Preface by Thomas Oliver, MD
NOT MEDICAL ADVICE
“Man is constantly standing, as if it were, on the brink of a precipice; he is continually on the threshold of disease. Every moment of his life he runs the risk of being overpowered by poisons generated within his system. Self-poisoning is only prevented by the activity of his excretory organs, chiefly kidney, and by the watchfulness of the liver, which acts the part of a sentinel to the materials brought to it by the portal vein from the alimentary canal. Disease is not something altogether apart from the individual.” – Thomas Oliver, MD
“The healthy man, as I have said, is both a receptacle and a laboratory of poisons. He receives them in his food, he creates them by disassimilation, and he forms them in his secretions. The human body is the theater of the toxic elaborations carried on by the normal microbes which constantly inhabit the alimentary canal. And yet man is not poisoned. He is defended in various ways against poisoning”. - Charles Bouchard
Bouchard deals, in his “Auto-Intoxication”, with subjects of everyday interest to the medical practitioner. Many of the facts therein alluded to can no longer be ignored. Putrefactive processes in the intestinal canal and the development of physiological and pathological alkaloids (nitrogenous organic compounds (morphine, quinine, strychnine) play an important part in many diseased processes until lately unknown or misunderstood. These lectures may, therefore, be regarded as an inquiry into the operation of poisons introduced from without or generated within the body of man, and the part they play in health and disease. No subject commands a greater interest; none demands more serious study.
Death frequently carries off in a few hours or days individuals who are in the prime of life and in apparent good health, and at whose post-mortem the most careful examination fails to reveal alterations of structure such as can explain the fatal stroke. Epidemics, not a specific character, but traceable to poisoned water or food, have unexpectedly appeared in certain neighborhoods; or members of a marriage party have died without much warning; death being attributed, and very properly, to some article of diet partaken of at the wedding feast. These are the cases that have aroused public opinion and awakened professional interest in a subject toward the elucidation of which the pathological chemist has vied with the bacteriologist.
The investigations of Selmi, Brieger, Pasteur, Frankel, Hankin, Martin, and Bouchard, not to mention others, have shown how disease may depend upon the presence in the system of substances capable combining with acids to form salts, and which correspond to inorganic and vegetable bases. It was to these substances that the Italian toxicologist, Selmi, gave the name of ptomaines, (any of a group of amine compounds of unpleasant taste and odor formed in putrefying animal and vegetable matter and formerly thought to cause food poisoning) -- by which is meant chemical compounds basic in character, and formed by the action of bacteria upon organic matter. It is owing to these basic properties and their resemblance to vegetable alkaloids that Ptomalines are sometimes spoken of as putrefactive or vegetable alkaloids, -- the term leucomaines, or animal alkaloids, being reserved for those basic substances resulting from tissue metabolism in the body.
Without discussing the question as to whether Ptomaines are poisonous or not, - for Bouchard in these pages confines himself rather to the general action of animal poisons than to a designation of them – it is sufficient to state that all Ptomaines are not poisonous. Some are quite inert. Brieger restricts the term Ptomalines to non-poisonous basic products, whilst those that are poisonous he calls “toxins’. Ptomalines contain nitrogen, and in this respect, they resemble vegetable alkaloids. Many of them contain oxygen, whilst in others the fact that the products secreted as the result of microbial activity react upon the organisms themselves, and thus limit their longevity.
It is the function of the gastro-intestinal juices, aided by the movements of the stomach and intestine, to convert foods into such soluble forms that they can be utilized by the economy…Many fission fungi (Patrick Jordan) –e.g. BACILLUS SUBTILIS and the SPIRILLUM of cheese (version of Spirochete) – can produce a peptonizing ferment; so that a small amount of the peptonizing done in the intestine may be due to microbes. This, though not proved, has been rendered probable by the experiments….it has been shown that certain of these micro-organisms secrete soluble ferments identical in their action with the ferments of digestive juices. Vignal states that certain of these organisms contribute to the dissolution of food in the intestine. In this connection we cannot fail to remember that bacteria by their action can produce in albuminous fluids albumoses and peptones, and that the former bodies are now regarded by bacteriologists as substances which play an important role in many pathological processes.
Bouchard, in his “Auto-Intoxication”, clearly indicates to us that man is constantly standing, as if it were, on the brink of a precipice; he is continually on the threshold of disease. Every moment of his life he runs the risk of being overpowered by poisons generated within his system. Self-poisoning is only prevented by the activity of his excretory organs, chiefly kidney, and by the watchfulness of the liver, which acts the part of a sentinel to the materials brought to it by the portal vein from the alimentary canal. Disease is not something altogether apart from the individual. The patient and his disease are too often found living under identical conditions.
“…Chemical investigation has shown that disease depends upon the products of putrefaction and fermentation, rather than upon the direct action of the microbes upon the tissues. It is this fact which renders knowledge of the life-history of bacteria so valuable to us; for long after the microbes have been destroyed by enzymes, or ferments, which they formed continue to act, and are not destroyed by a temperature which is destructive to the organisms themselves…
…Bouchard’s lectures devoted to typhoid fever and cholera contain suggestions of considerable value from a therapeutic view. It is only lately we have come to recognize that, once dangers incidental to typhoid fever have been successfully overcome, there are risks yet to be met; in a word, auto-intoxication from poisons generated within the intestinal canal. There are few medical men who hae not had some experience of the success which has followed the administration of intestinal anti-septics in enteric fever. In my own consulting practice, I have used Beta-Naphthol with excellent results. I can recall one case in particular…of a gentleman whose life I consider was saved by Beta-Naphthol and other alimentary antiseptics. We know that Naphthalin is sparingly soluble, and that it passes to a large extent unchanged through the alimentary canal. Salol, or the Salicylate of Phenol, has also given excellent results….it has the disadvantage of being poisonous, so Betol or Salicylate of Beta-Naphthol is to be recommended instead. All substances belonging to the Phenol Class may be regarded as antiseptics in the largest sense of the word. They are antiseptics as long as they are not absorbed.
A fairly large experience of the treatment of certain diseases in which the blood is poisoned – e.g. puerperal fever, certain forms of pneumonia, ulcerative endocarditis, etc. – has led me to place considerable on the efficacy of phenols. When absorbed they no longer exercise a direct action upon the germs, but they exert another action, viz, a de-poisoning one…in the small intestine Salols and Phenols are split up into their antiseptic constituents: Salol into Salicyllic and Carbolic acid, Betol into Salicyllic Acid and Beta-Naphthol, while Guaicol Carbonate…decomposes into Guaicol and Carbonic Acid.
Chemical disintegration and re-combinations undoubtedly occur, and to these must be attributed, by the process of de-poisoning just alluded to, the good results that follow the administration of antiseptics in certain forms of blood poisoning. Under all circumstances a rigid intestinal antisepsis cannot but be of the greatest possible utility.
[Note: Phenols are found in high amounts in berries, cocoa, coffee and tea, cloves, anise, and lesser in curcumin. Arugula, an edible leafy plant in the broccoli family, is high in phenols].
Thomas Oliver, preface to translation, 1894.
Product (non-endorsed): Power Phenols, Dr. Steven Gundry MD – LINK.
A Guide to Polyphenols – LINK.
Hey Wayne, Huge topics to deconstruct.
Phenols are a Superfamily of chemicals and Polyphenols do indeed exist under that umbrella but it is apples and orangutans.
Conversely, there is a very strange relationship with the existence of the Benzene STRUCTURE that is present as 6 carbon atom constructs inside of DNA but they are NOT benzene. This is why Benzene is so highly toxic and genetically damaging because it can slip into where it doesn't belong thus throwing a molecular spanner in the works.
I cover the intricate names/relationships of misunderstood biochemicals in my book Prion Agenda including the most misused non-understood word of: Fiber.
Gallic Acid Protects from Sepsis-Induced Acute Lung Injury,
Suleyman Kardas, Dept. Emergency Medicine,Kiziltepe State Hospital, Mardin, Turkey
Curr. Issues Mol. Biol. 2024, 46(1), 1-10; https://doi.org/10.3390/cimb46010001
Submission received: 20 November 2023
Abstract
Sepsis, a leading global cause of morbidity and mortality, involves multiple organ dysfunction syndromes driven by free radical-mediated processes. Uncontrolled inflammation in early sepsis stages can lead to acute lung injury (ALI). Activated leukocytes generate reactive oxygen species, contributing to sepsis development. Gallic acid, a phenolic compound, is known for its antimicrobial properties. This study aims to observe gallic acid’s protective and restorative effect on the lungs in an experimental sepsis model. Male Wistar albino rats were subjected to a feces intraperitoneal injection procedure (FIP) to induce sepsis. Four groups were formed: normal control, FIP alone, FIP with saline, and FIP with gallic acid. Gallic acid was administered intraperitoneally at 20 mg/kg/day. Blood samples were collected for biochemical analysis, and computed tomography assessed lung tissue histopathologically and radiologically. Gallic acid significantly decreased malondialdehyde, IL-6, IL-1β, TNF-α, CRP levels, oxidative stress, and inflammation indicators. Lactic acid levels decreased, suggesting improved tissue oxygenation. Histopathological examinations revealed reduced lung damage in the gallic-acid-treated group. Computed tomography confirmed lower lung density, indicating less severe inflammation. Arterial blood gas analysis demonstrated improved oxygenation in gallic-acid-treated rats. Gallic acid exhibited anti-inflammatory and antioxidant effects, reducing markers of systemic inflammation and oxidative stress. The findings support its potential to protect against ALI during sepsis. Comparable studies underline gallic acid’s anti-inflammatory properties in different tissues. Early administration of gallic acid in sepsis models demonstrated protective effects against ALI, emphasizing its potential as an adjunct therapy to mitigate adverse outcomes. The study proposes gallic acid to reduce mortality rates and decrease the need for mechanical ventilation during sepsis-induced ALI.