameters and the disorders of the studied eating behaviour. P <0.0001.
Disinhibition of hyperphagia score /32 |
Cortisol decreased more than 50% of baseline | Total | Eta | ||
NON | OUI | ||||
10 | 1 | 0 | 1 | 0.737** | |
12 | 1 | 0 | 1 | ||
13 | 0 | 1 | 1 | ||
14 | 0 | 1 | 1 | ||
15 | 0 | 3 | 3 | ||
17 | 1 | 2 | 3 | ||
18 | 1 | 2 | 3 | ||
19 | 0 | 1 | 1 | ||
20 | 0 | 3 | 3 | ||
21 | 1 | 3 | 4 | ||
22 | 0 | 2 | 2 | ||
23 | 0 | 1 | 1 | ||
Total | 25.00 | 1 6 |
0 19 |
1 25 |
** Eta tends to 1= high degree of association
Hungry sensation score/20 | Cortisol decreased more than 50% | Total | Eta | ||
NON | OUI | ||||
5 | 0 | 1 | 1 | 0.591** | |
6 | 0 | 1 | 1 | ||
8 | 2 | 2 | 4 | ||
10 | 1 | 4 | 5 | ||
11 | 0 | 3 | 3 | ||
12 | 0 | 1 | 1 | ||
13 | 0 | 2 | 2 | ||
14 | 2 | 1 | 3 | ||
15 | 1 | 1 | 2 | ||
17 | 0 | 3 | 3 | ||
Total | 6 | 19 | 25 |
** Eta tends to 1= High degree of association
Cognitive restriction score/24 |
Cortisol decreased more than 50% |
Total |
Eta |
||
NON |
OUI |
||||
8 |
0 |
1 |
1 |
0.824** |
|
9 |
2 |
1 |
3 |
||
10 |
1 |
4 |
5 |
||
11 |
0 |
1 |
1 |
||
12 |
0 |
1 |
1 |
||
13 |
0 |
6 |
6 |
||
14 |
0 |
3 |
3 |
||
15 |
1 |
0 |
1 |
||
16 |
1 |
0 |
1 |
||
17 |
1 |
0 |
1 |
||
18 |
0 |
2 |
2 |
||
Total |
6 |
19 |
25 |
** Eta tends to 1= High degree of association
Compared variables |
P value |
Cortisol difference vs.Disinhibition of hyperphagia |
<0.0001** |
Cortisol différence vs. Hungry sensation |
<0.0001** |
Cortisol difference vs. Cognitive restriction |
<0.0001** |
**p < 0.05 = Association
The diagnosis of a hypercortisolism involves several tests including either the ODST, or the increase of the urinary free cortisol (UFC) on the 24-hour urine . No test has a superiority over the other. ODST was suitable in this study because it is easily achievable and reproducible, therefore it represents the ideal test for outpatient screening of hypercortisolism [12].
After ODST, 76% patients suppressed cortisol by at least 50% baseline, while 24% had an insufficient suppression of cortisol. This might suggest, that these subjects would have hyperactivation of their corticotropic axis and thus subclinical Cushing’s syndrome as described in the literature [13-14]. Indeed, subclinical Cushing’s syndrome predisposes to a higher prevalence of obesity and other elements of the metabolic syndrome. This situation needs to be confirmed by others tests as late midnight salivary or serum cortisol or UFC; because effect exists in individuals a threshold of sensitivity to DXM [14]. The analyzes showed that there is a strong association between disinhibition of hyperphagia, cognitive restriction, feeling hungry and cortisol suppression by > 50% post ODST (eta = 0.7; 0.5 and 0.8 respectively). Studies have shown that disinhibition of hyperphagia and feeling of hunger influence weight gain. In Algeria, Koceir et al found that disinhibition of hyperphagia and hunger positively correlated with BMI [15]. In our study, BMI is strongly associated with disinhibition of hyperphagia (P <0, 0001). These results are similar to those of Anglé in 2009 in Finland [16]. In fact, disinhibition of hyperphagia is a frequent eating disorder in obese subjects, the weight gain occurs because of the imbalance of the energy balance with a massive food intake. All this is responsible for the onset of the metabolic syndrome and hormonal dysfunction including hormones involved in energy metabolism (cortisol, insulin resistance). Severe obesity is recognized as a cause of pseudo-Cushing, which could explain absence significant suppression of cortisol observed in some of our obese participants.
Regarding the different eating disorders we found that our participants had high scores, with a maximum of disinhibition of hyperphagia of 25/32, 17/20 and 18/24 respectively for the feeling of hunger and cognitive restriction. Several data in the literature have focused on the relationship between disinhibition hyperphagia and BMI in obese subjects [17]. Other studies have shown that disinhibition of hyperphagia is the major determinant of weight gain. Strong disinhibition is associated with the degree of adiposity [18]. Indeed, despite a high leptinemia, in obese patients, the sensation of hunger and the decrease in energy expenditure were strongly correlated with eating disorders [3]. Thus, a strong leptinemia does not decrease the appetite of the obese but rather continues to be accompanied by hyperphagia and weight gain. This is explained by a leptin resistance at both the peripheral and central level, as it has been proposed for insulin [19].
DXM: Dexamethasone
HDL-C: High density lipoprotein-cholesterol
LDL-C: Low density lipoprotein-cholesterol
NOC: National Obesity Center
ODST: Overnight Dexamethasone Suppression Test
TC: Total cholesterol
TFEQ: Three Factor Eating Questionnaire
TG: Triglycerides
UFC: Urinary Free Cortisol
Availability of data and materials
Data will be made available by the corresponding author upon reasonable request
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