Atmospheric Pollution and Toxicological Aspects of Helicobacter pylori Infection: Background, Pathophysiology and New Innovative Hypotheses

Abstract

A strange phenomenon characterized by numerous pathologies occurred in DR Congo and in some other countries of Subsaharian Africa since a few decades. While the entire population is convinced of massive poisonings provoked by a ritual poison from the eastern Africa, named Karuho, we incredibly established, since 2010, the responsibility of Helicobacter pylori in the phenomenon, thanks to cross-sectional epidemiological studies. Our findings have been published in international journals and presented in international scientific forums. The purpose of this chapter is to describe the background and conduct of this research, the pathophysiology of the Helicobacter pylori involvement, as well as the new innovative hypotheses on Helicobacter infection generated by this research.

1. Introduction

Discovered in 1875 by German researchers and discovered again in 1982 by two Australian researchers, J. Robin Warren and Barry J. Marshall, Helicobacter pylori remains in the human stomach, despite the high acidity of this medium. Its discovery in the stomach, along with the announcement of its role in gastritis, gastric ulcer and stomach cancer by J. Robin Warren and Barry J. Marshall, caused great controversy worldwide for more than two decades. Since 2005, when the two Australian researchers won the Nobel Prize, the controversy has stopped as the two researchers’ findings have been fully confirmed by other researchers around the world [1, 2, 3, 4].

It is now known that Helicobacter pylori tolerates little oxygen, and releases carbon dioxide and ammonia gas into the stomach but is normally unable to cause poisoning because the gases, after their release, become liquid, which prevents them from crossing the digestive barrier. Proton Pump Inhibitors (PPIs) are crucial in the therapy of this infection since the symptoms are primarily digestive [5, 6].

The present research undertaken in the Democratic Republic of Congo since 1990 has established that, contrary to what is reported in the literature, infection with Helicobacter pylori can well cause intoxication. Indeed, the carbon dioxide and ammonia it generates in the stomach, can well, under certain circumstances, pass into the blood and produce numerous extradigestive pathologies.

2. Background

2.1 Research design

The research was not designed to study Helicobacter pylori infection but to deal with suspicions of massive poisoning that appeared in DR Congo in the early 1980s, almost at the same time as HIV, first in northeastern DR Congo, mainly in Goma and Bukavu, before gradually spreading throughout the country, including the city of Kinshasa. The poison concerned would be a mythical and ritual poison from the east of the country and even from East Africa, extremely virulent, called Karuho poison. Its nature and its symptoms were unknown. Any foreigner traveling to the east of the country, mainly, to Goma and Bukavu, had to develop the unusual symptoms attributed to this unknown mythical poison. The patients were cared for only by traditional healers and self-proclaimed toxicologists, presenting themselves as the only specialists in this poison, since this phenomenon was unknown in the hospital [7, 8, 9].

The traditional diagnosis of poisoning, carried out on saliva, is very rudimentary. Early in the morning, the supposedly poisoned person spits into a glass of water after scraping his throat. In the event of a positive test, saliva flows to the bottom of the glass. The treatment is based on honey and various plant extracts, including strong laxatives. The results are more or less good. As the Karuho phenomenon was unknown in hospitals and following the failures of traditional healers’ treatments, people suspecting poisoning began to come to the Toxicology Department of the University of Kinshasa to meet the toxicologist. The flow of patients continues until today. The Toxicology Laboratory of the University of Kinshasa is practically the only operational toxicological laboratory in DR Congo, since 1974, although poorly equipped.

Suspicions of poisoning arouse a strong fear of immediate death, everywhere across the country in all walks of life: family, professional, school, academic, political and even religious. This phenomenon increases the country’s already very heavy economic and health burdens through the burden of communicable and nutritional diseases. They lead to dissension in the population, allow charlatans to manipulate the population, reduce the population’s confidence in the national health system, oppose the population to the political authorities and increase the East-West geopolitical divide in the country.

It was necessary to start research, first to understand what was really happening and then to try to find a valid scientific response to secure the population. The flow of patients, which was initially low, has increased over time so that today, not a day goes by without new cases coming from all over the country, sometimes even from outside the country.

2.2 General objective

The general objective of this research was to study the phenomenon of poisoning in the Democratic Republic of Congo and some other countries in sub-Saharan Africa.

2.3 Specific objectives

The specific objectives were to: assess the extent of the problem, determine the target population, determine the profile of patients, identify symptoms, establish the route of patients until their arrival at the Toxicology Department, evaluate traditional and modern means of control, study the possible influence of HIV, investigate the factors involved, generate hypotheses on the real identity of the Karuho phenomenon and propose appropriate solutions.

2.4 Methodology

2.4.1 Study population

The study population included all patients who, as mentioned above, have been coming to the Toxicology Department of the University of Kinshasa since 1990, for better care.

2.4.2 Study site

The headquarters of the study was the Toxicology Department of the University of Kinshasa. The analysis of biological parameters was carried out at the Biochemistry Laboratory of the Faculty of Pharmaceutical Sciences of the University of Kinshasa. Medical examinations were carried out in specialized laboratories of hospitals, when the patients’ pockets allowed it.

2.4.3 Methods

2.4.3.1 Data collection

Data collection was done by means of a questionnaire. However, listening to patients was a golden rule because it was essential to use patients as partners in this research.

2.4.3.2 Study variables

The variables of interest were: age, sex, marital status, education, province or country of origin, residence, nature and circumstances of onset of symptoms, medical itinerary before arrival at the Toxicology Department, testing, diagnosis and traditional treatments, test, diagnosis and modern treatments, medical history, chronic diseases: diabetes, hypertension, gastralgia and others, opinion on “poisonings”, opinion on the poison Karuho: origin, nature, mechanism of action, psychological state of the patient and the family members, who referred them to the Toxicology Department, common food: (meat, fish, chicken, vegetables, fruits and dairy products (milk, curd, cheese, yogurt, beans, …), common drinks: (water, sparkling water, alcohol (beer, wine and liquors), sugary soft drinks, non-alcoholic beer, traditional drinks and natural fruit juice.

2.4.3.3 Toxicological screening

The toxicological screening was conducted according to the “Basic Analytical Toxicology” of R.J. Flanagan et al., published in 2003 by the World Health Organization, in collaboration with the United Nations Environment Programme and the International Labour Organization, which offers researchers in developing countries simple analytical techniques but highly effective, able to solve complex toxicological problems with reduced material and financial resources. Thus, toxicological screening was carried out by urine tests, thin-layer chromatography on mini-plates and ultraviolet spectrophotometry [10, 11].

2.4.3.4 Biological parameters

The biological parameters examined were: haemoglobin, white-blood cell formula, fasting blood glucose, sedimentation rate, alanine aminotransferase, aspartate aminotransferase, urea, creatinine, thick gout, dimers, typhoid fever and Helicobacter pylori.

2.4.3.5 Medical examinations

The medical examinations were as follows: electrocardiogram, cardiac ultrasound, abdominal ultrasound, renal ecography, electroencephalogram, spirometer and CT scanner.

2.4.3.6 Data interpretation

In accordance with the literature, data interpretation used toxicoepidemiology. The world toxicological history informs that the Congolese are not the only ones or the first to face an unknown danger, exciting their imagination. Indeed, leprosy was considered a curse, the intoxication of Minamata Bay as a bad fate and for the Fire of Saint Anthony, the sick were accused of witchcraft. Toxicology also indicates that epidemiology has been the appropriate weapon for solving toxicological puzzles, including that of toxic cancer [12, 13, 14, 15, 16, 17, 18, 19].

This is why our research used toxicoepidemiology in the face of imaginary poisonings in DR Congo. It was supplemented by induction inference, allowing to go from the particular to the general, as well as by Mill’s criteria, to identify the causes of pathologies, and explain their distribution within the population and Bloom’s taxonomy, a tool of pedagogy by objective which, by a logical deduction, makes it possible to create new knowledge from a first simple knowledge [20, 21].

2.5 Results

The toxicological screening was negative for most of the patients. Table 1 shows that of the 1572 patients who were examined, 1430 (90.7%) were negative. The 142 (9.3%) patients who tested positive were for the paracetamol that these patients were taking to combat stomach pain. Helicobacter pylori was positive in all patients with a score of 100%. Iron deficiency anemia was identified in 95 (6%) patients. The liver parameters aspartate-amino-transferase (ASAT) as well as alanine-amino-transferase (ALAT) were normal in most cases, 1382 (87.8%) and 1387 (88.1%) respectively. Most cases of abnormal ASAT and ALAT were due to the presence of excess paracetamol. Urinary parameters, creatinine and urea were also normal in most cases, i.e. 1496 (95%) for creatinine and 1512 (96%) for urea. The disruption of renal parameters most often came from the uncontrolled treatments that patients received during their visit to traditional practitioners before their arrival at the Toxicology Department.

Variables	Patients	Percentages
Population of study
Unmarried	377	24
Married	1084	69
Formerly married	110	7
Total	1572	100
Age
0–5	12	0.8
6–20	217	13.8
21–50	1183	75.2
More than 50	160	10.2
Total	1572	100
Gender
Male	1038	66
Female	534	33.9
Residence
Kinshasa	1037	66
Other provinces	487	31
Other countries	48	3
Total	1572	100
Education
No education	172	11
Primary	188	12
High	408	26
Higher	801	51
Total	1572	100
Patients progression from 2005 to 2023
2005–2016	402	25.5
2017	186	11.8
2018	220	13.9
2019	245	15.5
2020–2021	53	3.3
2022	124	7.8
2023	342	21.7
Total	1572	100
Toxicological screening
Negative	1430	90.7
Positive	142	9.3
Helicobacter pylori
Positive	1575	100
Negative	0	0
Hemoglobin
Normal	1477	94
Anormal	95	6
Aspartate aminotransferase (ASAT)
Normal	1382	87.8
Anormal	193	12.2
Alanine aminotransferase (ALAT)
Normal	1387	88.1
Anormal	188	11.9
Creatinin
Normal	1496	95
Anormal	79	5
Urea
Normal	1512	96
Anormal	63	4

Table 1.

Results of variables of interest.

Comments: The study was carried out from July 2005 to May 2023 on a total number of 1572 patients distributed as follows: 347 (24%) single, 1084 (92%) married and 110 (7%) widowed. The age of the majority of respondents ranges from 21 to 50 years, with 1183 (75.2%) sick. There were 12 (0.8%) children aged under 5 years. There were more men: 1038 (66%) compared to 534 (34%) women. While at the beginning, the patients only came from the North-East of the country, mainly from the city of Goma, the city of Kinshasa, the most populous province of DR Congo, took the lead with 1037 (66%) sick. A total of 48 (3%) patients came from abroad, from Cameroon and the Republic of Congo. In terms of education, academics come first with 801 (51%) sick people. The number of patients was low at the beginning with an average rate of 33 (2.05%) patients per year during the first 12 years. Then it started to increase: 186 (11.8%) in 2017, 220 (13.9%) in 2018 and 245 (15.5%) in 2019. In 2020 and 2021 the number fell to 53 (3.3%) for both years due to COVID-19 infection. It then increased to 124 (7.8%) patients in 2022 and 342 (21.7%) patients in 2023, until May.

2.6 Helicobacter pylori role

It was in 2010 that the unexpected discovery of Helicobacter pylori as the cause of suspected poisoning in DR Congo was established. It all started with a young doctor from a public company in the city of Kinshasa who recommended a patient suspected of poisoning, presenting the same many and singular symptoms as the others who came to the Toxicology Department. However, this patient also had recurrent iron deficiency anemia requiring repeated blood transfusions. The young doctor who had been our toxicology student at the Faculty of Medicine of the University of Kinshasa thought that the patient could be poisoned with lead.

Lead, is indeed a very dangerous toxic of the group of heavy metals or metal trace elements, which can cause recurrent iron deficiency anemia in humans. Indeed, it inhibits the enzyme “ALAD” (deltaminolevulinic acid), which allows the conversion of porphyrin into hemoglobin, which leads to the accumulation of porphyrins in the blood. It also opposes the incorporation of iron at the level of protoporphyrin and weakens red blood cells, thus shortening their average lifespan [22, 23, 24].

Fortunately, like some other cumulative toxicants, lead poisoning already manifests itself during the preclinical phase, by three very early warning signs of poisoning. These are Burton’s line, black stool staining and accumulation of coproporphyrin in urine. The patient did not have Burton’s line, which is a simple but significant gray line visible at the base of the gums, attesting to the deposit of dental lead. His stools were not black either. In addition, analyses of urinary coproporphyrin and lead were carried out with a visible spectrophotometer using the Schwartz method, Zieve and Watson for coproporphyrin and analysis at the wavelength of 515 nm, after complexation with dithizone in chloroform for lead, also gave negative results [25, 26, 27].

Fortunately, the literature on Helicobacter pylori reminded us that, since 1993, Helicobacter pylori had been implicated in several cases of unexplained iron deficiency anemia. It seemed useful to us at any chance to explore this new path after that of lead [28, 29, 30, 31].

2.7 Acceptance into international conferences

Very quickly, this new track, which seemed very uncredible at first, turned out to be the right one, as evidenced by our results, which were accepted in international journals and validated in several of the following international forums:

• “9th International Symposium on Recent Advances in Environmental Health Research, Jackson State University, USA”. Poster presentation: “Helicobacter pylori responsible of poisoning suspicion in the democratic republic of Congo: about 56 cases”.

• 2016, “3rd Euro-Global Experts Meeting on Medical Case Reports (Euro Case Reports 2016), June 30-July 2, Valencia, Spain”. Oral presentation:

  “Surprising unknown H. pylori epidemic in the Democratic Republic of the Congo”.

• 2017, “5th European Conference on Clinical and Medical Case reports, September 7-8, 2017, Paris, France”. One oral and three following poster presentations:

Oral presentation: “Meanders of an atypical research work on Helicobacter pylori in the Democratic Republic of the Congo: influence of HIV and other factors and study of some interesting cases”.

Tree poster presentations:

“Profile of Helicobacter pylori patients received at the laboratory of Toxicology of the University of Kinshasa from July 2016 to July 2017”.

“Opinion of population of Kinshasa City on Helicobacter pylori phenomenon responsible of numerous extra-digestive pathologies in DR Congo”.

“About the management of Helicobacter pylori infection expressing numerous extra-digestive pathologies in DR Congo”.

• 2017, “7th International Conference on Predictive, Preventive and Personalized Medicine & Molecular Diagnostics, September 14-15, 2017, Edinburgh, Scotland”.

  E-Poster presentation: “Helicobacter pylori digestive and extra-digestive pathologies collected in the Democratic Republic of the Congo”.

• 2018, “Joint Pharmaceutical conference Democratic Republic of Congo Kinshasa and Republic of Congo Brazzaville, at Pointe Noire city”: Oral Presentation: “Karuho poison and Helicobacter pylori: Two features, One issue, One solution”.

• 2018, “Joint Event on International Conference on Pharmaceutics and Novel Drug Delivery Systems & 19th International Conference on Cellular and Molecular Medicine & 19th Annual Congress on Psychiatry and Psychiatric Disorders, held in Narita, Japan”.

“Toxicological aspects of Helicobacter pylori infection established in Democratic Republic of the Congo consecutively to massive poisoning suspicions all over the country”.

• 2018, “7th International Conference on Predictive, Preventive and Personalized Medicine & Molecular Diagnostics October 26-27, 2018, Boston, USA”. Oral presentation: “Successful toxicological Helicobacter pylori infection treatment conducted in a male Congolese patient with severe hemoglobin deficiency in the Democratic Republic of the Congo”.

• 2019, “ 2nd world congress and expo on Toxicology and Pharmacology” , October 28-29, Rome, Italy.

  Oral presentation: “Unexpcted interesting Toxicological trends in Helicobacter pylori infection in Democratic Republic of Congo, A case report” .

• 2019, “2nd world Congress an Expo on Dentistry and Oral Health”, October 30-31, 2019, Rome, Italy”.

  Oral presentation: “Impact of Helicobacter pylori intoxication in Throat, Mouth, Eyes and Face Skin Health in the Democratic Republic of Congo”.

2.8 Digestive and extra-digestive symptoms collected from patients

Several symptoms have been observed during the study. These symptoms collected from patients are presented in Table 2.

Digestive symptoms	General symptoms	Nervous symptoms
Heat in the stomach that can radiate to the chest Strong abdominal pain Belly buzzing Dry throat Burning of the tongue Dry lips Taste of chili on the lips Bitter or bland taste of food and drink Hyper-salivation Nausea Vomiting Regurgitation Hiccups Bloody sputum Constipation Belly bloating Increased pH and viscosity of saliva: saliva becomes alkaline and sticky Sensation of something in the throat	Pronounced weight loss Strong heat in other parts of the body, even on the feet Hyperthermia Heavy sweating Tingling and tingling Skin blackening and signs of early aging General fatigue Sexual weakness Heart palpitations Choking and shortness of breath Difficult breathing Hormonal disorders Anemia Skin allergies Swelling of the feet Dry cough Lack of appetite Oxygen desaturation Deposition of ammonium carbonate in the lungs	Dizziness and feeling high Imbalance Frequent and throbbing headaches Sensation of something moving in the head Blurred vision Ringing in the ears Intermittent tremors of legs and hands Memory disturbance with frequent forgetfulness Mental confusion Strong desire to sleep with sometimes loss of consciousness, mental confusion and temporary amnesia Visual hallucinations Electroencephalogram disruption Tingling and tickling Frequent insomnia

Table 2.

Symptoms collected from patients.

Comments: The most common symptoms are constipation, weight loss, loss of appetite, stomach pain and bloating. Then comes gas in the stomach, heat that can spread throughout the body, heavy sweating, heart palpitations, dry mouth and throat, dry cough, sputum, burning of the tongue, small sores in the mouth, bland, spicy or bitter taste, stuffy or runny nose, ear pain, blurred vision and darkening of the skin. Dizziness, headache, insomnia, memory disturbance, asthenia, sexual weakness, back pain, pain, heat or swelling of the legs, itching, cramps in the feet and hands, disturbance of menstruation and itching of the private parts in women. Difficulty breathing, shortness of breath, premature aging, dehydration, hypovolemia, allergy, seizures, headaches, fever, coma and death. Abundant nausea and vomiting which can also lead to death.

3. Pathophysiology

3.1 Description

Helicobacter pylori appears to be under the control of blood pH which modulates the acid-base balance of the body. When the pH of the blood is normal, the amount of acid in the stomach is normal too. Helicobacter pylori stays then in the gastric mucosa, protected by gastric mucus, for as long as necessary, without ever harming its host.

When the pH of the blood increases, gastric acidity decreases as a result of the action of bicarbonate. This occurs when the body is in a state of chronic respiratory acidosis or compensated respiratory acidosis. Respiratory acidosis is a primitive increase in the amount of carbon dioxide in the blood. When bicarbonate increases to compensate for this excess carbon dioxide, it is called chronic respiratory acidosis or compensated respiratory acidosis.

Blood pH is normally low but can also be close to normal. Helicobacter takes advantage of this situation of chronic acidosis to consolidate its position in the gastric mucosa by attaching more firmly to the epithelial cells of the gastric mucosa and activating certain virulence genes such as cagA and vacA that govern stomach inflammation and cancer genesis. It also secretes cytotoxins and mucolytic enzymes that can damage gastric epithelial cells and promote pathogenesis. Aggression of the mucus barrier can lead to gastritis, peptic ulcer, gastric cancer or gastric lymphoma.

When, on the other hand, the pH of the blood decreases, which happens especially in this case, where there is sudden inhalation of atmospheric air rich in carbon dioxide, gastric acidity increases. There is acute respiratory acidosis. Respiratory acidosis is acute when the increase in carbon dioxide is not accompanied by a concomitant increase in bicarbonate, compensating for the excess carbon dioxide. Helicobacter pylori faces excess gastric acidity. In this case, it naturally uses its urease enzyme to produce carbon dioxide and ammonia that can protect it from this excess acidity [32, 33, 34].

Normally, after their production, both gases are eliminated in the stool in liquid form. But, in case of respiratory acidosis that leads to acidification of the intestinal environment, modifying the bacterial flora and disrupting digestion, strong constipation occurs in patients. Constipation can also be a side effect of respiratory acidosis, as excess carbon dioxide can reduce intestinal peristalsis and promote stool retention. Following this constipation, gas accumulates in the stomach and intestines. There is bloating and appetite is disturbed, leading to weight loss. The pressure of bloating causes gases to rise along the oesophagus with strong heat that burns the throat, mouth, nose, ears, brain and lungs. Once in the lungs, carbon dioxide and ammonia gas generate another highly caustic toxicant, ammonium carbonate, before passing into the blood through the pulmonary alveoli. Ammonium carbonate causes dry cough, sputum, chest heaviness and heart palpitations. All these symptoms are felt by our patients. Ammonium carbonate could also cause pulmonary fibrosis and, even, lung cancer. Ammonia is a very violent gas that can cause obstruction of the upper pulmonary tract and even pulmonary oedema. It can also solubilize in mucosal water to form ammonium hydroxide, a very strong and very caustic base and hydroxyl ions in an exothermic reaction, releasing a strong heat that patients can hardly tolerate [35, 36, 37, 38, 39].

There is thus first environmental poisoning, by nasal inhalation of atmospheric carbon dioxide, leading to acute respiratory acidosis. To this first poisoning is added a second one, caused by ammonia and carbon gases produced by Helicobacter pylori in the stomach. Both gases also reach the lungs but, through the larynx and not through the nose. This is a special internal inhalation poisoning. Similar intoxication, by internal inhalation, is described in the literature. It concerns in particular ruminant bovains fed, at the end of the 70s, with large quantities of urea. This bovine poisoning lends credence to our discovery of Helicobacter pylori poisoning, as both involve the urease enzyme, producing carbon dioxide and ammonia from urea, reaching the lungs by internal inhalation [40, 41, 42, 43, 44, 45].

If carbon dioxide and ammonia are inhaled at the same time, the pH of the blood may vary depending on the concentration and duration of exposure to the gases. Carbon dioxide dissolves in the blood and forms carbonic acid, which lowers the pH of the blood (respiratory acidosis). Ammonia dissolves in water in the lining of the respiratory tract and increases the pH of the blood (respiratory alkalosis).

Both gases are very hot and, as said above, they burn the mucous membranes very strongly starting with the upper nasal and pulmonary mucous membranes, before extending to the mucous membranes of the other parts of the body. With regard to carbon dioxide, in 1986, the limnic eruption at Lake Nyos, Cameroon, in the English-speaking North-West region, allowed the world to discover the highly calorific properties of carbon dioxide. More than 1700 people died in this natural disaster but above all, most of the victims had deep burns that were observed for the first time and that were recognized as caused by carbon dioxide [46, 47, 48].

The consequence of this kind of internal boiler is heavy perspiration, especially during the night, when the patient is sleeping. This heavy perspiration has as a corollary, a strong dehydration that affects all parts of the body, among others: the skin, especially that of the face, all mucous membranes, especially oral and ones, blood volume (hypovolemia), saliva and darkening of the skin. If dehydration reaches the intracellular level, convulsions, headache, high fever, coma and death are noted [49, 50].

In this regard, here is the situation experienced by a patient for a year, from April 2019 to May 2020, commented by his daughter:

• Dad began his ordeal on April 7, 2019, with small convulsions, as if he were epileptic. The next day, a high fever appeared. The thermometer reached up to 39.40°C. Dad was committed to the hospital for a month and every day a high fever was present. He was sweating and shivering profusely. The traditional saliva test performed by a tradipratician smuggled into the hospital by the family came back positive. The family then took Dad out, claiming lack of means. The tradipratician followed us home. Two days after the traditional treatment began, Dad suddenly went into a coma. It took 4 days of intensive care in the hospital for Dad to come back to life. Sometime later, he flew to Europe for treatment. Here too, a surprise awaited him but still happier although really unexpected. Indeed, 3 weeks later, while the doctors were still doing their investigations, suddenly, the fever stopped on its own without any treatment. Dad was asked to remain at the doctors’ disposal until the fever resumed. He would have liked to do it but, another surprise, came to upset everything, the COVID-19 epidemic. In December 2019, Papa had to leave Europe in a hurry to return to Kinshasa. In January 2020, another surprise, this one unfortunate, emerged; the resumption of a fever, as strong as before his departure to Europe. Dad was committed to another hospital where he spent 4 months without the slightest relief! Eventually, he had to leave the hospital and was taken home with his fever. He could no longer stand up and eat. His weight loss had reached frightening proportions. A traditional healer was brought in once again. The traditional test turned out once again positive, while in the hospital it had been thought to attribute this fever to COVID-19. The treatment of the new tradipratician brought no relief either.

This case was very helpful. First, the fever was stopped by eliminating gas with strong adsorbents and laxatives and intensive oral rehydration. Secondly, it was then possible, thanks to Mill’s criteria, to establish the role of carbon dioxide and ammonia released by Helicobacter pylori in the stomach, in the phenomenon of suspected poisoning in DR Congo. On the other hand, it has been possible, still thanks to Mill’s criteria, to determine environmental pollution as the factor present in Kinshasa and managed in Europe, responsible for fever, and activating factor of Helicobacter pylori, as already described in our presentations at international conferences as well as in our publications. One of our publications even reported the results of an autopsy performed on one of our deceased patients which showed the swelling of the intestines and stomach, as well as the burning of the brain, lungs and feet by gas. The nature of these gases is beyond doubt since the signs of asphyxiation by carbon dioxide were clearly reported: blackened nails and toes, red eyes and self-bite of the tongue (Figures 1–6) [51].

Figure 1.

Gut distending photo Forensic Medicine Kinshasa.

Figure 2.

Stomach distending photo Forensic Medicine Institute/Kinshasa.

Figure 3.

Brain congestion photo Forensic Medicine Institute/Kinshasa.

Figure 4.

Right lung congestion photo Forensic Medicine Institute/Kinshasa.

Figure 5.

Fingers and toes cyanosis photo Forensic Medicine Institute/Kinshasa.

Figure 6.

Feet swelling photo Shafali/Kinshasa. Comments: Figures 1–6 are taken from one of our publications published in 2018. It reports the results of an autopsy carried out at the Institute of Forensic Medicine of the Kinshasa General Hospital, after a suspicious death of a patient known to have chronic gastritis to Helicobacter pylori. This autopsy showed various abnormalities as follows: swelling of the intestines, swelling of the stomach, cerebral congestion, congestion of the lungs, cyanosis of the lips, fingers and toes, biting of the tongue, pallor of the palms of the hands and pallor of the soles of the feet, cardiomegaly, red colouring of the eyes, nosebleeds, gastric bleeding and asphyxia by carbon dioxide. All these anomalies lend credibility to the double intoxication by carbon dioxide and ammonia presented in this chapter.

The severe dehydration and alkalinization of saliva by ammonia gas scientifically justify the traditional test of “poisoning” practiced by traditional healers on the saliva of patients.

In the throat, there is dryness and sputum that can be bloody [45]. Patients sometimes have a sensation of something in the throat, which makes breathing difficult, with shortness of breath and suffocation at night. The voice can become hoarse, so singing and, even speaking, becomes difficult. Sometimes the voice even goes out. In case of tooth decay, the tooth can sometimes break or crumble on its own, because of the heat excreted by the gases in the mouth.

The bitter taste of food and drink is common among sick people. This symptom is also related to the high heat of the gases in the mouth, which here burn the taste buds of the tongue. It is a reason for dissension among the population. Indeed, it would seem to be the proof of poisoning and also the indication of the poisoner. Here are a few examples.

• My cross began during a ceremony organized within our Church between our Pastor and the new Pastor who came to replace him, said Mr. Josué, a fervent member of one of the many revival churches in the city of Kinshasa. I let myself be trapped like a child. Indeed, I knew well that our Pastor did not love me; and that he considered me responsible for the strong reactions of the members of our community against him which resulted in his departure! He even attacked me in some of his sermons. Despite all this, I agreed to be served first and from the first bites I immediately felt a strong bitterness in my mouth, as if I had a quinine tablet in my mouth! I ran to spit everything in the toilet but it was too late.

• Last Saturday, says Mrs. Esperance, I went to visit a friend and she offered me food. Until then, everything was normal. But when it was time to drink water, I felt that it was very bitter. Afterwards, I felt that my tongue was burned as if I had drunk water that was too hot and yet it was not. My lips were also burning, as if chili pepper had been applied to them. That’s how mean people can be!

Flu, angina and colds are regular. The nose is often stuffy. Sinusitis is often diagnosed in many of these patients. Hot gases, as said above, spare no part of the body. Vision is often blurred even if the person wears medical glasses. And cases of double cataracts are common. The ears ring, hiss, become painful or even sometimes, sometimes hearing decreases.

Hot gases reach the brain and cause dizziness, headaches, insomnia, imbalance and even memory disturbance. This is observed by frequent forgetfulness even for young patients. Even worse, the person sometimes becomes unable to continue his sentence because he forgets the beginning and loses the thread of ideas. It takes a while for him sometimes to find himself or someone has to help him. Insomnia is often strong, as well as sometimes, visual hallucinations, loss of consciousness, mental confusion, vision and hearing disorders and intermittent tremors of the legs and hands! Some patients sometimes feel discomfort in the head, difficult to define. Some others sometimes even feel a kind of temporary madness. The electroencephalogram is often disturbed.

Fatigue is almost permanent. There is drowsiness during the day. There is also strong sexual weakness in both men and women. Sexual strength and desire decrease. Some women become frigid. Sexual weakness leads to discord in homes and sometimes even leads to divorce.

Fatigue is caused by the attack of gases on the brain combined with oxygen desaturation which is common in almost all patients, and which also explains the sexual weakness that occurs even in young people still in their twenties. Lack of oxygen also leads to metabolic acidosis. The organic acids generated participate in the melting of muscles and the development of cramps in the hands and feet.

There is also itching, swelling of the legs, tingling in the legs and arms, heat or pain under the soles of the feet, allergies, hypertension and diabetic crises. Finally, there are signs of early aging: the skin darkens, the face becomes dry and wrinkled, the gait is hesitant, the hands or fingers sometimes tremble and there is an imbalance when walking or even when you suddenly stand.

3.2 Pathophysiological scheme of Helicobacter pylori poisoning

See Figure 7.

Figure 7.

Physiological scheme of Helicobacter pylori poisoning.

4. New innovative hypotheses

Helicobacter pylori is widespread throughout the world, colonizing more than half of the world’s population. In 80% of cases, the infection is asymptomatic. Symptoms of infection are observed in only 20% of patients and they mainly include acute gastritis, chronic gastritis, gastric ulcer and gastric cancer. Gastric cancer follows gastric ulcer disease and occurs in a small proportion of 1–3% of cases of gastric ulcer disease.

Despite the low frequency of stomach cancer linked to Helicobacter pylori, it is one of the deadliest cancers in the world and Helicobacter pylori infection is categorized as a class one carcinogen. The eradication of Helicobacter pylori in patients with gastric ulcers should be the solution to prevent this cancer. Unfortunately, Helicobacter pylori is one of the most resistant bacteria in the world. It is resistant to various treatments, including quadruple therapy, currently used, after tritherapy.

New treatment principles are therefore necessary.

Our research comes at the right time in this regard. Indeed, it reveals a new face of Helicobacter pylori infection, previously unknown, which states that Helicobacter pylori is sensitive to environmental pollution in the same way as humans. By protecting itself against this pollution, especially represented by atmospheric carbon dioxide, the bacteria cause intoxication by carbon dioxide and ammonia which is described in the present chapter and which has been considered impossible until now, in the literature.

This new face of Helicobacter pylori was discovered in the Democratic Republic of Congo, following the fact that any foreign person, colonized by Helicobacter pylori, symptomatic or asymptomatic, going to Goma and Bukavu, rich in environmental carbon dioxide released from the Nyiragongo Volcano and the Lake Kivu, develops, after a few days, the symptoms of carbon dioxide and ammonia poisoning described in this chapter, which the population until now considers to be massive poisonings perpetrated by evil people. These patients are valuable in our research because they attest both to the link between atmospheric pollution, urease and Helicobacter pylori infection, as well as that between gastritis and constipation, practically present in all of our patients.

Our research reveals that the intensity of poisoning is a function of the intensity of environmental carbon pollution. It is the latter which determines the degree of production of carbon dioxide and ammonia by Helicobacter pylori. The threshold at which air pollution activates the bacteria is currently in progress within our research team, by mathematical modelling. The second factor that plays a determining role in this poisoning is constipation, responsible for the accumulation of the two gases in the stomach, which allows them to rise along the oesophagus and pass into the blood through the pulmonary alveoli, as well as their distribution throughout the body.

Our research reveals that the inflammation that causes symptoms of Helicobacter pylori infection, from gastritis to gastric cancer, comes from the high heat accompanying the two gases released by Helicobacter pylori [52]. It is important to remember, in this regard, the strong inflammation produced by carbon dioxide during the limnic irruption that occurred in 1987 at Lake Nyos in Cameroon, which caused terrible burns on the victims.

Our research recommends changing the approach to combat the symptoms of Helicobacter pylori infection, from gastritis to gastric cancer as well as those described in this chapter. She advises not to concentrate on the bacteria but on the factors which make it dangerous: atmospheric pollution which is at the origin of the reaction of Helicobacter pylori, urease which allows the bacteria to react by producing gases ammonia and carbon dioxide, the ammonia and carbon dioxide gases responsible for inflammation, the cause of all the ills caused by the bacteria and, finally, strong and permanent constipation, which prevents the two gases from being eliminated in the stools in liquid form.

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4.1 Air pollution

Fighting air pollution at a time when greenhouse gases, mainly carbon dioxide, are in full expansion, is not easy. For example, the Democratic Republic of Congo hosts three important natural carbon dioxide production sites: the Nyiragongo Volcano, Lake Kivu and the peatlands of the equatorial forest [53, 54]. In addition to this natural production of greenhouse gases, there is another production of gas caused by man. The situation is not different in other Saharan African countries. Intensive reforestation is therefore essential. At the same time, we encourage studies of chemical conversion of environmental carbon dioxide into a less dangerous product, undertaken throughout the world. Finally, a study of the historical behaviour of Helicobacter pylori infection throughout human history, in light of the discovery of the influence of greenhouse gases on this infection, would be highly useful.

4.2 Urease and antiurease

Antiurease is the best solution to deal with infection or better, Helicobacter pylori poisoning. In fact, it prevents the production of the two gases that generate inflammation. Many studies relating to the search for antiurease are underway throughout the world but the solution is still lacking [55, 56, 57]. Our research team has been interested in this challenge for a long time and to our great surprise, an enzyme drug, found on the market, has given incredibly satisfactory results. Unfortunately, this drug was shortly after modified by the company which had designed it and its antiurease properties had been disrupted. Contact with this firm is strongly considered to be able to carry out tests with the old formula of this product.

4.3 Constipation

Constipation is the real cause of all the problems that Helicobacter pylori causes in the human body. Indeed, if there is no constipation, the ammonia and carbon dioxide gases produced by Helicobacter pylori become liquid, and are eliminated without difficulty in the stools. The patient is then completely asymptomatic. Thus, in the absence of an antiurease, treatment of constipation is the best response against this infection. Unfortunately, this constipation is very strong. This severe constipation is due respectively to the accumulation of gases in the digestive tract which slow down intestinal transit, the concentration and fermentation of more or less dry stools in the large intestine, the disruption of macrobiota with the development of bad bacteria and sometimes the occurrence of haemorrhoids. Our research in this regard is directed towards Congolese and African medicinal plants, but also to specialists in the study of constipation throughout the world.

5. Conclusion

The link established between suspected poisoning, the environment and Helicobacter pylori in the Democratic Republic of Congo sheds exceptional light on Helicobacter pylori infection. We learn that Helicobacter pylori is sensitive to environmental pollution, mainly atmospheric. If this pollution exceeds a certain threshold, a disruption of intestinal transit may result, the carbon dioxide and ammonia released by Helicobacter pylori in the stomach can accumulate and pass into the blood through the pulmonary alveoli. If atmospheric pollution constitutes the external factor responsible for this poisoning, urease and constipation constitute the internal factors which must be combated in the same way. The application of the principles set out in this chapter could also make it possible to effectively combat or better prevent gastric cancer linked to Helicobacter pylori.

Our team is open to international collaborations that could allow us to obtain the financial and material resources necessary to continue our research.