Cannabis: the Cancer Cure...

Existing Drug Becomes Cheap Cancer Cure In Canada

University of Alberta scientists do understand the cause of cancer. The dying off of old cells to be replaced by new cells is a normal part of our cellular life-cycle and keeps us well. It seems that in cancerous cells, our body has forgotten how to tell the aged cells how to die off and be replaced by healthy new cells.

This process is governed by the mitochondria and is known as "cell death" or "apoptosis". In a cancer cell, the mitochondria has lost the ability to direct the cell to die off - the sick cell becomes "immortal", spreading and making the person increasingly unwell.

Trials using  dichloroacetate (DCA) have proven this compound can reactivate the mitochondria restoring the cell's original function of "apoptosis" enabling shrinkage in tumor size and mass. Testimonials have shown reversal in illness, remission, clean health tests, increased health and vitality. Favourable results (scientifically measurable) have been accomplished within days (less than a week) of starting treatment with DCA.

"Dr. Evangelos Michelakis, a professor at the University of Alberta Department of Medicine, has shown that DCA causes regression in several cancers, including lung, breast, and brain tumors."

It sounds too good to be true: a cheap and simple drug that kills almost all cancers by switching off their immortality. The drug, dichloroacetate (DCA), has already been used for years to treat rare metabolic disorders and so is known to be relatively safe.

It also has no patent, meaning it could be manufactured for a fraction of the cost of newly developed drugs.

Evangelos Michelakis of the University of Alberta in Edmonton, Canada, and his colleagues tested DCA on human cells cultured outside the body and found that it killed lung, breast and brain cancer cells, but not healthy cells. Tumours in rats deliberately infected with human cancer also shrank drastically when they were fed DCA-laced water for several weeks.

DCA attacks a unique feature of cancer cells: the fact that they make their energy throughout the main body of the cell, rather than in distinct organelles called mitochondria. This process, called glycolysis, is inefficient and uses up vast amounts of sugar.

Until now it had been assumed that cancer cells used glycolysis because their mitochondria were irreparably damaged. However, Michelakiss experiments prove this is not the case, because DCA reawakened the mitochondria in cancer cells. The cells then withered and died (Cancer Cell).

Michelakis suggests that the switch to glycolysis as an energy source occurs when cells in the middle of an abnormal but benign lump dont get enough oxygen for their mitochondria to work properly (see diagram). In order to survive, they switch off their mitochondria and start producing energy through glycolysis.

Crucially, though, mitochondria do another job in cells: they activate apoptosis, the process by which abnormal cells self-destruct. When cells switch mitochondria off, they become immortal, outliving other cells in the tumour and so becoming dominant. Once reawakened by DCA, mitochondria reactivate apoptosis and order the abnormal cells to die.

The results are intriguing because they point to a critical role that mitochondria play:  they impart a unique trait to cancer cells that can be exploited for cancer therapy, says Dario Altieri, director of the University of Massachusetts Cancer Center in Worcester.

The phenomenon might also explain how secondary cancers form. Glycolysis generates lactic acid, which can break down the collagen matrix holding cells together. This means abnormal cells can be released and float to other parts of the body, where they seed new tumours.

DCA can cause pain, numbness and gait disturbances in some patients, but this may be a price worth paying if it turns out to be effective against all cancers. The next step is to run clinical trials of DCA in people with cancer. These may have to be funded by charities, universities and governments: pharmaceutical companies are unlikely to pay because they cant make money on unpatented medicines. The pay-off is that if DCA does work, it will be easy to manufacture and dirt cheap.

Cancer Can be Cured in Weeks

Doctor testing drug to ‘prevent’ lesbianism, interest in ‘male careers’

(Oh, this has to be the most ludicrous waste of time, money, and resources EVER! And how many poor dumb couples will risk harm to their baby by having this concoction administered to them so their little girl won't be gay? Sick, sick, sick!--jef)

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By John Byrne | Wednesday, June 30th, 2010

Dr. Maria New has a new strategy for treating unborn fetuses: the use of a potentially dangerous steroid aimed at preventing a rare congenital disorder that affects the adrenal gland, potentially consigning the future child to a lifetime regime of drugs.

It also prevents "some of the symptoms of [this disorder] in girls, namely ambiguous genitalia. Because the condition causes overproduction of male hormones in the womb, girls who are affected tend to have genitals that look more male than female, though internal sex organs are normal."

Dr. New offers pregnant women dexamethasone, a risky steroid aimed at female fetuses that may have this disorder. Many exposed to dexamethasone through this off-label use are not being enrolled in controlled clinical trials.

And yes, it gets worse. As columnist Dan Savage points out, Dr. New is also exploring the use of dexmethasone's effects on future fetuses' desires to explore "male careers" or have disinterest in becoming mothers.

The majority of researchers and clinicians interested in the use of prenatal “dex” focus on preventing development of ambiguous genitalia in girls with CAH. CAH results in an excess of androgens prenatally, and this can lead to a “masculinizing” of a female fetus’s genitals. One group of researchers, however, seems to be suggesting that prenatal dex also might prevent affected girls from turning out to be homosexual or bisexual.

Pediatric endocrinologist Maria New, of Mount Sinai School of Medicine and Florida International University, and her long-time collaborator, psychologist Heino F. L. Meyer-Bahlburg, of Columbia University, have been tracing evidence for the influence of prenatal androgens in sexual orientation.... They specifically point to reasons to believe that it is prenatal androgens that have an impact on the development of sexual orientation. The authors write, "Most women were heterosexual, but the rates of bisexual and homosexual orientation were increased above controls . . . and correlated with the degree of prenatal androgenization.” They go on to suggest that the work might offer some insight into the influence of prenatal hormones on the development of sexual orientation in general. “That this may apply also to sexual orientation in at least a subgroup of women is suggested by the fact that earlier research has repeatedly shown that about one-third of homosexual women have (modestly) increased levels of androgens.” They “conclude that the findings support a sexual-differentiation perspective involving prenatal androgens on the development of sexual orientation.”

And it isn’t just that many women with CAH have a lower interest, compared to other women, in having sex with men. In another paper entitled “What Causes Low Rates of Child-Bearing in Congenital Adrenal Hyperplasia?” Meyer-Bahlburg writes that “CAH women as a group have a lower interest than controls in getting married and performing the traditional child-care/housewife role. As children, they show an unusually low interest in engaging in maternal play with baby dolls, and their interest in caring for infants, the frequency of daydreams or fantasies of pregnancy and motherhood, or the expressed wish of experiencing pregnancy and having children of their own appear to be relatively low in all age groups.”

In the same article, Meyer-Bahlburg suggests that treatments with prenatal dexamethasone might cause these girls’ behavior to be closer to the expectation of heterosexual norms: “Long term follow-up studies of the behavioral outcome will show whether dexamethasone treatment also prevents the effects of prenatal androgens on brain and behavior.”

In a paper published just this year in the Annals of the New York Academy of Sciences, New and her colleague, pediatric endocrinologist Saroj Nimkarn of Weill Cornell Medical College, go further, constructing low interest in babies and men—and even interest in what they consider to be men’s occupations and games—as “abnormal,” and potentially preventable with prenatal dex:

“Gender-related behaviors, namely childhood play, peer association, career and leisure time preferences in adolescence and adulthood, maternalism, aggression, and sexual orientation become masculinized in 46,XX girls and women with 21OHD deficiency [CAH]. These abnormalities have been attributed to the effects of excessive prenatal androgen levels on the sexual differentiation of the brain and later on behavior.” Nimkarn and New continue: “We anticipate that prenatal dexamethasone therapy will reduce the well-documented behavioral masculinization...”

It seems more than a little ironic to have New, one of the first women pediatric endocrinologists and a member of the National Academy of Sciences, constructing women who go into “men’s” fields as “abnormal.” And yet it appears that New is suggesting that the “prevention” of “behavioral masculinization” is a benefit of treatment to parents with whom she speaks about prenatal dex. In a 2001 presentation to the CARES Foundation (a videotape of which we have), New seemed to suggest to parents that one of the goals of treatment of girls with CAH is to turn them into wives and mothers. Showing a slide of the ambiguous genitals of a girl with CAH, New told the assembled parents:

“The challenge here is... to see what could be done to restore this baby to the normal female appearance which would be compatible with her parents presenting her as a girl, with her eventually becoming somebody’s wife, and having normal sexual development, and becoming a mother. And she has all the machinery for motherhood, and therefore nothing should stop that, if we can repair her surgically and help her psychologically to continue to grow and develop as a girl.”

In the Q&A period, during a discussion of prenatal dex treatments, an audience member asked New, “Isn’t there a benefit to the female babies in terms of reducing the androgen effects on the brain?” New answered, “You know, when the babies who have been treated with dex prenatally get to an age in which they are sexually active, I’ll be able to answer that question.” At that point, she’ll know if they are interested in taking men and making babies.
In a previous Bioethics Forum post, Alice Dreger noted an instance of a prospective father using knowledge of the fraternal birth order effect to try to avoid having a gay son by a surrogate pregnancy. There may be other individualized instances of parents trying to ensure heterosexual children before birth. But the use of prenatal dexamethasone treatments for CAH represents, to our knowledge, the first systematic medical effort attached to a “paradigm” of attempting in utero to reduce rates of homosexuality, bisexuality, and “low maternal interest.”