In modern medicine, the concept of the spleen in the Donguibogam does not merely refer to the anatomical spleen. The spleen described here relates broadly to the digestive system, overseeing digestion and nutrient absorption. In particular, gastric atony can be understood clinically as decreased gastrointestinal motility, also termed gastric hypomotility or gastroparesis.
The stomach is not a passive reservoir, but an active organ governed by an intricate neural network and hormonal signals. Within the stomach wall, specialized interstitial cells of Cajal act like pacemakers, generating regular electrical impulses that drive intestinal peristalsis. When these cells falter, gastric movement declines and stagnation begins. Food remains in the stomach for prolonged periods, producing dyspepsia, abdominal distension, nausea, and early satiety.
The autonomic nervous system serves as the central regulator of this process, managing vital functions such as heartbeat, respiration, and digestion without conscious effort. Within the digestive tract, the parasympathetic nerve stimulates gastrointestinal motility and increases digestive enzyme secretion, while the sympathetic nerve acts to suppress motility. Under chronic stress or irregular routines, the body shifts into a sympathetic-dominant state of fight or flight. In response, the stomach suspends activity, concluding that it is not the time to digest. This shift frequently leads to indigestion, persistent abdominal discomfort, and a heavy head.
Decreased gastrointestinal motility may also stem from underlying diseases, including diabetes complications involving vagus nerve injury, thyroid dysfunction such as hypothyroidism, neurological disorders like stroke or Parkinson's disease, and medications such as opioid analgesics or anticholinergics. Recently, post-viral chronic gastrointestinal hypomotility has also been observed. Because of these varied origins, simple digestant use often proves insufficient, and one must evaluate both autonomic nervous system balance and underlying conditions.
Hormones governing digestive movement are equally critical. Gastrin, which stimulates gastric acid and regulates motility; cholecystokinin, which triggers bile and pancreatic juice secretion as food enters the small intestine; and motilin, which encourages peristalsis, must remain in balance. Disruptions in these hormones can contribute directly to gastric atony. Rather than simple inactivity, a sluggish stomach is often a distress signal from a complex regulatory network. Gut dysbiosis has also been shown to impair digestive function and gastrointestinal motility.
