|
|
 |
 |
 |
Systemic Enzymes - Moving Beyond The traditional Concepts
By Aftab J. Ahmed, PH.D.
Enzymes play a critical role in
nearly every metabolic and physiological response in the body. They ensure that
the cellular processes take place at the right time, to the right extent and in
the correct context. As such, enzymes are cellular workhorses that carry out
their function rapidly and efficiently. With advancing years, failing health,
poor nutrition or otherwise complicating circumstances, however, enzymes are
either quickly depleted or lose their potency. When one enzyme is even partially
functional, a ripple effect on other bodily reactions and in fact, overall
function becomes readily discernible. It is for a reason then that over the
decades systemic enzymes have been pivotal in the emergence of integrated health
care.
Enzymes are characterized as systemic that when ingested orally, are delivered
intact to the bloodstream over the gastrointestinal (GI) tract. Routinely
composed of proteases, they break down proteins in circulating blood and as a
result, exert their many beneficial effects. This property of systemic enzymes
has significant implications for human health and disease. Traditionally, by
virtue of the fact that they work throughout the body, systemic enzymes help
maintain the bodily homeostasis, which is critical in the maintenance of good
health.
The peripheral circulatory system is impressive in its structural complexity and
fluid mechanics.1 In the first instance its
function is to transport nutrients and oxygen to tissues and organs and to whisk
away metabolic waste products. The marvel of the vascular architecture is its
flexibility that allows the blood to remain at the requisite viscosity—a
balance actually between thickness and fluidity—in order for the bodily
functions to proceed unfettered. Thus the equilibrium between the yin of blood
thickening and the yang of its fluidity, or liquefaction, is a prerequisite in
maintaining the circulating blood at a certain viscosity to prevent uncontrolled
bleeding and conversely, clotting.
At the center of this equilibrium between normal thickness and liquefaction is
the protein fibrin, which is the “glue” that helps maintain blood at optimal
viscosity. Fibrin is present in nearly all types of cells in its inactive,
precursor form, called fibrinogen. Upon proper stimulus, a proteolytic enzyme
clips fibrinogen to its biologically active form fibrin.
In fact, there is a series of protein precursors that are sequentially activated
prior to fibrin activation (Fig. 1). The reason for this convoluted cascade in
fibrin activation is to ensure that it does not spin out of control.
Excessive fibrin release is as deleterious to human health as its production in
less than required amounts. How so? Fibrin facilitates a number of metabolic
processes. Whereas on the one hand it is beneficial in wound healing, on the
other, its out-of-context production over time could precipitate lifethreatening
occlusion of the arteries.
Accordingly, over-production of fibrin, or insufficient rate of its breakdown,
is emerging as an important mechanism in chronic diseases.
Under normal physiological conditions, controlled release of fibrin coats the
rather fragile inner walls of the blood vessels to protect them from sustaining
injuries from (ab)errant particles in the bloodstream and smooths any unevenness
in the vascular wall to promote unhindered blood flow. Importantly, in case of
an injury, fibrin is released to initiate blood thickening, which effectively
seals off the injury site by forming a fibrin plug. In wound healing,
transforming growth factor-b (TGF-b) is produced along with fibrin release to
complete the healing process.2 This sequence
of events is regulated such that, after the repair process is complete, the
blood is liquefied to prevent excessive fibrin production and therefore,
minimize scarring of the tissue. Under some circumstances, however, if
liquefaction is not initiated and fibrin release continues unabated, it could
cause fibrosis or hardening of the tissue. The hardened tissue progressively
loses its function. Fibrosis can occur just as easily in the internal organs as
it does on the skin surface. Among the internal organs susceptible to fibrosis
are the liver, lungs and the kidneys. Likewise excessive fibrin release could
cause keloids, fibrous growths resulting from unbridled production of TGF-b.
Simultaneous overproduction of fibrin and TGF-b desensitizes the tissue to
register the signals to stop the repair process. Repetitive injuries to one
tissue also results in this desensitization. Of course advanced age, disease,
poor nutrition and other compromising factors contribute to over-repair as well.
Aside from over-repair, excessive amounts of fibrin in the circulating blood
increase its viscosity, which could form clots that are sticky enough to adhere
to the vessel walls. Such clots serve as seeds for progressive accumulation not
only of fibrin but also cholesterol and cellular debris in the blood. As the
clots increase in size, the blood is forced to circumnavigate these
obstructions, causing the blood vessels to bulge. This constriction is the root
cause of venous insufficiency, as in the so-called “economy class” syndrome
and varicose veins. It takes considerable time for these clots to develop into
mature plaques that are responsible for coronary artery disease (CAD). The path
to maturity is fraught with danger, however. The younger plaques can easily
erupt, leaving literally millions of micro-clots in their wake.3
As such they could precipitate a potentially fatal coronary episode, even in the
absence of symptoms traditionally associated with CAD. Recent clinical data
establish that such coronary events are almost invariably caused by chronic
inflammation.
In fact inflammation is the major culprit in many chronic diseases, including
arthritis, CAD, Alzheimer’s disease and a host of other agerelated
afflictions. To wit, fibrin is central in inflammatory conditions. While
inflammation is the healing response of the body to recover
 |
| Figure 2: Effect of
Oral Nattobinase on Plasma tissue Plasmacinogen Activator (each data
point represents the mean ±sd) |
from an injury, if unresolved, it can over-activate the immune system.
Considerable evidence suggests that repeated activation of the body’s
defensive arsenal may keep the immune system activated constantly, which could
potentially induce autoimmunity. To an extent the epidemiological data
corroborate the contention that spuriously activated immune system underlies
autoimmune diseases. As the immune system gears into action, antibodies are
produced, as in arthritis, which then form aggregates known as circulating
immune complexes (CICs). Circulating ICs clutter the blood traffic that, in
turn, not only increases blood viscosity but also may give rise to secondary
antibody production, which further aggravates autoimmunity.
How does fibrin fit in this jigsaw puzzle? If excessive amounts of fibrin are
present, a protective coat is laid on the surface of CICs making them
“invisible” to the immune system. Each CIC carries an ID tag, in a manner of
speaking, which makes it vulnerable to detection and elimination by macrophages,
the foot soldiers of the immune system. Fibrin coating, however, masks the
telltale ID tag and therefore prevents their clearance from the body.
The foregoing underscores the fact that diverse mechanisms are involved in the
onset of chronic diseases. This is precisely the reason why chronic diseases
progress slowly over long periods of time. Since the human body has a wide
repertoire of self-healing processes, a process gone awry is relatively quickly
corrected. If metabolic attrition persists, however, the ripple effect mentioned
initially takes hold. In essence, it could be likened to the molecular road rage
in which the many different mechanisms become hopelessly tangled, as in the
wreckage of a roadside pile-up. As a consequence, when a chronic disease is
clinically presented, it may be too late already to undo the damage. While
intuitively obvious, it demonstrates how the convergence of numerous pathways
makes chronic diseases less amenable to therapeutic intervention. This
convergence creates its own dynamics. Each of the contributing mechanisms brings
about a different composite. In a sense, it is not unlike the pieces viewed
through the lens of a kaleidoscope. With each turn, while the pieces are the
same, a different configuration ensues. This analogy is recapitulated in the
onset and presentation of chronic diseases. Several mechanisms, some of which
might be otherwise perfectly innocuous, morph into abnormal physiology. This
complexity is reflected in chronic diseases and should underscore the necessity
of preventive regimens. Therefore, a preventive regimen may be a more expedient
approach in its management.
Notably second-generation systemic enzymes are instrumental in keeping the
diverse biochemical pathways well within the normal range. The example of
out-of-context release of activated fibrin makes the point poignantly. Excessive
fibrin could blunt the immune response over time. By the same token, it may
encourage fibrosis, which may cause hypertension and thus affect overall
function of the cardiovascular tree. In turn, this may result in less than
optimal blood flow, triggering a domino effect that could encompass the entire
body (for a detailed review, see Ref. 4). Again the second-generation systemic
enzymes provide an effective regimen to nudge the underlying mechanisms to
retain, and in some cases restore, homeostasis. Furthermore, the benefits of
systemic enzymes can be augmented by bioflavonoids, which modulate the immune
system by mitigating the function of those chemical messengers that stoke the
inflammatory fires.
A protelolytic enzyme activity in fermented soybeans effectively optimizes blood
viscosity. Thanks to this activity, fermented soybeans have been used for
centuries in Japan to promote heart health and normalize blood flow. This
enzymatic activity regulates excess fibrin by primarily mobilizing tissue
plasminogen activator native to the body (Fig. 2). Accordingly, this proteolytic
activity primes the latent health-promoting potential in the body. In
combination with other plant-derived systemic enzymes, it also helps slake the
inflammatory response.5 Powerful as this
activity is, it can be further bolstered by bioflavonoids, since different roads
lead to the proverbial Rome of inflammation. Thus, a proprietary
Rutobioflavonoid mix (RBE) is designed to regulate pro-inflammatory chemical
messengers in favor of those that can help still the fires raging in the joint.6
Importantly, robust flow of blood to various tissues is indispensable for
health. For example, joints ravaged by arthritis may have blocked arteries in
close proximity. Therefore, unplugging of arteries should promote better
delivery of nutrients and oxygen to the joint to heal itself. In short, in the
management of chronic diseases a nutraceutical approach should discourage the
entanglement of biochemical pathways detailed above. While metabolic pile-up
depends on numerous factors, nutritional intervention directed at the underlying
cause helps alleviate pain and suffering, if not checkmate the molecular road
rage over the long run.
|
|
|
| |
Annotated references*
- Ahmed, A. J. The Cycle of Life: Circulation and The Lymphatic System,
Manuscript in Preparation (2002).
- Letterio, J. and Roberts, A. “Regulation of Immune Responses by TGF-b,”
Ann. Rev. Immunol. (1998). Vol. 16 p. 137.
- Fuster, V. The Vulnerable Plaque: Understanding, Identification and
Modification, (1999). Futura Publishing Co., Inc., Armonk, New York.
- Ahmed, A. J. “C-Reactive Protein: A Coronary Trojan Horse,”
totalhealth (1999). Vol. 22, No. 2.
- Sumi, H., Hamada, H., Nakanishi, K. and Hiratani, H. “Enhancement of the
Fibrinolytic Activity in Plasma by Oral Administration of Nattokinase: Natto
VR 501,” Acta Haematologica (1994). Vol. 84 p. 139.
- Salvemini, D, Wang, Z., Zweier, J., Samouilov, A., Macarthur, H., Misko,
T., Currie, M., Cuzzosrea, J. Sikorski, J. and Riley, D., “A Nonpeptidyl
Mimic of Superoxide Dismutase with Therapeutic Activity in Rats,” Science
(1999). Vol. 286 p. 304.
|
|
|
|
THE END OF
Heart Disease
and Arthritis
Neprinol completely eliminates arthritis in just six months without the use of damaging drugs and pain
relievers.
Details
|
|
TMN
Health -
Neprinol Authorized Distributor
9938 W. Guinivere Drive Mapleton, IL 61547
309-697-6628
Mon - Fri
9am - 6pm CST
Phone In Orders & Unadvertised
Discounts
Call 1-800-630-3004
E-mail |
|
|
