Metabolic and Kidney Diseases in the Setting of Climate Change, Water Shortage, and Survival Factors.
Climate change (global warming) is leading to an increase in heat extremes and coupled with increasing water shortage, provides a perfect storm for a new era of environmental crises and potentially, new diseases. We use a comparative physiologic approach to show that one of the primary mechanisms by which animals protect themselves against water shortage is to increase fat mass as a means for providing metabolic water. Strong evidence suggests that certain hormones (vasopressin), foods (fructose), and metabolic products (uric acid) function as survival signals to help reduce water loss and store fat (which also provides a source of metabolic water). These mechanisms are intricately linked with each other and stimulated by dehydration and hyperosmolarity. Although these mechanisms were protective in the setting of low sugar and low salt intake in our past, today, the combination of diets high in fructose and salty foods, increasing temperatures, and decreasing available water places these survival signals in overdrive and may be accelerating the obesity and diabetes epidemics. The recent discovery of multiple epidemics of CKD occurring in agricultural workers in hot and humid environments may represent harbingers of the detrimental consequences of the combination of climate change and overactivation of survival pathways.
Division of Renal Diseases and Hypertension, University of Colorado Denver, Aurora, Colorado; Richard.Johnson@ucdenver.edu.
Richard J
RJ
Johnson
Division of Renal Medicine, Department of Clinical Science Intervention and Technology, Karolinska University Hospital, Stockholm, Sweden;
Peter
P
Stenvinkel
Division of Renal Diseases and Hypertension, University of Colorado Denver, Aurora, Colorado;
Thomas
T
Jensen
Division of Renal Diseases and Hypertension, University of Colorado Denver, Aurora, Colorado;
Miguel A
MA
Lanaspa
Division of Renal Diseases and Hypertension, University of Colorado Denver, Aurora, Colorado;
Carlos
C
Roncal
Division of Renal Diseases and Hypertension, University of Colorado Denver, Aurora, Colorado;
Zhilin
Z
Song
Institut National de las Santé et de la Recherche Medicalé UMRS 1138, Centre de Recherche des Cordeliers, Paris, France; and.
Lise
L
Bankir
Laboratory of Renal Physiopathology, Instituto Nacional de Cardiologia Ignacio Chávez, Mexico City, Mexico.
Laura G
LG
Sánchez-Lozada
D000818:Animals; D057231:Climate Change; D003681:Dehydration / Q000150:complications / Q000378:metabolism; D005632:Fructose / Q000378:metabolism; D006801:Humans; D007674:Kidney Diseases / Q000150:complications / Q000453:epidemiology / Q000209:etiology* / Q000378:metabolism; D008659:Metabolic Diseases / Q000150:complications / Q000453:epidemiology / Q000209:etiology* / Q000378:metabolism; D013534:Survival; D014881:Water Supply
D005632:Fructose
chronic kidney disease; metabolism; obesity; osmolality; vasopressin