Licorice Root for Cancer, Inflammation, Immune Boosting and Expectorant Qualities

Licorice Root for Cancer and Inflammation

Licorice Root Boost the Immune System

Licorice Root for Expectorant Effect

Hundreds of potentially healing substances have been identified in licorice as well, including compounds called flavonoids and various plant estrogens (phytoestrogens). The herb's key therapeutic compound, glycyrrhizin (which is 50 times sweeter than sugar) exerts numerous beneficial effects on the body, making licorice a valuable herb for treating a host of ailments. It seems to prevent the breakdown of adrenal hormones such as cortisol (the body's primary stress-fighting adrenal hormone), making these hormones more available to the body.

It has a well-documented reputation for healing ulcers. It can lower stomach acid levels, relieve heartburn and indigestion and acts as a mild laxative.

It can also be used for irritation, inflammation and spasm in the digestive tract. Through its beneficial action on the liver, it increases bile flow and lowers cholesterol levels.

Licorice also appears to enhance immunity by boosting levels of interferon, a key immune system chemical that fights off attacking viruses. It also contains powerful antioxidants. Glycyrrhizinic acid also seems to stop the growth of many bacteria and of viruses such as influenza A.

In the respiratory system it has a similarly soothing and healing action, reducing irritation and inflammation and has an expectorant effect, useful in irritating coughs, asthma and chest infections.

It has an aspirin-like action and is helpful in relieving fevers and soothing pain such as headaches. Its anti-allergenic effect is very useful for hay fever, allergic rhinitis, conjunctivitis and bronchial asthma. Possibly by its action on the adrenal glands, licorice has the ability to improve resistance to stress. It should be thought of during times of both physical and emotional stress, after surgery or during convalescence, or when feeling tired and run down.

Licorice with glycyrrhizin may help to:

Control respiratory problems and sore throat. Licorice eases congestion and coughing by helping to loosen and thin mucus in airways; this makes a cough more "productive," bringing up phlegm and other mucus bits. Licorice also helps to relax bronchial spasms. The herb also soothes soreness in the throat and fights viruses that cause respiratory illnesses and an overproduction of mucus.

Lessen symptoms of chronic fatigue syndrome and fibromyalgia. By enhancing cortisol activity, glycyrrhizin helps to increase energy, ease stress and reduce the symptoms of ailments sensitive to cortisol levels, such as chronic fatigue syndrome, cancer, and fibromylagia.

Such “miracle remedies” allow us to temporarily push disease from consciousness during times when complete healing seems out of practical or philosophical reach. However, when opting to alleviate your dog’s pain and suffering, it is important to realize that suppression of symptoms will seldom constitute a complete cure – especially when the effectiveness of an anti-inflammatory or analgesic drug prompts us to forget the real problems. Of course, our decisions to use such remedies are based largely on personal freedom of choice.

But what about our animals? They don’t enjoy such freedom of choice. Instead they must rely upon us to make weighty decisions on their behalf, and as caring guardians who are tormented by the sight of a suffering companion, we sometimes find ourselves with the difficult choice of providing comfort over cure.

Of course we wish for our companion animals to have a long, healthy life, without the liver-damaging effects of anti-inflammatory drug therapies or the immunosuppressive results of corticosteroid drugs – but we also wish for them to be comfortable.

Fortunately, there are a few herbs that stand out from all others in their ability to address both sides of this difficult issue. Some herbs can provide not only a holistic therapeutic approach, but also a measure of comfort and relief during periods of crisis. In fact, one of the best of these “near-miracle herbs” is easy to find, grows like a weed, and tastes like candy.

I am referring to the Glycyrrhizza species, licorice, an ancient medicine with a multitude of modern applications.

Healing history
The ethnobotanical use of licorice dates back thousands of years, and its history in veterinary applications is probably just as ancient. In Europe it has been considered a valued medicine and trade commodity for at least a thousand years. By the 13th century licorice was already being cultivated for international trade. And in China, licorice is still used in more applications than any other herb – even more than ginseng.

Licorice root is useful for maladies ranging from stomach upset and ulcers to the treatment of cancer. And unlike many botanical medicines that are seen by science as anecdotal curiosities, contemporary herbalists and modern researchers continue to validate the effectiveness of licorice with modern science. Literal libraries of information have been compiled on the attributes of Glycyrrhizza – and it appears that we have only begun to scratch the surface of what this wonderful herb has to offer.

Anti-inflammatory action
Most people who have taken their animals to a conventional veterinarian for treatment of a chronic inflammatory disorder have witnessed the bittersweet use of hydrocortisone and other corticosteroid drugs (such as prednisone). In many ways these drugs are close to “miracle medicines” in their ability to relieve inflammation, itchiness, and even the symptoms of cancer and nervous diseases.

But almost as quickly as we embrace the wonders of steroid therapies we are forced to recognize that they are seldom a “cure” for anything. The side effects associated with steroid drugs may be worse that the disease we wish to combat; almost immediately we can expect to see acute water retention and weight gain, and as time passes (often within two weeks), side effects may also include hypertension, altered mood and personality, heart attack, osteoporosis, and chronic illness due to depressed immune function. In many cases, antibiotics, strong diuretics, and mineral supplements become necessary just to antidote the corticosteroids.

To illustrate the implications of corticosteroid therapies all we need to do is look at how cortisone-like drugs actually work: they suppress the immune system functions and inflammatory responses that are responsible for an animal’s discomfort. By decreasing natural production of lymphocytes and antibodies, and by altering normal defensive functions of the body, corticosteroids can often make disease symptoms disappear very quickly. However, continued use of corticosteroids will eventually induce a serious state of immune deficiency that can be very difficult to reverse, and can even be fatal.


One of the problems with treating lick
granulomas is that dogs will inevitably
ingest any topical preparation you use.
This isn’t a problem with licorice.

Fortunately, licorice root may provide us with some safer options. Several studies have confirmed its usefulness as an effective, fast-acting, anti-inflammatory agent. In fact, many holistic practitioners use licorice as a substitute for anti-inflammatory drugs or to reduce an animal’s need for cortico-steroids.

The anti-inflammatory activity of licorice root is primarily attributable to a chemical called “glycyrrhizin” present in the plant. Glycyrrhizin is similar to the natural cortisone that is released by the body’s adrenal glands. Glycyrrhizin effectively stimulates the adrenals into action, while introducing its own anti-inflammatory, anti-microbial, immune-supporting corticosteroid-like actions to the body. As a result, licorice helps relieve pain, itching, and inflammation without completely bypassing normal anti-inflammatory functions, and without seriously compromising the immune system.

All of this makes licorice useful against a wide variety of inflammatory diseases. In a study where arthritis was induced into rats through injections of formaldehyde (I know this is terrible!), a by-product of glycyrrhizin called glycyrretic acid was produced in the body and was shown to have obvious anti-arthritic actions that are comparable to those of hydrocortisone.

Glycyrrhizin has also been shown to potentiate the effects of cortisone-like drugs in the body. This makes the herb a useful adjunct in corticosteroid therapies, as the drug-strengthening effect of licorice will allow for lower drug dosages without comprising therapeutic effectiveness. When used in this capacity licorice may help reduce the debilitating side effects of steroid drugs in long term therapies, and may also be useful in assuring safe withdrawal when the patient is weaned off of the steroids.

Skin benefits
The anti-inflammatory properties of licorice root are also useful when topically applied. Licorice tea, salve, or oil infusion can be used to relieve the uncomfortable symptoms of various skin disorders, such as psoriasis, eczema, contact dermatitis, and flea-bite allergies.

Liver benefits
In addition to its powerful anti-inflammatory actions, licorice root is also useful in the treatment and prevention of many forms of liver disease. Over the past two decades, medical researchers in China and Japan have found (through animal studies) that extracts of licorice root are useful in the treatment of chronic and chemically induced hepatitis, and that the herb has liver-protectant qualities that are no less significant than those offered by the popular liver herb, milk thistle (Silybum marianum).

However, the mechanisms by which licorice root works in the liver are quite different from those of milk thistle. While milk thistle has been shown to resist liver cell destruction largely through protection of the cell walls and by antioxidant actions, licorice works through a broader diversity of effects.

In addition to a protectant action that glycyrrhizin has upon the liver cells, licorice also enhances interferon and T-cell production, two natural actions that are critical to liver repair and general resistance to disease.

In Chinese medicine, licorice is commonly used as a “liver detoxifier” in the treatment of obstructive jaundice. And in several studies licorice has been shown to benefit animals who are suffering from liver damage due to absorbed or ingested toxins, such as carbon tetrachloride.

Immune system benefits
In a very recent study, the root of Glycyrrhizza uralensis (an Asian species of licorice) was found to have a potentiating effect on the reticuloendothelial system; the body’s first line of defense against infection. In essence, the reticulo-endothelial system is comprised of specialized cells whose jobs are to seek out and eliminate invading microbes and dead blood cells, and licorice helps to stimulate these little bloodstream warriors into action.

Using licorice
Like all herbal medicines, a major problem with the use of licorice in animals is getting it into them, or keeping it on them. Here licorice affords us another comfort; it’s naturally sweet! In fact the sweet flavor of licorice is often used to mask the unpleasant flavor of other herbs.

The next time you give your dog an herb she hates, try adding a small percentage of low-alcohol licorice root extract (say 5 - 10 percent) to the total volume of the dose. You may find that the sweet flavor makes the administration experience more pleasant for both of you, and even if the “taste test” fails, you have potentiated your other herbs with the healing benefits of licorice!



Contraindications
Like all herbal medicines, the primary rule is moderation and insight when using licorice. Most herbalists and practitioners will agree that the risks of adverse side effects from licorice are limited to those who recklessly abuse it.

I have never seen a case of licorice-induced toxicity – but if used in very large, highly concentrated doses (especially over long periods of time), it is conceivable that corticosteroid-like side effects could occur, including water retention, hypertension, and loss of potassium, sodium retention and other symptoms of adrenal hyperactivity. In human studies, the large majority of these side effects have been observed following the excessive consumption of European licorice candy, which is made from a very concentrated, pressed extract of the root. (Most licorice candy produced in America contains absolutely no real licorice, but instead an artificial flavoring or the extracts of other plants that taste similar). Nevertheless, licorice should not be used with reckless abandon.

Animals with pre-existing cardiovascular conditions should not be given licorice without professional guidance.

References

1. Madisch A, Holtmann G, Mayr G, et al. Treatment of functional dyspepsia with a herbal preparation. A double-blind, randomized, placebo-controlled, multicenter trial. Digestion. 2004;69(1):45-52.
2. Gupta VK, Fatima A, Faridi U, et al. Antimicrobial potential of Glycyrrhiza glabra roots. J Ethnopharmacol. Mar 5 2008;116(2):377-380.
3. Jo EH, Hong HD, Ahn NC, et al. Modulations of the Bcl-2/Bax family were involved in the chemopreventive effects of licorice root (Glycyrrhiza uralensis Fisch) in MCF-7 human breast cancer cell. J Agric Food Chem. Mar 24 2004;52(6):1715-1719.
4. Takahashi T, Takasuka N, Iigo M, et al. Isoliquiritigenin, a flavonoid from licorice, reduces prostaglandin E2 and nitric oxide, causes apoptosis, and suppresses aberrant crypt foci development. Cancer Sci. May 2004;95(5):448-453..
5. Newall CA, Anderson LA, Phillipson JD. Herbal Medicines: A Guide for Health-Care Professionals. 1st ed. London: Pharmaceutical Press; 1996.
6. Blumenthal M, Goldberg A, Brinckmann J, et al. Herbal Medicine, Expanded Commission E Monographs. Austin: American Botanical Council; 2000.
7. Tyler V. Herbs of Choice, the Therapeutical Use of Phytomedicinals. Binghamton: Pharmaceutical Press; 1994.
8. Miyamura M, Ono M, Kyotani S, et al. [Properties of glycyrrhizin in Kampo extracts including licorice root and changes in the blood concentration of glycyrrhetic acid after oral administration of Kampo extracts]. Yakugaku Zasshi. Mar 1996;116(3):209-216.
9. Badr AE, Omar N, Badria FA. A laboratory evaluation of the antibacterial and cytotoxic effect of Liquorice when used as root canal medicament. Int Endod J. 2010 Aug 31.
10. Kim YH, Shin EK, Kim DH, et al. Antiangiogenic effect of licochalcone A. Biochem Pharmacol.2010 Oct 15;80(8):1152-9.
11. Park SY, Lim SS, Kim JK, et al. Hexane-ethanol extract of Glycyrrhiza uralensis containing licoricidin inhibits the metastatic capacity of DU145 human prostate cancer cells. Br J Nutr. 2010 May 21:1-11.
12. Chandrasekaran CV, Deepak HB, Thiyagarajan P, et al. Dual inhibitory effect of Glycyrrhiza glabra (GutGard™) on COX and LOX products. Phytomedicine. 2010 Sep 21.
13. Gol'dberg ED, Amosova EN, Zueva EP, et al. Licorice preparations improve efficiency of chemotherapy and surgical treatment of transplanted tumors. Bull Exp Biol Med. 2008 Feb;145(2):252-5.

Lucy takes 1 Swanson Licorice Root capsule

Panax or Korean Red Ginseng and Cancer

Effects of Panax or Korean Red Ginseng on Cancer

Red or Panax ginseng is used in traditional Chinese medicine as a prophylactic, a stimulant, and a
treatment for various diseases. In addition, ginseng has been found to enhance the immune
system and possess an anti-tumor effect. Ginseng appears to stimulate humoral and cellmediated
immune responses and the subsequent increase in titers of lymphocytes and circulating
antibodies. Furthermore, ginseng's cancer-prevention properties seem to be mediated through
the increased production of interferons and cytokines, which activate natural killer and cytotoxic
T-cells that can served to lyse or inhibit growing tumors. Both clinical and epidemiological studies
indicated that Panax ginseng can reduce the incidence of cancer in vivo. These results suggest
that ginseng shows antitumor effects as an immunomodulator.

Introduction
Korean Red (Panax) Ginseng is a traditional Chinese medicinal herb that has occupied an esteemed
position among the tonic medications since antiquity and has become quite popular
among the patrons of health food stores. The term ginseng means "essence of man"
because it has been touted as a revitalizing agent. Ginseng has been used for several
thousands of years in the Orient as a tonic, prophylactic agent, and restorative. Other
people have found that it enhances the immune system and possess anti-tumor effects.
Recent studies have reported that saponin from Panax ginseng protects against
myocardial and cerebral ischemic damage in different animal models (1).

Perhaps one of the most fascinating and potentially therapeutic effects of Panax ginseng
is its ability to enhance the immune response in the body. Recent studies have
investigated the effects of ginseng on the immune system in order to find new possible
components that may support the treatment of infectious and immunodeficient diseases.

Ginseng has been shown to slow growing tumors and inhibit the incidence of lung
adenoma (6). In epidemiological studies, ginseng uptake reduces the incidence of human
cancer (6). It has been suggested that ginseng may increase activity in the nonspecific
resistance of an organism to combat tumor growth. This paper will evaluate the effects of
ginseng on the immune system in animal studies and recent clinical evaluations. Perhaps
by understanding the effects of Panax ginseng, we can study its possible effects of
preventing cancer.

Immuno-mediating Effects
The landmark paper which first evaluated the effect of ginseng extract on the expression
of humoral and cell mediated immune responses showed that the number of antibody
forming cells, as well as the titers of circulatory antibodies, are enhanced if test animals
are pretreated with ginseng extract. On the fourth day after the injection of the antigen
(sheep's red blood cells) in mice, the antibody titer of the ginseng treated group was twofold
higher than that of the control group; on the tenth day, the treated group showed a
four-fold higher titer. They also had data that showed elevated natural killer (NK) cell
activity in comparison to control animals. These experiments led the way in determining
ginseng's immunostimulatory effects (7).

The use of polysaccharides from plants and herbs as immunostimulants has aroused great
interest in recent years. Immunotherapy is currently receiving great attention as support
treatment modalities in the management of cancer and AIDS patients whose immune
function is compromised. The polysaccharides extracted from Panax ginseng have been
investigated to determine their effects on the immune system. These polysaccharide
fractions were all tested for their anticomplementary activities using human serum and
antibody-sensitized sheep RBC. Complement systems play an important role in fighting
against various infections and tumors. Those active polysaccharides were found to be
able to stimulate the complement system possibly by enhancing the production of
interferon y (INF-y) by activated T-cells. INF-y is important in immune defense against
various viral infections and in the regulation of cell-mediated immune response.
Interferons are secreted by an infected cell as an early, non-specific defense before
specific antibodies appear. Interferons can protect uninfected cells by stimulating the
production of proteins that inhibit viral replication. Furthermore, the defense is not virus specific;
interferons produced in response to one viral strain confer resistance to unrelated
viruses. Thus, interferons are most effective in controlling short-term infections, such as
cold and influenza. This effect of ginseng is confirmed by Scoglione et al. (11) which
shows that a standardized extract of ginseng could induce a higher immune response in
vaccination against influenza.

 In a randomized, placebo controlled, double blind investigation of 227 volunteers, the frequency of influenza or the common cold was significantly less (p<0.001) in volunteers who received daily oral doses of ginseng as opposed to a placebo group (11). By the eighth week, antibody titers rose to an average of 272 units in the treatment group as opposed to 171 units in the placebo group (p<0.0001).
At concentrations from nanomolar to low micromolar range, ginseng polysaccharides can
significantly induce the production of TNF-a by mouse peritoneal macrophages (8). TNFa
has profound effects in the immune system, including tumor, cytotoxic, antiviral, and
anti-parasitic activities. TNF-a also causes inflammation and endotoxic shock, which may
be responsible for some possible side effects of polysaccharides. Thus, one of the
hypothesized activities of ginseng extracts is that they stimulate the complement system
by enhancing the production of INF-y and TNF-a .

Ginseng has also significantly enhanced natural killer cell function, which is part of the
body's nonspecific defense mechanisms. The ability of ginseng to boost NK cell activity
hints at its cancer preventive mechanisms. NK cells do not attack microorganisms
directly, but rather destroy the body's own infected cells. The NK cells also assault and
lyse aberrant cells that could form tumors. Peripheral blood mononuclear cells (PBMC)
either from normal individuals or from patients with either AIDS or chronic fatigue
syndrome (CFS) were treated with increased concentration of Panax ginseng extract. For
each group, increased concentrations of the herb progressively increased both the
antibody dependant cellular cytotoxicity and natural killer cell function (9). The presence
of ginseng extract significantly enhanced NK-function by PBMC from normal controls at
concentrations of greater than 10 ug/ml and cells from patients with either CFS or AIDS
at concentrations of greater than 1 ug/ml. Thus, extracts of Panax ginseng enhance
cellular immune function of PBMC both from normal individuals and patients with
depressed cellular immunity. NK cells have been demonstrated to lyse HIV infected cells
(10). If the clinical efficacy of immune stimulation in CFS and/or HIV-infected patients
were eventually demonstrated, the use of immune modulators may be an attractive
therapeutic alternative.

Even in healthy individuals, ginseng has been shown to be an immunopotentiating agent.
A controlled, double-blind study with standardized Panax ginseng extract against a
placebo found that a randomized group of 60 healthy volunteers given ginseng showed
significant increases in chemotaxis and NK activity as well as rises in phagocytosis
function (12). This group also demonstrated significant (p < 0.001) increases in total
lymphocytes (T3) and helper T4 percentages after consuming a capsule (100-mg ginseng
extract) every 12 hours for eight weeks. These data show that ginseng extracts are able to
stimulate an immune response in humans.

Isolated fractions of an immunomodulator from ginseng were used to test its tumor
inhibitory activity. Ethanol-insoluble extracts of ginseng were first demonstrated to
generate active killer T- cells through endogenously produced IL-2 (13). Peripheral blood
lymphocytes derived from humans or animals can be activated by IL-2 and become
highly cytotoxic against various malignant cells. IL-2 is a cytokine that signals other
lymphocytes to grow and proliferate. Thus, they can increase the supply of T
lymphocytes that can differentiate into cytotoxic T-cells. Because cancer cells carry
distinctive non-self molecular markers, cytotoxic T-cells can target the cancer cells and
lyse them. The injection of IL-2 can therefore mediate regression of selected metastatic
tumors in mice and humans. Yun et al. tested whether the endogenously produced IL-2
mediated the in vivo anti-tumor activity through the activation of lymphocytes (14).
Isolated IL-2 fractions that activated natural killer cells were tested in a benzo[a]pyrene
(BP) induced autochthonous lung tumor model. BP is an environmental carcinogen. The
incidence of lung tumor in the BP alone group was 55% at the ninth week after BP
treatment and it was significantly deceased by the treatment with ginseng extract. The
incidence decreased by 60% (p<0.05) in mice concurrently administered drinking water
containing 2 mg/ml ginseng extract for 6 weeks(14). The inhibition of lung tumor
incidence was dose dependent, indicating that ginseng can have specific effects that can
be augmented by increasing concentrations. Furthermore, Yang (15) found that injection
of ginseng partially restored the number and colony of activity in bone marrow cells,
which significantly enhanced the production of interleukin-1, interleukin-3, and
interleukin-6 like substances from immune cells.
Since 1978 Yun et al. have set out to investigate if ginseng can inhibit carcinogenesis.
These researchers demonstrated that Panax ginseng extract has anticarcinogenic effects
against pulmonary tumors induced by various chemical carcinogens. Mice injected
subcutaneously with BP within 24 hours of birth and which continued to receive ginseng
extracts in drinking water showed a significant decrease in incidence of lung adenoma.
This report is consistent with the anticarcinogenic effects of Korean Red or Panax ginseng described
earlier. These researchers then began a human case-control study to further determine the
effect of ginseng consumption in cancer resistance. In a recent study of almost 2,000
patients and matched controls in the Korea Cancer Center, ginseng intake resulted in a
decreased risk for cancer (odds ratio= 0.5) (16). In addition, their results showed a
decreased risk with rising frequency of ginseng intake.


Conclusion
Ginseng has been used for nearly 2,000 years for its prophylactic and anti-tumor effects.
Also, as Panax ginseng sales and public use continue to grow nationally, it is important to
encourage efforts to study the efficacy of ginseng in humans.
The results of the above experiments and epidemiological studies confirm that Panax
ginseng has various anticarcinogenic and immunomodulatory effects. While the exact
mechanism of ginseng pharmacology remains to be solved, these studies suggest that
Panax ginseng contains ingredients that stimulated humoral and cell mediated immune
responses. Enhanced production of interferons can help to inhibit viral replication,
helping to prevent infection. Increased antibody and lymphocyte titers may be very useful
in helping cancer and AIDS patients, whose immune functions are compromised.
Stimulating NK can cytotoxic T-cell activity can lyse and help fight or prevent against
growing tumor cells. These promising results may perhaps one day offer a powerful
adjunct to immuno- and cancer therapy.

REFERENCES
1. Chen X. Cardiovascular protection by ginsenosides and their nitric oxide
releasing action. Clinical and Experimental Pharmacology and Physiology
1996;23:728-732.
2. Sotaniemi EA, Haapakoski E, Rautio A. Ginseng therapy in non-insulindependant
diabetic patients. Diabetes Care 1995;10:1373-1375.
3. Kwan CY. Vascular effects of selected antihypertensive drugs derived from
traditional medicinal herbs. Clinical and Experimental Pharmacology and
Physiology 1995;1:297-9.
4. Gillis CN. Panax ginseng pharmacology: a nitric oxide link? Biochemical
Pharmacology 1997;54:1-8.
5. Engels HJ, Wirth JC. No ergogenic effects of ginseng (Panax Ginseng C.A.
Meyer) during graded maximal aerobic exercise. Journal of the American Dietetic
Association. 1997;97:1110-5.
Nutrition Bytes, 4(1), Article 7 (1998)
6. Yun TK. Experimental and epidemiological evidence of the cancer-preventive
effects of Panax ginseng C.A. Meyer. Nutrition Reviews 1996;54:S71-S81.
7. Singh VK, Agarwal SS, Gupta BM. Immunomodulatory Activity of Panax
ginseng extract. Planta Medica 1984;6:462-465.
8. Gao H, Fengzhen W, Lien EJ, Trousdale MD. Immunostimulating
Polysaccharides from Panax notoginseng. Pharmaceutical Research
1996;13:1196-1200.
9. See DM, Broumand N, Sahl L, Tilles JG. In vitro effects of echinacea and ginseng
on natural killer and antibody-dependent cell cytotoxicity in health subjects and
chronic fatigue syndrome or acquired immunodeficiency syndrome patients.
Immunopharmacology 1997;35:229-235.
10. Jenkins M, Mills J, Kohl S. Natural killer cytotoxicity of human
immunodeficiency virus-infected cells by leukocytes from human neonates and
adults. Pediatric Research 1993;33:469-474.
11. Scoglione F, Cattaneo G, Alessandria M, Cogo R. Efficacy and safety of the
standardized ginseng extract G115 for potentiating vaccination against common
cold and/or influenza syndrome. Drugs Under Experimental and Clinical
Research 1996;22:65-72.
12. Scoglione F, Ferrara F, Dugnani S, Falchi M, Santoro G, Fraschini F.
Immunomodulatory effects of two extracts of Panax Ginseng C.A. Meyer. Drugs
Under Experimental and Clinical Research 1990;16:537-542.
13. West WH, Tauer K, Yannelli JR, Marshall GD, Orr DW, Thurman GB, Oldham
RK. Constant-infusion recombinant interleukin-2 in adoptive immunotherapy of
advanced cancer. New England Journal of Medicine 1987;316:898-905.
14. Yun YS, Lee YS, Jo SK, Jung IS. Inhibition of autochthonous tumor by ethanol
insoluble fraction from Panax ginseng as an immunomodulator. Planta Medica
1993;59:521-524.
15. Yang G. Immunologic effect of traditional Chinese drugs. Chinese Medical
Journal 1996;109:590-60.
16. Yun TK, Choi SY. Preventive effect of ginseng intake against various human
cancers: A case-control study on 1987 Pairs. Cancer Epidemiology, Biomarkers,
and Prevention 1995;4:401-408.

Lucy's still in nasal cancer remission Jan 2012

Lucy's STILL in nasal cancer remission Jan 2012.  She shows no nasal cancer symptoms. No mucous, no bleeding, no changes to palate, eye, snout, eating habits, or activity.

This is will be 21 MONTHS post diagnosis by rhinoscopy biopsy.

Cancer treatment only consists of my research (Tippner Protocol) based on a highly diversified Orthomolecular attack for treatment. There is no magic pill. The body is too complex.
Meaning boatloads of easily health food store type pills.... And real mostly homemade food that gets her to eat them.

I will post a video of her playing in our yard shortly.

Resveratrol activity in cancer

Research studies continue to find more interesting benefits from this compound, including potential anti-cancer and anti-aging activity. It is not surprising that extensive research from all over the globe indicates that it has a wide range of beneficial properties.

Resveratrol ( trans-3,5,4'-trihydroxystilbene ) is a protective compound produced by grapes and other plants in response to environmental stresses. Studies have demonstrated that it has potent antioxidant activity and also has the ability to inhibit platelet aggregation. These actions may help prevent free radical damage throughout the body and provide protective support to the cardiovascular system.

Where is it found?
  Much of the resveratrol sold in supplement form is from the herb Polygonum cuspidatum which is available in various extract potencies, ranging from 5 percent to 50 percent.
Potential benefits
Over the next few years we are likely to discover that resveratrol has potential in the therapy of many conditions. It is a potent chemical and studies show it has anti-inflammatory, antioxidant, anti-infective properties, and it activates the longevity gene in fruit flies and worms.

Anti-aging and longevity
As to its anti-aging potential, resveratrol activates a cell's survival defense enzyme, which prolongs the time cells have to repair their broken DNA. It acts on fruit flies and worms in the same way as a method known to extend the life of animals including monkeys -- sharply restricting how much they eat. Resveratrol has been found to help mice live longer. Thus far, the research has focused in animals, worms and fruit flies, and we have no idea what would happen if humans ingested this supplement for prolonged periods, and how it interacts with other supplements or medications. Most of the resveratrol supplements on the market are an extract, usually 5 to 40 percent, of an herb called Polygonum cuspidatum which has a very high content of the substance. Therefore, when you take a resveratrol pill, you are also ingesting many other substances found within this herb.Resveratrol improves health and survival of mice on a high-calorie diet.
Nature. 2006.

Blood flow to brain
Effects of resveratrol on cerebral blood flow variables and cognitive performance in humans: a double-blind, placebo-controlled, crossover investigation
American Journal of Clinical Nutrition, 2010.
The many putative beneficial effects of the polyphenol resveratrol include an ability to bolster endogenous antioxidant defenses, modulate nitric oxide synthesis, and promote vasodilation, which thereby improves blood flow. In this study, 22 healthy adults received placebo and 2 doses (250 and 500 mg) of trans-resveratrol in counterbalanced order on separate days. After a 45-min resting absorption period, the participants performed a selection of cognitive tasks that activate the frontal cortex. Administration resulted in dose-dependent increases in cerebral blood flow during task performance. Cognitive function was not affected.Cancer
Recent laboratory studies indicate that resveratrol has promising therapeutic activity in various cancers, including breast, prostate, and neuroblastoma. Human studies are lacking at this time.

Role of resveratrol in prevention and therapy of cancer: preclinical and clinical studies.
Anticancer Res. 2004.
Resveratrol exhibits anticancer properties as suggested by its ability to suppress proliferation of a wide variety of tumor cells, including lymphoid and myeloid cancers; multiple myeloma; cancers of the breast, prostate, stomach, colon, pancreas, and thyroid; melanoma; head and neck squamous cell carcinoma; ovarian carcinoma; and cervical carcinoma. The growth-inhibitory effects are mediated through cell-cycle arrest; upregulation of p21Cip1/WAF1, p53 and Bax; down-regulation of survivin, cyclin D1, cyclin E, Bcl-2, Bcl-xL and clAPs; and activation of caspases.

Breast cancer
Identification of a p53-dependent pathway in the induction of apoptosis of human breast cancer cells by the natural product, resveratrol.
J Altern Complement Med. 2004.

Glioma
Resveratrol suppresses the angiogenesis and tumor growth of gliomas in rats.
Clin Cancer Res. 2004.

Lung cancer
Consumption of red wine is associated with a slight but statistically significant reduction in the development of lung cancer, as reported in the journal Thorax.

Neuroblastoma
NB is an aggressive childhood cancer of the peripheral nervous system arising from neural crest sympathoadrenal progenitor cells.

Curcumin and resveratrol induce apoptosis and nuclear translocation and activation of p53 in human neuroblastoma.
Anticancer Res. 2004.

Prostate cancer
Coral Lamartiniere, at the University of Alabama at Birmingham's Department of Pharmacology and Toxicology, gave male mice resveratrol, the equivalent of that found in a bottle of red wine in humans, and discovered that the mice were significantly less likely to develop prostate cancer.

Curcumin synergizes with resveratrol to inhibit colon cancer.
www.ncbi.nlm.nih.gov/pubmed/19838927
by AP Majumdar - 2009 - Cited by 36 - Majumdar AP, Banerjee S, Nautiyal J, Patel BB, Patel V, Du J, Yu Y, Elliott AA, Levi E, Sarkar FH .

Resveratrol inhibits pancreatic cancer stem cell characteristics in ...
www.ncbi.nlm.nih.gov/pubmed/21304978
by S Shankar - 2011 - Cited by 40 - Related articles
Jan 31, 2011 – Resveratrol inhibits pancreatic cancer stem cell characteristics in human and KrasG12D transgenic mice by inhibiting pluripotency maintaining ...
Role of resveratrol in prevention and therapy of cancer: preclinical ...

www.ncbi.nlm.nih.gov/pubmed/15517885
by BB Aggarwal - 2004 - Cited by 704 - Related articles
Role of resveratrol in prevention and therapy of cancer: preclinical and clinical studies. Aggarwal BB, Bhardwaj A, Aggarwal RS, Seeram NP, Shishodia S, ...
Resveratrol: a review of preclinical studies for human cancer ...
www.ncbi.nlm.nih.gov/pubmed/17306316
by M Athar - 2007 - Cited by 292 - Related articles

Nov 1, 2007 – Resveratrol: a review of preclinical studies for human cancer prevention. Athar M, Back JH, Tang X, Kim KH, Kopelovich L, Bickers DR, Kim AL.

Resveratrol - Wikipedia, the free encyclopedia
en.wikipedia.org/wiki/Resveratrol
There have since been many studies of the anti-cancer activity of resveratrol in animal models. ..... //www.ncbi.nlm.nih.gov/pmc/articles/PMC2893585/.

Cancer prevention

In 1997, Jang reported that topical resveratrol applications prevented skin cancer development in mice treated with a carcinogen.[33] There have since been many studies of the anti-cancer activity of resveratrol in animal models.[12]

Resveratrol has been shown to induce apoptosis in platelets,[34][35] and smooth muscle.[36][36][37]

Clinical trials to investigate the effects on colon cancer and melanoma (skin cancer) are currently recruiting patients.[39] The study of pharmacokinetics of resveratrol in humans concluded, however, that even high doses of resveratrol might be insufficient to achieve the resveratrol concentrations required for the systemic prevention of cancer.[40]

This is consistent with the results from the animal cancer models, which indicate the in vivo effectiveness of resveratrol is limited by its poor systemic bioavailability.[41][42] The strongest evidence of anticancer action of resveratrol exists for tumors it can contact directly, such as skin and gastrointestinal tract tumors. For other cancers, the evidence is uncertain, even if massive doses of resveratrol are used.[38]

Thus, resveratrol (1 mg/kg orally) reduced the number and size of the esophageal tumors in rats treated with a carcinogen;[43] and in several studies, small doses (0.02–8 mg/kg) of resveratrol, given prophylactically, reduced or prevented the development of intestinal and colon tumors in rats given different carcinogens.[38] Similarly, topical application of resveratrol in mice, both before and after the UVB exposure, inhibited the skin damage and decreased skin cancer incidence, however, oral resveratrol was ineffective in treating mice inoculated with melanoma cells. Resveratrol given orally also had no effect on leukemia and lung cancer;[38][44] however, injected intraperitoneally, 2.5 or 10 mg/kg of resveratrol slowed the growth of metastatic Lewis lung carcinomas in mice.[38][45]

Resveratrol treatment appeared to prevent the development of mammary tumors in animal models; however, it had no effect on the growth of existing tumors. Paradoxically, treatment of prepubertal mice with high doses of resveratrol enhanced formation of tumors. Injected in high doses into mice, resveratrol slowed the growth of neuroblastomas.[38]

Anti-inflammatory effects

The anti-inflammatory effects of resveratrol have been demonstrated in several animal model studies. In a rat model of carrageenan-induced paw edema, resveratrol inhibited both acute and chronic phases of the inflammatory process.[84] Similarly, preincubation with resveratrol decreased arachidonic acid release and COX-2 induction in mouse peritoneal macrophages stimulated with tumor promoter PMA, ROI, or lipopolysaccharides (LPS).[85] In an experimental rabbit inflammatory arthritis model, resveratrol showed promise as a potential therapy for arthritis. When administered to rabbits with induced inflammatory arthritis, resveratrol protected cartilage against the progression of inflammatory arthritis.[86]

Resveratrol interferes with all three stages of carcinogenesis—initiation, promotion and progression. Experiments in cell cultures of varied types and isolated subcellular systems in vitro imply many mechanisms in the pharmacological activity of resveratrol. These mechanisms include modulation of the transcription factor NF-κB,[138] inhibition of the cytochrome P450 isoenzyme CYP1A1[139] (although this may not be relevant to the CYP1A1-mediated bioactivation of the procarcinogen benzo(a)pyrene),[140] alterations in androgenic [141] actions, and expression and activity of cyclooxygenase (COX) enzymes. In vitro, resveratrol "inhibited the proliferation of human pancreatic cancer cell lines." In some lineages of cancer cell culture, resveratrol has been shown to induce apoptosis, which means it kills cells and may kill cancer cells.[141][142][143][144][145][146] Resveratrol has been shown to induce Fas/Fas ligand mediated apoptosis, p53 and cyclins A, B1, and cyclin-dependent kinases cdk 1 and 2. Resveratrol also possesses antioxidant and anti-angiogenic properties.[11



I give Lucy a 85# Lab 8 years old, 1   100mg Resveratrol capsule in AM meal.

N-acetyl cysteine (NAC) blocks cancer development and helps mucous

Cancer 



What You Need to Know: NAC N-Acetyl Cysteine’s Broad-Spectrum Benefits 

N-acetyl Cysteine  NAC also helps with mucus

For more than three decades, a safe, low-cost readily available compound has provided millions of people relief from the coughing, wheezing, and thick phlegm associated with cold and flu. Of course, pharmaceutical companies long ago co-opted it for profit by actually incorporating it into various patented drugs.

NAC is so effective at reducing nasal and bronchial congestion that according to one frequently quoted, now classic, study published in 1997, many people don’t even notice they are sick. De Flora et al enrolled 262 mostly older subjects and gave them either 600 mg of NAC twice a day or placebo for a 6-month period from fall until spring. Treatment with NAC significantly reduced flu-like episodes. Yet at the end of the study similar percentages of treatment and placebo groups showed they had caught the flu when their blood antibodies were tested. Of those who tested positive for the flu, only 25% of the NAC takers reported noticing symptoms while 79% of those receiving the placebo group had been noticeably sick.

Long relegated to infrequent use in unusual circumstances, the amino acid-derived compound N-acetyl cysteine (NAC) has drawn much increased scientific attention. 

NAC replenishes levels of the intracellular antioxidant glutathione (GSH), which is often deficient with advancing age and in chronic illness.
NAC also regulates expression of scores of genes in the pathways that link oxidative stress to inflammation.
These dual effects give NAC a unique role in the prevention and treatment of many common diseases, both acute and chronic.
NAC reduces the frequency and duration of attacks of chronic obstructive pulmonary disease (COPD) and may slow the clinical course of idiopathic pulmonary fibrosis (IPF). (MUCOUS AWAY!)NAC improves insulin sensitivity in people with some of the most difficult-to-treat metabolic disorders.   (CANCER LOVES GLUCOSE)NAC blocks cancer development at virtually every step in the process, and through multiple mechanisms, making it an important cancer chemopreventive agent.

Though most human individuals gain benefits from 600-1,800 mg/day, clinical studies have found that doses of up to 2,000 mg/day are safe and effective. A recent study demonstrated the safety of 2,800 mg/day for 3 months in patients with COPD.23



The strong and growing links between oxidative stress, inflammation, and cancer make NAC a natural go-to compound for cancer chemoprevention. True to form, NAC has multiple anti-cancer activities acting at multiple targets to provide layers of cancer protection against a large variety of cancer types. NAC induces programmed cell death (apoptosis) in multiple types of human cancer cells.62 In human gastric cancer cells, NAC not only induces apoptosis, but also stops DNA synthesis, preventing cancer the cells from replicating.63 In melanoma cells, NAC inhibits NF-kB, preventing expression of signaling molecules needed by the cancer for growth.64 NAC inactivates and promotes destruction of c-Src, a chemical control molecule that is overproduced in many human cancers, providing a completely unique means of slowing or stopping tumor development.65 Finally, NAC protects DNA from breakage induced by ionizing radiation, but does not prevent cell destruction by radiation.66 That’s a vital finding because it means that NAC might allow radiation therapy to effectively kill cancer cells while minimizing the risk of so-called secondary cancers that could otherwise arise as side effects of the radiation.

Animal studies strengthen the case for NAC still further. NAC protects mice from cigarette smoke-induced lung cancers and other lung changes, a finding with enormous implications not only for current smokers but for ex-smokers and people exposed to second-hand smoke.67 NAC protects rats from chemically-induced liver cancers immediately following tumor initiation.68 This early interference with cancer development bodes well for NAC as a chemopreventive agent in the many human toxin-related cancers.

Human studies are similarly encouraging, even in the most challenging patient groups such as smokers. A randomized, double-blind chemoprevention trial of NAC 600 mg twice daily for 6 months vs. placebo in otherwise healthy smokers showed a significant reduction in formation of damaged or oxidized DNA segments, telltale early markers of cancer development in lung fluid.69 The same study also demonstrated reductions in abnormal, pre-cancerous cell changes in the mouths of supplemented smokers. These effects support the scientists’ conclusion that NAC can reduce tobacco smoke carcinogenicity in humans.

Colon cancer is another malignancy with strong links to oxidative stress and inflammation. Preliminary studies in humans show a 40% reduction in colorectal polyps in patients given 600 mg per day of NAC, compared with controls.70 In a group of people with a previous history of pre-cancerous colonic polyps, 800 mg per day of NAC for 12 weeks significantly reduced the proliferative index, indicating a decreased risk of colon cancer.71

Supplementing with 600-1,200 mg per day of NAC appears to be an entirely appropriate means of adding to your general cancer-prevention strategy.


An Underutilized Intervention

NAC is a slightly modified version of the sulfur-containing amino acid cysteine. When taken internally, NAC replenishes intracellular levels of the natural antioxidant glutathione (GSH), helping to restore cells’ ability to fight damage from reactive oxygen species (ROS).

NAC has been used in conventional medicine for more than 30 years, primarily as a mucolytic (mucous-thinner) inhaled to manage conditions such as cystic fibrosis, in which mucous is abnormally thick and tenacious. While there is little in the scientific literature to support its use as an inhalant, NAC administered in this form remains highly popular among experienced pulmonary speclialists.4,5

NAC given intravenously or orally, on the other hand, saves lives every year as a treatment for acute poisoning with acetaminophen-containing pain-relieving drugs. Acetaminophen is sold as Tylenol® and combined with other drugs to create analgesic compounds, including Vicodin® and Percocet®.6 Overdoses with acetaminophen are the number one cause of acute liver failure in the United States.6-8 Too much acetaminophen overwhelms the body’s glutathione reserves, which creates widespread and irreversible liver damage. NAC quickly restores protective levels of glutathione, averting catastrophe.7

Beyond this particular application, NAC has remained a relatively obscure and poorly understood compound until quite recently. Scientists all over the world are now beginning to understand just how vital glutathione metabolism really is, and how many disease states involve glutathione deficiency.9 According to Stanford University’s Dr. Kondala R. Atkuri, “NAC has been used successfully to treat glutathione deficiency in a wide range of infections, genetic defects and metabolic disorders, including HIV infection and COPD. Over two-thirds of 46 placebo-controlled clinical trials with orally administered NAC have indicated beneficial effects of NAC measured either as trial endpoints or as general measures of improvement in quality of life and well-being of the patients.”9
Multitargeted Regulation of Gene Expression


Much of NAC’s beneficial activity derives from its capacity to modulate expression of genes for myriad signaling molecules in the inflammatory response.10-12 NAC inhibits expression of pro-inflammatory cytokines following exposure to bacterial cell components and infection with influenza A virus.13,14 NAC suppresses the “master signaling molecule” nuclear factor-kappaB (NF-kB), which in turn prevents activation of multiple inflammatory mediators.15,16 NAC also regulates the gene for COX-2, the enzyme that produces pain- and inflammation-inducing prostaglandins in a wide array of chronic conditions.17

NAC’s ability to replenish the intracellular glutathione supply and mitigate oxidative damage is a separate and equally powerful mechanism that affords protection against DNA damage and cancer development, even in smokers.18 NAC’s inhibition of inflammatory cytokine production is another mechanism credited with cancer reduction in various body tissues.19

Gene expression modifications induced by NAC may also help reduce the acute oxidant-provoked inflammatory response following exercise, making vigorous activity safer and even more beneficial.20 Finally, obesity-associated insulin resistance, which arises from production of inflammatory signaling molecules in fat cells, can be sharply mitigated by NAC through regulation of their genes.21,22

The recent explosion of scientific evidence for NAC’s multi-targeted health benefits is matched only by the willful ignorance of the mainstream medical community. Some even question its safety, despite nearly 40 years of use in a variety of clinical conditions, which have established the safety of this compound, even at very high doses and for long-term treatments.18 One study demonstrated the safety of 1,800 mg per day for 142 days, while another study demonstrated the safety of 2,800 mg per day for 3 months.23


Summary

N-acetyl cysteine is a broad-spectrum compound traditionally under-utilized in conventional medicine. A burst of new clinical research reveals that NAC exerts dual effects, functioning both as a powerful antioxidant that replenishes cellular antioxidant systems (glutathione in particular) and also as a potent modulator of gene expression, regulating inflammation at multiple, fundamental levels. It has been shown to be an effective intervention against influenza, chronic lung diseases (helps mucous), cancers, insulin resistance, and gastritis caused by H. pylori. NAC’s further value is shown in its ability to mitigate otherwise inevitable metabolic and immunological disturbances caused by exercise.

A synthetic N-acetyl derivative of the endogenous amino acid L-cysteine, a precursor of the antioxidant enzyme glutathione. Acetylcysteine regenerates liver stores of glutathione. This agent also reduces disulfide bonds in mucoproteins, resulting in liquification of mucus. Some evidence suggests that acetylcysteine may exert an anti-apoptotic effect due to its antioxidant activity, possibly preventing cancer cell development or growth.

Chemotherapy benefit
There is a condition called "chemo-brain," which effects a large number of cancer patients receiving chemotherapy patients. Patients with this condition suffer from memory loss and have difficulty with focus and concentration. Dr. Gregory W. Konat at West Virginia University School of Medicine in Morgantown first gave one group of rats to two drugs commonly used to treat cancer, Adriamycin and Cytoxan. These drugs led to memory problems. However, memory loss was prevented when the rats were given n-acetylcysteine injections three times per week during chemotherapy. Metabolic Brain Disease, 2008.

N acetyl cysteine prevents cisplatin induced ototoxicity in rats
Hearing Res 2004.
Animals were treated with acetylcysteine or saline 15 or 30 minutes before receiving cisplatin or 4 hours afterward. The treated rats showed no significant change in auditory brainstem response with cisplatin therapy. In contrast, the saline-treated animals displayed marked ototoxicity (damage to hearing).



Kidney disease and peritoneal dialysis
In patients with chronic kidney disease, inflammation and oxidative stress are cardiovascular risk factors. A study looked at the effect of oral NAC on plasma levels of inflammatory and oxidative stress markers in peritoneal dialysis patients. The eight week, placebo-controlled study included 30 patients on regular peritoneal dialysis. Twelve patients were treated twice daily with 600 mg of NAC and the remaining ten patients received placebo. NAC significantly decreased IL-6 levels without adverse side effects. Treatment reduced the inflammatory response in peritoneal dialysis patients. Nascimento MM, Suliman ME. Effect of oral N-Acetylcysteine treatment on plasma inflammatory and oxidative stress markers in peritoneal dialysis patients. Perit Dial Int. 2010.

N Acetyl cysteine in nephrology; contrast nephropathy and beyond.
Curr Opin Nephrol Hypertension. 2004.
At least 19 randomized trials evaluating acetylcysteine for the prevention of radiocontrast-induced nephropathy, at least five meta-analyses, and several reviews on that topic have been published within the past few years. One study indicated that long-term antioxidative treatment with acetylcysteine significantly reduced cardiovascular events in patients with end-stage renal failure. Although there are controversies on dosing and timing, its use together with hydration should be considered to protect patients from radiographic contrast media-induced nephropathy.

Nephropathy prevention
Researchers randomly assigned 354 consecutive patients undergoing primary angioplasty to one of three groups: 116 patients were assigned to a standard dose of N-acetylcysteine (a 600-mg intravenous bolus before primary angioplasty and 600 mg orally twice daily for the 48 hours after angioplasty), 119 patients to a double dose (a 1200-mg intravenous bolus and 1200 mg orally twice daily for the 48 hours after intervention), and 119 patients to placebo. Intravenous and oral N-acetylcysteine may prevent contrast-medium–induced nephropathy with a dose-dependent effect in patients treated with primary angioplasty and may improve hospital outcome.

NAC is so effective at reducing nasal and bronchial congestion that according to one frequently quoted, now classic, study published in 1997, many people don’t even notice they are sick. De Flora et al enrolled 262 mostly older subjects and gave them either 600 mg of NAC twice a day or placebo for a 6-month period from fall until spring. Treatment with NAC significantly reduced flu-like episodes. Yet at the end of the study similar percentages of treatment and placebo groups showed they had caught the flu when their blood antibodies were tested. Of those who tested positive for the flu, only 25% of the NAC takers reported noticing symptoms while 79% of those receiving the placebo group had been noticeably sick.


References

1.Chun LJ, Tong MJ, Busuttil RW, Hiatt JR. Acetaminophen hepatotoxicity and acute liver failure. Clin Gastroenterol. 2009 Apr;43(4):342-9.

2.Simonsen L, Taylor RJ, Viboud C, Miller MA, Jackson LA. Mortality benefits of influenza vaccination in elderly people: an ongoing controversy. Lancet Infect Dis. 2007 Oct;7(10):658-66.

3.Konturek PC, Konturek SJ, Brzozowski T. Helicobacter pylori infection in gastric cancerogenesis. J Physiol Pharmacol. 2009 Sep;60(3):3-21

4.Henke MO, Ratjen F. Mucolytics in cystic fibrosis. Paediatr Respir Rev. 2007 Mar;8(1):24-9.

5.Rogers DF. Mucoactive agents for airway mucus hypersecretory diseases. Respir Care. 2007 Sep;52(9):1176-93; discussion 93-7.

6.Marchetti A, Rossiter R. Managing acute acetaminophen poisoning with oral versus intravenous N-acetyl cysteine: a provider-perspective cost analysis. J Med Econ. 2009;12(4):384-91.

7.Saito C, Zwingmann C, Jaeschke H. Novel mechanisms of protection against acetaminophen hepatotoxicity in mice by glutathione and N-acetyl cysteine. Hepatology. Jan;51(1):246-54.

8.Chun LJ, Tong MJ, Busuttil RW, Hiatt JR. Acetaminophen hepatotoxicity and acute liver failure. J Clin Gastroenterol. 2009 Apr;43(4):342-9.

9.Atkuri KR, Mantovani JJ, Herzenberg LA. N-Acetyl cysteine—a safe antidote for cysteine/glutathione deficiency. Curr Opin Pharmacol. 2007 Aug;7(4):355-9.

10.Blesa S, Cortijo J, Mata M, et al. Oral N-acetyl cysteine attenuates the rat pulmonary inflammatory response to antigen. Eur Respir J. 2003 Mar;21(3):394-400.

11.Majano PL, Medina J, Zubia I, et al. N-Acetyl-cysteine modulates inducible nitric oxide synthase gene expression in human hepatocytes. J Hepatol. 2004 Apr;40(4):632-7.

12.Siddiqui A, Ancha H, Tedesco D, Lightfoot S, Stewart CA, Harty RF. Antioxidant therapy with N-acetyl cysteine plus mesalamine accelerates mucosal healing in a rodent model of colitis. Dig Dis Sci. 2006 Apr;51(4):698-705.

13.Geiler J, Michaelis M, Naczk P, et al. N-acetyl-L-cysteine (NAC) inhibits virus replication and expression of pro-inflammatory molecules in A549 cells infected with highly pathogenic H5N1 influenza A virus. Biochem Pharmacol. Feb 1;79(3):413-20.

14.Jiang XF, Zeng WY, Pu J, Liu YM. Effect of N-acetyl cysteine on lipopolysaccharide stimulating IL-8 expression of human uterine smooth cell. Sichuan Da Xue Xue Bao Yi Xue Ban. 2008 Mar;39(2):235-8.

15.Kim H, Seo JY, Roh KH, Lim JW, Kim KH. Suppression of NF-kappaB activation and cytokine production by N-acetyl cysteine in pancreatic acinar cells. Free Radic Biol Med. 2000 Oct 1;29(7):674-83.

16.Chen G, Shi J, Hu Z, Hang C. Inhibitory effect on cerebral inflammatory response following traumatic brain injury in rats: a potential neuroprotective mechanism of N-acetyl cysteine. Mediators Inflamm. 2008;2008:716458.

17.Origuchi T, Migita K, Nakashima T, et al. Regulation of cyclooxygenase-2 expression in human osteoblastic cells by N-acetyl cysteine. J Lab Clin Med. 2000 Nov;136(5):390-4.

18.De Flora S, Izzotti A, D’Agostini F, Balansky RM. Mechanisms of N-acetyl cysteine in the prevention of DNA damage and cancer, with special reference to smoking-related end-points. Carcinogenesis. 2001 Jul;22(7):999-1013.

19.Seo JY, Kim H, Kim KH. Transcriptional regulation by thiol compounds in Helicobacter pylori-induced interleukin-8 production in human gastric epithelial cells. Ann N Y Acad Sci. 2002 Nov;973:541-5.

20.Kerksick C, Willoughby D. The antioxidant role of glutathione and N-acetyl-cysteine supplements and exercise-induced oxidative stress. J Int Soc Sports Nutr. 2005;2:38-44.

21.Lin Y, Berg AH, Iyengar P, et al. The hyperglycemia-induced inflammatory response in adipocytes: the role of reactive oxygen species. J Biol Chem. 2005 Feb 11;280(6):4617-26.

22.Unoki H, Bujo H, Yamagishi S, Takeuchi M, Imaizumi T, Saito Y. Advanced glycation end products attenuate cellular insulin sensitivity by increasing the generation of intracellular reactive oxygen species in adipocytes. Diabetes Res Clin Pract. 2007 May;76(2):236-44.

23.Dauletbaev N, Fischer P, Aulbach B, et al. A phase II study on safety and efficacy of high-dose N-acetyl cysteine in patients with cystic fibrosis. Eur J Med Res. 2009 Aug 12;14(8):352-8.

24.Us D. Cytokine storm in avian influenza. Mikrobiyol Bul. 2008 Apr;42(2):365-80.

25.De Flora S, Grassi C, Carati L. Attenuation of influenza-like symptomatology and improvement of cell-mediated immunity with long-term N-acetyl cysteine treatment. Eur Respir J. 1997 Jul;10(7):1535-41.

26.Knobil K, Choi AM, Weigand GW, Jacoby DB. Role of oxidants in influenza virus-induced gene expression. Am J Physiol. 1998 Jan;274(1 Pt 1):L134-42.

27.Kujime K, Hashimoto S, Gon Y, Shimizu K, Horie T. p38 mitogen-activated protein kinase and c-jun-NH2-terminal kinase regulate RANTES production by influenza virus-infected human bronchial epithelial cells. J Immunol. 2000 Mar 15;164(6):3222-8.

28.Lowy RJ, Dimitrov DS. Characterization of influenza virus-induced death of J774.1 macrophages. Exp Cell Res. 1997 Aug 1;234(2):249-58.

29.Ungheri D, Pisani C, Sanson G, et al. Protective effect of n-acetyl cysteine in a model of influenza infection in mice. Int J Immunopathol Pharmacol. 2000 Sep-Dec;13(3):123-28.

30.McCarty MF, Barroso-Aranda J, Contreras F. Practical strategies for targeting NF-kappaB and NADPH oxidase may improve survival during lethal influenza epidemics. Med Hypotheses. Jan;74(1):18-20.

31.Garozzo A, Tempera G, Ungheri D, Timpanaro R, Castro A. N-acetyl cysteine synergizes with oseltamivir in protecting mice from lethal influenza infection. Int J Immunopathol Pharmacol. 2007 Apr-Jun;20(2):349-54.

32.Ghezzi P, Ungheri D. Synergistic combination of N-acetyl cysteine and ribavirin to protect from lethal influenza viral infection in a mouse model. Int J Immunopathol Pharmacol. 2004 Jan-Apr;17(1):99-102.

33.Jariwalla RJ, Roomi MW, Gangapurkar B, Kalinovsky T, Niedzwiecki A, Rath M. Suppression of influenza A virus nuclear antigen production and neuraminidase activity by a nutrient mixture containing ascorbic acid, green tea extract and amino acids. Biofactors. 2007;31(1):1-15.

34.Deryabin PG, Lvov DK, Botikov AG, et al. Effects of a nutrient mixture on infectious properties of the highly pathogenic strain of avian influenza virus A/H5N1. Biofactors. 2008;33(2):85-97.

35.Reichenberger F, Tamm M. N-acetylcystein in the therapy of chronic bronchitis. Pneumologie. 2002 Dec;56(12):793-7.

36.Sadowska AM, van Overveld FJ, Gorecka D, et al. The interrelationship between markers of inflammation and oxidative stress in chronic obstructive pulmonary disease: modulation by inhaled steroids and antioxidant. Respir Med. 2005 Feb;99(2):241-9.

37.Stav D, Raz M. Effect of N-acetyl cysteine on air trapping in COPD: a randomized placebo-controlled study. Chest. 2009 Aug;136(2):381-6.

38.Foschino Barbaro MP, Serviddio G, Resta O, et al. Oxygen therapy at low flow causes oxidative stress in chronic obstructive pulmonary disease: Prevention by N-acetyl cysteine. Free Radic Res. 2005 Oct;39(10):1111-8.

39.De Benedetto F, Aceto A, Dragani B, et al. Long-term oral n-acetyl cysteine reduces exhaled hydrogen peroxide in stable COPD. Pulm Pharmacol Ther. 2005;18(1):41-7.

40.van Overveld FJ, Demkow U, Gorecka D, de Backer WA, Zielinski J. New developments in the treatment of COPD: comparing the effects of inhaled corticosteroids and N-acetyl cysteine. J Physiol Pharmacol. 2005 Sep;56 Suppl 4:135-42.

41.Cai S, Chen P, Zhang C, Chen JB, Wu J. Oral N-acetyl cysteine attenuates pulmonary emphysema and alveolar septal cell apoptosis in smoking-induced COPD in rats. Respirology. 2009 Apr;14(3):354-9.

42.Meyer A, Buhl R, Magnussen H. The effect of oral N-acetyl cysteine on lung glutathione levels in idiopathic pulmonary fibrosis. Eur Respir J. 1994 Mar;7(3):431-6.

43.Demedts M, Behr J, Buhl R, et al. High-dose acetylcysteine in idiopathic pulmonary fibrosis. N Engl J Med. 2005 Nov 24;353(21):2229-42.

44.Tomioka H, Kuwata Y, Imanaka K, et al. A pilot study of aerosolized N-acetyl cysteine for idiopathic pulmonary fibrosis. Respirology. 2005 Sep;10(4):449-55.

45.Cottin V, Cordier JF. Idiopathic pulmonary fibrosis. Presse Med. 2008 Nov;37(11):1581-90.

46.Felton VM, Borok Z, Willis BC. N-acetyl cysteine inhibits alveolar epithelial-mesenchymal transition. Am J Physiol Lung Cell Mol Physiol. 2009 Nov;297(5):L805-12.

47.Peake J, Suzuki K. Neutrophil activation, antioxidant supplements and exercise-induced oxidative stress. Exerc Immunol Rev. 2004;10:129-41.

48.Quadrilatero J, Hoffman-Goetz L. N-Acetyl-L-cysteine prevents exercise-induced intestinal lymphocyte apoptosis by maintaining intracellular glutathione levels and reducing mitochondrial membrane depolarization. Biochem Biophys Res Commun. 2004 Jul 2;319(3):894-901.

49.Vassilakopoulos T, Karatza MH, Katsaounou P, Kollintza A, Zakynthinos S, Roussos C. Antioxidants attenuate the plasma cytokine response to exercise in humans. J Appl Physiol. 2003 Mar;94(3):1025-32.

50.Koechlin C, Couillard A, Simar D, et al. Does oxidative stress alter quadriceps endurance in chronic obstructive pulmonary disease? Am J Respir Crit Care Med. 2004 May 1;169(9):1022-7.

51.Zembron-Lacny A, Szyszka K, Szygula Z. Effect of cysteine derivatives administration in healthy men exposed to intense resistance exercise by evaluation of pro-antioxidant ratio. J Physiol Sci. 2007 Dec;57(6):343-8.

52.Aguiar AS, Jr., Tuon T, Soares FS, da Rocha LG, Silveira PC, Pinho RA. The effect of n-acetyl cysteine and deferoxamine on exercise-induced oxidative damage in striatum and hippocampus of mice. Neurochem Res. 2008 May;33(5):729-36.

53.Quadrilatero J, Hoffman-Goetz L. N-acetyl-l-cysteine protects intestinal lymphocytes from apoptotic death after acute exercise in adrenalectomized mice. Am J Physiol Regul Integr Comp Physiol. 2005 Jun;288(6):R1664-72.

54.Quadrilatero J, Hoffman-Goetz L. N-acetyl-L-cysteine inhibits exercise-induced lymphocyte apoptotic protein alterations. Med Sci Sports Exerc. 2005 Jan;37(1):53-6.

55.Kruger K, Frost S, Most E, Volker K, Pallauf J, Mooren FC. Exercise affects tissue lymphocyte apoptosis via redox-sensitive and Fas-dependent signaling pathways. Am J Physiol Regul Integr Comp Physiol. 2009 May;296(5):R1518-27.

56.Evans JL, Maddux BA, Goldfine ID. The molecular basis for oxidative stress-induced insulin resistance. Antioxid Redox Signal. 2005 Jul-Aug;7(7-8):1040-52.

57.Anuradha CV. Aminoacid support in the prevention of diabetes and diabetic complications. Curr Protein Pept Sci. 2009 Feb;10(1):8-17.

58.Guo Q, Mori T, Jiang Y, et al. Methylglyoxal contributes to the development of insulin resistance and salt sensitivity in Sprague-Dawley rats. J Hypertens. 2009 Aug;27(8):1664-71.

59.Song D, Hutchings S, Pang CC. Chronic N-acetyl cysteine prevents fructose-induced insulin resistance and hypertension in rats. Eur J Pharmacol. 2005 Jan 31;508(1-3):205-10.

60.Masha A, Manieri C, Dinatale S, Bruno GA, Ghigo E, Martina V. Prolonged treatment with N-acetyl cysteine and L-arginine restores gonadal function in patients with PCO syndrome. J Endocrinol Invest. 2009 Apr 15.

61.Fulghesu AM, Ciampelli M, Muzj G, et al. N-acetyl-cysteine treatment improves insulin sensitivity in women with polycystic ovary syndrome. Fertil Steril. 2002 Jun;77(6):1128-35.

62.Guan D, Xu Y, Yang M, Wang H, Wang X, Shen Z. N-acetyl cysteine and penicillamine induce apoptosis via the ER stress response-signaling pathway. Mol Carcinog. 2010 Jan;49(1):68-74.

63.Li J, Tu HJ, Dai G, et al. N-acetyl cysteine inhibits human signet ring cell gastric cancer cell line (SJ-89) cell growth by inducing apoptosis and DNA synthesis arrest. Eur J Gastroenterol Hepatol. 2007 Sep;19(9):769-74.

64.Yang J, Su Y, Richmond A. Antioxidants tiron and N-acetyl-L-cysteine differentially mediate apoptosis in melanoma cells via a reactive oxygen species-independent NF-kappaB pathway. Free Radic Biol Med. 2007 May 1;42(9):1369-80.

65.Krasnowska EK, Pittaluga E, Brunati AM, et al. N-acetyl-l-cysteine fosters inactivation and transfer to endolysosomes of c-Src. Free Radic Biol Med. 2008 Dec 1;45(11):1566-72.

66.Reliene R, Pollard JM, Sobol Z, Trouiller B, Gatti RA, Schiestl RH. N-acetyl cysteine protects against ionizing radiation-induced DNA damage but not against cell killing in yeast and mammals. Mutat Res. 2009 Jun 1;665(1-2):37-43.

67.Balansky R, Ganchev G, Iltcheva M, Steele VE, De Flora S. Prevention of cigarette smoke-induced lung tumors in mice by budesonide, phenethyl isothiocyanate, and N-acetyl cysteine. Int J Cancer. 2010 Mar 1;126(5):1047-54.

68.Nishikawa-Ogawa M, Wanibuchi H, Morimura K, et al. N-acetyl cysteine and S-methylcysteine inhibit MeIQx rat hepatocarcinogenesis in the post-initiation stage. Carcinogenesis. 2006 May;27(5):982-8.

69.Van Schooten FJ, Besaratinia A, De Flora S, et al. Effects of oral administration of N-acetyl-L-cysteine: a multi-biomarker study in smokers. Cancer Epidemiol Biomarkers Prev. 2002 Feb;11(2):167-75.

70.Ponz de Leon M, Roncucci L. Chemoprevention of colorectal tumors: role of lactulose and of other agents. Scand J Gastroenterol Suppl. 1997;222:72-5.

71.Estensen RD, Levy M, Klopp SJ, et al. N-acetyl cysteine suppression of the proliferative index in the colon of patients with previous adenomatous colonic polyps. Cancer Lett. 1999 Dec 1;147(1-2):109-14.

72.Huynh HQ, Couper RT, Tran CD, Moore L, Kelso R, Butler RN. N-acetyl cysteine, a novel treatment for Helicobacter pylori infection. Dig Dis Sci. 2004 Nov-Dec;49(11-12):1853-61.

73.Kim MH, Yoo HS, Kim MY, et al. Helicobacter pylori stimulates urokinase plasminogen activator receptor expression and cell invasiveness through reactive oxygen species and NF-kappaB signaling in human gastric carcinoma cells. Int J Mol Med. 2007 Apr;19(4):689-97.

74.Zala G, Flury R, Wust J, Meyenberger C, Ammann R, Wirth HP. Omeprazole/amoxicillin: improved eradication of Helicobacter pylori in smokers because of N-acetyl cysteine. Schweiz Med Wochenschr. 1994 Aug 9;124(31-32):1391-7.

75.Gurbuz AK, Ozel AM, Ozturk R, Yildirim S, Yazgan Y, Demirturk L. Effect of N-acetyl cysteine on Helicobacter pylori. South Med J. 2005 Nov;98(11):1095-7.

76.Palmer LA, Doctor A, Chhabra P, et al. S-nitrosothiols signal hypoxia-mimetic vascular pathology. J Clin Invest. 2007 Sep;117(9):2592-601.

77.Stenmark KR, Meyrick B, Galie N, Mooi WJ, McMurtry IF. Animal models of pulmonary arterial hypertension: the hope for etiological discovery and pharmacological cure. Am J Physiol Lung Cell Mol Physiol. 2009 Dec;297(6):L1013-32.

78.Sajkov D, McEvoy RD. Obstructive sleep apnea and pulmonary hypertension. Prog Cardiovasc Dis. 2009 Mar-Apr;51(5):363-70.

79.Kaldararova M. Why is pulmonary hypertension so frustrating? Bratisl Lek Listy. 2009;110(9):536-43.

80.Hoshikawa Y, Ono S, Suzuki S, et al. Generation of oxidative stress contributes to the development of pulmonary hypertension induced by hypoxia. J Appl Physiol. 2001 Apr;90(4):1299-306.

81.Marsden PA. Low-molecular-weight S-nitrosothiols and blood vessel injury. J Clin Invest. 2007 Sep;117(9):2377-80.

82.Lachmanova V, Hnilickova O, Povysilova V, Hampl V, Herget J. N-acetyl cysteine inhibits hypoxic pulmonary hypertension most effectively in the initial phase of chronic hypoxia. Life Sci. 2005 May 27;77(2):175-82.

83.Chuang IC, Liu DD, Kao SJ, Chen HI. N-acetyl cysteine attenuates the acute lung injury caused by phorbol myristate acetate in isolated rat lungs. Pulm Pharmacol Ther. 2007;20(6):726-33.

84.Liu DD, Kao SJ, Chen HI. N-acetyl cysteine attenuates acute lung injury induced by fat embolism. Crit Care Med. 2008 Feb;36(2):565-71.

85.Hildebrandt W, Alexander S, Bartsch P, Droge W. Effect of N-acetyl-cysteine on the hypoxic ventilatory response and erythropoietin production: linkage between plasma thiol redox state and O(2) chemosensitivity. Blood. 2002 Mar 1;99(5):1552-5.

86.Iturriaga R, Rey S, Del Rio R, Moya EA, Alcayaga J. Cardioventilatory acclimatization induced by chronic intermittent hypoxia. Adv Exp Med Biol. 2009;648:329-35.



I HAVE BEEN GIVING LUCY 1 800gm capsule of NAC at AM Meal.