*HumicAcid.

info Editor's Note:

The term (Humic Acid) or (Humic Acids) or (Humic Substances) has been substituted in
the following statements where the original wording was in scientific terms that detailed
chemical compositions of Humic Acid.
Extracts From:
"Medical Aspects and Applications
of Humic Substances"
Regarding the Anti-Inflammatory Activity of
Humic Substances
Prof. Dr. Renate Klocking & Dr. rer. nat. Bjorn Helbig
Institute for Antiviral Chemotherapy,
Friedrich Schiller University,
Jena, Germany

ANTI-INFLAMMATORY EFFECTS
Various healing effects of peat therapy were attributed to the anti-inflammatory activity
of (Humic Substances). Taugner (1963) showed in the rat paw edema model that
sodium humate significantly inhibits the development of various edemas compared with
untreated controls.
As found by Klocking et al. (1968) in the same model, ammonium humate isolated from
peat water exceeds the anti-inflammatory effect of sodium humate and is twice as
effective as acetylsalicylic acid (aspirin) and amino-phenazone, respectively. Amosova
et al. (1990), in evaluating the biologic activity of HA from Tambukan therapeutic mud in
animals, found (Humic Acid) (10 mg/kg) to suppress both phases of the inflammatory
process: the exudation (by 44 %) and the proliferation process (by 50-55%).
The anti-inflammatory effect of (Humic Substances) has been supported by a plausible
biochemical explanation. As demonstrated by Schewe et al. (1991), naturally occurring
(Humic Acid), and even more synthetic (Humic Acid)-like polymers, inhibit the
lipoxygenase pathway of the arachidonic acid (AA) cascade. AA is an integral part of
the cell membrane, and the substrate for the synthesis of eicosanoid-based
inflammation mediators such as leukotrienes, thromboxane and prostacyclin.
Recently, (Humic Acid) (sodium humate) as well as various synthetic HA-like polymers
were also found to suppress the heat-induced (42 8C, 6 h) AA release of human pro-
monocytic U937cells (Dunkelberg et al., 1997; Klocking et al., 1997). The inhibition of
AA release was most pronounced in cells treated with nontoxic concentrations (20
 mg/mL) of 3,4-DHPOP (96%) and 3,4-DHTOP (92%), respectively (Table 3). CHOP,
sodium humate, KOP and BOP protected cells from membrane damage at 65 ± 90%.
These findings may be indicative for membrane-protective activities of (Humic Acid)
type substances.
Unlike 5-lipoxygenase, phospholipase A (porcine pancreas), the rate-limiting key
enzyme of the AA cascade, is strongly activated at low (Humic Acid) concentrations (0.1
± 1 mg/mL) and normalized or slightly inhibited at high (Humic Acid) concentrations
(Klocking et al., 1999). The shape of the dose-response curve suggests (Humic
Substances) to have a regulatory function on PLA activity.
In referring to the function of (Humic Substances) as electron donor-acceptor system,
Jurcsik (1994) discussed the behavior of (Humic Substances) as the consequence of a
`buffering effect'; this means that (Humic Acids) are able to produce as well as to bind
activated oxygen species. This regulatory system is assumed to be important for the
favorable influence of (Humic Substances) on wound healing and killing of cancer cells
(Jurcsik, 1994).

DISCLAIMER: This website presents a collection of statements from around the world
about the benefits of Humic Acid. This information is provided for informational purposes
only. These statements were variously made over several decades of time. There are many
sources of Humic Acid around the globe, and they differ significantly in their physical and
chemical properties. This website does not intend to provide medical advice, nor does it
intend to suggest that all Humic Acid preparations will be of equal benefit. Nothing herein is
intended to be an endorsement of or a solicitation to purchase any particular Humic Acid
preparation. The FDA has not evaluated any statement made on this website. The
information herein is not intended to diagnose any disease, nor is it intended to prescribe
any preparation that claims to diagnose, treat, cure or prevent any disease.

Back to Anti-Inflammation Index