The Management of Chronic Diseases via Different Therapeutic Modalities with Peptic Ulcer Disease as an Example

Following two experiences I published here in this blog only last night, a few hours ago on my chronic neck pains and how I managed it with almost instant relief without the use of drugs, and analgesics and non-steroidal anti-inflammatory drugs (NSAIDs) here: 

A https://scientificlogic.blogspot.com/2023/04/an-almost-instant-cure-for-neck-to.htmln 

 I promised I would produce two different opinions on how peptic ulcer disease (PUD) is managed.

The first part is how a medical doctor who depends solely on conventional drug-based medicine to treat PUD looks at it, and the second part also by a medical doctor who uses an integrated approach in medicine to much better improve the therapeutic outcome in the management of PUD.

This is also to compare two different systems of medicine: one a more broad-spectrum, more holistic approach using natural and or a more integrated therapeutic modalities combined in the practice of medicine.

 https://www.tiktok.com/@natsolphc/video/7138152476045266219

There is also another video presentation by Dr. Peter Glidden sent to me by a medical colleague and friend of mine on conventional drug-based allopathic medicine.  

https://www.bitchute.com/video/e7JzINEL47ov/

However, I need to stress that all systems of medicine have their strengths and shortcomings. For instance, I need to emphasize that a lot of drugs used in emergency situations and for the management of acute and life-threatening diseases are absolutely necessary and lifesaving. For example about emergency drugs I wrote here published on Saturday, March 4, 2023.

https://scientificlogic.blogspot.com/search?q=emergency+drugs

Unfortunately drug-based conventional treatment for most chronic diseases, especially lifestyle diseases failed miserably with an integrated approach where the root causes need to be first addressed and the patient needs to be educated.

There are of course tens of hundreds of diseases that we need to discuss and write here, but this would run into dozens of volumes of textbooks on medicine, and alternative / complementary medicine each volume containing at least 1,500 pages. This is far, far beyond the scope of this article from the views of two MD doctors who would best write all of them separately. We will only reproduce two views, one using just solely drug-based approach, and the other using a more holistic and integrated approach on the management of peptic ulcer disease (PUD).

Part One: 

Petic Ulcer Disease. A Drug-based Approach: 

  

Petic ulcers disease (PUD) are mucosal defects in the in the gastroduodenal mucosa whose regenerative properties have been overcome by increased hydrochloric acid production or prostaglandin depletion by Non-Steroidal Anti-inflammatory Drugs (NSAIDs). Risk factors include cigarette use, alcoholism, NSAID use, familial history, gastric outlet obstruction, infection with Helicobacter pylori, CPD, hepatic cirrhosis, and renal failure.

Clinical features:

Peptic ulcer disease classically presents with burning epigastric pain 1 to 3 hours after meal, often awakening the patient at night. Although the patient may relate relief with food, more classical is relief with antacids or vomiting. Elderly patients or those using NSAIDs tend to have less pain associated with their ulcers. History may provide confirming clues, such as tobacco use, NSAIDs or alcohol consumption, or familial predisposition to ulcers.

A history of frequent vomiting, weight loss, early satiety, or nausea should suggest gastric outlet obstruction. Hemodynamic instability, hematemesis or melena all confirm hemorrhagic complications. Although bleeding is not common, perforation will usually present with severe pain or peritoneal signs.

 Diagnosis and Differential Diagnosis:

Typically, the diagnosis of peptic ulcer disorder is based on history and examination. The patient may have very mild epigastric tenderness. A succussion splash in the presence of excessive vomiting suggests gastric outlet obstruction. Directed laboratory work may confirm associated illness and can include blood cell count, creatinine, and calcium. Rectal examination and possible nasogastric aspiration may aid in diagnosing bleeding complications. in the presence of bleeding complications. In the presence of bleeding, one should consider clotting studies and, perhaps, liver function tests. A nasogastric tube may aid in the diagnosis of perforation by allowing the instillation of 250 ml air prior to an upright chest radiograph, specifically checking for air under the diaphragm. Definitive diagnosis of peptic ulcer disorder can only be made with an GI series using barium or by gastro endoscopy through direct vision, such tests can be reserved for patients with severe pain or bleeding. Serological tests for H. pylori and a serum gastrin may be useful in cases of persistent or recurrent peptic ulcer.

Many disorders can mimic peptic ulcers in pattern and location of pain. Pancreatitis is usually associated with worse pain and more commonly radiates to the back. With gastroesophageal reflux the patient may relate positional pain originating substernally.   Clues to biliary colic include a history of fatty food intolerance rather than pain with food in middle-aged obese females. The most serious diagnosis confused with peptic ulcer is myocardial ischemia or infarction, which should be considered in any patient over 40 or with cardiac risk factors.

Conventinal Management:

Treatment is primarily done on an outpatient basis unless complications exist.

1. Pain can be relieved with liquid antacids such as aluminum hydroxide gel, 30 – 60 ml to be continued 1 hour and 3 hours after each meal, and at bedtime.
2. Peptic ulcers are most conveniently treated with H₂ receptor antagonists such as cimetidine, 300 mg IV or 400 mg po bid, ranitidine, 50 mg IV or 150 mg po bid; famotidine, 20 mg IV or 40 mg po qhs (; and nizatidine, 150 to 300 mg po qhs. More recently the use of proton pump inhibitors such as Omeprazole, Esomeprazole (Nexium) is indicated for persistent peptic ulcers. This works by blocking an enzyme called H+/K+ ATPase to inhibit the production of acid in the stomach. Sucralfate and misoprostol are secondary drugs that may be considered.
3. Dietary modification should be the mainstay of the treatment.

 with the avoidance of caffeine, alcohol, and NSAIDs.

 Patients who demonstrate any complication of peptic ulcer disorders should be stabilized and admitted to a hospital. For haemorrhage, this includes intravenous fluids (RL or NS) with packed red blood cells (PRBC’s) and fresh frozen plasma (FFP) as clinically indicated. Gastric lavage with room temperature water will help assess extent of bleeding and prepare the patient for both diagnostic and therapeutic gastro-endoscopy. Perforation requires nasogastric suction, broad-spectrum antibiotics, KIV surgical intervention. Pyloric stenosis requires correction of fluid and electrolyte abnormalities, with referral for surgical management.

Part Two: 

An Integrative Medical Approach for PUD: Nutrition and Other Therapeutic Modalities : 

Pathophysiology:

PUD is one of the most common diseases clinicians see regularly. Many of them are undiagnosed. PUD is caused by disturbances in the gastrointestinal mucosa. These disturbances are due to the loss of protective elements and / or damaging insults that result in mucosal erosions, most commonly located in the duodenum or stomach. People with PUD commonly complain of epigastric pain particularly a few hours after meals, bloating, nausea, early satiety, altered bowel habits and heartburns.

Pain is usually improved with food or antacids. PUD may also occur without symptoms, particularly in older adults. Peptic ulcers may cause GI bleeding, which is a potentially life-threatening emergency necessitating urgent endoscopy and intensive care unit consideration. Ulcers may rarely perforate leading to intense pain and acute peritonitis, which is a surgical emergency. Patients with significant weight loss and PUD symptoms should undergo endoscopy to investigate potential malignant diseases.

The loss of gastrointestinal mucosal integrity is typically multifactorial, with diminished protective elements predominantly decreased acid buffering, reduced immune system functioning, and slowed wound healing. And insults primarily Helicobacter pylori infection, the use of nonsteroidal anti-inflammatory drugs (NSAIDs), increased acidity, and inflammation. Treatment efforts are focussed on restoring protective factors and reducing harmful affronts.

 Peptic ulcers may occur at any time in life, although the incidence gradually increases with age. In the early twentieth century, PUD was diagnosed in men at twice the rate as in women. However, PUD is now nearly equally distributed between genders, although gastric ulcers tend to be more common in women and duodenal ulcers more common in men.

 Historically, investigators were aware that smoking, stress, use of NSAIDs, caffeine, and family history increases risk three times with an afflicted first-degree relative contributing to peptic ulcer formation. However, prior to the late 1970s, allopathic medicine (as already discussed above) had limited success in treating PUD until the arrival of two revolutionary developments: the intervention of pharmaceuticals that reduced the amounts of acids the stomach produced such as the use of proton pump inhibitors (PPIs) like Omeprazole / Esomeprazole (Nexium) as already discussed above, and the discovery of the Heliobacter pylori bacterium.

 The development of gastric acid-suppressing medications, with the advent of histamine-2 receptors antagonists (H₂ blockers) in the late 1970s and proton pump inhibitors in the 1980s heralded a new chapter in conventional allopathic treatment of PUD. Previous efforts had focussed on reducing risk factors, administering acid buffers such as calcium carbonate for symptom relief, and surgery associated with significant morbidity and mortality. With the invention and administration of acid-reducing medication, the majority of the cases of PUD are quickly attenuated. The approach has drastically reduced the need of surgery and the increased the role of pharmaceuticals in PUD therapy.

 H. pylori was identified in 1982, a discovery for which Dr J. Robin Warren and Dr Barry J. Marshell won the Nobel Prize for medicine in 2005. The more the medical world learns about this unique bacterium, the more our thinking about PUD treatment evolves. H. pylori infection has been shown to increase the incidence of PUD by at least four-fold. Rates of H. pylori infection vary worldwide according to age and economic status. Younger, more affluent individuals have rates as low as 20 %, whereas up to 60 % of all individuals in the developing world, and 50 % of individuals older than 60 years are colonized by this bacterium. Living in harsh acidic environment of the human stomach, H. pylori appears to increase the risk of PUD by directly damaging the protective mucus lining of the GI tract and allowing for increased acidic damage. H. pylori also triggers an immune response that causes damaging inflammation. Besides PUD, H. pylori has been linked to increased rates of gastric cancer, dyspepsia, vitamin B₁₂ deficiency, iron deficiency, and idiopathic thrombocytopenia (ITP). H. pylori may not be without benefits, with some studies indicating a correlation between H. pylori colonization and decreased rates of asthma, allergies, gastroesophageal reflux disorder (GERD), obesity, and oesophageal cancer. Whether H. pylori is predominantly a symbiotic bacterium that has been with humanity for millions of years, occasionally running amok and causing PUD and stomach cancer, or strictly a pathogen that has an increasing niche in the modern world warranting global. The pending answer to this question will likely guide approaches to PUD treatment in the decades to come. 

 Although there have been promising H. pylori vaccines studies in animal models, indicating vaccines may eventually become the most powerful tool for treating PUD, successful clinical vaccine trials have yet to be reported. Even with a potential vaccine, complete global eradication of H. pylori is logistically challenging, despite H. pylori exclusively residing in humans, because there are currently an estimated 5 billion people infected worldwide.  Further, only 10 % to 20 % of H. pylori-infected

 Individuals develop PUD. Thus, current treatment screening of asymptomatic individuals for H. pylori is not advised. H. pylori and NSAIDs, in combination with other risk factors, account for the majority of the cases of PUD. The remaining cases are attributable to other independent risk factors and a few clinical “zebras”, such as Zollinger-Ellison tumours, carcinoid syndrome, other drugs, radiation, cytomegalovirus, and systemic mastocytosis.

 Pharmaceutical acid suppression, the discovery and subsequent antibiotic treatment of H. pylori, resulted in optimism that PUD was on the verge of elimination at the end of the 21^st century. However, due to increasing antibiotic resistance, increasing knowledge of the harm of long-term pharmaceutical acid suppression, in addition to evidence of the potential benefits of H. pylori infection, there is now a requirement for more judicious use of antibiotics and the incorporation of more integrative approaches to PUD management in the years and decades ahead.

Diagnosis:

The overlapping constellation of PUD symptoms with other diseases, such as gastritis, irritable bowel syndrome, gastroesophageal reflux disease, Crohn’s disease, pancreatitis, gallstones, and malignancy, makes the initial diagnosis of PUD challenging, particularly because endoscopy which is invasive and expensive for current standard diagnostic testing. The next best tool is the barium GI series that has radiation risk, cost and potential inaccuracy. A study reported that the physical examination finding of epigastric tenderness decreases the likelihood of PUD. Thus, it is not surprising that many clinicians, and patients without signs of serious disease such as bleeding or weight loss, hesitate in electing to pursue these invasive diagnostic measures. Accordingly, the majority of PUD may never be diagnosed with certainty. H. pylori testing in symptomatic patients increases the number of people diagnosed with H. pylori infection, but a positive test result indicates only a bacterial infection and cannot differentiate between conditions such as gastritis and more serious PUD. although initial management is largely the same. There are various tests for H. pylori, but the stool antigen and urea breath tests are consistently the best for determining active infection.

Once a diagnosis of PUD is established, recurrence is reported in up to 74 % of patients. PUD management therefore focuses on the prevention and symptomatic treatment, a good fit for an integrative approach in medicine not just using pharmaceuticals.

 Dietary constituents were linked to PUD long before the discovery of H. pylori infection. Accordingly, nutrition is considered a key component of ulcer prevention and symptom management.

Meal timing influences PUD, with skipping breakfast and consuming large meals shortly before bedtime shown to increase the risk of PUD.

Fruits and vegetable intake reduces the risk of developing ulcers, with epidemiological studies demonstrating that a diet high in plant-based fiber and vitamin A, especially carrots, spinach, mango, sweet potatoes, and apricots helps protect against PUD. Flavonoids, compounds found throughout the plant kingdom have been found to be protective against H. pylori infection and are present in concentrated amounts in citrus, berries, onions, parsley, green tea, red wine, and dark chocolate. Sulforaphanes, which are phytochemicals found in vegetables such as brussels sprouts, broccoli, cabbage, cauliflower, bok choy, turnips, and radishes, are also protective against H. pylori infection.

Studies have specifically shown that virgin olive oil (30 g daily for 2 weeks) or broccoli (70 g a day for 8 weeks) have the ability to decrease and potentially eliminate H. pylori. Foods containing capsaicin (chili) have been shown to be protective against ulcers. Other common foods demonstrating protective effects against P. pylori include banana, honey, garlic, ginger, okra, pomegranate, and apple. There is likely a synergy in consuming combinations of these beneficial foods as ‘let food be thy medicine’.

However, milk increases PUD risk, likely due to the increased stimulation of acid production. However, fermented milk products such as yogurt, aged cheese, and sauerkraut that have probiotics have been demonstrated to have a protective action against H. pylori. Although there is no evidence that caffeine and coffee are risk factors for PUD, the evidence is lacking, although there are risk factors for reflux disease.

Physical Activity:

Numerous studies have shown that regular exercise and physical activities compared to sedentary lifestyles is more protective against PUD One study particularly showed that the risk of duodenal ulcers was 62 % less in men who cumulatively walked or ran more than 10 miles a week. Routine exercise should be recommended for almost all patients, especially those who have a previous history of PUD.

Stress Reduction:

The relationship between stress and PUD is a classic example of the need for clinicians to keep in mind the social determinants of health, over which our patients have varying degrees of control. Stress is largely a product of the social and environmental milieu, and convincing evidence indicates that stress plays a role in PUD. It is well known that people with stressful jobs such as directors, managers, executives, doctors among others are more prone to suffer from PUD than others. When the discovery of H. pylori linked to PUD was discovered they dismissed stress as one of the causes by putting this bacterium solely to be blamed. However, immunologists know that stress compromises the immune system by allowing the H. pylori and other infectious agents to take hold. The connection between stress and PUD is established early in life. Childhood stress in the form of traumatic events, such as an illness or death in a family, financial strains, or family conflict and relationship is shown to be associated with nearly 50 % higher rates of PUD in adulthood. Studies have also shown that the GI ulceration increases with both chronic stress and in times of acute stress, such as during an earthquake or war. A multipronged approach to stress reduction, in comparison with any single method, appears to provide more protection against PUD. As a clinician, recommending individually tailored stress reduction programmes, including yoga, tai chi, meditation and other coordinated movements inclusive of focussed breathing and any other culturally applicable relation techniques will likely be beneficial.

Sleep:

Inadequate sleep is a risk factor for PUD, likely the result of increased stress levels causing immune dysfunction and impaired lifestyle decisions. Maintaining good sleep hygiene is an important component of ulcer avoidance.

Cigarette Smoking:

Smoking increases rates of PUD up to four times when compared with non-smokers, likely due to decreased wound healing. According, smoking cessation is essential in addressing PUD.

Alcohol Avoidance or in Moderation:

Alcohol in large amounts has also been shown to be linked to PUD, probably due to mucosal damage. One epidemiological study showed that those who consumed more than 42 drinks per week had a greater than four-fold increase in the incidence of bleeding ulcers compared to those who consumed one or less than one drink per week. However red wine was reported to be protective against H. pylori infection possibly due to the presence of bioactive substances such as flavonoids. Avoidance of alcohol especially in high doses and in frequency is prudent for those with a history of PUD or its symptoms whereas a moderate consumption of red wine may be useful.

Nonsteroidal Anti-Inflammatory Drugs:

There is evidence that the use of NSAIDs increases the risk of PUD by up to 5 times and the risk of bleeding ulcers associated with conformed PUD up to five times also. NSAIDs inhibits prostaglandin production, and such an event compromises the protective muco-protective coats in the GI tract. However, there is evidence that medications such as sucralfate or misoprostol together with NSAIDs can relieve the symptoms of PUD and prevent its recurrence NSAIDs should be avoided as much as possible in patients with PUD or with patients with a history of PUD. However more than 80 % of patients on NSAIDs never develop PUD and may not be necessarily harmful to those with asymptomatic PUD or with a history of peptic ulcers. 

Nutritional Supplements:

Certain useful microorganisms have been shown to be useful in the management of PUD. The use of probiotics for instance, has been shown to decrease the recurrence of peptic ulcers. There is a straight-line correlation between higher intake of probiotics and lower incidences of H. pylori infection. Its mechanism is unclear, probably due to increased GI mucus production, competition for mucosal binding sites as bacterial competitors and the production of compounds unsuitable for H. pylori. Results of studies in animal models showed probiotics decrease the inflammatory response to H. pylori. The majority of the studies were conducted using Lactobacillus strains commonly found in yoghurt but other strains of probiotics are also useful. We believe that the incorporation of yogurt and other probiotic rich foods regularly into the diet may be useful in PUD prevention and its recurrence. Many clinical studies have confirmed that probiotics like Lactobacillus and Saccharomyces boulardii have synergy with antibiotic therapy for H. pylori eradication and can decrease antibiotic-related side effects such as diarrhoea, bloating nausea and abdominal pains. There are some evidences showing probiotics alone with antibiotics can improve PUD symptoms and perhaps suppress or eradicate H. pylori infection

Vitamin C:

Vitamin C or ascorbic acid has also been shown to have an effect on the eradication of H. pylori. There is one study demonstrating a 10 % eradication rate with 2 weeks daily dose of 1000 mg of vitamin C. Additionally, vitamin C enhances the effect of antibiotics regimens against H. pylori eradication. This has been shown in at least two studies. There was a 5-year Japanese study demonstrating lower rates of PUD in groups taking vitamin C supplementation. A constant intake of dietary intake of vitamin C is recommended for individuals with symptoms of PUD, a previous history or family history of PUD, or other risk factors associated with PUD,

Zinc:

A clinical trial has reported zinc accelerates the healing of peptic ulcers up to three times compared to placebo groups. This observation was strengthened in animal model studies. The role of zinc may be due to its ability to enhance tissue repair. Zinc supplementation has been used in Europe and East Asia among other countries for PUD and was found to be effective in numerous other studies.

There are also many other nutrients and nutritional adjuncts such as polyunsaturated fatty acids, glutamine, as well as botanical medicines such as Curcuma longa (turmeric), De glycyrrhizinate  Liquorice  (Glycyrrhiza glabra), mastic (Pistacia lentiscus), cabbage (Brassica oleracea), chili (Capsaicin), cranberry (Vaccinium  oxycoccos), neem (Azadirachta indica) and hundreds of other botanical medicines among them just to name a few more like peppermint, wormwood, cinnamon, chamomile, gingko, nutmeg, hops, sage, green tea, red ginseng. Aloe, fenugreek, and mugwort among many, many more far too long to list them here, let alone discuss their scientific studies, mode of action in phytotherapy (pharmacognosy) and their therapeutic role in the prevention and relief of symptoms of peptic ulcer disease.  

Conventional approaches use acid-suppressing drugs, antacids, sucralfate.

Others: 

Other alternative / complementary medicine against PUD includes acupuncture, massage, Traditional Chinese Medicine and osteopathy.

All studies and references quoted above, please refer online to:

ExpertConsult.com