obesity is one of the most significant and rapidly increasing health problem today , giving rise to an explosion in health care costs .
the amount of energy we consume and how much we move around are the key factors in body weight regulation , but why a positive energy balance emerges in the majority of individuals in societies with access to abundant food calories is not completely understood .
our lifestyle has changed dramatically since the beginning of industrialization , and some of these changes probably affect energy balance in ways that favour weight gain .
some experts consider the dogma that voluntary changes in food intake and physical activity are the principal causes of the obesity epidemic to be circumstantial .
moralizing the problem and socially stigmatizing the obese has done nothing to stem the epidemic .
results from both human and animal studies indicate the existence of an intricate homeostatic system for maintaining body weight within a fairly narrow range and the presence of a powerful hedonic system that can interfere with this relatively finely tuned regulation . if central mechanisms in this homeostatic system , which involves endocrine feedback from the periphery to the brain , are influenced by changes in the environment , then even small environmental changes could potentially cause changes in body weight .
we propose a novel hypothesis involving a mechanism in which a small change in blood ph caused by increased concentrations of co2 in our environment may contribute to the development of obesity .
coinciding with the sharp increase in the prevalence of human obesity over the last 50 years , weight gain has also been observed in animals . a recent study found that 24 populations of 8 different species , including laboratory animals that had been fed the same diets for decades , all displayed significant weight gain .
this suggests that a shared environmental factor , favouring weight gain , may be involved in the regulation of energy balance .
the atmospheric concentration of co2 has remained between 180280  p.p.m . over the past two million years . however , with the increasing industrialization of modern societies , co2 concentration has risen to 400  p.p.m . , with an additional increase to 550  p.p.m .
thus , the partial pressure of co2 in the outside air has increased by nearly 40% over the last century .
henry 's law states that the solubility of a gas is directly proportional to the partial pressure of that gas above the solvent , so we can assume that humans now absorb around 40% more co2 in body tissue .
this increased acidic load is only partially counterbalanced by increased excretion of renal acid ( h ) .
it is therefore reasonable to assume that blood and cerospinal fluid are now slightly more acidic than 100 years ago .
additionally , in industrialized cultures , we spend 8090% of our time indoors , where co2 concentrations are often higher .
it is well established that acidity of the blood increases ( decreased ph ) with increasing co2 concentration in the inhaled air . in a number of studies of a duration of several weeks
, a lower ph was maintained throughout , indicating that full renal compensation did not occur .
acidosis is also compensated by increased ventilation , but apparently , this does not happen before co2 concentration in inspired air is about 10  000  p.p.m .
in parts of the brain ( hypothalamus ) , there are specialized nerve cells ( orexin neurons ) , which are involved in the regulation of appetite , energy metabolism , wakefulness , feeding behaviour and libido .
these orexin neurons are extremely sensitive to changes in ph , a decrease of only 0.1 ph units leading to a doubling in their activity . given the observed increase in atmospheric co2 concentration from 280 to 400  p.p.m .
, and the decrease in the ph of blood observed in animals and humans exposed to co2 concentrations ranging from 7000 to 15  000  p.p.m . , we estimate that the firing rate of the orexigen neurons has increased by approximately 1% in the course of the last century .
the basis for the calculation : if the ph decrease with 0.1 ph units , the firing rate will change nearly 100% . during the past century
additionally , we assume that there is a linear relationship between the ph in the blood and the co2 concentration in the inspired air .
two studies was identified where blood ph was measured in relation to exposure to low concentration of co2 . a human study with exposure to 7000  p.p.m .
co2 and a blood ph decrease of 0.05 units and a guinea pigs study with exposure to 15  000  p.p.m .
( 7000400  p.p.m . ) . according to ( williams et al . , ) will a drop in ph of 0.05 ph units means a 50% increase in the firing rate .
a rough estimate of the proposed increase in the firing rate would be : 50%/6600  p.p.m.=0.008%/p.p.m
we hypothesize that a lower blood ph , caused primarily by rising co2 concentrations in air , indoors as well as outdoors , leads to elevated activity in parts of the hypothalamus , resulting in increases in appetite and energy intake .
these ph - sensitive neurons also regulate wakefulness , and increased activity in the neurons will lead to increased wakefulness , which has also been associated with weight gain .
interestingly , numerous studies have shown an association between short sleep duration and increased body mass index .
the national sleep foundation ( www.sleepfoundation.org ) finds that sleep duration has been decreasing steadily over the past century .
activation of the orexin system will lead to less sleep , and lack of sleep has been reported to decrease levels of the satiety hormone leptin , increase levels of the hunger hormone ghrelin , and alter glucose homeostasis .
additionally , in patients with obstructive sleep apnoea , characterized by both a hypercapnic and a hypoxic state , energy expenditure ( ee ) has been found to decrease with increasing severity of the affliction .
leptin concentrations in these patients are only half that found in healthy control subjects matched for age , sex , body mass index , waist / hip ratio and fat mass .
leptin is involved in the regulation of both energy intake and of ee , and narcoleptic patients , despite eating less than normal people , they still become obese .
lower orexin levels decrease appetite , so the weight gain may be a result of decreased ee caused by lower circulating plasma leptin levels .
this effect of leptin may be the same as that linking shorter duration of sleep to obesity .
orexin neurons are inhibited by glucose and leptin , and leads to decreased appetite , wakefulness , sympathetic stimulation , libido and need for pleasure / reward .
in addition , the orexin neurons stimulate centres in the brain forming adrenocorticotrophic hormone , which in turn leads to increased production of cortisol by the kidneys . increased cortisol levels
are known to increase appetite and favour abdominal energy storage in pathological doses ( cushing disease ) .
interestingly , short sleep duration and chronic stress cause increased levels of cortisol and have resulted weight gain in some individuals .
if elevated environmental levels of co2 reduce blood ph , and this then leads to an increased firing rate in the orexin neurons in the hypothalamus , then several key processes in the brain could be affected , leading to greater appetite and increased energy storage .
the relationship between increased exposure to co2 and the processes described above has not been investigated previously . an obvious way to test
the hypothesis is to conduct long - term animal studies , in which the effects of exposure to elevated levels of co2 , as the sole intervention factor , on the amount of food eaten , weight gain , growth rate , and if there are measurable effects , whether they might be explained by a decrease in blood ph . by use of metabolic cages with different co2 concentrations , differences in ee ( respiratory calorimetry ) and
ideally , the animals should be followed over several generations , because the acidic stress is likely to influence the production of cortisol , which is known to induce foetal programming , resulting in increased risk of obesity and related diseases in the offspring .
long - term studies in humans prohibited by ethical considerations , but short - term studies to test the effects of moderately elevated levels of co2 on appetite regulation could be performed in respiration chambers .
we conducted a small , short - term , crossover design , pilot study , with 6 young healthy males ( body mass index 2025  kg  m and 2235 years ) randomly exposed to ambient air or 8000  p.p.m .
the study was reviewed by the science ethics committee for the capital region of denmark , journal number : h-4 - 2011-fsp , and the committee judged that because of the very limited intervention that the project was not notifiable . before the study , we have obtained informed consent from all the participants .
subjects ' ad libitum energy consumption increased numerically by 6.1% when exposed to co2 ( 95% ci : 5.7 to 17.9% , s.d . : 14.8% ) .
though not statistically significant , probably due to insufficient statistical power , the results was in the expected direction and suggests that the hypothesis is worthy of exploration in larger cohorts , both animal and human , using suitable designs to minimize individual variability in the measured outcomes .
the cost of health care for an increasingly overweight and obese population has increased dramatically , and efforts to halt the obesity epidemic have failed .
we propose that exposure to increasing amounts of co2 in the atmosphere changes regulatory neuronal mechanisms in the hypothalamus , resulting in decreased ee and sleep , and increased appetite and obesity .
if substantiated , this could prove to be an additional mechanism in the multifactorial causes of obesity , which will necessitate major political , economic and environmental interventions to combat the obesity epidemic .
 human obesity has evolved into a global epidemic . 
 interestingly , a similar trend has been observed in many animal species , although diet composition , food availability and physical activity have essentially remained unchanged . 
 this suggests a common factor  potentially an environmental factor affecting all species . 
 coinciding with the increase in obesity , atmospheric co2 concentration has increased more than 40% . 
 furthermore , in modern societies , we spend more time indoors , where co2 often reaches even higher concentrations . increased co2 concentration in inhaled air decreases the ph of blood , which in turn spills over to cerebrospinal fluids . 
 nerve cells in the hypothalamus that regulate appetite and wakefulness have been shown to be extremely sensitive to ph , doubling their activity if ph decreases by 0.1 units . 
 we hypothesize that an increased acidic load from atmospheric co2 may potentially lead to increased appetite and energy intake , and decreased energy expenditure , and thereby contribute to the current obesity epidemic . 
Background
A possible connection between the obesity epidemic and the environment
How can increased atmospheric CO
Testing the hypothesis
Conclusion