One of the most common problems that afflict modern society is acid reflux, commonly called heartburn. This symptom is usually caused by the regurgitation of acid from the stomach into the esophagus. Not only is it an unpleasant sensation, but if left untreated it can sometimes lead to esophageal cancer. While H2 acid blockers, such as ranitidine, and the newer proton pump inhibitors, such as omeprazole, are often effective, some people do not get relief from them. While not widely known, honey can be a very effective remedy, as discussed in a CTV.ca/health blog I originally posted in 2010.

Curing heartburn when pills don’t work: A honey of a suggestion
by Dr. Lorne Brandes  December 8, 2010
 
"I feel fine except for my chronic heartburn," a young woman told me a few months ago during a follow-up visit. Happily, with tests indicating that her breast cancer remained in remission, we had the luxury of focusing that day on her dyspepsia.
Bad heartburn symptoms had started during a pregnancy 10 years earlier (not uncommon) but persisted after delivery. She saw a specialist, had the usual tests for ulcers and hiatus hernia (none found), was told she had "hyperacidity" and was prescribed a series of antacids; none worked. "Now my doctor has me on Pariet [a proton pump inhibitor]; even that doesn’t give me good relief of my symptoms," she lamented.
Desperate for any alternative suggestion, I gave her one. "I want you to try a tablespoon of liquid honey before breakfast and at bed time every day. If your symptoms go away within a week or two, try stopping the Pariet, and stay on the honey until I see you in three months," I instructed. She promised she would try my "home remedy".
She returned for her next visit with a big smile on her face. "It’s unbelievable," she blurted out before I could pop the question. "The honey completely stopped my heartburn within two weeks. I stopped the Pariet and have not needed it since. This is the first time in ten years I don’t feel as though there is a fire in my stomach." Even I was impressed!
So, you may ask, how did I know to tell her about honey? It all started two years ago when I received an e-mail from my youngest brother, Ken, a self-employed entrepreneur/businessman who is also one smart and very funny fellow. I kid you not, here is what he had to say:
"To: The family doc (Revised scene from The Graduate)
Me: I just want to say one word to you – just one word.
You: Yes, sir.
Me: Are you listening?
You: Yes, I am.
Me: HONEY.
You: What exactly do you mean?
Me: There’s a great future in HONEY. Think about it. Will you think about it?
You: Yes, I will
"For 60 years I have lived with the world’s most cantankerous stomach. I invented acid reflux when no one had ever heard those two words side by side….diagnosed "colicky" as a new-born, "nervous" stomach as an adolescent, "type A" in my 20’s, "occupational hazard" of being a retailer in my 30’s, "probably allergic" in my 40s-50s.
"There was always some doctor telling me my stomach was what my stomach was, and prescribing the usual antacids each and every decade… but they never worked for more than 30 minutes before the aching, burning discomfort started up again… that is the reason I have never been able to sleep more than 2 consecutive hours in my entire life on the planet. No sooner would I assume the prone position, and all would be quiet on the Western front, when a Vietnam war-era flame thrower would shoot a plume of burning gas straight up the old gullet… at least, that is how I always pictured what was going on internally.
"So I resigned myself to the fact that it would always be thus and life would have to go on. Years of experimenting with diet never achieved any lasting results, although I eliminated meat, anything sweet, milk, etc… but nothing worked… meditation didn’t work, yoga didn’t work. Anyway, as Darwin predicted, I acclimated to my constant "sleepus interruptus", adjusted to it and became inured to the constant discomfort of heartburn.
"[Now] fast forward to 30 days ago. For the last 3 months I had tried blender drinks for breakfast – a few ounces of water, 6 ounces lactose-free skim milk, [various fruits], 3 teaspoons of yogurt and a sprinkling of [natural grain cereal]….hit the liquefy button and wait a couple of minutes….anyway, as much as I am addicted to these "health" drinks they are murderous to my alimentary canal….I wake up in the morning with a mixture of bile and fruit concoction in the back of my throat, afraid to belch for the fact that it would spew out my mouth.
"Then one day… for whatever divine reason… I decided my concoction needed HONEY…. so I purchased some liquid Munro honey, made by Sunshine brand in Alvinston, Ontario.
"As I was making my morning drink last month I decided to just squirt some honey straight into my mouth (I have that luxury as a person who lives alone). As someone who has not had sweets for 45 years, it was quite satisfying… anyway, I added some to my drink and downed it and that was that… by mid afternoon, I noticed I didn’t have the usual regret for having eaten earlier in the day.
"I then ingested some more honey at dinner time and an hour before bed….I repeated this the next day and the next….to make this rather tedious story short, I have not had one episode of acid reflux, day or night in over 30 days… just like that... just like a miracle! For the first time in my life, I am never aware of my stomach or its contents….whatever microbe, bacteria, nematode or alien that had been lurking somewhere in my alimentary canal my entire life is now history.
"Now I sleep 6 hours straight. I can’t tell you the overall feeling of well being I have….and it is not a placebo effect….I have pushed the envelope, so to speak… I have never been able to eat past 6 or 7 pm without dearly paying the consequences, so for the last week I have purposely been eating my dinner between 8 and 9… then I take a heaping dose of honey 3 times a day plus 1 hour, or so, before bed and sleep like a log….I also have been eating spicy foods that normally would kill me… things like: spicy pasta sauces, curried vegetable sautés (with white onions!). I can even eat peanut butter, which was always instant death for me and wrecked my entire day.
"I started wondering if I was going nuts thinking that honey had cured my illness… so, last week I googled "the curative powers of honey". Your main man, Hippocrates, extolled the virtues of honey as a cure for digestive-related problems… and the anecdotal testimonies about honey from the ancient Greeks, Hebrews, Arabs go on and on.
"So there you have it… I have handed you the holy grail…you are the scientist in the family… you are the genius… you are the scientifically learned and gifted one… go explore this further.
"Just do me one favour – keep it in its simple, unadulterated form….don’t go finding the active ingredient in honey, isolate it, synthesize it, manufacture it in pill form that can only be purchased by prescription for $29.99 for a package of 12, that cannot be taken by people using beta-blockers, who have a history of high blood pressure, glaucoma, ulcers, rheumatoid arthritis, urinary tract or yeast infections, psoriasis, phlebitis, are pregnant or thinking of becoming pregnant…
"Don’t create side effects like dizziness, drowsiness, sexual dysfunction, bloating, diarrhea, blurred vision and heart palpitations….if you want to throw in an erection than lasts over 4 hours, okay, but no other side effects….if you promise me that, I will release all claims to any future royalties you receive, as well as any claim to earnings you get from the Nobel prize…..Deal? Deal."
"Coulda been a doc but no stomach for it…
Ken Brandes"
As you can now plainly see, insanity runs in my family. Yet the dividing line between insanity and brilliance is often razor-thin. Not only did my insanely brilliant brother stumble anew on the healing properties of honey, he humorously hit the nail squarely on the head when it comes to drug companies attempting to commercialize a natural substance!
Still, the question is begged: could pure, unadulterated honey, as a result of its antibacterial stomach-healing effects, out-perform the best, most expensive and side-effect-prone pills known to big pharma? Don’t hold your breath for industry to run a phase 3 trial testing that possibility! On the other hand if you have chronic heartburn that doesn’t respond well to those expensive prescription pills, try a dollop of natural liquid honey twice a day for a few weeks, see how you do, and let me know.
By the way, Ken reports that, after one false start, he was able to stop the honey altogether a few months back. He remains symptom-free, eats what he wants, and sleeps like a baby.
 
 

The latest U.S. and Canadian task force study recommendations for screening mammograms are that only women at high risk for developing breast cancer, such as those with a family history, need be screened annually starting at age 40. For women at average to low risk, with no clinical concerns, screening mammograms every 2 to 3 years starting at age 50 may suffice. But other than those with a strong family history of breast cancer, who else should be considered at high risk? The answer in my CTV.ca/health blog from 2011 may surprise you!  

​Are you at average risk for developing breast cancer? The answer may surprise you!
by Dr. Lorne Brandes  November 30, 2011 
 
Predictably, last week’s release of new breast cancer screening guidelines by the Canadian Task Force on Preventive Health Care (CTFPHC), like those issued by a similar U.S. task force in 2009, provoked a fierce public debate among advocates and opponents of mammography.
My major criticism of the report stemmed from the fact that all of its recommendations, from who should get screening mammograms (and at what interval), to women and doctors not performing routine breast examinations, were categorized by the CTFPHC panel as “weak”, meaning that, for each, “appreciable uncertainty” exists and that the level of evidence is not high. “Then why make them?” I asked .
Of all the recommendations, the greatest controversy surrounded the suggestion that, since breast cancer is much less common before age fifty, women aged 40 – 49 should not be routinely screened with mammograms.
The reason? Based on the large number needed to screen (2,100 per life saved), the 3.6% rate of unnecessary biopsies resulting from false-positive findings on mammograms (estimated at 327 per 1,000), and the anxiety provoked in such instances, the panel concluded that the harm of screening this younger group “probably” outweighed the benefit, despite the fact that, by its own account, mammograms every 1 to 2 years cut breast cancer deaths in this age group by 18%, saving an average of 474 lives per million women tested!
In publishing its new guidelines, the panel stressed that, regardless of age, its recommendations apply only to women considered at “average risk” for developing breast cancer, which it defined as: no previous breast cancer; no family history of breast cancer involving 1st-degree relatives; no known breast cancer gene mutations ( BRCA 1 or 2); no previous radiation to the chest wall.
But now, a paper just presented at the annual meeting of the Radiological Society of North America ( RSNA ) in Chicago, takes direct aim both at the CTFHPC screening guidelines for women 40-49 and at one bastion of the “average risk” equation: family history.
Radiologist, Dr. Stamatia Destounis, and her colleagues at the Elizabeth Wende Breast Care centre in Rochester, New York, studied over 1,000 women, aged 40 – 49, who had been diagnosed with breast cancer. Of those, 373 were diagnosed on a screening mammogram. And while 39% picked up on the mammogram had a family history of breast cancer, 61% did not . Moreover, the type and stage of cancer, determined at surgery, was identical in the two groups.
“In the 40 – 49 age group, we found a significant rate of breast cancer and similar rates of invasive disease [and lymph node involvement] in women with and without [a] family history. We believe this study demonstrates the importance of mammography screening for women in this age group, whether or not they have a family history, which is in opposition to the recommendations issued by the [U.S. and Canadian] task force[s]," Dr. Destounis said.
And, while I am in complete agreement with Dr. Destounis’ message, there are ten additional proven risk factors for breast cancer, not included in the CTFPHC or U.S. guidelines, that are highly important for every woman to know. They include:

• Obesity (greater than 20% over ideal body weight)
• Enlarged thyroid (including Hashimoto’s thyroiditis)
• Diabetes
• Never having been pregnant (nulliparity)
• First pregnancy age 32+
• Regular alcohol (all types) consumption starting in teenage years
• Smoking, including chronic exposure to second-hand smoke
• Prolonged use of oral contraceptives during reproductive years
• Hormone replacement therapy (HRT) after menopause
• Dense breast tissue on previous mammograms

Taking into account this information, are you really at “average risk” for developing breast cancer? If one or more items in this list apply to you, then your risk is significantly higher than average and I suggest you opt for regular screening mammograms starting at age 40!
And remember, this advice comes not from a panel of non-experts that issues broad statistical guidelines (which can never apply to a single individual), but from an oncologist who, for many decades, has specialized in the diagnosis and treatment of breast cancer and, quite frankly, has “seen it all”. 

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​At ASCO 2016, Oncologists reported the results of MA.17R, a randomised trial in which doubling the duration (from 5 to 10 years) of a daily oral dose of the aromatase inhibitor, letrozole,  in postmenopausal women with early stage breast cancer, resulted in a significant decrease in the risk of disease recurrence. However, the side effects of letrozole, including hot flashes, decreased libido, insomnia, joint pains and an increased risk of bone fractures can be hard on many women. This can make the decision to take letrozole for an additional 5 years very difficult for those at risk of recurrence who struggle with side effects. But did you know that women who have side effects with anastrazole, an aromatase inhibitor virtually identical to letrozole, actually have a lower risk of recurrence than women who don't have symptoms? Read more in this CTV.ca/health blog I posted in 2008.

Why Antiestrogen Side Effects May Predict Decreased Risk of Breast Cancer Recurrence
by Dr. Lorne Brandes  November 5, 2008 
 
A just-published article in The Lancet Oncology suggests that women with breast cancer who develop some common side effects (hot flashes, night sweats or joint pain) within three months of starting tamoxifen or the newer aromatase inhibitor drug, anastrazole (Arimidex), are less likely to have a recurrence of their disease when compared to women who do not.
These latest findings stem from an ongoing analysis of the clinical outcome in thousands of post-menopausal women with early breast cancer who, several years ago, participated in a large international phase three clinical study called ATAC.
Following initial surgery, radiation and/or chemotherapy, patients were randomized to receive five years of therapy with anastrazole alone, tamoxifen alone or both drugs in combination. The object of the trial was to determine which, if any, of the three hormonal regimens was superior to decrease recurrence.
After several years of follow up, it was observed that women who developed joint pains within three months of starting anastrazole had a 14 per cent recurrence rate, whereas women in whom the drug did not cause this symptom had a 23 per cent recurrence rate. Excluding joint pain (a side effect limited to anastrazole), women who developed hot flashes or night sweats within three months of starting either tamoxifen or anastrozole had a recurrence rate of 18 per cent compared to a 23 per cent recurrence rate in those who did not report these symptoms.
The authors concluded that the increased beneficial response associated with these somewhat unpleasant symptoms of antiestrogen therapy should be discussed with patients when deciding on whether to continue the treatment for the full five years.
Given the size of the ATAC study, the difference in recurrence rates, depending on the presence or absence of early side effects associated with tamoxifen or anastrazole, is a significant finding that should be taken seriously. Yet, how can we explain it?
The short answer is that the hot flashes, sweating and bone pain probably indicate an optimal concentration of the drug in the body.
There are at least three variables that determine concentration: how much of the drug is absorbed from the bowel; once absorbed, how efficiently the drug is metabolized in the liver (either broken down or converted to an active form); and whether other substances are present, such as fruit juices or certain medications, that may interfere with bowel absorption and/or liver metabolism of the drug.
The walls of cells lining the bowel are richly endowed with tiny pumps that transport drugs and other substances from the gut into the bloodstream. Recently it has been found that bowel absorption of many medications is significantly decreased when pills are washed down with various fruit juices that block the action of the pumps. Do women who drink juice to help them swallow tamoxifen or anastrazole have significantly lower bowel absorption than women who down their pills with water? A fundamental but most important question that requires an answer!
Perhaps the best studied variable is how drugs such as tamoxifen are broken down in the liver, where a large family of metabolizing enzymes, called P450, reside. To be clinically effective, tamoxifen first must be converted by certain P450 enzymes to two active forms: endoxifen and 4-hydroxy-tamoxifen.
However, significant genetically-determined variations in the P450 enzymes that metabolize tamoxifen have been observed. A 2005 study, published in the Journal of Clinical Oncology, linked the presence of a “normal” enzyme profile to both the occurrence of hot flashes and improved disease-free survival. Women who had one or more variant enzymes, associated with impaired conversion of tamoxifen to the active forms, tended not to have hot flashes and also had significantly worse clinical outcomes.
Finally, many drugs, including antidepressants such as fluoxetine (Prozac) and paroxetine (Paxil), can interfere with the metabolism of tamoxifen, resulting in lower concentrations of the antiestrogen. This likely occurs because they compete with tamoxifen for the same P450 liver enzymes, thereby decreasing the conversion of tamoxifen to its two active metabolites.
Some advice: if you have recently started therapy with tamoxifen or an aromatase inhibitor (including Arimidex, Femara and Aromasin) and are experiencing hot flashes and/or joint pain, try to stick with the medication. Those side effects may be telling you that you have an increased chance of benefit down the road.
However, if you are NOT experiencing side effects, first determine whether you are using a fruit juice to swallow your pill or check to see whether you may be taking one or more interfering medications. If neither is the case, speak to your oncologist about whether your metabolism of tamoxifen can be assessed (a tissue sample can be obtained using a buccal swab to obtain cells from the lining of the cheek). In the case of aromatase inhibitors, a check of residual estrogen levels in the blood can be carried out by most hospital labs. The answer may be of great importance to the outcome of your treatment.
 

Advances in the treatment of multiple myeloma were highlighted at the recent ASCO meeting in Chicago. However, a gentle approach with 2 old drugs, cyclophosphamide and prednisone (CP), first reported by yours truly and Dr. Lyonel Israels in the 1980s, remains an option for older patients who can't tolerate aggressive chemotherapy. Moreover, CP has been shown to benefit myeloma patients who have failed bone marrow transplantation. Read more in my re-posted CTV,ca/health blog from 2009.

Progress in treating multiple myeloma: New respect for a simple old treatment
December 16, 2009 07:21 by Dr. Lorne Brandes
 
Multiple myeloma (which means “many marrow tumours”) is a type of bone marrow cancer involving plasma cells that normally produce antibodies to protect us from infection. Because malignant plasma cells don’t function well, patients with myeloma may suffer frequent bouts of bacterial and viral illness.
 Moreover, as they divide, the cancerous plasma cells form chemical-secreting tumours that literally dissolve the bone around the marrow cavity, causing painful holes that can easily fracture. Almost always a fatal disease, multiple myeloma used to kill its victims within a few months to a year.
Interestingly, in 1949, Dr. Carman Weder, a Saskatoon physician, was the first to observe that the chemical, urethane, was effective in a patient with myeloma. Ultimately, the drug was abandoned after a clinical trial in 83 patients showed it to be both toxic and ineffective as compared to a placebo.
The modern era in myeloma treatment arrived with the synthesis, in the early 1950s, of a drug, called melphalan, at London’s Chester Beatty Research Institute (now called The Institute of Cancer Research).
Melphalan was first tested in humans by my mentor at the Royal Marsden Hospital, Dr. David Galton (see my post on Dr. Galton). He found that it predictably killed malignant plasma cells in the marrow, helped affected bones to heal, and appeared to prolong life. Melphalan was even more active when given along with a steroid drug, called prednisone. That combination, given the acronym “MP”, increased survival by two to three years, on average. As a result, MP became the gold standard against which any new treatment for myeloma was, and continues to be, compared.
Yet, although still in use all these years later, melphalan has a dark side. Because it is also very toxic to normal blood cells in the bone marrow, it increases the risk of infection and bleeding. This can be a major problem, especially in older people, in whom the disease is most frequent. As fate would have it, in the early 1980s, I stumbled across a much gentler drug treatment for myeloma.
Confronted with a gentleman whose bone marrow could not tolerate melphalan, I decided to substitute another active drug, called cyclophosphamide. However, because his blood counts were already perilously low and he needed transfusions, I settled on a much smaller single intravenous (IV) dose than usual. He was also given a prednisone pill to take every other day, rather than daily, to keep side effects to a minimum.
“Come back next week so we can check your blood,” I somewhat nervously advised after his first treatment.
When he reported back seven days later, everything was fine. His blood cells were holding their own. We gave him the same small IV dose of cyclophosphamide again and continued the prednisone pill every other day. With each weekly visit and treatment came an improvement in his condition. After three months, not only was he feeling much better and continuing to tolerate the drugs well, he no longer needed transfusions. All his blood counts had gone up while the plasma cells in the bone marrow were down by over half
"Can I tell you about a patient of mine?” I asked my illustrious boss, the late Dr. Lyonel Israels. An internationally-renowned hematologist, Lyonel had also spent time with Galton, in 1955, helping him develop another new cancer drug, CB1348, later called chlorambucil.
After listening to my story, Lyonel was eager to try the treatment on one of his own elderly patients who had stopped MP because of the side effects. A few months later, she too had improved significantly, and without appreciable toxicity.
Over the next four years, the two of us treated 20 patients with this simple regimen of weekly low-dose IV cyclophosphamide and alternate day oral prednisone; 10 had a major response while an additional five stabilized or improved.
"In myeloma, less is more," Lyonel quipped.
A country-wide trial followed, carried out by the National Cancer Institute of Canada. In confirming our findings, the researchers concluded that “the regimen of weekly cyclophosphamide and alternate-day prednisone may be as effective as more aggressive regimens in the treatment of patients with myeloma who have failed MP therapy.”
Yet, aside from a few Canadians, and David Galton and his colleagues in the U.K., nobody else seemed to be paying attention. The “zeitgeist” in the late 1980s, especially among American oncologists was that, where myeloma treatment was concerned, the more aggressive the better.
“Since it gets no respect, we should call it the ‘Rodney Dangerfield regimen’,” I lamented to Lyonel and my other Winnipeg colleagues.
And so it remained for the next 20 years, as stronger and stronger drugs were tried with much toxicity but little improvement in the outcome. Bone marrow transplants were pursued with modest success, but the mortality rate from the procedure remains considerable and most patients ultimately relapse.
Then, in 2005, came vindication… suddenly and without warning (at least to me). A study, published in the Mayo Clinic Proceedings, found that weekly cyclophosphamide and alternate-day prednisone (CP) “first introduced by Brandes and Israels” was “an effective, well-tolerated and convenient regimen” in patients with multiple myeloma who had failed a bone marrow transplant! Thirty-six of 66 patients responded to CP with a median survival of 28.6 months.
Subsequently, a 2008 study combining the CP regimen with bortezomib (Velcade) found “an unprecedented response rate [more than 50% complete remissions] and encouraging one-year survival [83%] in relapsed/refractory patients with [multiple myeloma].”
Now, as we head into 2010, myeloma patients have increasing reason to be optimistic, according to a statement just issued by the International Myeloma Foundation. Among the promising treatments cited by the foundation: a variation of the CP regimen, combined with bortezomib and another promising drug, called lenalidomide (Revlimid).
Respect has come late for our simple CP regimen. But come it has. How do I feel? To quote Jackie Gleason, “How sweet it is!”
 
 
 

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​As most readers know, mammography remains at the forefront of screening for early breast cancer, but not without controversy. As a result of in-depth meta-analyses assessing the number of lives saved per number of women screened, as well as the psychological trauma associated with biopsy following a possible "finding" (often a false-positive), the United States Preventive Services Task Force (USPSTF), along with its Canadian counterpart, has backed away from recommending yearly screening mammograms except in women considered at higher than average risk for developing breast cancer. But did you know that some suspect breast cancers on a mammogram may disappear with further followup? Read about the findings of a Norwegian study in this re-posted CTV.ca/health blog I wrote in 2008.

Why some early breast cancers may spontaneously disappear
November 30, 2008 13:33 by Dr. Lorne Brandes
 
​“I know I need to be screened, but every time I go for that test, I dread what my mammogram might show,” a patient recently confided to me.
She’s not alone. In the back of everyone’s minds is the thought that bad news could be forthcoming. Yet the assurance that, if diagnosed early, most breast cancers can be cured keeps women going back for the ordeal every year or two. After all, they (and we) are told that the more often breast cancer is caught and treated while the lump is too small to feel, the less likely the disease will become invasive, spread and, eventually, kill.
Now, the conventional wisdom of this notion has been shaken to some degree by a large new mammography study just published in the Archives of Internal Medicine. Norwegian doctors compared breast cancer incidence over a six-year period among 120,000 women between the ages of 50 and 64 who had three screening mammograms (one every two years) and 110,000 similarly aged women who had only a single mammogram at the end of the six-year period.
The doctors assumed that, regardless of when they were detected, the number of breast cancer tumours ultimately would be the same in each group, but the results came as a surprise. While, as expected, the cumulative number of breast cancers detected over six years in the screened group (1,909 cases per 100,000 population) was higher than in the control group (1,564 cases per 100,000 population), what was not expected was that, as compared to the screened group, the control group had 22 per cent fewer cancers detected on the single mammogram carried out at the end of the sixth year.
This outcome could not be explained by any obvious differences between the two groups. Therefore, the study’s authors raised the provocative possibility that “the natural course for some screen (mammogram)–detected breast cancers may be to spontaneously regress,” adding, for emphasis, “although many clinicians may be skeptical of the idea, the excess incidence (of cancer diagnoses) associated with repeat mammography demands that spontaneous regression be considered carefully.”
If this hypothesis is correct (and I, for one, believe it may be), what is the mechanism whereby up to one-in-five early breast cancers picked up on mammograms might shrink away without the need for treatment?
A major clue may be the age (50-64 years) of the population studied. What natural event occurs in most women between the ages of 50 and 55?
It’s the menopause, of course. Given that approximately two out of three breast cancer tumours are estrogen-driven, the sudden drop-off in ovarian estrogen at menopause may starve those estrogen-requiring cancers of the very hormone that drives their growth and development. As a result, they may either disappear over time or, in some cases, shrink and lie dormant without further growth.
There are other strong precedents in support of the “hormone hypothesis for spontaneous regression”: removing the ovaries, a common procedure for many decades in the treatment of metastatic breast cancer, often led to a dramatic, if temporary, shrinkage of large tumours. We can accomplish the same result today with specific drugs, called aromatase inhibitors, which block fat cells from producing estrogen.
Moreover, with the widespread discontinuance of hormone replacement therapy (HRT) for menopausal symptoms, the incidence of breast cancer world-wide has fallen rather dramatically over a very short period of time, consistent with a potent biological effect of hormone withdrawal to inhibit the development of breast cancer.
In an editorial accompanying the Norwegian study, cancer experts Drs. Robert M. Kaplan and Franz Porzsolt write: “If the spontaneous remission hypothesis is credible, it should cause a major reevaluation in the approach to breast cancer research and treatment. Certainly it is worthy of further evaluation.” I agree.
 

​A new study suggests that type-2 diabetics who take metformin following a diagnosis of breast cancer lower their risk of dying of the disease by 50%. Here is a re-posting of my CTV.ca/health blog from 2009 reporting on the science behind the story.

Is the anti-diabetic pill metformin also effective against cancer?
June 17, 2009 07:49 by Dr. Lorne Brandes
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In my June 9 blog, I explained why off-patent drugs usually are not developed for new uses, such as cancer treatment. It generally boils down to money: because of the ready availability of cheaper generic versions, major pharmaceutical companies are reluctant to invest tens, or hundreds, of millions of dollars in the clinical cancer trials required to gain regulatory approval of a new use for their old drug.
Well, I have just learned that one old drug could prove to be an exception to that rule (As we say in medicine, “Never say ‘never’ and never say ‘always’”).
Its name is metformin, an oral medication widely used to treat adult (type 2) diabetes mellitus (DM2). Although its composition patent lapsed in 2002, and despite the fact that cheaper, FDA-approved, versions are now made by at least fifteen generic drug companies, metformin is still marketed under the trade name Glucophage by its original developer, Bristol-Myers, Squibb.
Given the increasing epidemic of DM2 in affluent countries of the western world, it seems that everyone still manages to reap a profit from this effective old warhorse!
Now comes exciting new evidence that what works in diabetes may also work in cancer. Here’s the story.
For some years, DM2 has been recognized as a risk factor for developing cancer. The association may be largely indirect, through obesity, which is prevalent in type 2 diabetics.
Too much body fat often results in what is called “insulin resistance”: far from producing too little insulin, the pancreas in obese subjects with DM2 produces too much of the hormone in response to the increased blood sugar. High levels of insulin and insulin-like growth factors (IGFs) are strongly implicated in the causation of cancer in laboratory rodents and in humans.
Metformin is especially effective in obese diabetics who overproduce insulin. By activating an important enzyme, called adenosine monophosphate kinase (AMPK), metformin prevents the liver from breaking down starch into sugar and stimulates uptake of sugar by the body’s muscles. As a result of this one-two punch, blood sugar and insulin levels fall.
Now for the cancer connection.
By activating the same AMPK enzyme in cancer cells, metformin inhibits malignant growth in the test-tube and in mice. The AMPK enzyme also interacts with other genes and proteins involved in aggressive malignant behaviour. Indeed, metformin is highly active in the test-tube against cells derived from “triple negative” breast cancer, a form of the disease with an especially poor prognosis.
Based on the accumulating laboratory data, researchers at Scotland’s University of Dundee compared the risk of cancer in 983 patients with DM2 who took metformin and 1,846 diabetic controls who did not in a study published in the British Medical Journal. They found that diabetic patients who took metformin had a significantly lower cancer rate. Those taking the highest doses of metformin for the longest period of time, had the lowest cancer rate (a 44% decrease as compared to diabetic controls who did not take metformin).
Now, with a just-released study published in the Journal of Clinical Oncology (JCO), the metformin train appears to be leaving the station.
Doctors at Houston’s M.D. Anderson Cancer Center assessed the effects of chemotherapy, given before surgery, on locally advanced breast cancer among 88 patients with DM2 who took metformin, 87 patients with DM2 who did not take metformin, and 2,374 non-diabetic patients. After the chemotherapy, all patients underwent mastectomy or lumpectomy; lymph nodes draining the breast were sampled in all cases.
Pathologists closely examined each surgical specimen under the microscope to determine the presence or absence of residual cancer cells. Cases in which there was no residual cancer following the chemotherapy were called “pathological Complete Responses (pCR)”.
The study found a significantly higher rate of pCR (24%) in patients with DM2 who took metformin at the time of chemotherapy than in patients with DM2 who did not take metformin at the time of chemotherapy (8% pCR). Non-diabetic patients also had a lower pCR rate (16%) than patients with DM2 who took metformin, but the difference did not reach significance.
In an accompanying JCO editorial entitled, “Metformin in breast cancer: Time for action,” the University of Toronto’s Dr. Pamela Goodwin and her colleagues announced plans for a large international phase 3 study to be led by the Clinical Trials Group of the National Cancer Institute of Canada. It will compare the effect of adding metformin or a placebo to chemotherapy following surgery for early breast cancer. The study will include both patients with DM2 and high insulin levels, and non-diabetic women.
Will metformin, the old, wildly successful anti-diabetic drug, morph into metformin, the new, wildly successful anti-cancer drug? Although nobody yet knows, one thing is certain: a positive outcome should generate even more hefty profits for both Bristol-Myers and its generic competitors!
 


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The Women's Health Initiative study suggested that taking estrogen modestly increases the risk of breast cancer in post-menopausal women. But estrogen is a double-edged sword. High doses actually shrink breast cancer! Learn more from my CTV.ca/health blog, originally posted in 2009.

​Treating advanced breast cancer: The estrogen paradox
by Dr. Lorne Brandes  August 24, 2009 

Is anything in science and medicine ever completely new? Occasionally, perhaps, but usually not. As a biblical sage once observed (Ecclesiastes 1:9-14): “What has been will be again, what has been done will be done again; there is nothing new under the sun.”
So, when a new study, showing that estrogen treatment can shrink advanced breast cancer, appeared in this week’s edition of the Journal of the American Medical Association (JAMA), the words of the sage immediately came to mind.
To put the study’s findings into context, we must first review the causal relationship between estrogen and breast cancer.
Large, widely-reported studies have shown that taking estrogen as part of hormone replacement therapy (HRT) significantly increases breast cancer risk. In addition, scientists have repeatedly linked estrogen-driven breast cancer with being overweight. Why? Fat cells produce lots of estrogen that fuels this type of breast cancer. In contrast, drugs (called aromatase inhibitors) that block fat cell estrogen can both decrease the recurrence rate of early breast cancer, and shrink metastases if the disease spreads.
At this point, one would be right to question why, if estrogen often propels the growth of breast cancer, it also can be used in its treatment. It is a paradox to be sure, one that had its beginning in the 1940s, when Sir Alexander Haddow, a brilliant Scottish chemist, first proposed that cancer-causing chemicals themselves might be effective to treat cancer.
Not only did his hypothesis prove to be correct (and became known as “The Haddow Effect”), it led scientists under his direction to discover a series of anti-cancer drugs, themselves carcinogens that are still in clinical use today.
One carcinogen pegged by Haddow as a possible breast cancer treatment was the synthetic estrogen, diethylstilbestrol (DES). Once again he was right. Although the drug was often toxic at the high doses required to be effective, and worked only about one-third of the time, for the next quarter-century it was widely used to shrink advanced breast cancer in post-menopausal women. The “estrogen paradox” was evident even then!
When tamoxifen (itself a weak estrogen that can cause uterine cancer) proved almost as effective as, but significantly less toxic than, DES, it became the drug of choice in the 1980s. DES was ultimately banned in most countries after it was linked to reproductive tract abnormalities, including vaginal cancer in young girls whose mothers took it in pregnancy to decrease the risk of bleeding, premature labour and miscarriage.
Despite the demise of DES, natural estrogens, such as estradiol (contained in Premarin, for example), continue to be approved for use in treating inoperable breast cancer. However, in the “modern era” they have been rarely prescribed for this purpose.
Now, with the just-published study in JAMA, that is almost certain to change.
The study’s rationale stemmed from earlier laboratory experiments with cultured breast cancer cells that could grow in the absence of estrogen (mimicking resistance to treatment with an aromatase inhibitor). It was found that when small amounts of estradiol were now added to the culture medium, the cells died.
To determine whether these findings might carry over to the clinic, oncologists assessed the effect of high (30 mg) and low (6 mg) daily doses of estradiol on the growth of estrogen-dependent breast cancer in 66 women whose disease had stopped responding to aromatase inhibitor drugs. Consistent with the previous experience with DES, 9 of 32 women responded to high-dose estradiol. What may not have been anticipated, but in keeping with the preceding lab data, an equal number of women (10 of 34) responded to low-dose estradiol, and with significantly fewer side-effects. As a result, low-dose estradiol will be adopted for future studies.
The study additionally found that positron emission tomography (PET) body scans performed twenty-four hours after the first dose of estradiol were highly predictive. Only patients in whom the PET scan detected increased glucose (sugar) metabolism in the tumours (a sign of early growth-stimulation) responded to treatment. In other words, an early stimulation of tumour cells by estradiol was soon followed by the reverse effect (shrinkage or stability of the cancer). A paradox, indeed.
Finally, there was one more bit of icing on the cake: two of seven women regained a response to their previous aromatase inhibitor after the estradiol improvement wore off.
 While the study was relatively small and the findings preliminary, I think it is likely that they will quickly change how oncologists treat late-stage estrogen-dependent breast cancer. Since generic estradiol is commercially available and already approved in breast cancer, oncologists can easily prescribe the 6 mg daily dose to women who stop responding to aromatase inhibitors. Moreover, a PET scan performed one day after the first dose will quickly indicate who should continue and who should stop.
Maybe something is new under the sun after all!

A story in today's news about how to safely dispose of prescription pain killers, often only months or up to three years beyond their expiry dates, prompts me to re-post this blog I wrote for CTV.ca/health in 2011.













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​Drug expiry dates: Should you use outdated medicine?
July 8, 2011 11:04 by Dr. Lorne Brandes

A recent e-mail from a friend immediately “caught my eye” (the pun will be evident in a moment). He thought I would be interested in a 2002 article , entitled, “Do Medications Really Expire?” by writer, Richard Altschuler.
“Does the expiration date on a bottle of a medication mean anything? If a bottle of Tylenol, for example, says something like ‘Do not use after June 1998,’ and it is August 2002, should you take the Tylenol? Should you discard it? Can you get hurt if you take it? Will it simply have lost its potency and do you no good?” Altschuler asked.
“In other words, are drug manufacturers being honest with us when they put an expiration date on their medications, or is the practice of dating just another drug industry scam, to get us to buy new medications when the old ones that purportedly have ‘expired’ are still perfectly good?” he added.
I paused to reflect on those important questions. A few weeks earlier, my ophthalmologist had given me some sample eye drops. “According to the date on the box, they expired last month. Are you okay with that, or would you prefer that I write you a new prescription?” she asked. “I… think… I’m okay with the samples,” I replied hesitantly.
There followed a discussion about how it makes no sense that a drug with an expiry date of December 31st suddenly stops working on January 1st. Yet, as I left her office, thanking her for the free samples, I wondered whether I might be playing Russian Roulette with my eye pressures.
Now, based on the information in my friend’s e-mail, I suspect that I wasn’t.
To begin, Altschuler explains that drug expiry dates are not a money grab cooked up by Big Pharma, but rather, the result of a 1979 federal law, mandated by the FDA.
He goes on to explain, “…the expiration date… specifies only the date the manufacturer guarantees the full potency and safety of the drug - it does not mean how long the drug is actually ‘good’ or safe to use…. [M]edical authorities uniformly say it is safe to take drugs past their expiration date - no matter how ‘expired’ the drugs purportedly are. Except for possibly the rarest of exceptions, you won't get hurt and you certainly won't get killed.”
Perhaps not hurt or killed. But what about potency? How long do drugs, such as those eye drops, remain effective? Happily, a more recent publication goes a long way in answering that question.
According to a comprehensive 2006 paper, published in the Journal of Pharmaceutical Sciences by scientists at the FDA’s Center for Drug Evaluation, we now know quite a lot about the shelf-life of many pharmaceuticals, thanks to the American military. Why?
Because the U.S. Department of Defense (DoD) maintains a billion dollar stash of drugs (called the Strategic National Stockpile), including a host of antibiotics, anesthetics, narcotics, anti-allergics, anti-toxins, anti-malarials, anti-convulsants, vaccines and intravenous solutions. It’s part of the DoD’s Medical Readiness Strategic Plan for war or natural disasters.
But just like the everyday consumer, the DoD’s drugs have those same expiry dates. Replacing such a huge cache of unopened/unused drugs every 3 to 5 years is not only potentially wasteful, but hugely expensive for the taxpayer. Therefore to gain a handle on the question of drug stability, the DoD, in conjunction with the FDA has, for the last twenty years, monitored 122 of its drugs in a shelf life extension program, known by the acronym “SLEP”.
Here’s how it works, as described in the journal paper: “Certain lots of drug[s] that are approaching their labeled expiration date are selected… [and]… subjected to a battery of tests… If a lot fails any [original] specification…the shelf life for that lot is expired. [If a drug lot passes all the tests] and the [predicted] remaining expiration period is longer than 1 year, the [drug lot] is granted a new expiration date.”
What has the program found? Fully 88% of the 3000 drug lots tested have an average extended shelf-life of 5.5 years beyond the original expiry date! Indeed, many pills, powders and liquids have been found to be stable for an extra ten or more years, while only 10 of the 122 drugs failed to gain an extension beyond their original expiry date. Even in those cases, the drug lots often failed for reasons other than loss of potency, such as a change in appearance.
So what do I advise? Extrapolating from the SLEP findings, if an unopened medication, such as my ophthalmologist’s eye drop samples, are stored according to the manufacturer’s recommendations, they should retain their safety and effectiveness for a year or more beyond their expiry date. Opened eye drops, on the other hand, should be discarded after a month or two, not necessarily because of a decrease in potency, but because of concern over bacterial contamination , especially at room temperature.
As for the majority of opened prescriptions and over the counter medications, such as aspirin, Tylenol, antibiotic pills or capsules, blood pressure pills, antihistamines and acid blockers, it is very likely that they, too, will remain safe and effective for months or even years beyond their expiry date if stored properly in a closed container.
However, there is one important exception: if any drug falls into the category of “lifesaving”, its expiry date should be heeded irrespective of any potential for a longer shelf life. In serious disease situations, no one should take a chance with the effectiveness of their medication!
 
 

This week, a story appeared on CTV news about the failure of Health Canada to regulate cosmetics containing potentially dangerous ingredients. Here is a a blog I wrote on that subject in 2009.













Skin care products and cancer: What manufacturers don’t tell you
October 14, 2009 11:15 by Dr. Lorne Brandes
 
On a recent visit to a department store cosmetics counter, I was amazed at the number and variety of “rejuvenating” skin creams and lotions for sale -- and not just for women!
“How much did all that cost?” I asked warily as the smiling clerk handed the Visa card back to my wife.
“If they help my skin look younger, it’s worth it,” was all she would say.
It now appears that her faith in the products she bought may have been misplaced: a new report in the Journal of Clinical Oncology (JCO) warns that an ingredient in some skin creams may have serious long-term health consequences for women with, or at risk for, breast and uterine cancer. The offending substance? Estrogen!
The story began with an alert oncologist. He observed that the skin of a woman he was treating for estrogen-driven breast cancer looked more youthful since her previous visit. The doctor quickly ascertained that, starting four weeks earlier, his patient had been applying a new moisturizing skin cream after her daily bath.
His interest was immediately piqued. For years, it has been known that one of the benefits of taking estrogen for relief of menopausal symptoms is younger-looking skin. Could the cream she was putting on her skin contain estrogen? The product information provided no indication that it did.
His suspicion aroused, the oncologist sent a sample of the patient’s skin moisturizer, along with 15 other skin products, to an independent lab for analysis. The price of the creams ranged from $10 to several hundred dollars. Each was chosen based on the manufacturer’s claim that it rejuvenated, or enhanced the youthful appearance, of the skin. None listed estrogen as an ingredient.
The results supported the doctor’s concern: six -- almost 40 per cent -- of the creams contained significant amounts (up to 0.61%) of estriol or estrone, two potent forms of estrogen. As a comparator, Estrase, a vaginal cream prescribed to treat symptoms of vaginal dryness in post-menopausal women, contains up to 60 times less estrogen!
In publishing these results, it was decided not to provide the brand names of the estrogen-containing creams. While I suspect that the authors (or the journal’s editors) may have been concerned about potential lawsuits, an alternative reason was given: “…since cosmetic companies frequently change their formulations, contents of each product may not currently be similar to those obtained [at the time of analysis, in April 2007].”
Cosmetic companies are not currently required to submit their products for regulatory approval to agencies such as the FDA or Health Canada. Rather, as noted in a recent scientific review, complex skin formulations that contain potentially harmful ingredients are largely regulated by the cosmetic manufacturers themselves. And, as we have just learned, these same manufacturers generally do not feel inclined to divulge the presence of “problematical” ingredients like female hormones.
Should we be worried about the estrogen content of facial creams and other skin care products? In short, yes.
While skin absorption of ingredients in topically-applied creams and lotions can vary depending on the formulation and length of exposure, one extreme example has been published. A 93-year-old woman, who had applied an estrogen-containing cream to her skin for seven decades went to her doctor with uterine bleeding and a breast lump. She was found to have a uterus “as large as that of a normal adult menstruating woman,” while the breast lump proved to be malignant. The authors believed that both findings were likely related to prolonged use of the skin cream.
More to the point, women with breast cancer who are under treatment with an estrogen-lowering aromatase inhibitor should be especially concerned about any product that, without their knowing it, could work against this treatment by raising the level of blood estrogen through the skin. Similarly, healthy women at risk for breast or uterine cancer should also beware of the increased exposure to environmental estrogen inherent in some rejuvenating skin preparations.
To quote the authors of the JCO report, “We believe that women, especially patients with a history of breast cancer, should be able to understand the potential risks when exposed to estrogenically active molecules in commercially available topical moisturizers. Because our testing methodology was only intended as a screening process, we strongly encourage the scientific community and the U.S. Food and Drug Administration to repeat and expand on the results of these screening tests.”
I agree. And in light of a new warning just issued by noted scientist, Dr. Samuel Epstein, on the potential cancer-causing hormonal agents in cosmetics, their recommendation for FDA involvement is well-justified.
 
 

Since I started reposting my CTV.ca/health blogs, some of you have asked me to include written about Jack Layton. Here it is.

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​Did prostate cancer kill Jack Layton?
September 12, 2011 09:39 by Dr. Lorne Brandes
 
Few can forget their shock over Jack Layton’s gaunt appearance and raspy voice at the July 25th news conference where he stunned the country by announcing that, less than three months into the job, he was temporarily stepping down as Opposition leader “to fight a second type of cancer.” His previous prostate cancer “was no longer a threat,” he said.
Like all Canadians, I was very saddened. But, as an oncologist who treats prostate cancer, I was not surprised by this unhappy turn of events; as to the “different” cancer that Mr. Layton said he was now battling, I was doubtful. Let me tell you how I arrived at my conclusions and why I think the issue of his cancer is important to discuss from a medical and political perspective.
To begin, I remember being very concerned when he first made his diagnosis public in February, 2010. Only a week earlier, he had suffered pain from a “back injury” sustained while exercising. Now, painful back injuries can happen to anyone (fit like Jack, or not), but with a diagnosis of prostate cancer coming immediately on the heels of the back pain, I wondered whether there was a link. Did x-rays of his spine show something more concerning? If not caught early, prostate cancer can spread to the bones and cause pain.
Far from being reassured, my worry increased when Mr. Layton declared , “This year, more than 25,000 Canadian men are going to be diagnosed with treatable prostate cancer. And I've recently learned that I'm one of them.” He also told reporters that “he had already started a program of treatments for the cancer”, and that “so far the treatments are going well.”
But what exactly did he mean by “treatable”? Being the supreme optimist that he was, why did he not say “curable”? Both advanced and early prostate cancer are treatable, but only early prostate cancer is potentially curable. In the absence of further information, an air of uncertainty surrounded the type of “treatment” he was undergoing.
From an oncology perspective, the recommended treatment for a fit, healthy 60 year-old man with early prostate cancer is usually radical prostatectomy ; a second choice for localized disease is radical radiation therapy with curative intent. Yet, from his statement that he was “already on treatment”, it is clear that surgery had been discounted.
What about curative-intent radiotherapy? With the exception of pure brachytherapy treatment in carefully-selected (and often, older) patients, it is generally a complex treatment , in many instances preceded and/or followed by months of hormonal therapy, first to shrink the tumour and then prevent recurrence. Moreover, it usually takes a significant amount of time to carefully map out the radiation field, followed by five to six weeks of treatment and a period of recovery, often taking several weeks to a few months before a person is able to return to full activity.
But Jack’s return to Parliament Hill was only a matter of six weeks from the start of his “treatments”. Looking fit and, as always, upbeat, it was clear that he had come through them well. Yet, I could not shake the suspicion that, because the time interval was fairly short, they were palliative in nature, consisting of a week or 10 days of radiation to treat painful metastases in his spine (the “back injury”) and oral and/or injectable medications to block testosterone , the usual approach to treating Stage 4 (metastasized) prostate cancer.
Then, in March, 2011, 15 months after he was first diagnosed, came the revelation that he would require immediate surgery to repair a painful hip fracture. A hairline break, diagnosed a few weeks earlier, had suddenly gotten much worse on conservative management with pain killers and crutches.
After recovering from the operation, probing questions from reporters about the nature and treatment of the fracture, and whether his health problems would allow him to lead his team into the expected federal election were met with generalities and assurances that he would be up to the task.
When asked specifically whether he was still being treated for prostate cancer, Mr. Layton answered, “ Well, I work with my doctors on an ongoing basis like most people with cancer to monitor the situation. They’re happy with how things are going.” Any other details would remain a private matter between Jack and his doctors.
All the while, many in the oncology community, including me, suspected something more sinister was brewing. In the absence of trauma, benign hip fractures are extremely uncommon in a man his age. If it was not an “innocent” occurrence, two possibilities were bone thinning (osteoporosis) due to testosterone-blocking therapy or, even more ominously, a progressively-worsening fracture caused by prostate cancer cells destroying the bone. In that case, his disease was no longer responding to whatever treatment he had been receiving.
Whatever the cause, “the happy warrior” rallied after his hip surgery and, cane in hand, limped and then danced from strength to strength as he led the NDP to a remarkable showing in the general election, becoming Leader of Her Majesty’s Loyal Opposition in the process.
But his victory was to be short-lived. Like Moses at the river Jordan, Jack Layton would not enter the promised land. A return of intense pain, accompanied by sweating, tiredness and weight loss were evident by early June.
Describing his “new battle with a second cancer” in his July news conference, Mr. Layton explained that his PSA test remained very low; therefore, the new problem was unrelated to his previous prostate cancer. His doctors appeared to concur, releasing a statement that “new tumours were discovered which appear to be unrelated to the original cancer.”
However, that opinion is subject to debate. Why? As cancer of any type progresses, the cells can change in appearance as their biological behaviour becomes more aggressive. And so it is with prostate cancer, where the tumour cells can become “dedifferentiated” (primitive in nature), metastasizing rapidly throughout the skeleton as well as to the liver, lungs and brain. Moreover, unlike the cells earlier in the disease, dedifferentiated prostate cancer cells may no longer produce PSA .
Therefore, an alternative explanation is that Mr. Layton’s “unrelated tumours” were really his old prostate cancer in a new form. A pathologist examining them under the microscope might not be able to state with certainty their exact nature or origin, as appeared to be the case here.
At the end of the day, from a medical and personal perspective, the identity of the new tumours mattered little. With such an aggressive cancer ravaging his body, and despite any attempts to slow down the process, Mr. Layton soon succumbed and all of Canada mourned his untimely passing.
Yet, questions persisted. When the nature of the “new cancer” that took her husband’s life came up in an interview, Olivia Chow demurred , telling the CBC’s Peter Mansbridge that no further information would be forthcoming so as not to “dash the hopes of other cancer patients suffering from the same illness.”
In the overall context of the information gap surrounding specific details of Jack Layton’s illness, Ms. Chow’s answer seems ingenuous at best, and evasive at worst.
If, as seems likely in my opinion, Mr. Layton, a candidate for Prime Minister of Canada, was diagnosed with incurable stage 4 prostate cancer prior to the general election, was his failure to come clean about the seriousness of his situation an abrogation of his responsibility to voters? Was Ms. Chow’s subsequent refusal to discuss the nature of the “second cancer” motivated by fear that admitting everything was related to advanced prostate cancer would hurt her late husband’s credibility and the future of the NDP?
If so, it appears she need not have worried. In response to an article in the Globe and Mail that asked whether Apple’s Steve Jobs and, likewise, Jack Layton, should have been more forthcoming about the details of their medical diagnoses, the vast majority of readers replied, “Ain’t nobody’s business.”
However, there were a few dissenters when it came to Mr. Layton:
“A politician with a serious illness should disclose the illness when running for office because people may vote differently if they know the facts….,” said one.
“Layton should have been clearer about the extent of his illness as he ran for re-election,” opined another.
“If he actually ran knowing he was in big trouble health wise, then perhaps…[a] debate…needs to occur as to whether this is proper or not,” commented a third.
I guess I’m in the minority, but given the facts as I see them, I agree with the dissenters, as well as with Globe and Mail writer, Andre Picard, that, like their American counterparts, Canadian politicians, especially those running for high office, owe the public full health disclosure.
After all, should we not subscribe to the premise that, in politics as in life, honesty is the best policy?