Rudolf Virchow, a contemporary of Pasteur and one of the formulators of “the cell theory”: the foundation of modern biology, reflected: “If I could live my life over again, I would devote it to proving that germs seek their natural habitat: diseased tissue, rather than being the cause of diseased tissue.”
The enduring popularity of the Germ Theory is attributable, in part, to its portrayal of disease onset as being a thunderbolt in a previously clear sky. This absolves the individual of the responsibility to live in accordance with the Laws of Nature that govern health, the violation of which leads to enervation and autotoxemia: the most common causes of disease.
In Part I of this series of three articles, I discussed the Germ Theory, the actual role of bacteria within the scheme of Nature and the fact that, in most cases, physical derangement precedes the appearance of pathogenic (disease-causing) bacteria within the body, and not vice versa.
This article, Part II of this 3-part series, will focus upon the nature of viruses, contagion, and Professor Antoine Beauchamp’s identification and observation of what he termed microzymas.
If you have not already read Part I, I suggest you do so as it will provide crucial context for Part II, below. To access Part I, click on the following link: Read Part I
The Nature Of Viruses
Bacteria and viruses, while both classified as microbes, are actually vastly different. To begin with, bacteria are often 1,000 times larger than viruses. In fact, some groups of viruses, called bacteriophages, actually infect bacteria.
Viruses also differ from bacteria in that they are not (technically speaking) living organisms, as they do not metabolize food nor produce energy. A virus consists of a protein coat surrounding a core of nucleic acid (i.e., genetic material). Lacking metabolic function, energy production and the raw materials for organic synthesis, they cannot reproduce themselves. Instead, they attach themselves to host cells (cells whose environs they invade and use for their own purposes) that manufacture new virus particles based upon the genetic blueprints furnished by the virus.
Once a virus attaches to a host cell, it inserts its own genetic material in one of three ways:
- deceives the cell into uptaking the virus, mistaking it as a nutrient moiety
- certain viruses with sticky coatings will fuse with the host cell’s cell membrane (the “border guard” of the cell, which surrounds the cell and controls ingress and egress), and then penetrate its defenses;
- forcibly pierces the host cell’s membrane, enters the cell and injects its DNA into the host.
Once the parasitic link-up to the host cell is established, the virus then uses that cell’s own enzymes (which help facilitate cellular functions) to build the proteins it needs to reproduce. The cell then performs like a genetic factory, producing viral components that are assembled into clones of the virus. Many of the other cell functions are shut down to conserve energy for viral replication. Ultimately, some cells die from exhaustion, disintegrate and discharge their viral load into the extracellular (outside the cell) environment.
Other viruses move out into the body by dissolving the cell membrane. Once the viruses enter the fluids outside of the cells, they can proceed to infect other host cells, extending the infection until either the virus is immunologically contained or the person perishes.
During the course of their evolution, viruses have acquired the ability to target specific cells. For example, the pneumonia virus is capable of latching on to lung cells. The hepatitis virus is programmed to infect liver cells. The human immunodeficiency virus (HIV) has developed the capacity to parasitize white blood cells.
Unlike bacteria, viruses do not propagate upon, and decompose, food waste and dead cells; rather, they invade devitalized cells wherein they are reproduced, often destroying said host cell in the process. Like bacteria, however, viruses do not attack healthy cells, which are far more resistant to their predations.
Microbiologists are continually discovering new information about the vital roles bacteria play in the body. But the purpose in Nature that viruses serve is not well understood. Nevertheless, viruses have inhabited the earth far longer than humans and have all along been performing tasks according to Nature’s blueprint.
Recent studies suggest that viruses may play some role in the adaptations through which species evolve over time. Geneticists have observed fragments of viral DNA incorporated into animal cells. While the host cells were reproducing, these fragments of viral genetic material became part of the fabric of the host’s genes. These hybridized genes have since been passed along through the thousands of generations of human existence.
Astonishingly, viral DNA accounts for nearly half of the human genome (the sum total of human genetic material). Some scientists now believe that this viral genetic material is one of the vital engines of human evolution. It has been hypothesized that certain viral genes may have initiated some of the changes in human form and behavior that facilitated the evolutionary branching off of man from other primates that occurred 6 million years ago.
Conceivably, viruses may fulfill the same role within the organism that predatory animals, such as wolves and lions, do in Nature: the cutting of weakened and aged animals from herds to insure the continuedgenetic vitality of the prey-species. Body cells have a limited lifespan, at the end of which they reproduce and give rise to a new generation of like cells. Viruses, in their capacity of “weak-cell terminators,” may help to preserve cellular genetic integrity, and thus, discourage the genetic mutations which play a primary role in the processes of aging and degenerative disease.
Viruses also act as catalysts for cellular immune response. Interferon is a protein produced by host cells in response to a viral challenge. The interferon released cannot save the host cell, but it diffuses into the body fluids and mobilizes the defenses of other, as yet unaffected, cells.
Under normal circumstances, viruses perform certain useful scavenging and immune-enhancement functions. This is not to say that we should celebrate and welcome them. Anyone who suffers from Herpes simplex, influenza, Hepatitis C or AIDS, knows full well the suffering they engender. However, aside from behavioral judiciousness, the most crucial defense against communicable viral infection is not risky immunization, but rather, the maintenance of a healthy internal terrain and robust immunological resisting power.
Undoubtedly, microorganisms can be transferred from one host to another. If this were not so, yogurt could not be made (via inoculation of milk) from a few tablespoons derived from a previously cultured batch.
When body tissues become congested, devitalized and lose resisting power via the offices of enervation (depleted vital force and nerve energy) and autotoxemia (systemic accrual of metabolic waste and other toxins beyond the body’s threshold of tolerance), the resultant corrupted cellular milieu, overabundance of weakened cells, in concert with a decline in vigor of immunological-limiting mechanisms (which govern microbial activity), can metamorphose a containable viral incursion into a, destructive pillage.
Germs stimulated into frenzied activity by the accumulation of toxic substances in the blood and the devitalized tissue elements of a given host can be transferred to the mucous membranes of another individual. Yet, the latter will only develop the same disease if he or she is similarly enervated and autotoxemic, thus providing the requisite culturing conditions for potentially pathogenic microorganisms.
During the influenza (Spanish flu) epidemic of 1918-19, the U.S. Navy performed an experiment exploring the dynamics of contagion. Sixty-eight young, healthy volunteers were selected; some were injected with pure cultures of Pfeiffer’s bacillus (Haemophilus influenzae – a pathogenic bacterial species sometimes associated with influenza virus infections), while others had their nasal membranes sprayed and their throats swabbed with these germs. The researchers found no resultant incidence of disease among the test subjects. Over the years, hundreds of similar test studies (again, using healthy volunteers) have been performed yielding similar findings.
At the time, Pfeiffer’s bacillus was thought to actually be the causative agent of the influenza. This was ultimately disproved and we now know that influenza is a viral infection. Nevertheless, Pfeiffer’s bacillus was found in many of those suffering with the Spanish flu, and it is an undeniably pathogenic species that can cause meningitis and severe upper respiratory infections, including pneumonia.
Martha Wollstein M.D., a researcher at The Rockefeller Institute for Medical Research, wrote in 1919: “It has been shown that the serum [i.e., the clear, yellowish fluid obtained upon separating whole blood into its solid and liquid components after it has been allowed to clot] of patients convalescent from influenza yield reactions for antigens [any substance such as a toxin that stimulates an immune response in the body] of Pfeiffer’s bacillus.
“These reactions appear constantly at the end of the first week, increase in intensity during the second week, and remain demonstrable for a period of two to four months. They were most complete in the serum of patients suffering from post-influenza pneumonia. It has also been demonstrated that the strains of Pfeiffer’s bacillus isolated during the epidemic were morphologically and biologically similar to the strains isolated from influenza cases in other years. The patients’ serological reactions indicate the parasitic nature of the bacillus, but are not sufficiently stable and clean-cut to signify that Pfeiffer’s bacillus is the specific inciting agent of epidemic influenza. They do, however, indicate that the bacillus of Pfeiffer is at least a very common secondary invader in influenza, and that its presence influences the course of the pathological process.”
While it has been established that Pfeiffer’s bacillus does not directly cause the flu, it may play some role in the development and severity of the disease. Does the flu virus open the door for the bacterial complication or do the pathological actions of the bacteria predispose an individual to the virulent viral infection?
Although the U.S. Navy study did not prove anything regarding transmission of the flu virus, it did demonstrate that the direct transmission of a disease-causing bacteria (which are, at the very least, associated with certain flu complications) did not evoke symptoms in healthy subjects.
G.T. Stewart, professor of epidemiology and pathology at the University of Glasgow, writes: “If two subjects are exposed to equal doses of the same germ and one develops infection while the other does not, the factor governing the development of infection clearly lies outside the germ.”
This predisposing factor to developing a communicable infectious illness such as the flu is the confluence of enervation (i.e., lowered vitality and resisting power) and autotoxemia (i.e., tissues overburdened with impurities). Due to faulty maternal health habits during the gestation period, many infants are enervated and autotoxemic at birth.
Children who are sustained on a denatured diet of processed foods, junk foods and sugar-laden beverages, drugged for every symptom they present with and enervated by sensory over-stimulation and insufficient rest, have attenuated powers of resistance and are ripe candidates to serve as hosts to communicable, pathogenic microorganisms.
Naturally, the same is true for adults whose lifestyles violate the most basic rules of Nature by paying little heed to the fundamental elements of life and health, such as nutritious diet, adequate exercise, sunlight, fresh air, rest and sleep. Older adults are particularly vulnerable in this regard as the vitality of their immune systems is diminished, not only by habitual unhealthy lifestyle, but also by the erosive action of an aging process whose momentum is unhindered by the anti-aging counteractions of nutritious diet, daily exercise and adequate fresh air, sunlight, rest and sleep.
Germs may act as the exciting cause or catalyst for a potentially life-threatening toxic crisis, yet, lacking the necessary disordered milieu, they can rarely be its cause. The increased tissue-congestion and waste-production (which is a feature of the accelerated performance of the natural decomposing function of bacteria), coupled with sluggish elimination and lowered resisting power (which characterizes enervation), act as a flame of ignition. Still, without the powder keg of autotoxemia, there can be no explosion.
When bacteria feed upon the waste material that has accumulated in the body, they are only performing their intended function. The earth is a closed system that contains a limited amount of the life-sustaining raw materials (carbon, hydrogen, nitrogen, oxygen, etc.) that have to be perpetually recycled. Bacteria are the key players in this reference. For instance, underwater bacteria annually produce 330 billion pounds (150 billion kilograms) of oxygen every year – 50% of all the oxygen utilized by living organisms.
Similarly, bacteria in the body are charged with breaking down waste and recycling vital raw materials that can then be utilized gainfully by body cells. However, the greater the waste accumulation, the greater the population of bacteria that will develop to feast upon it. This feeding frenzy gives rise to a production of a huge amount of bacterial metabolic waste which then expands and complicates the indigenous state of autotoxemia. It also taxes the immune system whose responsibility it is to restrict the populations of bacterial decomposers in order to keep them within constructive limits.
Once again, it all boils down to autotoxemia and enervation. If the extracellular milieu (the environment of the fluids which surround the cells) is healthy, the feeding bacteria serve a positive, symbiotic role with no downside. On the other hand, if the extracellular milieu is corrupted by autotoxemia and the immune system handicapped by enervation, the bacteria overwhelm the body’s powers of resistance and push the total toxic load beyond the threshold point of tolerance into the red zone of disease. Essentially, this is the pathological pattern that characterizes most common infectious and inflammatory diseases.
Professor Antoine Beauchamp, a contemporary of Pasteur, was one of the greatest biologists of the modern era. Beauchamp’s experiments are almost flawless paradigms of scientific procedure. He discovered that cells are built of even smaller molecular units, which he named microzymas (i.e., “smallest ferments”).
It was Beauchamp’s idea that when the microzyma’s habitat: the body cell becomes devitalized or dies, said microzymas convert themselves into specific bacterial forms utilizing cellular material for the purpose of dissolving decaying cellular debris.
If Beauchamp’s conclusions are valid (and, to this day, they have the support of many eminent scientists), then contagion from without is not the primary source of the pathogenic microbes found in association with diseased tissue. Instead, the host organism creates them in accordance with its need for their unique sanitizing and scavenging services.
Beauchamp declared: “Disease is born of us and in us, and that is as it should be, because the life of man, and every other creature, is no more delivered over to chance than the course of the stars. Life would be delivered over to chance if it depended upon primitive germs created [solely] for destructive purposes.”
Part III of this 3-part series will focus specifically upon the flu and present some elements of Dr. Berkowsky’s Natural Health Science System therapeutic protocol.