While studies show that reduced saturated fat intake (butter, meat fat) lowers the amount of LDL (bad cholesterol) in the blood, the research needs to be evaluated in the context of what we replace saturated fats with. Generally, if we replace the saturated fats in our diet with unsaturated plant-source fats that are usually liquid at room temperature, we benefit by reducing our levels of LDL cholesterol and reducing our chances of experiencing cardiovascular disease. However, if this dietary change is combined with a higher carbohydrate intake (particularly refined carbs), this can lead to insulin resistance, Type 2 diabetes, and increased atherosclerotic heart disease.
So it’s worth remembering that, first, the amount we eat will ultimately determine the health of our heart. And second, fat is not necessarily Dietary Enemy No. 1. When nutritionalists say “balanced diet,” they indeed mean balanced in all directions, not just substituting one set of molecules for another!
REFERENCES
Krauss, R., F. Hu, P. Siri-Tarino. Saturated fat, carbohydrate, and cardiovascular disease. Am J ClinNutr, vol. 91, no. 3, 2010, pp. 502–509.
Lundell, D. Heart surgeon speaks out on what really causes heart disease. Health and Wellness, March 2012. https://www.sott.net/article/242516-Heart-surgeon-speaks-out-on-what-really-causes-heart-disease.
21 SHOULD WE ALL BE ON GLUTEN-FREE DIETS?
IS GLUTEN SENSITIVITY a new epidemic or a myth? Some of us would say both!
Celiac disease, a gastrointestinal absorption impairment, was first described in 250 AD in Cappadocia in ancient Greece, by Aretaeus, a renowned follower of Hippocrates although he lived a few centuries later. But it wasn’t until 1952 that a Dutch pediatrician linked the symptoms of sufferers of this condition to wheat proteins. We then knew that gluten, a fragment of wheat, could cause damage to the lining of the small bowel, and that removing wheat from the diet could lead to a remarkable remission of symptoms, particularly chronic diarrhoea and weight loss.
Nowadays, celiac disease (gluten enteropathy) is readily diagnosable through a blood test for celiac antibodies and confirmed with a small bowel biopsy, done usually with a scope. In most western countries, the incidence of the disease is less than 1 percent. However, on the Celtic fringe (western Scotland, Ireland, and Brittany), the incidence is much higher. In persons who have Type 1 diabetes, it’s 8 percent, a very high figure suggesting that, like diabetes, celiac disease is probably an autoimmune disorder — a condition in which the body’s immune system attacks its own healthy cells.
Numerous books have been written describing the role of gluten in everything from sports performance to memory loss, depression, and autism. In the past 15 years, a multi-billion dollar industry has built up around “gluten sensitivity” and the benefits of a gluten-free diet. Gluten-free products range from bread to restaurant meals and beer. Some studies report people feeling better mentally and emotionally on a gluten-free diet. These include people without celiac disease, leading to the concept of another condition (six times more common), called Non-Celiac Gluten Sensitivity (NCGS). Science is saying that these people don’t have medically proven celiac disease, yet their symptoms are very similar to the classic symptoms of gluten intolerance.
So if 1 percent of Canadians have celiac disease and 30 percent of us are avoiding gluten, are we medics missing something?
In 2011, a symposium of gastroenterologists in Oslo set about defining NCGS and determining the terminology to define it as a separate entity. A landmark article by three gastroenterologists in Italy published in the World Journal of Gastro-enterology in 2015 suggested diagnostic and treatment criteria for this group. In essence, these people may be sensitive to some other component of wheat. Remember, we have only been eating wheat for 10,000 years — a short time in human evolution.
As to the validity of gluten-induced behavioural changes, research is at an exploratory stage. It is far more difficult to define and quantify mental health symptoms than gastrointestinal complaints. Many parents of children with autism are following the GFCF diet, which is both gluten-free and casein-free (casein is dairy protein). While there is a lack of scientific evidence to support any benefit for children with autism, there are anecdotal descriptions of improvements in behaviours from parents who have used this diet. So, given the lack of options for these parents, should they not give the GFCF diet a try?
Well, there are practical issues when it comes to adherence to any diet. Firstly, youngsters on the autism spectrum are among the most difficult children to nourish. Swallowing immaturity and extreme food aversions are common. Combine this with the fact that a GFCF diet involves eliminating most bread and grain products — pasta, cereals, and pizza, for example — and much dairy-related nourishment, and you may have a problem with providing the basics of the four food groups to any child. Supplementation can make up for the lack of some nutrients, but not for the lost calories.
For my part, I’m grateful to the industry for manufacturing gluten-free products, as it significantly improves the available choices and quality of life for many — be that 1 percent or 30 percent of the population.
REFERENCES
Elli, L., L. Roncoroni, M.T. Bardella. Non-celiac gluten sensitivity: Time for sifting the grain. World J Gastroenterol vol. 21, no. 7, 2015, pp. 8221–8226.
Cronin, C.C., and F. Shanahan. Why is celiac disease so common in Ireland? PerspectBiol Med, vol. 44, no. 3, 2001, pp. 342–352.
Peters, S.L., J.R. Biesiekierski, G.W. Yelland, J.G. Muir, P.R. Gibson. Gluten may cause depression in subjects with non celiac gluten sensitivity. Aliment PharmacolTher, vol. 39, no. 10, 2014, pp. 1104–1112.
MEDICAL CONTROVERSIES
22 PLACEBO: IS A “DUMMY PILL” ETHICAL?
BACK TO LATIN again. The word placebo in that language means “I will please.”
It can be used in two contexts:
A harmless pill, medicine, or procedure prescribed more for the psychological benefit of the patient than for any proven medical effect.
A substance (often a pill) used in a randomized controlled trial designed to test the efficacy of medical treatments (usually a new drug). In this context, the placebo is given to participants who do not know whether they are receiving the active drug, or a “dummy” drug — the placebo. To prove a medicine is effective, a pharmaceutical company must show not only that their drug has the desired effects, but that these effects are significantly greater than those of the placebo (dummy drug) group.
Although placebos have been described in the medical literature for more than 200 years, they have probably been around since the dawn of medicine. Perhaps the three biggest questions on this topic are:
Do placebos actually work?
Whether they do or not, is it ethical for a doctor to
take part in such deception?
Is there a placebo component to most treatments?
So great is the scope of this topic that Professor Ted Kaptchuk of Harvard Medical School has spent the last few years as director of the Harvard-wide program in Placebo Studies. Along with his colleagues, he has been able to study the impact of placebos in various illnesses, and the neurobiological, psychological, and cultural basis for the effect.
Do placebos work? Let’s start with the fact that clinical trials commonly report 30 percent of respondents benefiting from the placebo drug. (Obviously, the respondents were unaware that they were taking a placebo at the time.) When we add to this that the placebo is not going to produce any side effects, we can see why Professor Kaptchuk’s research is so important. His work at Harvard has determined that placebo treatments (with no active chemical) can stimulate real physiological responses. These include changes in heart rate and blood pressure, and even chemical activity within the brain in cases involving pain, depression, and anxiety.
But what is the basis of these physiological changes? Are they based on emotions, faith, or the perception of the caring physician? More importantly, are there certain people who are susceptible to placebo responses, and can the
y be identified? (Similar arguments apply to hypnosis.)
Is it ethical, then, for a doctor to prescribe a placebo or dummy pill? Not without the consent of the patient! In the case of clinical trials, however, the experimental subject signs a consent that clearly states that one of the blind treatments will be a sugar pill or dummy medicine. This is to protect the patients from accidental reports of new medications.
What if we were to tell patients that we proposed to give them a placebo to treat their symptoms? Until recently, the deceptive nature of placebo treatments was felt to be an insurmountable ethical barrier to their use. However, in the case of irritable bowel syndrome, a condition of chronic abdominal pain, and of constipation or diarrhoea, two studies have shown open-label placebo to be equal or more effective than the main drug available to treat the disease. Placebo response in one study was 59 percent. So will patients accept the use of a placebo if they are shown evidence that it is effective? Maybe!
And lastly, do all or most medications have a combination of biochemical and placebo effects? This must be true in everyday practice. Differences of only one or two percentage points have been found in some studies comparing anti-depressant use to placebo. Also, the relief resulting from being prescribed an antibiotic for a winter respiratory infection must be part placebo effect, as it’s estimated that 80 percent of these infections are caused by viruses, which are unresponsive to antibiotics.
The ultimate answers will probably involve the identification of “responders” and “non-responders.”
REFERENCES
Kirsch, I. The placebo effect has come of age. Journal of Mind-Body Regulation, vol. 1, no. 2, June 2011, pp. 106–109.
Kienle, G.S., et al. The powerful placebo effect: Fact or fiction. Jclin Epidemiol, vol. 50, no. 12, 1997, pp. 1311–1318.
Feinberg, C. The placebo phenomenon. Harvard Magazine, January 2013, pp. 1–10. http://harvardmagazine.com/2013/01/the-placebo-phenomenon.
23 THE HIGH COST OF DYING
IT IS NO MYTH that all of us are going to die at some point. But are exorbitant end-of-life costs a myth or a reality?
The picture of one’s last days spent attached to a machine, undergoing a thousand tests, is more and more familiar these days. In an age of awareness of health spending, it’s common to see headlines like “60 percent of health dollars used in last six months of life,” or “1 percent of population using 30 percent of health budget.”
If health policy analysts tell us that 60 percent of this budget is being spent on persons in the last six or twelve months of their life, could they be correct? Could it be, then, that the rest of us are collectively left with 40 percent — less than half the pot?
One of the problems with this topic is that the headlines are coming from different health centres in different countries with diverse demographics and variable cultural and legal challenges. The staff at Nuffield Trust in London’s West End were not convinced of these figures and thought that they were in fact a myth. They decided to add up care costs in their population over the 90 days that preceded death. In their study of a population of more than 200,000, they had 21,000 deaths. Computing the costs of family doctor visits, community nurse contacts, residential nursing care, hospice care, and in-patient hospital care, costs averaged out per person were £6,500 (approximately $10,000).
For sure, health-care costs escalated in the final weeks of life — but hardly by 60 percent. The American Journal of Public Health recently published data showing that only 11 to 13 percent of care costs are incurred in the final year of life.
So, whence the myth and hyperbole? I can only surmise that hospital economists may have been quoted out of context. Perhaps 60 percent of costs in that hospital, with that demographic, or in that ICU?
So, then, it’s not age as such that elevates spending. Healthy elderly seniors may not cost our health-care systems much more than folks in middle age. However, it’s a fact that most countries do find that proximity to death rather than age is the key factor in health-care spending.
We are all aware that hospital stays are very expensive and that home care is more cost-effective. This is particularly the case in palliative care, where people are able to live out their days in the home and family environment, with skilled hospice support. Clearly, the funding for home care needs to follow the patient home and not be a form of cliché or lip service.
Also, to this point, we have equated “end of life care” with “elder care.” But having worked in neonatal pediatrics for many years, I know that the costs for end-of-life care in the youngest demographic in our population — premature infants — is considerable. This is another form of ICU care, called NICU (neonatal intensive-care unit). Premature infants make up less than 10 percent of births but are responsible for 50 percent of the in-patient budget for infants. Mortality in this group is far higher than the average, as are the long-term disabilities.
REFERENCES
Aldridge, M., and A. Kelley. The myth regarding high cost of end of life care. American Journal of Public Health, vol. 105, no. 12, 2015, pp. 2411–2415.
Georghiou, T., and M. Bardsley. Research report: Exploring the cost of care at the end of life. Nuffieldtrust.org.uk. September 2014.
24 VACCINE CONTROVERSIES
WHEN AN ENGLISH SURGEON named Edward Jenner discovered a vaccine for smallpox in the late 1700s, he could hardly imagine the controversies that would thwart his science 200 years later.
Smallpox was first reported in New France in 1616 near Tadoussac, brought by French settlers. Because the Aboriginal peoples in the area had no immunity, they were ravaged by the disease, which quickly spread to other tribes.
Smallpox had devastated Europe in epidemics for hundreds of years. Jenner noted, however, that milkmaids in pastoral England were rarely afflicted with the disease. He deduced that this immunity was probably related to their coming into contact with cowpox through the udders of cows. Cowpox, a milder virus that causes minimal rash and other symptoms, belongs to the same poxvirus family as the variola virus that causes the devastating smallpox.
Jenner found that scratching the fluid of cowpox lesions into the skin of healthy individuals inoculated them against both cowpox and smallpox. From his insight came the concept of innoculation, in which the serum of recovered patients contained a substance that could protect others from that disease.
And so….
The Pertussis (Whooping Cough) Vaccine Controversy
I arrived in Liverpool in 1978 to train as a pediatrician. Merseyside had Britain’s second-biggest children’s hospital, known as Alder Hey Children’s Hospital. With 800 beds, it served an area of several million people in north England and Wales. Its wards stretched through 26 attached buildings and rose three storeys high. The wards were labelled from A all the way to Z — the ward where we resident junior doctors slept, if such a chance arose.
Distance within the hospital was complicated by the fact that the Casualty or Emergency Department was on A ward, and thus one mile from the doctors’ sleeping quarters. A hospital bylaw allowed the on-call house officer to ride a bicycle in the corridors between Z ward and A ward — after 8 pm.
D3 had a unit called the “Pertussis ward,” with 20 to 30 beds for one disease only: whooping cough. This devastating respiratory condition, sometimes known as the “100-day cough,” can cause apnoea (cessation of breathing), pneumonia, and even seizures. Most pertussis deaths occur in the first six months of life, when the vaccine has not yet taken. The spasms of coughing are dramatic, and followed by a whoop as the child breathes in.
Liverpool, once the second city of the Empire, went into decline after the demise of the shipbuilding industry. The Beatles had departed nine years earlier, and the Cavern Club was now the Cabin Club. We managed to get a flat around the corner from Penny Lane and settled into this unique city, still possessing the charms of its people and its history.
However, one topic was never far from the minds of pediatricians and parents. Pertussis, having
been almost eradicated, was making a comeback. Vaccination rates had dropped to 20 percent. In Britain from 1974 to 1979, there were 103,000 cases of pertussis. Forty-one children died, most of them aged under a year. A second epidemic was to follow in the 1980s. The reason? Controversy about safety of the vaccine.
Media reports of this vaccine causing neurological damage led to a sharp decline in public acceptance of the safety of this immunization. The reports tended to be sensationalized by the tabloid press, while the dangers of the disease itself were given little attention.
Scepticism among the medical profession itself regarding the administration of this vaccine condemned it to a controversy that would last for decades.
But some truth lies behind most myths. The whole-cell vaccine used from 1950 to 1990 had been developed in early 1900s. It could cause fevers, and sometimes even seizures (approximately 5 percent of infants are prone to develop seizures with febrile illness). As whooping cough became less common, stories began to appear regarding neurological damage from this vaccine.
A wave of legal battles, and vaccine compensation ensued. It is impossible to tell what caused the neurological damage in these unfortunate children. There were no MRIs or genetic tests to confirm diagnoses then.
In 1981, a landmark survey of children aged six months to 36 months determined that the risk of neurological damage after whooping cough vaccine was three per million — very close to the risk for those unimmunized. The irony is that the disease itself causes seizures in 10 percent of infants.
A second improvement in uptake occurred with the development of an acellular vaccine, which is purer and causes less fever.
Of Plagues and Vampires: Believable Myths and Unbelievable Facts from Medical Practice Page 6
