Nausea and vomiting with abdominal pain and early satiety?
By Stephanie Ogura, ND and Melanie Kusznireckyj, ND
Gastroparesis is defined by delayed gastric emptying without mechanical obstruction of the stomach. It is a disorder of gut-brain interaction that is defined by impairment of gastric mobility resulting in prolonged food retention in the stomach and the presence of associated symptoms: nausea, vomiting, bloating, abdominal pain, postprandial fullness, and early satiety. Delayed gastric emptying is when more than 60% of the meal is still present in the stomach after 2 hours, and/or more than 10% of the meal is present after 4 hours.
Gastroparesis stats [ii],[i],[iii],[iv]:
- Prevalence of gastroparesis ranges widely in studies. Prevalence ranges from 13.8 to 267.7 per 100,000 adults;
- Prevalence of anxiety and depression, and gastroparesis is 49% and 39% respectively;
- Up to 50% of individuals with gastroparesis report having a poor or fair quality of life;
- 30% report they are not working due to gastroparesis;
Etiologies[v]:
- Idiopathic (11.3%-39.4%)
- Diabetic mellitus (37.5%-57.4%)
- Drug-induced (11.8%-19.6%)
- Postsurgical (1.1%-15%)
- Rare etiologies include connective tissue disorders like scleroderma, collagen storage disorders, and neurodegenerative diseases; viral or bacterial infections, or renal insufficiency
- female:male prevalence is nearly 2:1, and peak prevalence late 50–60 years of age.
Pathophysiology [vi]:
- Gastric electrical dysrhythmia: loss of pacemaker interstitial cells of Cajal (ICCs), ICCs are crucial for regulation of smooth muscle contractility as they initiate and propagate the gastric electrical slow waves. ICC damage could result from chronic high blood sugar levels leading to oxidative stress and inflammation, and from vascular diseases leading to ischemia and the lack of oxygen and nutrients to ICC.
- Impaired gastric accommodation (adequate relaxation of the fundus and the proximal gastric body induced by food ingestion and regulated by the nitric oxide-mediated vagal reflex): advanced glycation end-products (AGEs), produced during hyperglycemia, can inhibit the expression of intestinal nNOS
- Antral hypomotility: hyperglycemia inhibits antral contractions.
- Abnormalities in pyloric function and duodenal motility. Hyperglycemia stimulates pyloric contractions.
Naturopathic principles are well suited to improve the overall well-being of individuals with gastroparesis, and to guide individuals with predisposing factors or early symptoms on prevention strategies.
- Dietary modification
- Vagal nerve stimulation[vii]
- Dandelion: increases gastric emptying[viii]
- Celery & artichoke: luteolin may be a vascular protective agent by directly acting on vascular ECs to stimulate NO-dependent vascular dilatation.[ix]
- Hesperidin: polarization of interstitial cells of Cajal pacemaker potential and increase in gastrointestinal motility[x]; stimulates production of nitric oxide (NO) from vascular endothelium
- Quercetin: Restoration of density of interstitial cells of Cajal[xi]
- Address underlying causes such as glycemic control.
- Address concomitant symptoms such as anxiety
From a Naturopathic Medicine perspective, gastroparesis can be addressed by keeping in mind glucose control and the microvasculature to the stomach. Vitazan Professional selected their top three products to address this in our August Gastroparesis monthly awareness promotion.
REFERENCES:
[i] Huang, I-Hsuan et al. “Worldwide prevalence and burden of gastroparesis-like symptoms as defined by the United European Gastroenterology (UEG) and European Society for Neurogastroenterology and Motility (ESNM) consensus on gastroparesis.” United European gastroenterology journal vol. 10,8 (2022): 888-897. doi:10.1002/ueg2.12289
[ii] Araujo-Duran, Jorge et al. “Gastroparesis for the nongastroenterologist.” Cleveland Clinic journal of medicine vol. 91,6 373-383. 3 Jun. 2024, doi:10.3949/ccjm.91a.23078
[iii] Overs, James et al. “Comparing the prevalence and association between anxiety, depression and gastrointestinal symptoms in gastroparesis versus functional dyspepsia: A systematic review and meta-analysis.” Journal of psychosomatic research vol. 183 (2024): 111834. doi:10.1016/j.jpsychores.2024.111834
[iv] https://cdhf.ca/en/digestive-conditions/gastroparesis/
[v] Sato, Hiroki, and Madhusudan Grover. “Gastroparesis and Functional Dyspepsia: Spectrum of Gastroduodenal Neuromuscular Disorders or Unique Entities?.” Gastro hep advances vol. 2,3 (2023): 438-448. doi:10.1016/j.gastha.2022.10.005
[vi] Oh, Jung Hwan, and Pankaj J Pasricha. “Recent advances in the pathophysiology and treatment of gastroparesis.” Journal of neurogastroenterology and motility vol. 19,1 (2013): 18-24. doi:10.5056/jnm.2013.19.1.18
[vii] Dougherty, Michael I et al. “Improvement in Symptomatic Gastroparesis With Increased Vagal Nerve Stimulation.” Neurology. Clinical practice vol. 11,1 (2021): e18-e19. doi:10.1212/CPJ.0000000000000775
[viii] Jin, Y-R et al. “The effect of Taraxacum officinale on gastric emptying and smooth muscle motility in Rodents.” Neurogastroenterology and motility vol. 23,8 (2011): 766-e333. doi:10.1111/j.1365-2982.2011.01704.x
[ix] Si, Hongwei et al. “The flavonoid luteolin induces nitric oxide production and arterial relaxation.” European journal of nutrition vol. 53,1 (2014): 269-75. doi:10.1007/s00394-013-0525-7
[x] Hwang, Minwoo et al. “Hesperidin depolarizes the pacemaker potentials through 5-HT4 receptor in murine small intestinal interstitial cells of Cajal.” Animal cells and systems vol. 24,2 84-90. 26 Mar. 2020, doi:10.1080/19768354.2020.1746398
[xi] Vieira Frez, Flávia Cristina et al. “Restoration of density of interstitial cells of Cajal in the jejunum of diabetic rats after quercetin supplementation.” Revista espanola de enfermedades digestivas vol. 109,3 (2017): 190-195. doi:10.17235/reed.2016.4338/2016