If you have breast cancer, it’s possible your doctor is going to use tamoxifen to fight it. This drug has been around for at least two decades. So we know what the drug is going to do. We know that it can fight cancer. But we also know that it often has debilitating side effects.
To help mitigate the side effects, doctors often prescribe another drug along with the tamoxifen. But there’s a major problem with this drug.
I received a letter from Eve. She was a 72-year-old female with cancer. And her doctor prescribed tamoxifen to treat it. She wrote to tell me: “The cancer isn’t going away. I also take an SSRI to help with the depression. I recently read that the SSRI can help with the tamoxifen side effects. It seems to help. Should I continue to take the tamoxifen even though it isn’t working?”
Here’s what I told Eve:
You should stop taking the SSRI. Here’s why:
A new study says the SSRI can negate the cancer-killing abilities of the tamoxifen.
The problem, which turns out to be alarmingly common, came into the public spotlight earlier this year. Sean Hopkins, a clinical pharmacy specialist in breast cancer at the Ottawa Hospital Regional Cancer Centre in Ottawa, Canada, made the presentation. He released startling information on the interaction between the anti-cancer drug tamoxifen and SSRI drugs.
SSRI drugs are some of the most commonly prescribed drugs in the world. Most of those prescriptions are for depression. But doctors will often prescribe SSRIs to women to treat the side effects that commonly happen when you take tamoxifen. Mr. Hopkins showed that while SSRIs can reverse the side effects of tamoxifen, they also can decrease the cancer-fighting abilities of tamoxifen.
So if your oncologist has you taking tamoxifen, and another doctor has you on one of these SSRI drugs, you’re not getting the benefit from the tamoxifen therapy that you wanted. The reason has to do with the liver enzyme CYP2D6. It works like this.
Tamoxifen, all by itself, does not have an anti-cancer activity. Your liver has to convert it endoxifen. It is endoxifen that has the anti-cancer effect. CYP2D6 is the enzyme that makes that conversion possible. The problem with the SSRI drugs is that they inhibit CYP2D6. This makes it impossible for the liver to convert tamoxifen to endoxifen. And, thus, it blocks the anti-cancer effect of tamoxifen.
Tamoxifen has been on the market for at least 20 years. And the SSRIs have been out for longer than that. How many women have been suffering the side effects of tamoxifen treatment during all those years, while at the same time diminishing its anti-cancer effect by taking another drug to help them with the side effects of the first drug? And, by the way, SSRIs are not the only drugs that block CYP2DA. Here’s a list of other drugs to avoid: Amiodarone (Cordarone), Chlorpheniramine (Chlor-Trimeton), Chloroquine (Aralen), Chlorpromazine (Thorazine), Cinacalcet (Sensipar), Diphenhydramine (Benadryl), Halofantrine (Halfan), Haloperidol (Haldol), Imatinib (Gleevec, Perphenazine (Trilafon), Propafenone (Rythmol), Propoxyphene (Darvon)
Quinacrine (Atabrine), Quinidine (Quinidex, etc), Quinine, and Terbinafine (Lamisil).
And how many other drugs are doctors using together that tend to cancel each other out in ways that we don’t yet know about? God bless all the doctors out there who go out of their way to find natural solutions to their patient’s problems, and thus decrease or even eliminate their need to rely on drugs.
If you’re taking tamoxifen and an SSRI or one of the other drugs that inhibit CYP2DA, make sure you show this article to your doctors and discuss possible alternatives to the SSRI – including the one I’m going to tell you about now.
This Natural Hormone Could Save Millions of Breast Cancer Patients
Did you know that when a surgeon removes a breast-cancer tumor, the doctors can check it to see if it has estrogen and progesterone receptors on it? If it has estrogen receptors, that means that estrogen will stimulate the cancer to grow faster. And, in that case, doctors give therapies designed to stop the estrogen stimulation. Conventional “wisdom” suggests that when breast cancers are progesterone positive, it means that progesterone will act like estrogen and will stimulate the growth of the cancer. But, is this true?
Actually, nothing could be further from the truth. And here’s why this ignorance gets to me so much.
Not long ago, I was giving a lecture to a group of oncologists on how effective ozone therapy is as a part of an overall anti-cancer program. And while I had their attention, I put a question to the audience: “Can any of you give me a single reference in the medical literature supporting the idea that giving progesterone to a woman with a progesterone-receptor-positive breast cancer will stimulate the cancer to grow faster?” The room suddenly became very quiet. The audience started looking around for raised hands, but to no avail. Not one of those doctors had any proof at all for the theory. So now let me bring you to a real live case that happened just the other day.
One of my patients had a breast cancer biopsied and it turned out to be both estrogen- and progesterone-receptor positive. So one of the first things I did was to give her high doses of progesterone. The data shows that giving high doses of progesterone before surgery in progesterone-positive cancers results in better outcomes. Well, it wasn’t too long after that before she got back to me and said that her oncologist said she needed to avoid progesterone because everybody knows that if she took progesterone her cancer will grow faster. And to add to her concern, she had done her homework. She checked out the website for the American Cancer Society and, indeed, they very clearly said that taking progesterone would stimulate her cancer to grow faster.
I know that taking progesterone actually slows down progesterone-receptor-positive breast cancer because I’ve been using it to do just that for years. And anybody in the alternative medical world knows that progesterone can offset many of the effects of estrogen. But it’s hard to battle with the big boys. Both the American Cancer Society and every single oncologist I’ve ever talked to keep repeating the same uninformed mantra with absolutely no proof at all to back them up. How many women have been injured out of this ignorance? I can only guess. So imagine my excitement when I found a series of studies that proves beyond a doubt that one of the best things a woman can do if she has breast cancer that is both estrogen- and progesterone-receptor positive is to take progesterone. Here are the details.
The Proof I Was Looking For....
The researchers took a group of mice and grafted estrogen-positive breast cancers on them. They exposed some of the mice to estrogen. And they exposed some of the mice to estrogen combined with a very high dose of progesterone. After 25 days, they measured how much the cancers had grown. And guess what? The cancers in the mice exposed to the high-dose progesterone grew much more slowly and were much smaller than the ones without the progesterone. They concluded that, “progesterone inhibited tumor formation.” Not bad for a natural therapy. But that was not enough. Then they wanted to see what would happen on real human breast cancer cells.
To do the experiment they used breast-cancer cells from 14 real breast-cancer patients. All of the cancers were estrogen- and progesterone-receptor positive. Then they grew the cells in a culture. They exposed some of the cells to estrogen alone, some to progesterone, and some to both estrogen and progesterone combined. They found the same results as before. Not only did the progesterone not stimulate the cancers to grow faster, it actually inhibited their growth. And it inhibited the growth even when the mice were simultaneously receiving estrogen. In their words, the results showed “that progesterone can antagonize estrogen-induced growth in primary human breast tumors cultivated as explants.” But they didn’t stop there. They still wanted to know if combining progesterone treatment with estrogen blockage was better than estrogen blockage alone. So here’s the last experiment.
They grafted breast cancers that were estrogen- and progesterone-receptor positive on another group of mice. Then they gave some of the mice the drug tamoxifen. Tamoxifen is a drug that oncologists commonly give to their estrogen-positive breast cancer patients because it interferes with the way that estrogen can stimulate cancer growth. They gave another group progesterone. And they gave the last group both tamoxifen and progesterone. Once again, the results were very impressive for progesterone therapy. Though both tamoxifen and progesterone successfully inhibited cancer growth, “the combination of tamoxifen plus progesterone had the greatest tumor inhibitory effect.” But once again our hot-on-the-trail researchers kept going.
The results of the last experiment were so spectacular that they repeated it again with different breast-cancer cells. The same thing happened again: “Confirming the finding that tumor volume was inhibited by progesterone alone, but the greatest degree of tumor inhibition was observed under conditions where an estrogen antagonist (tamoxifen) was coupled with progesterone.” Additionally, using special microscopic and staining techniques, the researchers were able to discover why progesterone works so well. It’s because when progesterone interacts with the progesterone receptor on the cancer cell, it stimulates a series of reactions that decreases the impact of estrogen on the estrogen receptor.
Women on tamoxifen therapy are subject to a long list of serious side effects that progesterone can offset. Their quality of life will be much better with the combination, not to mention a better cancer-response rate. So if you have breast cancer, take this article to your oncologist and ask for some progesterone. It could save your life – and it will make tamoxifen more tolerable and more effective.
Mohammed, H., I.A. Russell, et al. “Progesterone receptor modulates ERα action in breast cancer.” Nature. 2015 July 16;523(7560):313-7.
“Breast cancer and drug interactions: Making sure patients get full benefit of tamoxifen treatments,” March 29, 2010.
DePinho, Robert A. “Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient micePDF file,” Nature, January 6, 2011.