So it transpired that children on leukemia treatment in New York, Christchurch, and Kingston, Ontario, could receive the exact same treatment protocol, and that data during the course of treatment could be shared with other centres for the benefit of all. Not only were patient details shared and reviewed, but the events and responses to relapses were also shared. This collaboration led to a 44 percent reduction in mortality from relapse between 2000 and 2005.
Adults with leukemia do not fare as well as children. This is because adults tend to acquire a more aggressive form of leukemia.
Genetics and ethnicity may also affect outcome. This again relates to the sub-type of leukemia. For instance, in Canada, two-thirds of children will have the lower risk variety. In North Africa, the statistics are inverted, and two-thirds will have the higher risk type.
So these are meaningful gains and improvements in the lives and families of childhood sufferers. We also have some way to go. Our goal is 100 percent intact, long-term survival. The last part of this battle may be the hardest.
The caring, loving families of children with cancer will frequently ask us, “Can we treat her with natural products?” This question may reflect their fear of toxicity of chemotherapy agents. Perhaps they are partly correct. For now, though, we need to define what we mean by standard medical care and what we understand to be “natural medicine.”
Standard medical care (also referred to as mainstream medicine) is medicine practised by health professionals who hold an MD degree. They are frequently joined by nursing specialists, called nurse practitioners.
Complementary medicine is a form of treatment used along with standard medical care. These are not standard treatments but could take the form of, say, acupuncture, to help lessen the pain of cancer treatments.
Alternative medicine is usually what people are referring to when they speak of “natural medicine.” These are treatments that are used instead of standard medical treatments. An example might be using a special diet instead of chemotherapy to treat cancer.
Physicians are sometimes criticized for dismissing so-called natural therapies in favour of mainstream medicine. Commonly, I am asked, “But doctor, what harm can it possibly do?”
In the previous chapter I explained that Vitamin B (folic acid) can actually accelerate the course of cancer and result in early demise. The herb kava kava, used to reduce anxiety, can cause liver damage. St. Johns wort can interfere with the efficacy of some chemotherapy agents. We ask that patients inform us of any or all of the products and dietary supplements they are taking, so our pharmacists can check whether they could interact negatively with mainstream treatment.
Fundamentally, the word natural does not mean safe.
REFERENCES
Hunger, P., X. Lu, M. Devidas, B. Camitta, P. Gaynon, N. Winick, G. Reaman, W. Carroll. Improved survival for children and adolescents with acute lymphoblastic leukemia between 1990 and 2005: A report from Children’s Oncology Group. J ClinOnc, March 2012.
Kaatch, P. Epidemiology of childhood cancer. Cancer Treatment Reviews, vol. 36, no. 4, 2010, pp. 277–285.
16 DOES WEARING SUNSCREEN PREVENT SKIN CANCER?
NOT ALL SKIN CANCERS are equal. To emphasize the differences, we talk in this chapter about melanoma skin cancer and non-melanoma skin cancer.
Malignant melanomas (MMs) make up only about 2 percent of skin cancers, and yet they are responsible for more than 80 percent of deaths from skin cancer, often following a change in a pre-existing mole. The past three decades have seen an increase in the incidence of melanoma in persons over 50. The incidence of the disease in younger people is stable, but people are living longer, and the incidences of all cancers are increasing in the older population.
The other types of skin cancers (non-melanoma) are less malignant and make up the other 98 percent of all skin cancers. They consist of basal cell carcinoma and squamous cell carcinoma. They involve more benign lesions and are related to prolonged sun exposure. While these lesions rarely progress beyond local skin lesions, some, especially squamous cell carcinoma (which are even less common), can spread to nearby tissues.
Genetics is known to play a role in the development of malignant melanoma. If you have a first-degree relative (a parent or sibling) with MM, the risk of your developing it is doubled. Certain genetic patterns are more commonly seen in people with MM. For instance, CDKN2A is a tumour suppressor gene that can undergo mutation (change) and allow the malignancy to occur.
Before we dig into micromolecular structures, there are very obvious patterns in the distribution of skin cancer that tell us more about its natural history. Malignant melanoma is 25 times more common in whites than in people of African descent. It is also less common in people who tan well. For instance, it is five times less common in Hispanic and East Indian folks than in Caucasians.
Evidence shows the role of sun exposure in the causation of MM to be “sun injury” — a bad sunburn — rather than sun exposure. Basal cell and squamous cell carcinoma are a feature of “prolonged sun exposure,” not necessarily sun injury. Basal cell carcinoma tends to occur on each side of the nose and also at the tops of the ears — areas of maximum exposure. For that reason, many golfers concentrate their sunscreen on those skin areas.
So where do we find the biggest incidence of non-melanoma skin cancers? Wait for it: the top three countries are Switzerland, Ireland, and Canada (especially Manitoba). How does this make any sense, especially when the lowest incidence in the United States is in California? To further confuse you, California has a high population of Hispanics, but in fact it’s the white population of that state that has the lowest incidence of skin cancer.
I can tell you personally, from 30 years living in each of Ireland and Canada, that exposure to the sun, let alone the appearance of the sun, can be a rare event. Manitoba has glorious winter sunshine, but I’ve yet to see people sunbathe in minus 30 degrees. So, if the cloudiest country in the world (Ireland, surely) has the second-highest incidence of skin cancer, surely more than just sunshine is to blame. It is conceivable that when the sun does shine, people are more prone to expose themselves to extreme amounts of sun over short periods of time.
Where does sunscreen come into the picture? Is it the answer to preventing skin cancers? Maybe not….
So far, sunscreen has not been shown to reduce the incidence of either melanoma or non-melanoma skin cancers. In fact, the availability of sunscreen has led to longer periods of intentional sun exposure, and more frequent sunburns. Over the two decades or so in which we have seen generalized use of sunscreens, the incidence of skin cancer has actually risen. This may go partway to explaining why MM is more common in indoor desk workers than in outdoor field workers!
In 1977, Bob Marley went to his doctor for removal of a wart on the undersurface of his foot. This wart turned out to be a malignant melanoma, which was to cause his death in 1981. Certainly, this was not due to sun exposure. Bob was also Anglo-Jamaican. His father was a British naval officer from Liverpool.
Melanoma can also occur in the rectum and in the vagina. Very confusing, isn’t it?
It seems to be a myth that sunscreen is going to prevent deaths from skin cancer. We need to acknowledge, however, that even though people with an indoor lifestyle can die of skin cancer, sun damage frequently plays a causative role.
REFERENCES
Huncharek, M., and B. Kupelnick. Use of topical sunscreen, and the risk of malignant melanoma: Results of a meta-analysis of 9,067 patients from 11 case control studies. American Journal of Public Health, vol. 92, 2002, pp. 1173–1177.
Chestnut, C., and J. Kim. Is there truly no benefit with sunscreen use and Basal Cell Carcinoma? A critical review of the literature and the application of new sunscreen labelling rules to real world sunscreen practices. Journal of Skin Cancer, vol. 11, 2012.
Planta, M. Sunscreen and melanoma: Is our prevention message correct? J Am Board Fam Med., vol. 24, 2011, pp. 735–739.
17 “FRIDAY LEUKEMIA”
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IT MUST BE THE WORST day of our life when we or a loved one receive a devastating diagnosis such as leukemia. These days, outcomes are more favourable for people with acute leukemia, particularly children, but this disease is still a life-threatening event and a life-altering experience.
I have always remarked on how frequently these dramatic encounters with patients and their loved ones occur on a Friday. Maybe it’s just life. For instance, we always hit the supermarket when the lines are busiest, or I always visit the library on the day when they close early.
You can surmise that the admission and diagnoses on a Friday are due to only skeleton services being available at weekends and the need to wrap decisions on a Friday. However, after decades of care and consoling of these families, it’s no coincidence that my weekends have been filled with these family conferences after diagnoses on a Friday.
In 2010, a group of German oncologists published an article called “Friday Leukemia” in a journal of research in blood disorders. This group of cancer specialists reviewed 197 cases of leukemia over three and a half years. They looked back at these cases, and found that 23 percent were admitted and diagnosed on a Friday. The next closest day of admission was Monday, at 16.8 percent.
The German oncologists further analyzed their cohort of the Friday folks as to their outcomes. The conclusions they drew were that this group did not have any significant difference in disease type and their outcomes did not differ from people diagnosed on other days of the week.
Were there differences in the outcomes, there might have been an argument for assigning a sub-classification to the Friday Leukemia group!
Robinson Crusoe, after all, named his desert island companion Man Friday because this was the day the man saved his life. Could there be more to this Friday “myth”?
REFERENCE
Wilop, S., O. Galm, L. Thompson, R. Osieka, T.H. Brummendorf, E. Jost. Friday leukemia. Blood, vol. 115, no. 4, January 2010.
WE ARE WHAT WE EAT
18 CRANBERRY JUICE PREVENTS URINARY INFECTIONS
OF THE COUNTLESS women who have suffered from recurring urinary tract infections, many will tell you that their grandmother, or better still, their grandmother’s grandmother, swore by cranberry juice as a preventative agent for these infections (also called UTIs, cystitis, pyelitis, or bladder/kidney infections).
When native Americans first introduced the Pilgrims to cranberries in the 1600s, they noticed how fond cranes were of devouring the berries. This gave rise to the name “craneberries.” Cranberries later became part of the New World tradition of Thanksgiving dinner.
Although commercial harvesting of cranberries did not start till the 1800s, it was not long before medical folklore got hold of the potential benefits of this fruit for the prevention of urinary infections, well before the antibiotic era. Apart from family members, countless doctors (myself included) have recommended this route for those afflicted — not so much as a cure, but as a preventative.
So were we right? And, more importantly, is there a scientific basis for this theory? Well, it’s not merely an old wives’ tale, for two scientific reasons:
Cranberry juice is highly acidic, and bacteria are inhibited in an acid urine. However, it is unclear whether cranberry lowers the pH of the urine enough for the acidic urine to be effective against bacteria.
Cranberry juice contains a chemical called Proanthocyanidin. Laboratory studies have shown that this chemical can inhibit the adherence of E. Coli bacteria to the bladder wall.
So on both counts we know that cranberry could prevent the colonization of the bladder with bacteria. The question is — does it?
The trouble is that we don’t know how much cranberry, at what concentration, and over what period of time is necessary to inhibit bacterial growth properly. We don’t really have good studies showing the degree of acidity achieved by a glass of cranberry juice. Some studies are done with a juice concentrate and some with a cranberry capsule.
There have been multiple trials on this question, many fraught with dropouts and low numbers. Many trials were also not placebo controlled. In 2007, a review concluded that cranberry was effective in decreasing the number of UTIs in women over a 12-month period. Our friends at the Cochrane database concluded that there was some evidence to support the use of cranberry for prevention of UTIs, but they called for standardization of dosage and method of administration. An update on that review in 2012 reversed the conclusion. And then a year later, in 2013, a report of meta-analysis from the Cleveland Clinic concluded that cranberries reduced the occurrence of UTIs in women with recurrent UTIs, compared to a placebo.
We still need a more definitive study. This study should involve women of comparable age and medical condition, with a defined dose of cranberry, compared to a placebo.
So where does all this leave us?
Well, in patients with complex medical histories and fragile health, we will probably continue to use preventative antibiotics. But it’s worth remembering that these meds have side effects and allergy profiles and will stop helping the patient as soon as they are discontinued.
Cranberry is safe and pleasant to drink, and it may well be effective if used by the 60 percent of women who experience cystitis (milder lower urinary tract infections). Therefore, if you are one of this group and you have a choice between drinking apple, orange, or cranberry juice, I think you know what my advice will be.
You may therefore wish to categorize this myth as a believable one!
REFERENCES
Craig, J., R. Jepson. Cranberries for preventing urinary tract infections. Cochrane Renal Group Intervention Review. Published online, 23 January 2008. http://www.cochrane.org/CD001321/RENAL_cranberries-for-preventing-urinary-tract-infections.
Mathers, M.J., F. Von Runstedt, A.S. Brandt, M. Konig, D.A. Lazica, S. Roth. Myth or truth: Cranberry juice for prophylaxis and treatment of recurrent urinary tract infections. Urologe A, vol. 48, no. 10, 2009, pp. 1203–1209.
19 DOES EATING CHOCOLATE CAUSE ACNE?
IN MEDICAL SCHOOL LECTURES on adolescent medicine, one talk was labelled the “Sex and Pimples” lecture, trivializing a condition that is the bane of many teenagers’ lives. Tending to strike somewhere between 14 and 18 years of age, this affliction has troubled the lives of countless self-conscious young people in the years transitioning to adult life. Even the medical name of this condition — Acne Vulgaris — is enough to destroy the self-esteem of any young teen.
Many sufferers report being abused or bullied because of their acne. Such is the anguish of affected teens that up to 20 percent report that they have considered suicide.
A controversial drug for acne, called Accutane, has been associated with an increase in attempted suicide. The claim is hard to substantiate, as those taking Accutane were the group worst affected by acne and were more likely to have been suicidal before starting the medication.
Popular culture frequently looks for a cause in the lifestyle of these young folk. “It’s that awful fast food, and poor hygiene.” However, we have studies now that show that the consumption of burgers, fries, and chocolate have no impact on acne. Likewise, washing one’s face too often may actually worsen acne.
At some point in our lives, 75 percent of us suffer from acne. One-quarter of those affected have severe acne. In teenage life, boys are more commonly affected, while in adult life, women are more commonly affected.
We know that there are two verified mechanisms in the causation of acne:
An increase in sebum, which is under the control of androgens. Sebum is that oily fluid secreted by the sebaceous glands. Girls secrete androgens as well as estrogens in puberty. In women, the balance between androgen and estrogen (with estrogen fluctuations) can cause similar acne problems in later adult life.
Colonization of the sebaceous ducts by the acne bacterium (Propionibacterium Acnes).
While androgens, not chocolate, cause acne, there have been reports of high dairy intake being associated with worsenin
g of acne.
Overall, the prognosis for acne is good. Topical creams and oral medication mean that it is no longer necessary for young people to suffer the physical and mental health consequences of acne. These days, the aim should be to avoid the physical and psychological scars of teenage years as much as possible.
REFERENCE
Pappas, A. The relationship of acne and diet: A review. Dermato-Endocrinology, vol. 1, no. 5, pp. 262–267.
20 IS THE BEST HEART DIET AN ULTRA LOW FAT DIET?
PERHAPS THE TITLE of this chapter should refer to a low fad rather than low fat diet being best for our health.
Some years ago I heard a New York cardiologist speaking at a medical meeting. The topic was “Nutritional Aspects of Heart Disease.” The speaker stood on the podium for only a short time and repeated, “Eat less, eat less, eat less.” His talk was not well received by his colleagues, and the physician in question was ultimately sanctioned by his regulatory body for contempt.
But think about it. Had he stood up for 40 minutes, and showed graphs, histograms, and models of cholesterol molecules, he would have been praised effusively. A week later, most people would have forgotten what he had said. Instead, we are still talking about the event years later. The cardiologist was frustrated with seeing overweight middle-aged patients, all day, every day, whose problem was the amount they ate rather than the content of their diet. Oversized portions have invaded our culture and our hearts.
For more than half a century, the conventional wisdom among nutritionists and public health officials was that fat is Dietary Enemy No. 1. The fact is, we actually need fats in our diet. These include mono-unsaturated fats, as found in olive oil and avocados, and some poly-unsaturated fats, as found in fish and walnuts.
Of Plagues and Vampires: Believable Myths and Unbelievable Facts from Medical Practice Page 5
