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Obstructive Sleep Apnea (OSA)
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andGastroenterology
CarlosA.Cortez-Hernández andJoseC.Cessa-Zanatta
13.1 Obstructive Sleep Apnea (OSA) andGastroenterology
Obstructive sleep apnea (OSA) is a disease with a high prevalence worldwide. High
costs are needed for identifying the disease and for the treatment and care of associated conditions such as obesity and metabolic syndrome. The severity of sleep apnea
and chronic intermittent hypoxia is thought to be the key trigger for inammation
that causes progression of nonalcoholic fatty liver disease (NAFLD). Colorectal cancer represents the third most common cancer in men, and the second in women, the
hypoxia caused by OSA could be associated with the development and growth of
colorectal tumors, and if this is conrmed in future studies, OSA could be considered
an additional risk factor for starting screening programs at a younger age. Finally, the
association with OSA and gastroesophageal reux disease (GERD) can be associated with hormonal disorders observed in OSA, but more studies are needed before
concluding that there is a solid relation between both diseases.
Obstructive sleep apnea (OSA) is a disorder with a very high prevalence all
around the world, and it is associated with negative health outcomes. It is associated
with many metabolic disorders, which include metabolic syndrome. In addition, it
has been associated with nonalcoholic fatty liver disease (NAFLD) in adult and
pediatric populations.
NAFLD is a disease with a very high prevalence in obese patients, affecting more
than 70% of this population [1]. The rst studies describing the association of OSA
severity with the progression of NAFLD were published 20years ago. To date, more
than 20 studies in different populations have conrmed this association.
13
C. A. Cortez-Hernández (*) · J. C. Cessa-Zanatta
Faculty of Medicine, Gastroenterology Service and Department of Internal Medicine,
Hospital Universitario Dr. José E.González, Universidad Autónoma de Nuevo León,
Monterrey, Mexico
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
P. M. Baptista et al. (eds.), Obstructive Sleep Apnea,
https://doi.org/10.1007/978-3-031-35225-6_13
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C. A. Cortez-Hernández and J. C. Cessa-Zanatta
The severity of sleep apnea and, specically, its manifestation, chronic intermittent
hypoxia (CIH), is the critical trigger for higher levels of stress oxidative and generation of reactive oxygen species (ROS), which cause the liberation of inammatory
cytokines, provoking systemic inammation that causes exacerbation of NAFLD and
progression to liver brosis. CIH results in reduced oxygen tension in the liver, specically in the hepatocytes surrounding the central vein (zone 3), and causes the
expression of hypoxia-inducible factors (HIFs), which are fundamental oxygen sensors that regulate the capacity of the cell to respond to a hypoxic environment. HIFs
are implicated in developing hepatic steatosis, insulin resistance, and liver brosis,
resulting in a fundamental link between OSA and NAFLD [2].
OSA severity and, specically, its manifestation, chronic intermittent hypoxia
(CIH), triggers high levels of oxidative stress and reactive oxygen species (ROS),
which release inammatory cytokines, producing systemic inammation with exacerbation of NAFLD and progression to liver brosis. CIH results in reduced oxygen
tension in the liver, specically in the hepatocytes surrounding the central vein
(zone 3), and causes hypoxia-inducible factors (HIFs), which are fundamental oxygen sensors that regulate the capacity of the cell to respond to a hypoxic environment. HIFs are implicated in the development of hepatic steatosis, insulin resistance,
and liver brosis, resulting in a fundamental link in the association of OSA and
NAFLD [2].
A French study of 1285 patients with OSA found a linear relationship between
OSA severity and hepatic steatosis index [3].
Continuous positive airway pressure (CPAP) therapy has proved to prevent serious coronary events and reduce blood pressure [4]. In patients with OSA, treatment
with CPAP in a chronic way diminishes mortality risk in the OSA population, but
the effect of CPAP treatment on liver disease in patients with OSA is controversial [5].
The pathogenesis of NAFLD has not been fully elucidated, but a “Two-hit”
model has been proposed as the mechanism underlying the pathogenesis of
NAFLD.The insulin resistance and excess hepatic lipid accumulation due to the
dysregulation of fatty acids cause the rst hit, while oxidative stress and inammation cause the second hit.
These mechanisms are suggested to be signicant risk factors in the progression
of NAFLD.OSA is consistently associated with some of these risk factors, including insulin resistance, dyslipidemia, visceral fat deposition, increased serum leptin
levels, and low-grade inammation. CPAP may positively affect the liver by interfering with these factors of the “Two-hit” model [6, 7] (Fig.13.1).
Despite the “Two-hit” hypothesis being very popular and is often quoted, recent
data show that it is not enough to explain the elaborated interaction of the multiple
factors involved in the development of NASH.Some other factors and mechanisms
that participate in the pathogenesis of NASH are included in the “Multiple-hit
hypothesis” [8].
This hypothesis places insulin resistance as a key factor in the progression of
nonalcoholic fatty liver disease (NAFLD) [9] because it causes a chain of reactions
including higher peripheral lipolysis, with an increased ux of free fatty acids
CPAP: continuous positive airway pressure
13 Obstructive Sleep Apnea (OSA) andGastroenterology
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CPAP
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Lean Mass
Fig. 13.1 Effect of CPAP on components of “two-hit.” CPAP continuous positive airway pressure
Adiponectin
Insulin
resistance
First Hit
Leptin
Dyslipidemia Inflammation
Oxidative
stress
Second Hit
(FFAs), and also more hepatic de novo lipogenesis (DNL). Insulin resistance also
affects adipose tissue, causing altered secretion of adipokines and increased levels
of inammatory cytokines, interleukin (IL)-6, and tumor necrosis factor (TNF)-α.
Alteration of gut microbiome causes high gut permeability, systemic levels of lipopolysaccharides, and absorption of FFAs [10].
All of these factors cause an increased ux of FFAs into the liver. This results in
excess triglyceride (TG) deposition in the liver (hepatic steatosis) that parallels the
generation of lipotoxic metabolites of FFAs. Further, these toxic metabolites cause
mitochondrial dysfunction with increased oxidative stress, generation of ROS, and
endoplasmic reticulum stress, which manifests in hepatocyte injury and
inammation.
As mentioned before, CIH is the most crucial trigger for increased oxidative
stress, generation of ROS, and release of inammatory cytokines, resulting in systemic inammation that drives the exacerbation of NAFLD and progression to liver
brosis.
CIH raises sympathetic activity and induces a state of insulin resistance. This
promotes lipolysis in the adipose tissue and increased ux of FFAs in the liver.
Under normal oxygenation conditions, FFAs are metabolized by oxygen-dependent
mitochondrial combustion through β-oxidation. Hence, hypoxia creates a state of
excess FFAs and their reduced utilization through mitochondrial β-oxidation. More
FFAs become available for TG and cholesterol synthesis, resulting in fatty liver,
liver injury through oxidative stress, and NASH.CIH has also been shown to selectively inactivate the adipose tissue lipoprotein lipase and reduce the very low density lipoproteins (VLDL) clearance from circulation. In summary, CIH can cause
dyslipidemia by upregulating de novo lipogenesis (DNL) and lipoprotein secretion,
reducing lipoprotein clearance, and enhancing peripheral lipolysis and inux of
FFAs in the liver.
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Also, obstructive sleep apnea is related to liver brosis. Stellate cells and portal
broblasts are essential sources of brillar collagen and lysyl oxidase (LOX)
enzymes in the normal liver and after early hepatic injury. Hypoxia is a potent stimulator of LOX activity, which plays an essential role in the covalent cross-linking of
collagen and elastin, increasing liver stiffness. This increased stiffness causes
increased mechanical tension that is crucial for the differentiation of hepatic stellate
cells and portal broblasts into myobroblasts, which are responsible for the deposition of extracellular collagen and, eventually, the development of brosis. Mesarwi
and colleagues have recently demonstrated that serum LOX is elevated in patients
with NAFLD-associated hepatic brosis relative to those without brosis [11].
These same investigators also proposed the potential role of serum LOX as a biomarker of liver brosis in patients with severe obesity and OSA.HIF-1α has also
been independently implicated in the development of liver brosis in a mouse model
of NAFLD [12]. Hence, it can be concluded that hypoxia induces HIF-1α, which in
turn causes the expression of the LOX enzyme and the subsequent development of
brosis.
Given that CIH plays a vital role in mediation of NAFLD in OSA, treatment with
CPAP would be expected to yield unequivocal benets in NAFLD patients. However,
the available studies have yielded mixed results.
C. A. Cortez-Hernández and J. C. Cessa-Zanatta
13.2 Obstructive Sleep Apnea (OSA) andColorectal Cancer
Colorectal cancer is the third most common cancer in men, and the second most
common in women, accounting for almost 10% of all cancers in both groups [13].
Elevated rates of colorectal cancer in western countries suggest that lifestyle could
play an essential role in the etiology of this disease [14].
Today, there is strong evidence that healthy habits like being physically active,
consuming whole grains, and foods containing dietary ber decrease the risk of
colon cancer. In addition, consuming red meat, processed meat, or two or more
alcoholic drinks per day, and being overweight or obese increase the risk of colorectal cancer [15]. Plus, low consumption of fruit and nonstarchy vegetables could be
associated with an increased risk of colorectal cancer [16].
Less than 10% of colorectal cancer cases account for hereditary causes, like
those with hereditary nonpolyposis colorectal cancer or familial adenomatous polyposis. Most cases are related to sporadic colorectal cancer with genetic and environmental causes, emphasizing the importance of being aware of these risk factors
and taking action to change them [17].
The studies to nd the association between OSA and colorectal cancer are not
easy because they have many confounding factors because most of these patients
are obese, and obesity may contribute to the development of colorectal neoplasia.
The association between OSA and colorectal neoplasia remains unclear. But
some studies have found an association between OSA and the development of
colorectal neoplasia.
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