Monthly Archives: July 2014
With symptoms including a runny nose, sore throat, sneezing, cough, headaches and fever, the common cold can leave you feeling rotten for up to two weeks.
As the name suggests, they’re annoyingly common, with the average adult likely to get two or three colds a year, while children average ten.
Common colds are caused by more than 200 different viruses and tend to be milder than the flu. But while the influenza vaccination can prevent against the most common circulating strains of the flu, there’s no equivalent for the common cold.
So, can you prevent the common cold? Or treat it once you have it? Let’s put four popular therapies to the test: echinacea, garlic, vitamin C and zinc.
Echinacea is a group of flowering plants common in North America, and was a traditional Native American medicine. These days you can buy the product in capsules, tablets or drops.
Around one in 20 Australians take echinacea, in the hope that extracts will stimulate immunity and kill off any bugs encountered.
In terms of prevention, taking echinacea products daily to avoid the common cold may slightly reduce the risk of getting a cold, but the evidence is rather murky. If we pool the results from studies that compared Echinacea to placebo treatment, people who took Echinacea seemed to get fewer colds. But there is major inconsistency between the individual studies, so combining them together this way isn’t very valid.
In terms of treatment, there is no convincing clinical evidence that taking echinacea products at the onset of symptoms can cure a cold or reduce the duration of illness.
However, it’s difficult to come to any clear conclusions or recommendations about echinacea’s effect on the common cold because the preparations studied have varied, with different species, parts of the plant, preparation method and dosage.
Echinacea products are not without side effects, such as allergic reactions in children which, though uncommon, can be severe.
Garlic has been promoted as a natural preventative against the common cold, taken in commercial products or eaten raw.
It too is seen to have antiviral and antimicrobial properties, and manufacturers claim it boosts the immune system. The mechanisms behind these actions are unclear but the chemical allicin, which is responsible for the aroma of fresh garlic, may be the active agent.
There is a dearth of quality scientific evidence about the effect of garlic on colds. The recent Cochrane systematic review which set out to answer this question could find only one study suitable for analysis.
Participants who took a garlic capsule (with a standardised dose of allicin powder) daily for three months reported fewer days of illness from colds than those who took a placebo. But they were more likely to suffer from side effects such as skin rash, and body odour.
These results may appear promising but need to be approached cautiously until replicated. It’s always possible there are biases in a single study – for instance, the study author appears to sell medicinal garlic products.
The lack of quality evidence precludes a recommendation for using garlic supplements for the common cold. But, of course, people who like eating garlic should continue to do so.
Vitamin C is commonly found in fresh fruits and vegetables and is one of the most common supplements taken by Australians. The use of vitamin C for the common cold became popular in the 1970s, following its promotion by American chemist Linus Pauling who believed it had many health benefits.
There is good study data on the effect that vitamin C has on the common cold: for the most part, it isn’t effective.
Taking vitamin C daily as a preventative has no effect on the likelihood of getting a cold in the general community. It might have a small effect on the severity of symptoms, and on the duration of illness (about a half day for a usual cold).
But taking vitamin C as treatment (taking a dose after you get a cold) does not have an effect on the duration or severity of symptoms.
This same data found that vitamin C can be beneficial for people undergoing heavy acute physical stress, such as marathon runners and alpine skiers. But this is an unusual and specific context and the results can’t be generalised for regular community settings.
This mineral is an essential nutrient and is found in both plant and animal sources. Foods that are particularly rich in zinc include oysters, sun-dried tomatoes, beef and various seeds (including pumpkin, sunflower, sesame, and pine nuts). Oral zinc is widely available in a number of different formulations.
Interestingly, oral zinc does appear to have a beneficial effect for the common cold, but with a number of major caveats.
When taken as a treatment at the onset of the cold, zinc appears to reduce the duration of a cold, but only at higher doses (more than 75 milligrams a day). Zinc might be more effective in adults than in children, and when taken as lozenges, particularly in the zinc acetate form.
There is little data on using zinc as a regular preventative, and you might not want to because it comes with a number of unpleasant side effects, such as nausea and bad taste.
It’s important to note that the results vary between studies and there is some evidence of publication bias. So it may be that the estimate of the effectiveness of zinc for the common cold is exaggerated.
When we step back, it isn’t really that surprising that nothing really works, or works that well for preventing or treating colds. Given how common it is, any truly effective therapy would be a massive commercial blockbuster and hardly a secret.
General practice registrars Dr Samuel Cheng and Dr Catherine Lip, from the GP Unit, Fairfield Hospital, co-authored this article
Julia Child, goddess of fat, is beaming somewhere. Butter is back, and when you’re looking for a few chunks of pork for a stew, you can resume searching for the best pieces — the ones with the most fat. Eventually, your friends will stop glaring at you as if you’re trying to kill them.
That the worm is turning became increasingly evident a couple of weeks ago, when a meta-analysis published in the journal Annals of Internal Medicine found that there’s just no evidence to support the notion that saturated fat increases the risk of heart disease. (In fact, there’s some evidence that a lack of saturated fat may be damaging.) The researchers looked at 72 different studies and, as usual, said more work — including more clinical studies — is needed. For sure. But the days of skinless chicken breasts and tubs of I Can’t Believe It’s Not Butter! may finally be drawing to a close.
The tip of this iceberg has been visible for years, and we’re finally beginning to see the base. Of course, no study is perfect and few are definitive. But the real villains in our diet — sugar and ultra-processed foods — are becoming increasingly apparent. You can go back to eating butter, if you haven’t already.
This doesn’t mean you abandon fruit for beef and cheese; you just abandon fake food for real food, and in that category of real food you can include good meat and dairy. I would argue, however, that you might not include most industrially produced animal products; stand by.
Since the 1970s almost everyone in this country has been subjected to a barrage of propaganda about saturated fat. It was bad for you; it would kill you. Never mind that much of the nonsaturated fat was in the form of trans fats, now demonstrated to be harmful. Never mind that many polyunsaturated fats are chemically extracted oils that may also, in the long run, be shown to be problematic.
Never mind, too, that the industry’s idea of “low fat” became the emblematic SnackWell’s and other highly processed “low-fat” carbs (a substitution that is probably the single most important factor in our overweight/obesity problem), as well as reduced fat and even fat-free dairy, on which it made billions of dollars. (How you could produce fat-free “sour cream” is something worth contemplating.)
But let’s not cry over the chicharrones or even nicely buttered toast we passed up. And let’s not think about the literally millions of people who are repelled by fat, not because it doesn’t taste good (any chef will tell you that “fat is flavor”) but because they have been brainwashed.
Rather, let’s try once again to pause and think for a moment about how it makes sense for us to eat, and in whose interest it is for us to eat hyperprocessed junk. The most efficient summary might be to say “eat real food” and “avoid anything that didn’t exist 100 years ago.” You might consider a dried apricot (one ingredient) versus a Fruit Roll-Up (13 ingredients, numbers 2, 3 and 4 of which are sugar or forms of added sugar). Or you might reflect that real yogurt has two or three ingredients (milk plus bacteria, with some jam or honey if you like) and that the number in Breyers YoCrunch Cookies n’ Cream Yogurt is unknowable (there are a few instances of “and/or”) but certainly at least 18.
Many things have gone awry with the way we produce food. And it isn’t just the existence of junk food but the transformation of ingredients we could once take for granted or thought of as “healthy.” Indeed, meat, dairy, wheat and corn have become foods that frequently contain antibiotics and largely untested chemicals, or are produced using hybrids or methods that have increased yield but may have produced unwanted results.
The best current answer to that: It’s possible to eat as much meat as we do only if it’s grown in ways that are damaging. They’re damaging to our health and the environment (not to mention the tortured animals) for a variety of reasons, including rampant antibiotic use; the devotion of more than a third of our global cropland to feeding animals; and the resulting degradation of the environment from that crop and its unimaginable overuse of chemicals, soil and water.
Even if large quantities of industrially produced animal products were safe to eat, the environmental costs are demonstrable and huge. And so the argument “eat less meat but eat better meat” makes sense from every perspective. If you raise fewer animals, you can treat them more humanely and reduce their environmental impact. And we can enjoy the better butter, too.
When it comes to food, we’re told to eat what’s in season, buy locally and avoid “food miles” – for good reason. But not everyone has access to grower’s markets, or the time and resources to source and…
But not everyone has access to grower’s markets, or the time and resources to source and prepare ingredients from multiple locations. Even buying fresh and cooking from scratch is a struggle for some.
Foods that have been preserved by freezing, canning or drying are certainly not in vogue but this doesn’t mean they’re nutritionally inferior. Preserved foods are often a nutritious, cheap and convenient alternative to fresh produce.
Frozen vegetables are harvested ripe, at their prime, when they have optimal nutrient content. They’re then snap frozen, often on the site of production, locking in most of the nutrients.
While there may be minor losses of water soluble vitamins such as vitamin C due to the initial blanching, most of the vitamin and mineral content remains intact.
The texture of frozen vegetables does change due to the formation of ice crystals that break down some of the plant cell walls, making them less crispy. But this doesn’t significantly damage the fibre content.
In comparison, fresh fruit and vegetables are often harvested before they’re ripe, placed in cold storage or transported long distances and spend time in storage at markets and supermarkets. This process leads to continued losses of the less stable vitamins.
Studies comparing the nutrient content of frozen and fresh vegetables have often found the frozen varieties to be nutritionally superior, because loss of the water soluble vitamins is slowed considerably by freezing. Fat soluble vitamins and minerals are heat stable, so they’re less likely to be affected.
We know less about the effect of preserving on the phytonutrients in food. These compounds – such as anthocyanins in frozen berries – are not essential for the human body but seem to have health benefits.
Berries are extremely seasonal because they deteriorate quickly, meaning they are often unavailable or expensive. As a result, large proportions of berry harvests are frozen to allow maximum use of the crop and maximum availability. So far, studies have shown freezing berries results in only a small loss of anthocyanin.
Canning can lock in the nutrients of fruits and vegetables, making them edible for months or even years.
But when fruits and vegetables are heated during the canning process, the water soluble nutrients – vitamin C and Bs – decline considerably.
The heat-stable vitamins E and A are much less affected, as are carotenoids and minerals.
Perhaps surprisingly, canned tomatoes may be nutritionally superior to fresh varieties because of the increased presence of lycopene, a phytonutrient that may decrease the risk of cancer.
Lycopene is tightly bound to the fibre structures in tomatoes; the process of canning helps break down the fibre structures, releasing the lycopene and making it more easily absorbed by the body.
When it comes to canned fruit and vegetables, be wary of salt and sugar content. Buy canned fruit packed in natural juice rather than syrup and choose no added salt canned vegetables.
Dried fruit is a convenient way to add variety and improve nutrition. It’s compact, easily stored and transported, high in carbohydrates and fibre, and makes a great snack on the run.
Dried fruit is high in energy (kilojoules), as the drying process concentrates the sugars. But it also has higher concentrations of more stable nutrients such as calcium and iron, as well as phytonutrients.
Be aware that some dried fruit can contain sulphur dioxide, a pre-treating agent that maintains the original colour of the fruit, which causes sensitivity in some people, particularly asthmatics. If you’d rather avoid sulphur dioxide, buy the brownish rather than the orange dried apricots.
Fresh can be best when the food is in season, inexpensive and and at its peak for flavour, texture and nutrient content. But if foods are out of season, likely to have been stored for an extended time and are expensive, frozen, canned and dried fruit and vegetables are a good alternative to boost variety and nutrition.
You don’t need an expert to tell you obesity has become a major health problem worldwide. The World Health Organization estimates 35% of the world’s adults are overweight and 11% obese, double the rate…
You don’t need an expert to tell you obesity has become a major health problem worldwide. The World Health Organization estimates 35% of the world’s adults are overweight and 11% obese, double the rate in 1980.
Overweight and obese people have an increased risk of high blood pressure, type 2 diabetes and cardiovascular disease, as well as arthritis, obstructive sleep apnoea and liver disease. Obesity can reduce life expectancy by five to 20 years, and the obesity epidemic may soon reverse the gains that have been made in human longevity.
We could simply eat less and move more. But, of course, it’s not that simple; many of us find it impossible to consistently control our calorie intake. For those with severe obesity or diabetes who have tried all other medical options but failed to lose weight, bariatric surgery is the last-line option.
Bariatric surgery refers to a group of surgical procedures that make it more difficult to over eat and/or absorb food. It is recognised as the most effective treatment for obesity, resulting in both the largest and most sustained weight loss, and the greatest reduction in obesity-related disease and death.
But it is highly invasive, it comes with a number of risks and in some cases is not effective.
Types of surgery
There are three main types of bariatric surgery available in Australia: laparoscopic adjustable gastric band (LAGB), sleeve gastrectomy and gastric bypass. All of these procedures can now be performed with keyhole surgery.
Laparoscopic adjustable gastric band
LAGB is a relatively simple operation in which an adjustable silicone balloon ring is placed around the upper stomach. As well as restricting the volume of food the stomach can hold, the pressure created by food in the reduced upper stomach stimulates the vagal nerve, reducing appetite.
But it is easier to consume fluids than denser, healthier foods, reducing the quality of the diet, which might explain why LAGB results in less weight loss than other procedures.
For sustained weight loss, close follow up is needed, with optimal adjustment of the band; if the band is too tight, it’s difficult to eat healthy foods and obstruction may occur, if the band is too loose, appetite is not controlled.
Revision surgery is required in about 15% of patients within three years due to band slippage and erosion of the band into the stomach wall.
Side effects include gastric reflux.
In this procedure, most of the stomach is removed. It is technically simple and is reported to have a good safety profile in experienced hands.
The weight loss and improvement in diabetes is related to both reduced capacity of the stomach and an increase in hormones that reduce appetite and increase meal related insulin release.
Nutritional deficiencies are common and most people need supplements of nutrients normally absorbed by the stomach. Surgical complications include leakage or bleeding at the suture line.
This procedure is the newest and there is less long-term data than for other procedures.
This operation creates a small proximal stomach joined to the end of the jejunum (the lower small bowel) so that parts of the small bowel, where nutrients are absorbed, are bypassed. While a more extensive operation, it can be reversed because nothing is removed.
Gastric bypass results in more weight loss than the sleeve gastrectomy as there is both a reduction in the capacity of the stomach and reduced absorption of nutrients, including the beneficial changes in gut hormones seen with the sleeve gastrectomy.
In some patients, the weight loss is so great that they become malnourished and all patients require life-long supplements of vitamins, calcium and other minerals. There is also the risk of “dumping syndrome” due to the rapid transit of undigested food from the new, smaller stomach to the bowel, causing nausea, cramps, diarrhoea, and occasionally low blood sugar from very high insulin levels.
Surgical complications include leakage, bleeding and bowel obstruction.
Risks and long-term effects
There is also a reported increased incidence of suicide and substance abuse in patients who have had bariatric surgery. But there have been few controlled studies comparing the quality of life after surgery with patients who have not sought surgery.
It’s important to note that individuals do not need to attain the amount of weight loss achieved with surgery to have substantial beneficial health outcomes. A reduction in weight of 5% to 10% can improve the health of your heart and reduce obesity-related disease and early death, especially if combined with increased physical activity.
The current guidelines in most countries, including Australia, are that bariatric surgery is indicated in people with a body mass index (BMI, kg/m2) of greater than 40 or a BMI over 35 with serious health problems, such as type 2 diabetes.
These guidelines are based on those developed by the United States’ National Institute of Health (NIH) in 1991, when a different range of operations were available and surgery was not performed laparoscopically. Because of this, some researchers have recommended governments lower the threshold of eligibility to include people with a BMI over 30 without metabolic complications.
The reduction of the threshold may result in too many people having surgery inappropriately. While bariatric surgery is the most robust treatment for obesity, it is invasive, often irreversible and has associated risks.
Despite the proven efficacy of bariatric surgery, there is no way that it can be delivered on a mass scale. This surgery should be reserved for patients with severe obesity or patients with diabetes who have been compliant with treatment but have been resistant to medical treatments.
Furthermore, there are many new treatments in the pipeline that may mimic the beneficial effects of surgery, such as medications with effects on multiple hormone pathways and less invasive surgical procedures that may be as effective as the current operations with fewer complications.
Progesterone therapy, endothelial function and cardiovascular risk factors: a 3-month randomized, placebo-controlled trial in healthy early postmenopausal women
PLOS ONE, 02/11/2014 Exclusive Author Commentary Clinical Article
Prior JC, et al. – Progesterone is effective treatment for hot flushes/night sweats. The cardiovascular effects of progesterone therapy are unknown but evidence suggests that premenopausal normal estradiol with also normal progesterone levels may provide later cardiovascular protection. The authors compared the effects of progesterone to placebo on endothelial function, weight, blood pressure, metabolism, lipids, inflammation and coagulation. Results indicate that progesterone has short–term cardiovascular safety. Endothelial function, weight, blood pressure, waist circumference, inflammation and coagulation were unchanged as were lipids except for HDL–C. The statistically significant decrease in HDL–C levels was not clinically important (based on lack of Cardiovascular Risk Profile change).
What is important about these RCT data is that they fill a gap in knowledge about the physiological actions of progesterone. Although we carefully screened women enrolled in this study to be early in menopause (1-11 years since their last flow) and to have no cardiovascular risk factors, it may be that the effects of progesterone would be different in women with initial evidence for cardiovascular disease. For example, one study in hypertensive women and men show blood pressure lowering. There is a mechanism for this since in vitro progesterone has vascular smooth muscle relaxation effects. I’m also excited about these data because of my hypothesis that premenopausal normal progesterone and estradiol levels are needed for “women’s cardiovascular protection.” Given that silent (occurring within clinically normal menstrual cycles) ovulatory disturbances (anovulation and short luteal phases) appear to be common in premenopausal women (Li Epidemiologic Reviews 2014), this hypothesis becomes increasingly plausible
Alcohol and cancer is a topic that arouses a lot of controversy: many Australians like the odd drink but don’t want to make the connection to cancer, the world’s biggest killer. The World Health Organisation’s…
Alcohol and cancer is a topic that arouses a lot of controversy: many Australians like the odd drink but don’t want to make the connection to cancer, the world’s biggest killer.
The World Health Organisation’s new World Cancer Report 2014 shows cancer is responsible for 8.2 million deaths in 2012. Around 340,000 of those deaths were the direct result of alcohol consumption.
The link between alcohol and cancer itself is not news. Way back in 1988, the WHO’s International Agency for Research on Cancer (IARC) concluded that alcohol consumption was a group one carcinogen – a direct cause of cancer in humans.
What has evolved over the past 26 years is evidence showing alcohol caused more cancers than first thought. Alcohol has now been conclusively shown to cause breast cancer in women, bowel cancer in men, and cancers of the mouth, pharynx, larynx and oesophagus in everyone. There is increasing evidence that alcohol causes liver cancer in both women and men as well.
When it comes to cancer patters, the IARC is the best of the best – the world’s leading cancer scientists, analysing huge population studies within an exhausting evidentiary framework, to determine beyond doubt the causes of what is now the world’s biggest killer.
One of the most interesting aspects of the IARC’s work is that, despite the baseless catchphrase “everything gives you cancer”, the evidence shows there are only a handful of proven cancer-causing agents:
- the combined effects of obesity, poor diet and physical inactivity
- UV radiation
- alcohol consumption
- viral infections such as hepatitis and human papillomavirus
- industrial chemicals, many of which have been banned in countries such as Australia.
So in terms of risk, where does alcohol fit into the mix?
The new WHO report shows around 4.2% of all global cancer deaths are directly attributed to alcohol consumption. In Australia, the percentage is likely to be higher (6.5% according to some analyses). The reason for that is simple: the average Australian drinks more than the average individual from most other countries.
The risk equation in terms of alcohol exposure is straightforward: the more you consume, the higher the risk. As with most carcinogens, it’s continuous, long-term exposure that does the most damage.
To put some context around the stats, even by the most conservative estimates, more Australians die each year from an alcohol-related cancer than from melanoma.
The good news is that although alcohol is a proven cause of cancer, you can reduce your cancer risk by reducing your alcohol consumption. It’s all a matter of informed choice.
Australian guidelines recommend men and women consume no more than two standard alcoholic drinks on any given night to reduce the lifetime risk of alcohol-related harm. If you adhere to the guidelines, you will significantly reduce your cancer risk. But even one or two drinks a day, every day over an extended period, can increase your cancer risk – especially for women.
So, what can regulators do?
Increased awareness would help. We’ve long made the case for text warnings on alcohol products, just so people can make an informed choice about that extra drink. Warning labels would remind consumers of the risks whenever they’re exposed to the product.
Any potentially harmful product should carry a warning for the consumer. A box of matches does. And, while a misused match can cause death, we’re not losing more than 2,000 Australians each year to match-related fires and explosions, as we are to alcohol-related cancers.
We’ve also long made the case that Australia’s alcohol taxation system is wrong. Harmful products should be taxed on a proportional basis, linked – where possible – to the agent that causes the harm.
With alcohol products, it’s the level of alcohol (and ethanol in the alcohol) that causes cancer, and most the other alcohol-related health problems. The tax component should be linked to the alcohol volume.
That way, as well deterring people from purchasing the most harmful alcohol products, governments have a revenue source to help pay for all the problems alcohol causes and to fund public education programs. (The fact that some wines are cheaper than bottled water says it all.)
Until we get better public policy settings to reduce the impact of cancer-related alcohol, it’s up to you to make an informed choice
I very frequently am told by patients that their GPs and or specialists tell them that all hormones are the same, and the synthetic is the same as the natural. Here is another article (from the Journal of the American Association no less) disproving this. How much more evidence do we need? Premarin in Australia is also known as Premia.
Pfizer’s Premarin for Menopause Linked to Blood Clot Risk
Bloomberg News, 10/01/2013
Pfizer’s Inc. (PFE)’s Premarin for menopause may be tied to a higher risk of blood clots than another common estrogen treatment called estradiol, a study found. Women taking Premarin, also known as conjugated equine estrogens, had double the risk of a blood clot in the veins than women taking estradiol, a synthetic form of estrogen, according to research in JAMA Internal Medicine. No difference between the treatments was seen in the risk of stroke. The findings don’t mean women should stop taking Premarin, an estrogen gathered from the urine of pregnant horses, to ease their menopausal symptoms such as hot flashes, night sweats, mood swings and vaginal dryness, said Nicholas Smith, the lead study author. More research is needed to replicate the results so doctors can say for sure that different types of estrogen drugs carry varied levels of heart risks, he said. “The assumption has held that all oral estrogens have similar safety profiles. This may not be the case,” Smith, a professor of epidemiology at the University of Washington School of Public Health in Seattle, said in an e–mail. “More comparative safety studies of commonly used treatments are needed.”
Here is the full study, if you want more information.
Lower Risk of Cardiovascular Events in Postmenopausal Women Taking Oral Estradiol Compared With Oral Conjugated Equine Estrogens ONLINE FIRST
2Group Health Research Institute, Group Health Cooperative, Seattle, Washington
3Seattle Epidemiologic Research and Information Center, Department of Veterans Affairs Office of Research and Development, Seattle, Washington
4Department of Medicine, University Hospitals of Geneva, Geneva, Switzerland
5Department of Medicine, University of Washington, Seattle
6Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, the Netherlands
7Department of Biostatistics, University of Washington, Seattle
8Department of Statistics, University of Auckland, Auckland, New Zealand
9Department of Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, the Netherlands
10Department of Health Services, University of Washington, Seattle
Importance Little is known about the comparative cardiovascular safety of oral hormone therapy products, which impedes women from making informed safety decisions about hormone therapy to treat menopausal symptoms.
Objective To compare the relative clinical cardiovascular safety of 2 commonly used oral estrogen drugs—conjugated equine estrogens (CEEs) and estradiol.
Design, Setting, and Participants Population-based, case-control study from January 1, 2003, to December 31, 2009, comparing cardiovascular event risk associated with current CEEs and estradiol use in a large health maintenance organization in which the preferred formulary estrogen changed from CEEs to estradiol during the course of data collection. Participants were 384 postmenopausal women aged 30 to 79 years using oral hormone therapy.
Main Outcomes and Measures Incident venous thrombosis was the primary clinical outcome, and incident myocardial infarction and ischemic stroke were secondary outcomes. As validation, an intermediate clotting phenotype, the endogenous thrombin potential–based normalized activated protein C sensitivity ratio, was measured in plasma of controls.
Results We studied 68 venous thrombosis, 67 myocardial infarction, and 48 ischemic stroke cases, with 201 matched controls; all participants were current users of oral CEEs or estradiol. In adjusted analyses, current oral CEEs use compared with current oral estradiol use was associated with an increased venous thrombosis risk (odds ratio, 2.08; 95% CI, 1.02-4.27; P = .045) and an increased myocardial infarction risk that did not reach statistical significance (odds ratio, 1.87; 95% CI, 0.91-3.84; P = .09) and was not associated with ischemic stroke risk (odds ratio, 1.13; 95% CI, 0.55-2.31; P = .74). Among 140 controls, CEEs users compared with estradiol users had higher endogenous thrombin potential–based normalized activated protein C sensitivity ratios (P < .001), indicating a stronger clotting propensity.
Conclusions and Relevance In an observational study of oral hormone therapy users, CEEs use was associated with a higher risk of incident venous thrombosis and possibly myocardial infarction than estradiol use. This risk differential was supported by biologic data. These findings need replication and suggest that various oral estrogen drugs may be associated with different levels of cardiovascular risk.
Placebos have a longer history than medicine as we know it, and have a huge effect on all kinds of diseases and health conditions. But it may now be time to rethink their role. The placebo made its debut…
Placebos have a longer history than medicine as we know it, and have a huge effect on all kinds of diseases and health conditions. But it may now be time to rethink their role.
The placebo made its debut in the medical literature some 200 years ago, although the administration of inert agents in medical practice has a considerably longer history. In fact, such practice is probably as old as medicine itself.
Placebos took on a more studied role with the increasing application of the scientific method to health care that really took off around the middle of the last century. In this context, placebo interventions have been used as a control to test the efficacy of certain treatments.
What is it anyway?
Recently, the increasing incorporation of best-available scientific evidence into medical care (evidence-based practice) has sparked debate around placebos.
Most often, these debates centre on whether a particular treatment works only via placebo, and what implications this might have for policy-makers, clinicians, and patients.
Unsurprisingly, there’s also significant ethical controversy concerning the practice of clinicians knowingly providing inert treatments (placebos) to their patients.
But two important considerations are sometimes lost in the midst of these debates. The first is the question of just how powerful the placebo effect really is; that is, how much benefit do patients actually gain due to the administration of placebo intervention?
The second issue is possibly of even greater significance. It concerns the theoretical underpinning of placebos and placebo effects themselves.
Why we need to understand
Attempts to try and define placebos and placebo effects have a chequered history. The short version of the story is that no one has been able to propose a definition palatable to the bulk of the players in the field.
The problem with coming to an agreed definition stems from a logical paradox – how can an inert agent (a placebo intervention) have a real effect (a placebo effect)?
Some researchers have tried to overcome this problem by introducing terms such as “non-specific” or “contextual” to the placebo definition, but all of these require that the placebo itself is no longer inert.
This leads to questions about what is and isn’t a placebo, and blurs the lines between placebo interventions and “real” interventions.
Currently, the placebo exists as a kind of mysterious black box that sits between administration of a treatment that doesn’t work the way we think it should, and a beneficial effect for a patient. So what purpose does this black box serve?
If there is an effect (the patient gets better), then seeking the reason or cause of this effect would seem useful.
This work has already begun; the two most promising lines of research investigate how patients’ expectations affect their outcome, and explore the role of classical conditioning in the placebo effect.
There’s also research seeking to better understand the effect of manipulating the context of treatment and features of the patient-practitioner interaction – factors that often fall under the cloak of the placebo. These might include empathy shown by the practitioner, the connection or bond patients feel and the beliefs of the practitioner regarding the patient or condition.
Considering these factors as effective treatment components in their own right offers a way to understand how interventions work and, potentially, an insight into the nature of the condition being treated.
Improving understanding of how treatments work, and what features of the clinical context influence outcome has self-evident advantages for clinicians and their patients. And reconceptualising the outdated notion of an inert placebo can help resolve some of the ethical issues surrounding its use.
From a research perspective, hanging onto the placebo idea also appears to serve little purpose. Simply designating a control intervention as a “placebo” tells us nothing about what the control intervention actually controls for.
A number of different interventions may all be called placebos, and all of them may control for different aspects of the intervention being tested.
Dispensing with the idea of a placebo arm in clinical trials could have the benefit of forcing trial designers to more carefully consider and define what they seek to control for, and assist interpretation of clinical trials.
The placebo effect emerged and gained prominence in an era when health care was moving from a semi-mystical past toward the scientific present.
Over this time, numerous treatments have been abandoned as understanding of biology, anatomy and pathology improved. It’s possible the current concept of placebo, which served as a useful tool in the past, has reached its use-by date
It may seem like a fairly fundamental question, but there is still debate over whether viruses should be considered a form of life. The diversity of viral infections is immense. Viruses cause everything…
It may seem like a fairly fundamental question, but there is still debate over whether viruses should be considered a form of life.
The diversity of viral infections is immense. Viruses cause everything from common cold (rhinoviruses) to Ebola and warts (papillomavirus); from HIV/AIDS to influenza and smallpox. Many viruses can cause cancer: the hepatitis B virus is a known cause of liver cancer, and some types of human papillomavirus cause cervical cancer.
Although viruses exhibit some of the characteristics of living organisms — they have genes, evolve by natural selection and create copies of themselves — most biologists argue they aren’t alive because they can’t replicate by themselves.
To say that viruses are small is an understatement. If the human genome were “War and Peace”, the average bacterium would have a genome of about a page or two. On this scale, the influenza virus is about two words; the smallest virus, circovirus, merely a letter or two.
Essentially, viruses are snippets of genetic code that hijack the mechanics of living cells to replicate themselves, escape the cell and spread (the “computer virus” analogy is apt). Even their envelope – the coating that many viruses have to protect their contents – is derived from the cells of their hosts.
Some viruses that cause human disease can be prevented from doing so — with varying degrees of success — through vaccines.
The origin of the word vaccine (from the Latin for “cow”) comes from Edward Jenner’s observation that milkmaids appeared to be immune from smallpox. From this came the idea that infection with a closely related but less dangerous virus could protect against serious disease.
It was subsequently found that even inactivated viruses (such as those in the rabies and polio vaccines) or parts of viruses (such as those in the hepatitis B and influenza vaccines) were able to stimulate the immune system to remember and protect from infection on subsequent exposure.
Compared with antibiotics for treating bacterial infection, which were developed in the 1940s, antiviral treatments are a much more recent development.
Most antiviral medication attempts to block one or more points in the viral replication cycle. Many antiviral medications used to treat HIV and herpes simplex (which causes cold sores), for instance, jam the replication mechanism itself.
Other antivirals interfere with the mechanism viruses use to enter or exit host cells (such as oseltamivir for influenza), while others stimulate the immune system to seek and destroy virally-infected cells (such as interferon for hepatitis C).
Mega-, mimi-, or TRUC?
Humans (or at least doctors) take a very anthropocentric view of the world, but viruses can infect all living organisms, even bacteria (bacteriophages). And they seem to be everywhere.
J Craig Venter, the biologist and entrepreneur who was one of the first to sequence the human genome (interestingly, his own), circumnavigated the world in his yacht and sampled seawater as he went. When his team examined the samples, they found an incredible diversity of new viruses, with about 10 million copies of viruses per millilitre of water.
The recent discovery of new very large viruses has also blurred the lines between what does and does not constitute life. In 2003, the Mimivirus was found inside an amoeba in a cooling tower in England. It was named the “microbe mimicking virus” as it was visible under a microscope and had a genome that rivalled small bacteria.
The current biggest virus record holder is the Pandoravirus, found in a pond in Melbourne. Its genome approaches the complexity of a small parasite.
These recent discoveries have prompted a reconsideration of the nature and classification of life. Didier Raoult, the French biologist who led the team that discovered Mimivirus, has even proposed reclassifying complex organisms such as giant viruses as “truc”. This is French for “stuff”, as well as being an acronym for “things resisting [un]complete classification” — in other words, the “too hard” basket.
Are the seawater viruses the soup from which we subsequently evolved? More research may yield answers to these and other interesting questions. Whatever the case, it is clear that these tiny genetic parasites will always be problems for us to contend with.
Sugar MADNESS: How metabolic syndrome drives obesity and what you can do about it
It’s a complicated, but important story: Sugar MADNESS is a memory aid to learning about sugar, metabolic syndrome, and what to do about it.
Sugar consumption, especially from sugary drinks
- Metabolic syndrome
- Addictive properties of sugar
- Disorder of fat (energy) storage
- Stress reduction
- Sleep and exercise
View complete slide presentation go here: http://medepi.com/2014/02/02/sugar-madness/ (not able to embed slide presentation)