Estrogens and Obesity: Lack of will or hormonal disbalance?

We can not consider obesity as a "drugs deficiency", only "lack of will" or a simple behavioural disorder.
Neurophysiological signals are strongly influencing our current wheight.
Estrogens, for example, play an important role in regulating our food intake and satiety.

Before menopause, women are protected from obesity and associated disorders by estrogens, and the sudden fall in estrogens blood level around age 52 is often associated to wheight gain.

In the hypothalamus there are two estrogen receptors, estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ). Activation of ERα by estrogens reduces food intake and increases body weight.
This new research published in the current number of "Cell Metabolism" focus on estrogens activity on two different cell populations' receptors in the hypothalamus. This activity can cause wheight gain and eventually promote obesity.

Rerearchers focused their work on neurons in the hypothalamus of brain that carry an estrogen receptor alpha – a molecule that takes estrogen signals into the neurons. The hypothalamus links the nervous system to the endocrine system to regulate multiple physiological processes, including those controlling body weight.
Don't forget that estrogen receptors have been found in many peripheral tissues including adipose tissue. Their biological activity has not been completely explained.

Here you can read more on "estrogen receptors and obesity" and about the "Metabolic impact of sex horones in Obesity"

I am sure that this kind of research will help us to better undestand complexity
linked to obesity and chronic diseases and to find remedies for epidemic of obesity that is speading form the rich to the developing countries.

Adiposity in children and its correlation with BP

The effect of adiposity on blood pressure in children is minimal until the body mass index reaches the 85th percentile, at which point it intensifies, according to a study published online Oct. 3 in Hypertension.

Wanzhu Tu, Ph.D. followed 1,111 children for 4.5 years. Blood tests and BP were measured.

"There is a marked intensification of the influence of adiposity on BP when children reach the categories of overweight and obese. Among the possible pathways, leptin may be a potentially important mediator acting through the sympathetic nervous system (reflected in heart rate)," the authors write.



BMI was used in this study to meaure adiposity but a new index can give furter information about the real fat percentage.




This new index is called Body Adiposity Index (BAI) and it is calculated using Hip circumference and Height.





Try to calculate your BAI and compare it with your BMI.

Here you can calculate your BMI



Are the 2 indexes telling you the same story?

Iron deficiency in obese people linked to inflammation

It is difficult to think at obesity as a condition linked to nutritional carencies because we normally think that it is caused by excess of nutrients.

Obesity is not caused by excess of nutrients
It is caused by excess of empty calories and bad fats.

The paradox is that you can also witness nutritional carencies like hypoferremia (iron deficiency) in obese people.


A clinical trial with 172 healthy non-obese (BMI <30 kg/m2), and 234 obese (BMI ≥30 kg/m2) has been conducted to understand mechanisms involved in the hypoferremia of obesity. Results are published here.

Researchers found in obese patients:
- inadequate bioavailable iron relative to body weight
- diminished intestinal absorption
- decreased iron bioavailability induced by inflammatory adipokines

This study confiirms that obesity is a condition where inflammatory pathways are over-activated and nutritional carencies can be present despite the excess of food intake.

Falsely normal ferritin concentrations are commonly found and are likely increased by chronic inflammation. So this marker if measured alone can be misleading in obese people.

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