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  Vol. 302 No. 16, October 28, 2009 TABLE OF CONTENTS
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Tuberculosis and the Inflammatory Processes of Obesity in Human Evolution—Reply

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

In Reply: Dr Fantuzzi and I agree that obesity may provide some protection from tuberculosis1 and that tuberculosis may have affected evolution. She challenges my interpretation, positing that cytokines from adipocytes cannot be important in this arena because they are restricted to areas near their secretion site and do not reach the site of the infection, the lung. However, mycobacteria spread promptly from the primary site of infection via lymphatics and the bloodstream to hilar lymph nodes, apices of both lungs, and sites throughout the body, where they can remain dormant but viable, capable of reactivating disease at any time.2 With chronic tuberculosis, recurrent rounds of hematogenous spread can occur.2

Among nonobese adults, for persons in whom a larger fraction of the total body fat is of the subcutaneous type, the adipose tissue contributes a lower level of proinflammatory elements. Individuals with more of their fat in visceral type fat . . . [Full Text of this Article]

Jesse Roth, MD
jesserothmd@hotmail.com
Feinstein Institute for Medical Research
North Shore–Long Island Jewish Health System
Manhasset, New York



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RELATED LETTER

Tuberculosis and the Inflammatory Processes of Obesity in Human Evolution
Giamila Fantuzzi
JAMA. 2009;302(16):1754.
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