Probiotics already have a laundry list of health benefits, from helping to regulate the G.I. tract to boosting weight-loss efforts—and new research suggests that there may be another plus-side to loading up on the microorganisms: healthier blood pressure. People who consume probiotics tend to have lower blood pressures, according to a new study published in the journal Hypertension. Researchers analyzed nine key studies with a total of 543 participants, eight of which linked probiotic consumption to a reduction in systolic blood pressure (SBP). Eight of the studies also reported a drop in diastolic blood pressure (DBP), although only two were clinically significant. Researchers noted a greater reduction in blood pressure if participants consumed multiple probiotics and suggested the benefits may be greater for those with higher baseline blood-pressure levels. Researchers say the improvement in blood pressure is on par with the reduction you’d get from cutting back your salt consumption by about two grams per day—and that it could be a key step toward improving cardiovascular benefits for the general public.
Monthly Archives: October 2015
The Surprising Benefit of Eating Probiotics
Now there’s yet another reason to grab a container of yogurt.
There have still been issues with the telephone at the new clinic, but they (hopefully) have at last been rectified. Some of the path test have unfortunately gone to my old addresses, so make sure when having your blood tests to make sure it now goes to the Caboolture Superclinic. The article below shows that most alternative treatments for the menopause do not work. Stick to the Bioidentical HRT for best results.
Menopausal women misled by bad advice – study
A concerning number of middle-aged women are using alternative and complementary medicine (CAM) to treat menopausal symptoms despite any evidence of efficacy, say researchers from Melbourne’s Monash University.
They blame GPs, in part, for this “possibly dangerous” trend, pointing to a national survey that shows about a third of primary care doctors self-identify as practising complementary therapy.
“It is cause for concern that a sizable proportion of Australian practitioners are recommending ineffective therapies,” write Professor Susan Davis and colleagues in the Medical Journal of Australia.
Their research suggests that almost half a million Australian women aged between 40 and 65 could be using CAM for the treatment of menopause symptoms, in particular to combat vasomotor symptoms (VMS).
“The prevalence of use of at least one CAM for any menopausal symptoms was 39.16%,” they write.
Of the 2020 women in the study, 13% reported using CAM for VMS. Phytoestrogens were the most popular treatment (taken by 6% of women), followed by evening primrose oil (4%), ginseng (2%) and black cohosh (1%).
Less than 1% said they used CAM for sexual symptoms.
The results also show that just under a third of the women used at least one natural therapy for other symptoms, with a relatively high take-up rates for fish or krill oil and glucosamine.
The researchers note that none of these treatments have been shown to be any more effective than a placebo for treating menopausal symptoms, and in many cases they are potentially dangerous.
Adverse effects range from sleeplessness, diarrhoea and vaginal bleeding to hypertension and decreased insulin secretion.
“Given the lack of evidence regarding benefit of CAMs for alleviating VMS, as well as the potential adverse effects and their high cost, the continuing use of these CAMs for this purpose cannot be supported.”
The researchers suggest GPs need to more actively guide women in the management of VMS and other menopause symptoms.
“More judicious use of supplements such as fish oil and glucosamine, particularly by older women, is needed until their efficacy and safety profiles are better understood.”
How could a cashless economy make you gain weight? It’s all about the pain in your brain.
In early May, 2015, news services reported that Denmark would allow retailers to only offer card payment and allow them to ban cash as a means of transaction.
For quite a while, Scandinavia has been all about a cashless society. Sweden has taken it one step further with a vein scanner, where consumers can pay for their coffee by entering the last four digits of their mobile phone number into a sensor that scans their veins – presumably to see if they have Black, Platinum, Gold, Silver, or just boring old red blood.
But, will we ever see Australia go completely cashless?
I don’t think so. While Australians are also pretty good at adopting new technology, we are also pretty good at not giving up the old stuff. Prospect theory, which tells us that we value losses more than we value gains, would suggest that we are unlikely to give up the perceived usefulness of cash, at least in the short-term.
That said, at an incremental level, we are using our cards more and more, particularly in relation to the swipe and go PayWave and PayPass technology. According to a Westpac forecast made in 2014, there would be almost $3 billion in contactless transacations in Australia in 2015.
But, there are other reasons why we should be hesitant to give up cash totally, and these tend to be directly related to the hip-pocket nerve – well, kind of.
Research in psychology and neuroscience has suggested that there is a kind of emotional competition between the immediate pleasure of buying something, and an equally immediate pain of paying for that something.
A 2007 study published in the journal Neuron, found that the region of the brain associated with pain processing (the bilateral insula) activated when participants saw prices that were too high.
In the study, people were placed in an fMRI machine, given $20 cash and given the opportunity to buy something. What the researchers found was that the handing over of cash caused a sense of pain for them, or at least that’s what was observed happening in the brain.
We already know a lot of this from psychological experiments which show we have a tendency to “couple” or clump bits of information together in our minds. So, when we buy something with cash, we know straight away how much that thing is going to cost us. We also know that we no longer have that amount of money in our wallet or purse.
But when we use a plastic card, we are, ostensibly handing over something quite abstract. Whether it’s debit or credit, there is a degree of psychological and temporal distance. Most people don’t know exactly how much they have in their savings or credit account; they might have a general idea, but you can see that it is not the same as cash. It requires effort to check your credit or debit card balance, but looking in your wallet, as you are paying, requires next to no cognitive effort.
So, when you hand over your card, you don’t see the money disappear from your account (at least in any concrete way), and therefore, feel like you’ve lost anything. You’re also creating a kind of abstract distance between the payment of the bill, and the usage of the money that you have. And that is sometimes extended even more if you don’t actually get the bill for months after you have spent the money and consumed the product.
In addition, research tells us that people are more likely to buy unhealthy food, on average, when they pay using cards, as opposed to using cash. A study published in the Journal of Consumer Research in 2010 analysed the shopping behaviour of 1,000 households over a period of six months and found that using debit and credit cards led to a small, but statistically significant, increase in impulsive purchases of unhealthy products.
In one of the experiments, participants spent 40% more on “vice” product (such as chocolate biscuits or frozen cheesecakes) when they were using credit cards, than cash. The mode of payment didn’t affect the amount spent on “virtue” products (such as rolled oats).
The researchers even classified different types of spenders as “tightwads” and “spendthrifts”, and found that “tightwads” were likely to spend 56% more on impulse products when they used credit, than when they used cash. They also found that participants also thought “less” about their product when they chose vice products.
But, there is nuance in these broad findings. A different study found that if people were buying indulgent food such as chocolate cake for immediate consumption, the pain of using cash was offset by the excitement and anticipation of eating the delicious, exciting food.
So, the greater the pain of payment, the more we were to choose foods that we wouldn’t normally consider as part of a healthy diet, but only if we plan to eat them straight-away.
In one of the experiments, the researchers created a cafe afternoon snack menu, and found that people who paid with cash consumed close to 80 more calories than those who used a card. People who paid with cash consumed products higher in total fat (3g, or 15% more), salt (130 mg, or 17%), carbs (8g, or 13%) and sugar (1.5g or 6%), than those who used a card to pay.
Which returns us to the earlier idea that paying for something causes a sense of “pain”, and paying with cash hurts more than paying with a card. People are offsetting that pain by treating themselves to make themselves feel good after the trauma of spending money.
So, the moral to all of these stories? Put a freeze on your cards (maybe literally – stick your cards in the freezer for month and see how much you spend), don’t go shopping when you are in an fMRI machine, and eat more chocolate biscuits (well, that’s my interpretation of the findings).
Previously I have written about the breast protective effects of progesterone (not to be confused with progestogens, the synthetic form of progesterone.)
Here is more interesting information about this very important issue for women, seeing as progesterone is in most of the script I write for menopausal women.
The protective side of progesterone
Division of Medical Oncology A, Regina Elena Cancer Institute, Rome, Italy
Breast Cancer Research 2007, 9:402 doi:10.1186/bcr1792
See related commentary by Jerry, http://breast-cancer-research.com/content/9/2/102 and related research by Rajkumar et al., http://breast-cancer-research.com/content/9/1/R12
The electronic version of this article is the complete one and can be found online at: http://breast-cancer-research.com/content/9/6/402
|Published:||21 November 2007|
© 2007 BioMed Central Ltd
According to Jerry’s commentary , exogenous oestrogen and progesterone potently inhibit tumorigenesis, representing an interesting strategy to prevent breast cancer, but we feel that the concerns noted by Jerry deserve further comment.
According to the Million Women Study , when progesterone was included in the hormone replacement therapy (HRT) formulation, the odds ratio fell from 1.3 to 1.1, indicating a protective effect exerted by progesterone, though no significant difference in the relative risk of ovarian cancer was registered in the subgroups of women who used oestrogen only compared with those who used the combination. Long durations of use of unopposed oestrogen and of oestrogen plus progestin, especially sequential regimens, have been reported to be associated with increased ovarian cancer risk. In preclinical models, combined progestins circumvent the anti-apoptotic action of the long isoform of Fas-associating protein with death domain-like interleukin-1 beta-converting enzyme (FLICE)-like inhibitory protein, an anti-apoptosis mediator, representing an effective therapy for ovarian cancer cells . In premenopausal women, combined oral contraceptives (OC) have been described to be effective at decreasing the risk of epithelial ovarian carcinoma, even though the strongest risk reduction has been associated either with low- or high-potency progestin formulations.
Some synthetic progestins, when added to oestrogen in HRT for menopausal symptoms, have been reported to increase the risk of breast cancer more than oestrogen alone. Progestin use in breast cancer survivors is associated with an increased breast cancer risk compared with its non-use . However, outside pregnancy, progesterone endogenously produced or exogenously administered does not have a cancer-promoting effect on breast tissue. The greater breast cancer risk related to the use of HRT containing oestrogen and synthetic androgenic progestin (19-nortestosterone derivatives) could be due to the non-progesterone-like effects enhancing the oestrogen proliferative effect on oestrogen-sensitive cancer cells.
In postmenopausal women, progesterone is added to prevent the carcinogenic effect of oestrogen on the uterus . In premenopausal women, the potency of the progestin in most OC appears adequate to provide a protective effect against endometrial cancer. Higher progestin-potency OC may be more protective than lower progestin potency OC among women with a larger body habitus. Progestagens counteract the adverse effect of oestrogens on the endometrium, the effect being greater the more days every month that they are added to oestrogen and the more obese that women are.
Finally, because hormones may play a crucial role in the development of breast, endometrial and ovarian cancer, the impact on cancer risk of progestins included in HRT or OC formulations remains a major interest.
FLICE = Fas-associating protein with death domain-like interleukin-1 beta-converting enzyme; HRT = hormone replacement therapy; OC = oral contraceptive.
The authors declare that they have no competing interests.
- Jerry DJ: Roles for estrogen and progesterone in breast cancer prevention.Breast Cancer Res 2007, 9:102. PubMed Abstract | BioMed Central Full Text |PubMed Central Full Text
- Beral V, Million Women Study Collaborators: Ovarian cancer and hormone replacement therapy in the Million Women Study.Lancet 2007, 369:1703-1710. PubMed Abstract | Publisher Full Text
- Syed V, Mukherjee K, Godoy-Tundidor S, Ho SM: Progesterone induces Apoptosis in TRAIL-resistant ovarian cancer cells by circumventing c-FLIP(L) overexpression.J Cell Biochem 2007, 102:442-452. PubMed Abstract | Publisher Full Text
- Beral V, Million Women Study Collaborators: Breast cancer and hormone-replacement therapy in the Million Women Study.Lancet 2003, 362:419-427. PubMed Abstract | Publisher Full Text
- Beral V, Bull D, Reeves G, Million Women Study Collaborators: Endometrial cancer and hormone-replacement therapy in the Million Women Study.Lancet 2005, 365:1543-1551. PubMed Abstract | Publisher Full Text
To pose the question of whether we can love happiness feels a bit like asking whether the Pope is a Catholic. Most of us believe we not only can love happiness, but that we should!
This article is part of a series, On Happiness, examining what it means and how it might be achieved in the 21st century.
To pose the question of whether we can love happiness in today’s world feels a bit like asking whether the Pope is Catholic. Most of us believe we not only can love happiness, but that we should! Unfortunately, it is this very love of happiness that is leading many of us to experience more sadness.
Why, I hear you ask? Well let me start with an example. Imagine you have a goal and it is to become smarter. You decide to enrol in an science degree and major in astrophysics (being an astrophysicist is clearly going to make you smarter), you spend every spare minute playing Sudoku and purchase the latest “get smart quick” brainpower gimmick.
Over time you notice that indeed you are becoming smarter. You are winning more often at Scrabble and Trivial Pursuit and can amaze your friends with complex theories of black holes and dark energy.
Yet, you would still like to be smarter. You feel slightly disappointed that you are not as smart as you thought you might be. This feeling of disappointment motivates you to learn more and try harder until eventually you reach your goal.
Now imagine that your goal is to be happy. You buy the latest books on how to be happy, repeat positive sentiments to yourself in the mirror each morning and spend at least ten minutes a day holding a pencil between your teeth (it’s true, it actually does work!).
Upon reflection, however, you are not as happy as you would like to be. Now, the feeling of disappointment, rather than motivating you to try hard, tends to make you feel less happy. As a result, you are now further removed from your desired state of happiness.
The nature of goal pursuit itself predicts this ironic outcome. Aiming for a goal often involves feelings of disappointment along the way, which means that trying to be happy may be counter-productive.
The aim of this illustration is to show that the very act of trying to be happy ironically pushes happiness further away. The most powerful strategy for achieving happiness is to give up trying to be happy.
Living in a world of laughing clowns
Consistent with the above insights, current approaches within psychotherapy have begun to challenge how people relate to their own emotions. People walk out of these sessions more accepting of their negative emotions and holding less tightly to the need to be happy.
As they walk out of the therapist’s door, however, they are confronted with a world that is beset by happiness. From advertising on billboards and television screens to national campaigns designed to raise national levels of happiness, the value of happiness is promoted everywhere.
On the flip side, our Western world values sadness very differently. In some cases even everyday malaise is quickly pathologised and medicalised, and treated with drugs designed to return people to “normality”.
Indeed, there is an eerie similarity between our current approaches to our emotional worlds and the kind of dystopian society that Aldous Huxley envisaged in his book Brave New World.
Our own research has begun to highlight the possibility that “happiness cultures” may be responsible for reducing life satisfaction and increasing depression. This is especially true when people experience high levels of negative emotion and feel that these emotional states are socially devalued.
Experiencing this mismatch between our own emotional states and those that are considered valuable by the cultures that we live in may even leave us feeling lonely and socially disconnected.
So should we hate happiness?
I am certainly not suggesting we should all dress in black and revel in our shared despair. Being happy is a good thing and it is exactly this state that we are all so keen to achieve.
The point is that we often go about this in the wrong way. We fail to value negative experiences along the way and think that striving for more and more pleasure and enjoyment is the best way to achieve our happiness goals.
The fact is that endless pleasure, and endless happiness, quickly becomes very dull and even painful. For true well-being we need contrasts. Our negative experiences and negative feelings give meaning and context to happiness: they make us happier overall. As our own research suggests, pain has many positive consequences and experiencing pain is often a critical pathway to flourishing in life.
So can we love happiness? I think we can. It is not so much our love of happiness, but our dislike of sadness, the tendency to run away from pain and suffering and to see these experiences as a sign of failure, that leads to the problems I describe above.
Perhaps our problem with happiness comes about because we live in a world where we believe we can control everything in our lives. From our temperature-controlled homes to our capacity to insure against every possible risk, we believe we should have the same level of control over our emotional lives.
There is an oft-quoted saying (commonly found on a wall calendar at your grandmother’s house), “If you love something set it free”. Perhaps that is how we should be thinking about happiness?
This article is based on an essay in the collection On Happiness: New Ideas for the Twenty-First Century (UWA Publishing, June 2015).
You can read other articles in the series here.
Early menopause and other gynecologic risk indicators for chronic fatigue syndrome in women
Boneva, Roumiana S. MD, PhD; Lin, Jin-Mann S. PhD; Unger, Elizabeth R. PhD, MD
Objective: This study aims to examine whether gynecologic conditions are associated with chronic fatigue syndrome (CFS).
Methods: This study includes a subset of 157 women from a population-based case-control study in Georgia, United States, conducted in 2004-2009. Gynecologic history was collected using a self-administered questionnaire. Crude odds ratios (ORs) with 95% CIs and ORs adjusted for body mass index and other covariates, where relevant, were estimated for gynecologic conditions between 84 CFS cases and 73 healthy controls.
Results: Cases and controls were of similar age. Women with CFS reported significantly more gynecologic conditions and surgical operations than controls: menopause status (61.9% vs 37.0%; OR, 2.37; 95% CI, 1.21-4.66), earlier mean age at menopause onset (37.6 vs 48.6 y; adjusted OR, 1.22; 95% CI, 1.09-1.36), excessive menstrual bleeding (73.8% vs 42.5%; adjusted OR, 3.33; 95% CI, 1.66-6.70), bleeding between periods (48.8% vs 23.3%; adjusted OR, 3.31; 95% CI, 1.60-6.86), endometriosis (29.8% vs 12.3%; adjusted OR, 3.67; 95% CI, 1.53-8.84), use of noncontraceptive hormonal preparations (57.1% vs 26.0%; adjusted OR, 2.95; 95% CI, 1.36-6.38), nonmenstrual pelvic pain (26.2% vs 2.7%; adjusted OR, 11.98; 95% CI, 2.57-55.81), and gynecologic surgical operation (65.5% vs 31.5%; adjusted OR, 3.33; 95% CI, 1.66-6.67), especially hysterectomy (54.8% vs 19.2%; adjusted OR, 3.23; 95% CI, 1.46-7.17). Hysterectomy and oophorectomy occurred at a significantly younger mean age in the CFS group than in controls and occurred before CFS onset in 71% of women with records of date of surgical operation and date of CFS onset.
Conclusions: Menstrual abnormalities, endometriosis, pelvic pain, hysterectomy, and early/surgical menopause are all associated with CFS. Clinicians should be aware of the association between common gynecologic problems and CFS in women. Further work is warranted to determine whether these conditions contribute to the development and/or perpetuation of CFS in some women.
Post Reprod Health. 2015 May 19. pii: 2053369115577328. [Epub ahead of print]
Intravaginally applied oxytocin improves post-menopausal vaginal atrophy.
To explore the efficacy of local oxytocin for the treatment of post-menopausal vaginal atrophy.
Double-blinded randomised controlled trial.
Healthy post-menopausal women in Stockholm, Sweden.
Sixty four post-menopausal women between February and June 2012 at the Karolinska University Hospital Huddinge/Sweden.
MAIN OUTCOME MEASURES:
The efficacy of oxytocin for treatment of vaginal atrophy after seven weeks and cytological evaluation.
The percentage of superficial cells in the vaginal smears and the maturation values were significantly increased after seven weeks of treatment with vagitocin 400 IU (p = 0.0288 and p = 0.0002, respectively). The vaginal pH decreased significantly after seven weeks of treatment with vagitocin 100 IU (p = 0.02). The scores of vaginal atrophy, according to the histological evaluation, were significantly reduced after administration of vagitocin 100 IU (p = 0.03). The thickness of the endometrium did not differ between the treatment and placebo groups after seven weeks of treatment. The symptom experienced as the most bothersome was significantly reduced after seven weeks of treatment in the women receiving vagitocin 400 IU compared to women in the placebo group (p = 0.0089).
Treatment with intravaginally applied oxytocin could be an alternative to local estrogen treatment in women with post-menopausal vaginal atrophy.
© The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.
Estrogen; oxytocin; post-menopausal; vaginal atrophy; vagitocin
One of my patients had a DVT and wanted to know whether she could continue with the HRT, and did the BHRT cause the DVT. This is of course an important question. In the past we would have said yes to both those questions. However, we now know better and the research and evidence proves the opposite. I have had patients who have had DVTs and some even pulmonary emboli, who I have given BHRT knowing it was safe to do so. The difference is in the mode of delivery – as long as it is transdermal .(troches and creams) then it does not increase the DVT (VTE in medical lingo) risk.
Here is only some of the evidence I am referring to – I have dozens of other medical journal articles showing the same thing, as well as being included in the guidelines of all the major menopause and endocrine associations. I have highlighted the important bits – note VTE is venous-thrombo-embolism – viz a blood clot.
What’s new in hormone replacement therapy: focus on transdermal estradiol and micronized progesterone.
Department of Obstetrics and Gynecology, George Washington University, Washington, DC 20036, USA.
The original conclusions of the Women’s Health Initiative study have been questioned as a result of the availability of age-stratified data. Initial concerns regarding the risk of coronary heart disease (CHD) in association with the use of hormone replacement therapy (HRT) have been replaced with concerns regarding thromboembolic disease, encompassing venous thromboembolism (VTE), particularly in younger postmenopausal women, and stroke, particularly in older women. The original publication of the study results led to a dramatic decrease in the use of oral HRT; however, the use of transdermal HRT has increased over recent years. Guidelines from the North American Menopause Society, the Endocrine Society, the International Menopause Society, and specific guidelines from the European Menopause and Andropause Society for the management of menopausal women with a personal or family history of VTE all contain positive statements regarding both transdermal estradiol and micronized progesterone. Unlike oral estrogens, transdermal estradiol has been shown not to increase the risk of VTE, or stroke (doses ≤ 50 μg), and to confer a significantly lower risk for gallbladder disease. Unlike some progestogens, progesterone is also not associated with an increased risk of VTE, or with an increased risk of breast cancer. Based on these data, which are now included in the guidelines, the use of transdermal estradiol and micronized progesterone could reduce or possibly even negate the excess risk of VTE, stroke, cholecystitis, and possibly even breast cancer associated with oral HRT use.
Climacteric. 2012 Apr;15 Suppl 1:11-7.
Postmenopausal hormone replacement therapy and cardiovascular disease: the value of transdermal estradiol and micronized progesterone.
Department of Endocrinology and Menopause, Center of Women’s Health, University Women’s Hospital, Tuebingen, Germany.
Most available postmenopausal hormone replacement therapies (HRT) offer similar efficacy, but differ with respect to the cardiovascular risks associated with their use. There is a wealth of evidence to suggest that, unlike oral estrogens, transdermal estradiol does not increase the risk of venous thromboembolism, probably due to its lack of effect on the coagulation cascade, including thrombin generation and resistance to activated protein C, and does not increase the risk of stroke. It is cardioprotective, significantly reducing the incidence of myocardial infarction compared with non-users; it significantly reduces the incidence of new-onset diabetes, a risk factor for myocardial infarction. Micronized progesterone has also been shown not to increase the risk of venous thromboembolism and further reduced the incidence of new-onset diabetes when combined with transdermal estrogen. Micronized progesterone has a neutral effect on the vasculature, including a neutral or beneficial effect on blood pressure. Therefore, experimental and clinical data indicate that transdermal estradiol and micronized progesterone could represent the optimal HRT, particularly in women at risk of adverse events.
Finally, this study from the well respected British Medical Journal (BMJ)
Effect of hormone replacement therapy on cardiovascular events in recently postmenopausal women: randomised trialCite this as: BMJ 2012;345:e6409
Objective To investigate the long term effect of hormone replacement therapy on cardiovascular outcomes in recently postmenopausal women.
Results At inclusion the women on average were aged 50 and had been postmenopausal for seven months. After 10 years of intervention, 16 women in the treatment group experienced the primary composite endpoint compared with 33 in the control group (hazard ratio 0.48, 95% confidence interval 0.26 to 0.87; P=0.015) and 15 died compared with 26 (0.57, 0.30 to 1.08; P=0.084). The reduction in cardiovascular events was not associated with an increase in any cancer (36 in treated group v 39 in control group, 0.92, 0.58 to 1.45; P=0.71) or in breast cancer (10 in treated group v 17 in control group, 0.58, 0.27 to 1.27; P=0.17). The hazard ratio for deep vein thrombosis (2 in treated group v 1 in control group) was 2.01 (0.18 to 22.16) and for stroke (11 in treated group v14 in control group) was 0.77 (0.35 to 1.70). After 16 years the reduction in the primary composite outcome was still present and not associated with an increase in any cancer.
Conclusions After 10 years of randomised treatment, women receiving hormone replacement therapy early after menopause had a significantly reduced risk of mortality, heart failure, or myocardial infarction, without any apparent increase in risk of cancer, venous thromboembolism, or stroke.
Jodie McVernon receives funding from the Australian Government Department of Health, the Australian Research Council and the National Health and Medical Research Council (NHMRC). She leads an NHMRC funded Centre of Research Excellence in Infectious Disease Modelling to Inform Policy, on which all co-authors are co-investigators. She is a member of the Australian Technical Advisory Group on Immunisation and a Director of the Influenza Specialist Group.
James McCaw receives funding from the ARC and the NHMRC.
Joshua Ross receives funding from the Australian Research Council and the National Health and Medical Research Council.
Kathryn Glass receives funding from the ARC and the NHMRC.
Nicholas Geard receives funding from the Australian Research Council and the National Health and Medical Research Council.
The University of Melbourne provides funding as a founding partner of The Conversation AU.
Australian National University provides funding as a member of The Conversation AU.
Viruses have been described as “organisms at the edge of life”, unable to reproduce outside the cells of those they infect. But this status has not impeded their evolutionary success. Children, in particular, experience a multitude of viral illnesses during their early years, which gradually reduce over time as their natural immunity develops.
Viral infections may be fleeting (think influenza) or chronic (HIV, for instance), affecting various parts of the body to cause a diverse array of symptoms. These differences have important implications for the spread of that particular viral disease.
Reducing reproduction numbers
The most relevant factor is the infectiousness of a virus, often summarised in a measure known among epidemiologists as its “reproduction number”. This describes the average number of secondary infections produced by one ill individual.
Consider the most commonly transmitted viral illness, the flu: about 10% to 20% of the population is infected by one of the circulating influenza viruses each year. Symptoms vary from a mild “cold” through to severe respiratory infection requiring hospitalisation.
So it’s perhaps surprising that the reproduction number of influenza is relatively low; each infectious person infects only one and a half other people – or put another way, two infectious people produce, on average, three new cases of influenza. If we could get that reproduction number below one, incidence numbers would decline as, on average, each infected person would not necessarily produce a successor.
What makes the flu difficult to control despite its relatively low reproduction number is the fact that people are contagious for a day or two before they show any symptoms. Once they become unwell, they’re contagious for a couple more days. But by this stage they’re more likely to stay home and avoid contact with others.
As half or more of their secondary infections will have been produced before the ill people showed any symptoms, influenza control strategies that rely on identifying and isolating them aren’t necessarily going to effectively reduce the incidence of the illness in the community.
This incubation period – the time when a person is infected but not showing symptoms – is a vital consideration for controlling viral illness.
Consider the outbreak of a deadly strain of the coronavirus that caused Severe Acute Respiratory Syndrome (SARS) in 2003. Like influenza, SARS leads to fever and cough, and is mostly spread by close contact between people. Even though its reproduction number has been estimated to be between three and four, people carrying the virus are most contagious in the second week of their infection, after they have started to show symptoms of the disease.
It was this delay until contagion that made it possible to contain SARS: health-care workers were able to find and quarantine people who had contact with the disease before they infected others. Nonetheless, controlling its outbreak was not an easy task – it spread to around 30 countries and killed about 10% of those infected.
SARS appears to have been eradicated but the recently emerged Middle East Respiratory Syndrome (MERS), which also belongs to the coronavirus family, has many similarities. The majority of cases, including the recent outbreak in the Republic of Korea, have arisen from infection spread in health-care settings, where early infections are indistinguishable from other respiratory viruses.
Another virus that’s been grabbing news headlines of late is Ebola. While flu and SARS spread through coughing and sneezing, contracting Ebola requires direct contact with the blood or other bodily fluids of an infected person, or with items such as bedding or clothing contaminated with these fluids.
As with SARS, people infected with Ebola are not contagious until they begin to show symptoms, which include diarrhoea, vomiting and bleeding. Contagiousness increases as these symptoms worsen and peaks around the time of death. The body of a deceased person remains contagious after death. Safe burial practices were therefore an essential component in controlling the recent Ebola outbreak.
The reproduction number of Ebola in the latest outbreak was as high as four. But, as with SARS, the delay until contagion made it possible to trace and quarantine people who had been in contact with Ebola before they spread the disease any further.
The importance of vaccines
In stark contrast to these stories of successful disease control, the World Health Organisation estimates that 35 million people are living with human immunodeficiency virus (HIV) infection. And more than 39 million have died from the infection to date.
This toll is largely due to the fact that people with HIV infection may take anywhere between two and 15 years to develop symptoms of acquired immune deficiency syndrome (AIDS). Meanwhile, they unknowingly infect others over a period of many years, rather than days or weeks.
HIV spread can be effectively reduced by antiretroviral drugs, which lower virus levels in the blood. Unfortunately, WHO estimates that only a third of the people who need these drugs currently have access to them. Meanwhile, the quest for an HIV vaccine continues.
Vaccines, in fact, are one of the best ways to control the spread of viral illnesses. Consider the numerous childhood illnesses that are now contained thanks to vaccines.
Measles and chicken pox, for instance, are classically identifiable by their distinctive rashes. But they’re most infectious in the time between the appearance of non-specific symptoms, such as fever, runny nose and cough, and the development of this rash. This made it very difficult to control their spread until vaccines were developed.
As you can see, different viral diseases are most infectious at different times and this timing of contagiousness plays a key role in how successfully the diseases spread. Knowing a virus’ most infectious period is vital for working out the kinds of measures that are likely to work to control and perhaps even eradicate it from the community.
My new Tel no is 07 5315 8888. I may have given an incorrect number before.;