Prevennia works because it keeps the estrogen-DNA-adducts at low, normal, healthy levels. Best of all, Prevennia is all natural. Recent studies at Harvard Medical School and the Institute of Genetics and Molecular Biology have shown that resveratrol may radically reduce the risk of heart disease and age-related illnesses. But only Prevennia™ combines resveratrol perfectly with three other antioxidants.

NAC (N-Acetyl-L-Cysteine), reduces the amount of estrogen-DNA adducts and the resulting damage to DNA in two ways: first, it acts to block formation of the reactive estrogen metabolites and, second, NAC reacts itself with the reactive estrogen metabolites, thereby preventing them from reacting with DNA.

Lipoic Acid reduces the amount of estrogen-DNA adducts and the resulting damage to DNA in the same two ways as NAC, and it increases the amount of one of the estrogen-protective enzymes in cells.

Resveratrol also reduces the amount of estrogen-DNA adducts and the resulting damage to DNA in two ways: first, it acts to block formation of the reactive estrogen metabolites and, second, resveratrol increases the level of an enzyme in cells that converts the reactive estrogen metabolites to non-reactive metabolites, thereby limiting the formation of estrogen-DNA adducts.

Melatonin reduces the amount of estrogen-DNA adducts and the resulting damage to DNA by blocking formation of the reactive estrogen metabolites.

To distinguish healthy people at high or elevated risk for cancer (e.g., breast or prostate cancer), urine or blood samples can be analyzed for specific biomarkers, known as depurinating estrogen%u2010DNA adducts. For example, the ratio of these depurinating estrogen%u2010DNA adducts to their respective metabolites and conjugates serves as such a biomarker. It is important to not only determine the absolute levels of the adducts, but to also calculate the ratio of the adducts to their respective metabolites and conjugates to provide a more accurate diagnostic assay.

The testing methods developed by Drs. Cavalieri, Rogan and Jankowiak provide laboratory methods for identifying a person that is at an elevated risk for developing cancer. These methods determine the ratio of depurinating estrogen%u2010DNA adducts to their respective metabolites and conjugates in a biological sample from the subject. An increased level of the ratio, compared to controls (i.e., healthy, normal%u2010risk people), indicates whether the person is or is not at an elevated risk for developing cancer. At the present time these tests are not commercially available.

Figure 3. Second analysis of estrogen-DNA adducts in URINE from women.

Figures 4 and 5 depict depurinating estrogen–DNA adducts in the urine of healthy men and men with prostate cancer. Men in the healthy category have a significantly lower level of the depurinating estrogen%u2010DNA adducts than men with prostate cancer.

This research can trace its roots back to the 1960s, in Italy, when it was established that women working in shoe factories had very high levels of leukemia. The chemical benzene was used as the solvent. After elimination of benzene from the factories, cancer levels returned to normal. Since benzene has a pleasant aroma, this category of chemicals was called aromatic hydrocarbons.

Subsequent research into the chemical structure of estrogens showed that one of the four chemical "rings" that comprise estrogen is benzene. Unfortunately for humans, of the four ring structures in estrogens, the benzene ring is also the most reactive one. This reactivity led to further research by Dr. Cavalieri and Dr. Rogan on the ability of estrogens to cause cancer.

Estrogens are essential hormones in both men and women. In breast and prostate cancer, specific oxidative metabolites of estrogens, namely, catechol estrogen quinones, can react with DNA. DNA is repaired when damaged, but sometimes mistakes occur during this process. Thus, the catechol estrogen quinone metabolites are potential endogenous chemical carcinogens. The mutations generated by this DNA damage are thought to result in the initiation of breast and prostate cancer (Figure 6).

In the metabolism of the endogenous estrogens, estrone and estradiol, there are activating pathways that lead to the formation of the catechol estrogen quinones, which can react with DNA. There are also deactivating pathways that limit formation of the quinones and/or prevent their reaction with DNA.

Both stable and depurinating adducts are formed, but more than 99% of the estrogen-DNA adducts are depurinating adducts.Once the depurinating adducts are shed from the DNA, the release of these depurinating adducts generates apurinic sites (gaps) in the DNA, which, in turn, can induce mutations that lead to cancer. The initiation of cancer by estrogens is based on estrogen metabolism in which the homeostatic balance between activating and deactivating pathways is disrupted.

When estrogen metabolism is balanced, in other words in balance, the level of estrogen-DNA adducts in tissue and urine is low and/or the levels of estrogen metabolites and conjugates are high. In contrast, when estrogen metabolism is unbalanced, the level of DNA adducts in tissue and urine is high and/or the levels of estrogen metabolites and conjugates are low. It is the imbalance of estrogen metabolism, leading to relatively high levels of estrogen%u2010DNA adducts, that is thought to be a critical determinant of cancer initiation.

Cancer is a disease that begins with mutation of critical genes: oncogenes and tumor suppressor genes. Mutation of critical genes allows a cancer cell to develop and ultimately results in pathogenic loss of normal regulatory controls, leading to excessive cell proliferation of tumor cells in the human body. Conventional cancer treatments have focused mainly on killing cancerous cells. Such treatments threaten noncancerous cells, are inherently stressful to the human body, produce many side effects, and are of uncertain efficacy. Additionally, such treatment regimens are not necessarily directed toward the actual root of the cancer problem or its prevention.

One of the major obstacles in cancer research is that cancer is a problem of 200 diseases. This viewpoint has impeded researchers from looking at the etiology of cancers because the search would be prohibitively complex and expensive. For this reason, the etiology of breast, prostate and other human cancers remains virtually unknown. While the expression of various cancers coincides with the above concept, some scientist consider there to be a common origin for many prevalent types of cancer.

There is a widespread agreement in the scientific community that cancer is basically a genetic disease – not in the sense that most cancers are inherited, but in the sense that cancer is trigged by genetic mutations. Thus, cancer can be considered a disease of mutated critical genes that modulate cell growth and death. These include oncogenes and tumor suppressor genes, which give rise to transformation and abnormal cell proliferation. Understanding the origin of these mutations opens the door to strategies for controlling and preventing cancer. Drs. Cavalieri and Rogan have discovered a mechanism that initiates a cell, sending it on its way to becoming cancerous (Figure 6).

The catechol quinone metabolites of natural and synthetic estrogens, as well as benzene, react with DNA to form specific depurinating adducts that can lead to critical mutations responsible for initiating many prevalent types of cancer. Recognition of this unifying mechanism in the etiology of these diseases provides unique knowledge enabling development of strategies to assess risk and prevent cancer.

The dietary supplement, Prevennia, was formulated to reduce the levels of estrogen%u2010DNA adducts to healthy levels and to maintain people already at a healthy level (Figure 7).