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Phases of digestion

Digestion is the physiological process by which ingested food is broken down mechanically and chemically into absorbable nutrients, primarily occurring in the gastrointestinal tract through distinct phases: the cephalic phase, gastric phase, and intestinal phase.^[1] These phases involve coordinated mechanical actions, such as chewing and peristalsis, and chemical breakdown via enzymes and acids, enabling the extraction of carbohydrates, proteins, fats, vitamins, and minerals for energy, growth, and cellular repair.^[2] The process is regulated by neural and hormonal mechanisms across cephalic, gastric, and intestinal phases, ensuring efficient nutrient processing while preventing overload.^[3] In the cephalic phase, mechanical digestion begins with mastication in the oral cavity, where teeth grind food into smaller particles, and chemical digestion initiates through salivary amylase, which hydrolyzes starches into maltose and other disaccharides at a neutral pH of approximately 6.7–7.0; this phase is triggered by sensory cues like sight and smell.^[1] Lingual lipase also contributes by beginning triglyceride breakdown, while the formed bolus is propelled via swallowing into the esophagus, with minimal further processing there.^[2] This phase is largely under voluntary neural control but prepares the alimentary canal for subsequent involuntary actions.^[3] The gastric phase occurs in the stomach, where peristaltic contractions and antral grinding reduce food particles to less than 2 mm, mixing them with gastric juices to form chyme.^[1] Hydrochloric acid lowers the pH to 0.8–3.5, denaturing proteins and activating pepsinogen to pepsin for protein hydrolysis, while intrinsic factor aids vitamin B12 absorption later.^[1] Gastrin, released in response to stomach distension and peptides, stimulates further acid secretion, but somatostatin inhibits it as the stomach empties to maintain balance.^[3] During the intestinal phase, primarily in the small intestine, chyme mixes with pancreatic enzymes (including amylase, lipases, and peptidases), bile for fat emulsification, and brush border disaccharidases like maltase, lactase, and sucrase, completing macronutrient digestion into monosaccharides, amino acids, and fatty acids at a pH of 6–7.^[1] Hormones such as secretin and cholecystokinin, triggered by chyme entry, regulate pancreatic bicarbonate to neutralize acid and promote bile and enzyme release, while the large intestine focuses on water absorption and bacterial fermentation of remnants.^[2]^[3] Absorption of nutrients occurs mainly via enterocytes in the small intestine, with undigested material forming feces for elimination.^[1]

Overview of Digestive Phases

Definition and Significance

The phases of digestion refer to the sequential stages of gastrointestinal regulation, primarily dividing gastric and pancreatic secretion into the cephalic, gastric, intestinal, and basal states, which correspond to anticipatory, stimulatory, modulatory, and resting periods, respectively.^[4]^[5] These phases coordinate the digestive process by integrating sensory, mechanical, and chemical signals to optimize enzyme and acid release in response to nutrient intake.^[6] The concept of these phases originated in the early 20th century, with Ivan Pavlov first describing the cephalic phase through experiments on salivary and gastric responses to food cues in dogs around 1902.^[6] This framework was expanded in the mid-20th century to encompass the gastric and intestinal phases, following the discovery of key hormones such as gastrin in 1905 by John Edkins, who identified it as a chemical stimulant of gastric acid secretion extracted from antral mucosa.^[7] Subsequent research confirmed and refined these phases, highlighting their integration via neural pathways like the vagus nerve and hormones including gastrin and secretin as foundational regulators.^[8] The significance of these phases lies in their role in ensuring the timed release of digestive juices to align with food arrival in the gastrointestinal tract, thereby enhancing nutrient breakdown, absorption efficiency, and overall energy homeostasis while minimizing risks such as mucosal damage from excess acid that could lead to ulcers.^[6] For instance, the cephalic phase contributes approximately 20-30% of total gastric acid secretion during a meal, the gastric phase 50-60%, the intestinal phase 10-20%, and the basal state less than 10%, illustrating how these stages collectively account for meal-stimulated output while maintaining low inter-meal secretion.^[9]^[10]^[5]

Regulatory Mechanisms

The regulatory mechanisms of digestion are governed by integrated neural and endocrine systems that coordinate gastrointestinal motility, secretion, and absorption across its phases. Neural regulation involves central and peripheral pathways that respond to sensory cues and local stimuli. The central nervous system, particularly the hypothalamus and medulla oblongata, processes inputs from higher brain centers and autonomic nuclei to modulate digestive functions via descending pathways.^[11] Peripheral neural control is primarily exerted by the parasympathetic vagus nerve (cranial nerve X), which innervates the esophagus, stomach, pancreas, and proximal colon, promoting secretion and peristalsis through cholinergic stimulation of enteric neurons. The enteric nervous system (ENS), an intrinsic network comprising the myenteric plexus for motility and the submucosal plexus for secretion and blood flow, operates semi-autonomously but integrates extrinsic signals; it includes sensory neurons that detect luminal contents and motor neurons that execute responses. In the cephalic phase, cranial nerves IX (glossopharyngeal) and X (vagus) relay anticipatory signals from oral sensory receptors to the brainstem, initiating vagal efferent activity. Local reflexes in the gastric and intestinal regions are mediated by ENS circuits, such as the gastrocolic reflex, which link distension or chemical changes to coordinated contractions and secretions.^[11] Endocrine regulation is achieved through hormones secreted by enteroendocrine cells in the gastric and intestinal mucosa, fine-tuning digestive processes via bloodstream delivery to target organs. Gastrin, released by G cells in the gastric antrum and duodenum, binds to cholecystokinin-B receptors on parietal cells to stimulate hydrochloric acid secretion and mucosal growth. Histamine from enterochromaffin-like (ECL) cells in the gastric oxyntic mucosa potentiates gastrin's acid-stimulatory effects by activating H2 receptors on parietal cells, forming a key paracrine loop. Somatostatin, produced by D cells throughout the stomach and duodenum, exerts broad inhibition on gastrin release, acid secretion, and other GI hormones via somatostatin receptors. Secretin from S cells in the duodenal mucosa suppresses gastrin and gastric acid while stimulating pancreatic and biliary bicarbonate release to neutralize chyme. Cholecystokinin (CCK), secreted by I cells in the duodenum and jejunum, promotes pancreatic enzyme secretion (e.g., amylase, lipases, proteases) and gallbladder contraction for bile release, while also slowing gastric emptying through vagal and myenteric inhibition.^[12]^[13] These neural and endocrine elements integrate via feedback loops to maintain homeostasis and prevent digestive overload. The enterogastrone effect, primarily driven by duodenal hormones like secretin and CCK in response to acidic or fatty chyme, inhibits gastric acid secretion and motility through direct endocrine action and vagal reflexes, ensuring synchronized transit. Interstitial cells of Cajal (ICCs), specialized mesenchymal cells within the GI muscularis, serve as pacemakers by generating rhythmic slow-wave potentials via ion channel activity (e.g., calcium and potassium currents), which propagate to coordinate smooth muscle depolarization and peristalsis independent of neural input.^[12]^[14] Post-2021 research has elucidated the expanding role of the gut-brain axis in these mechanisms, with vagal afferent fibers detecting enteroendocrine cell-released hormones (e.g., CCK, GLP-1) to relay satiety and motility signals to the nucleus tractus solitarius in the brainstem. The gut microbiome further influences hormone release by producing metabolites such as short-chain fatty acids, which stimulate enteroendocrine cells to secrete GLP-1 and serotonin, modulating digestion and central regulation, although foundational neural and endocrine pathways remain unaltered.^[15]

Cephalic Phase

Sensory Triggers

The cephalic phase of digestion is initiated by a variety of sensory stimuli that signal the anticipation of food intake, priming the gastrointestinal tract for processing. These primary triggers include the sight, smell, taste, and even the cognitive thought of food, which evoke anticipatory responses without the physical presence of nutrients in the digestive system.^[16] Such stimuli are often amplified through conditioned associations from prior eating experiences, a process rooted in Pavlovian classical conditioning where neutral cues, like the environment or time of day linked to meals, elicit physiological preparations for digestion.^[6] Sensory information reaches the central nervous system via specialized pathways that converge to integrate signals and coordinate responses. Olfactory cues are transmitted through the olfactory nerve (cranial nerve I) to the olfactory bulb and subsequently to the hypothalamus and limbic structures, facilitating rapid detection of food aromas.^[16] Gustatory signals from taste buds travel primarily via the facial (CN VII), glossopharyngeal (CN IX), and vagus (CN X) nerves to the nucleus of the solitary tract (NTS) in the brainstem, where they are relayed to the hypothalamus for further processing.^[16] Visual stimuli, meanwhile, are processed through cortical pathways that project to the hypothalamus, contributing to the overall sensory orchestration. These pathways integrate in the NTS and hypothalamus, enabling a cohesive anticipatory signal that enhances vagal efferent activity to the gut.^[16] This phase physiologically commences seconds to minutes before swallowing and persists until food arrives in the stomach, ensuring timely preparation of digestive secretions. For instance, exposure to food aromas can account for approximately 30% of the salivary and gastric secretory response, demonstrating the potency of olfactory triggers in modulating digestive readiness.^[17] Psychological factors, such as heightened appetite, further influence these responses by increasing vagal tone, which amplifies the preparatory signals to the gastrointestinal tract.^[6]

Neural and Hormonal Responses

The cephalic phase of digestion is initiated by sensory triggers such as the sight, smell, or thought of food, prompting neural and hormonal signals that prepare the gastrointestinal tract for incoming nutrients.^[18] Neural responses primarily involve vagal efferents from the parasympathetic nervous system, which release acetylcholine (ACh) to stimulate gastric secretions. This ACh acts directly on parietal cells in the gastric mucosa, activating the H⁺/K⁺ ATPase proton pump to secrete hydrochloric acid (HCl) into the stomach lumen, and on chief cells to release pepsinogen, the inactive precursor to the proteolytic enzyme pepsin. These neural signals account for approximately 20-30% of the total gastric acid secretion during a meal, priming the stomach for protein digestion and pathogen defense.^[19]^[20]^[9] Hormonal responses complement these neural effects through early release of gastrin from G cells in the gastric antrum, stimulated indirectly by vagal ACh, which promotes further HCl production by parietal cells. Additionally, vagal stimulation triggers enterochromaffin-like (ECL) cells to secrete histamine, which binds to H₂ receptors on parietal cells, amplifying acid secretion via a paracrine mechanism. These initial hormonal signals enhance the preparatory environment without direct food contact.^[18]^[21] Beyond gastric effects, cephalic neural and hormonal responses increase salivation, including secretion of salivary amylase from acinar cells to initiate carbohydrate breakdown in the mouth, and enhance gastric motility through vagally mediated contractions that promote mixing and propulsion. Vagal efferents also prime pancreatic acinar cells for enzyme secretion, such as amylase and lipases, via ACh stimulation, ensuring coordinated downstream digestion. These preparatory responses typically last 10-60 minutes, fading as the phase transitions to gastric stimulation.^[22]^[23]^[17]

Gastric Phase

Mechanical Stimuli

The mechanical phase of gastric digestion is initiated by the physical distention of the stomach wall as food enters from the esophagus, activating specialized mechanoreceptors embedded in the gastric mucosa and muscular layers. These stretch-sensitive receptors, primarily low-threshold mechanoreceptors in the fundus and corpus, detect the volume and pressure changes caused by ingested material, triggering a cascade of local enteric reflexes that contribute to the stimulation of gastric secretory and motor activities during this phase. This mechanosensory input ensures that digestive processes scale with meal size, promoting efficient breakdown without relying solely on chemical cues. The primary pathways for mechanical stimulation involve both intramural enteric nervous system reflexes and extrinsic vagovagal pathways. Local reflexes within the stomach wall, mediated by the myenteric and submucosal plexuses, directly enhance smooth muscle contraction and glandular secretion upon stretch detection. Additionally, afferent fibers of the vagus nerve transmit signals to the brainstem's nucleus tractus solitarius, which in turn activates efferent vagal outflows to stimulate parasympathetic responses; this includes the release of acetylcholine from postganglionic neurons to parietal cells for acid production and gastrin-releasing peptide from enteroendocrine cells to amplify gastrin secretion. These coordinated mechanisms result in heightened gastric motility, characterized by increased peristaltic waves and mixing contractions that propel and triturate chyme, with responses increasing at food volumes around 50-150 mL for antral distension.^[24] In addition to stimulatory effects, mechanical distention incorporates inhibitory feedback to maintain gastric accommodation and prevent complications such as reflux. When stomach volume exceeds approximately 500 mL, high-threshold mechanoreceptors in the proximal stomach activate nitrergic inhibitory neurons within the enteric plexus, inducing receptive relaxation—a transient fundic dilation that accommodates larger boluses without excessive pressure buildup. This adaptive response, distinct from the excitatory peristalsis in the distal stomach, underscores the biphasic nature of mechanical regulation in the gastric phase.

Chemical Stimuli

The chemical stimuli in the gastric phase of digestion are initiated by the breakdown products of food, particularly peptides, amino acids, and partially digested proteins present in the stomach lumen. These substances are detected by chemoreceptors located in the gastric antrum and mucosa, which trigger local neural and hormonal responses independent of mechanical distention. This detection process ensures that gastric secretion is finely tuned to the nutrient content of the meal, promoting efficient protein digestion.^[25] The primary pathway involves direct stimulation of G cells in the antrum, leading to the release of gastrin, a key hormone that acts on enterochromaffin-like (ECL) cells to induce histamine secretion. Histamine then binds to H2 receptors on parietal cells, while acetylcholine from vagal nerves potentiates this effect, collectively driving acid secretion during the gastric phase. Additionally, gastrin directly enhances parietal cell activity through cholecystokinin-2 (CCK2) receptors. This coordinated response drives hydrochloric acid (HCl) production via the H+/K+ ATPase proton pump on parietal cell membranes and pepsinogen release from chief cells, which is subsequently activated to pepsin in the acidic environment. These secretions facilitate protein hydrolysis and maintain an optimal pH for enzymatic activity, sustaining the process for 2-4 hours as the meal is processed.^[25]^[26]^[27] Certain exogenous substances, such as alcohol and caffeine, serve as minor chemical stimulants by directly irritating the gastric mucosa or activating bitter taste receptors, thereby increasing gastrin and acid output. However, a negative feedback mechanism prevents over-secretion: as HCl accumulation lowers intragastric pH below 3, it stimulates D cells to release somatostatin, which inhibits G cell gastrin production and ECL cell histamine release. This pH-dependent regulation, primarily operating at pH levels between 2 and 3, protects the gastric mucosa from excessive acidity. Chemical stimuli synergize briefly with mechanical factors to amplify the overall gastric response during meal ingestion.^[25]^[28]^[29]

Intestinal Phase

Enteric Stimulation

The intestinal phase of digestion begins as partially digested chyme from the gastric phase enters the duodenum, where specific nutrients trigger stimulatory responses primarily aimed at pancreatic and biliary secretions. Fats in the form of monoglycerides, proteins as amino acids, and to a lesser extent carbohydrates in the chyme activate enteroendocrine cells in the duodenal mucosa, initiating hormonal and neural signals that account for approximately 10% of total gastric acid stimulation while serving as the primary driver for pancreatic exocrine function.^[30]^[12] Key pathways involve the release of cholecystokinin (CCK) from I cells in the duodenum and jejunum, which is secreted in response to fatty acids and protein breakdown products; CCK binds to receptors on pancreatic acinar cells to promote the secretion of digestive enzymes such as amylase, lipase, and proteases, while also stimulating gallbladder contraction to release bile into the duodenum for fat emulsification.^[12]^[31] Complementing this, secretin is released from S cells when the duodenal pH drops below 4.5 due to acidic chyme, prompting the pancreas to secrete a bicarbonate-rich fluid that neutralizes the acid and raises the luminal pH to 6-7, creating an optimal environment for enzymatic activity.^[32]^[33] These hormonal actions are reinforced by neural mechanisms, including vagovagal enteropancreatic reflexes that transmit signals via the enteric nervous system to enhance pancreatic enzyme output in coordination with nutrient arrival.^[34] The resulting responses facilitate further digestion by delivering enzymes for carbohydrate, protein, and lipid breakdown in the small intestine, while the bicarbonate infusion protects the duodenal mucosa and supports nutrient absorption. Additionally, CCK contributes to enhanced duodenal motility, promoting segmentation and peristalsis to mix chyme with secretions. This stimulatory phase is short-lived, typically lasting 30-60 minutes per bolus of chyme to synchronize with the rate of gastric emptying and prevent overload in the duodenum.^[35]^[36]

Enteric Inhibition

Enteric inhibition represents the primary feedback mechanism during the intestinal phase of digestion, where signals from the duodenum and proximal jejunum suppress gastric activity to prevent overload of the small intestine with chyme. This process is crucial for coordinating digestion, ensuring that the delivery of nutrients matches the absorptive and processing capacity of the intestine while protecting the duodenal mucosa from excessive acidity or osmotic stress.^[37] The mechanisms of enteric inhibition involve both hormonal and neural pathways. Hormonally, secretin released from duodenal S cells inhibits gastric acid secretion and slows gastric emptying by stimulating bicarbonate release from the pancreas, which neutralizes duodenal acid. Cholecystokinin (CCK), secreted by I cells in response to fats and proteins, further inhibits gastric motility and acid production while promoting gallbladder contraction and pancreatic enzyme release. Glucose-dependent insulinotropic peptide (GIP), produced by K cells upon exposure to glucose, amino acids, and fats, suppresses gastric acid secretion and motility, particularly at higher physiological doses. Additionally, somatostatin from D cells in the stomach and duodenum acts as a paracrine inhibitor, reducing the release of other hormones like gastrin and enhancing overall suppression. Neuronal mediation occurs via the enterogastric reflex, which is activated through extrinsic vagal and splanchnic nerves, integrating sensory inputs from the duodenum to dampen gastric function; this reflex is both hormonally augmented (e.g., by somatostatin and CCK) and directly neural, with hormonal components predominating in fat-induced responses.^[12]^[37]^[38]^[39] Triggers for these inhibitory responses include the arrival of acidic chyme (pH below 4.5), hyperosmolar solutions, and high concentrations of fats or proteins in the duodenum. Acidic chyme, with a threshold pH of 4.5, prompts secretin release proportional to the acid load, typically activating at duodenal H+ loads of 1-2 mEq to prevent mucosal damage. Fats and proteins stimulate CCK and GIP secretion even from small intestinal loads, while distension or osmolarity from nutrient-rich chyme further engages the enterogastric reflex and somatostatin release from D cells. These triggers collectively signal the need to modulate upstream gastric activity.^[40]^[12]^[39] The effects of enteric inhibition are profound, achieving up to 80-90% reduction in gastric acid secretion and motility during peak responses, such as those induced by duodenal fat, thereby terminating the gastric phase of digestion. Gastric emptying is slowed to approximately 1-2 mL/min for liquids, matching the intestine's processing rate and preventing duodenal hyperacidity or osmotic overload. This inhibition not only optimizes nutrient absorption but also safeguards the intestinal mucosa by maintaining a neutral pH environment through coordinated bicarbonate secretion. In balance with enteric stimulation, these inhibitory processes ensure efficient, phased progression of digestion.^[39]^[37]^[41]

Basal and Interdigestive Phases

Basal Secretion

Basal secretion encompasses the ongoing, low-level release of gastric juices during interdigestive periods, representing a steady-state process that persists in the absence of meal stimuli. In the stomach, this involves hydrochloric acid (HCl) production at rates typically ranging from 1 to 5 mEq/hour, accounting for less than 10% of the maximal stimulated output of approximately 20 to 40 mEq/hour. This output is predominantly mediated by constitutive levels of gastrin from antral G cells, which stimulate enterochromaffin-like (ECL) cells to release histamine; the histamine then binds H2 receptors on parietal cells to promote acid secretion, with negligible contribution from vagal neural pathways.^[42]00786-5/fulltext)^[43] Regulation of basal secretion follows circadian patterns, characterized by higher acid output at night—peaking between 10 PM and midnight—compared to lower daytime levels, reflecting endogenous rhythmic influences on parietal cell activity. Cortisol exerts a stimulatory effect on this process, as evidenced by reduced acid secretion in cortisol-deficient states like Addison's disease and restoration upon replacement therapy. Fasting conditions maintain minimal gastric motility, allowing the low-volume secretions to accumulate without significant mixing or propulsion.^[43]^[44]^[45] The key functions of basal secretion center on mucosal integrity and microbial defense: surface epithelial cells continuously produce a protective layer of mucus and bicarbonate to neutralize HCl and shield the gastric lining from autodigestion. The resultant acidic milieu (pH 1-2) inhibits bacterial proliferation, preventing overgrowth and potential enteric infections in the upper gut.^[25]00786-5/fulltext) Clinically, basal acid output (BAO) is assessed by nasogastric aspiration of gastric contents over a 60-minute fasting interval, titrating the acid concentration to yield normal values below 5 mEq/hour. Markedly elevated BAO, often surpassing 15 mEq/hour, signals hypersecretory disorders such as Zollinger-Ellison syndrome, driven by gastrinomas that pathologically amplify gastrin-mediated stimulation.^[46]^[47]

Basal Electrical Rhythm and Motility

The basal electrical rhythm (BER), consisting of slow-wave oscillations, underlies the rhythmic electrical activity in the gastrointestinal tract during fasting states. In the stomach, these oscillations occur at a frequency of approximately 3 cycles per minute (0.05 Hz) and are generated by networks of interstitial cells of Cajal (ICC), which serve as pacemaker cells within the myenteric plexus of the gastric corpus.^[48]^[49] These slow waves propagate distally, increasing in frequency to about 12 cycles per minute in the duodenum, where ICC in the proximal duodenum initiate annular wavefronts that coordinate smooth muscle depolarization without necessarily triggering contractions unless modulated by neural or hormonal inputs.^[49]^[50] This gradient ensures orderly aboral propagation, maintaining baseline tone between meals. Interdigestive motility is characterized by the migrating motor complex (MMC), a cyclic pattern that recurs every 90-120 minutes during fasting to clear residual contents from the upper gastrointestinal tract. The MMC comprises three phases: Phase I, a period of quiescence lasting about 40-60% of the cycle with minimal contractile activity; Phase II, featuring irregular contractions that build in intensity (up to 2-3 per minute in the stomach and 11-12 per minute in the small intestine); and Phase III, the most intense phase with high-amplitude peristaltic waves (propagating at 6-10 cm/min) that originate in the antrum or duodenum and sweep bacteria, debris, and secretions toward the lower gut, earning it the designation as the gut's "housekeeper."^[50] This housekeeping function prevents small intestinal bacterial overgrowth by limiting microbial proliferation in stagnant luminal contents.^[50] Regulation of the MMC involves hormonal, neural, and enteric mechanisms, with motilin peaking during Phase II to initiate progression toward Phase III via stimulation of antral contractility and serotonin release from enterochromaffin cells.^[51] Vagal efferents, activated through 5-HT3 receptors on afferent nerves, drive gastric Phase III, while enteric control via intrinsic primary afferent neurons and 5-HT4 receptors governs intestinal components, ensuring coordinated propagation.^[51] Disruptions in these pathways, such as impaired vagal signaling or reduced ICC networks, abolish or alter MMC cycling, contributing to fasting motility disorders like gastroparesis, where delayed emptying exacerbates symptoms.^[52] Recent models from 2023-2025 highlight the gut microbiome's influence on MMC via microbial metabolites, particularly short-chain fatty acids (SCFAs) produced by bacterial fermentation, which modulate ICC function and enhance motility homeostasis through receptor-mediated effects on pacemaker activity.^[53] These insights underscore the interplay between microbial ecology and electrical rhythmicity in maintaining interdigestive clearance. Alongside motility patterns, basal secretion provides continuous low-level glandular output to support this fasting state.^[49]

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The small intestine basic electrical rhythm (slow wave) frequency gradient ... Interstitial cells of Cajal generate electrical slow waves in the murine stomach.
[49]
Redefining the functional roles of the gastrointestinal migrating ...
Phase III of the MMC is the most active of the three and can start either in the stomach or small intestine. Historically this pattern was designated to be the ...
[50]
Mechanism of Interdigestive Migrating Motor Complex - PMC
Migrating motor complex (MMC) is well characterized by the appearance of gastrointestinal contractions in the interdigestive state.Missing: housekeeper | Show results with:housekeeper
[51]
The migrating motor complex: control mechanisms and its role in ...
Mar 27, 2012 · The migrating motor complex (MMC) is a cyclic, recurring motility pattern that occurs in the stomach and small bowel during fasting; it is interrupted by ...
[52]
The interplay of gut microbiota and intestinal motility in ...
Jul 5, 2025 · Key gut microbial metabolites that play a significant role in intestinal motility are short-chain fatty acids (SCFAs) and secondary bile acids.