Doctors are now prescribing this ‘treatment’ to fight cancer
Naveed Saleh, MD, MS, for MDLinx | December 09, 2019
Once upon a time, patients with cancer were advised to rest and relax, especially after cancer treatment such as chemotherapy, so as not to strain themselves. This isn’t so much the case today, when exercise is encouraged for this patient population—and even dosed into treatment regimens.
The ACSM recommends that all physicians ask their patients with cancer about physical activity, and if inadequate, recommend more.
In the 1990s and 2000s, evidence cropped up that contraindicated previous beliefs that exercise was bad for patients with cancer. In turn, these studies laid the foundation for the burgeoning field of exercise oncology. Today, there are more than 1,000 randomized, controlled trials on the topic.
In October 2019, the American College of Sports Medicine (ACSM) convened an expert panel to report recently updated guidelines regarding the role of exercise in cancer survivorship. Let’s take their results from the top, and focus on the role of exercise as a cancer treatment.
Benefits of exercise in cancer
“The ACSM panel found evidence that providing specific exercise prescriptions for a number of cancer-related health outcomes benefitted people living with or beyond cancer,” said former ACSM president and panel co-chair Kathryn Schmitz, PhD, MPH, professor, Departments of Public Health Sciences and Physical Medicine and Rehabilitation, Penn State College of Medicine, Hershey, PA. “As an example, we saw strong evidence that an exercise program consisting of a half hour of aerobic exercise three times weekly was sufficient to improve anxiety, depression, fatigue, quality of life, and physical function in cancer survivors.”
Concerns about lymphedema secondary to twice-weekly resistance training have been raised, but the panel found this type of exercise did not increase the risk of disease and even offered some health benefits. However, compared with resistance training alone, symptoms of depression and anxiety have only been shown to improve with resistance training combined with aerobic training.
It remains to be elucidated whether exercise also improves other cancer-related outcomes—including cardiotoxicity, peripheral neuropathy, pain, cognitive function, or chemotherapy completion rate—as well as whether exercise boosts treatment tolerance.
In terms of survivorship, exercise prescribed to patients with colon, breast, or prostate cancers has been linked to lengthened survival. However, not enough evidence exists regarding potential survival benefit in those with other types of cancer. On a related note, the ACSM recommends that all cancer survivors heed to general public health recommendations for physical activity, which is either 2.5 to 5.0 hours per week of moderate-intensity activity or 1.25 to 2.5 hours per week of vigorous activity.
Years ago, it was unclear to most that exercise is good for the heart, and now everybody knows this thanks to a paradigm shift. Similarly, the ACSM hopes for a paradigm shift in how providers, caregivers, and patients with cancer view exercise as beneficial and necessary in treatment.
“ACSM has just started a new initiative called Moving Through Cancer,” said Dr. Schmitz, “which focuses on increasing awareness of the value of exercise for cancer survivors, along with educating the cancer clinician workforce to refer, coordinate, and prescribe exercise; expanding opportunities to exercise; and shifting policy so that, by 2029, exercise is standard practice for all patients living with and beyond cancer.”
Importantly, any exercise regimen needs to be personalized to patient preference and functional status. Factors including age, cancer type/stage, adverse effects of treatment, and comorbidities should be taken into consideration.
Lots of people with cancer don’t exercise. These patients should be advised to try some type of physical activity as a means to improve their health. Simply going from no exercise to some exercise is a great improvement. The ACSM recommends that all physicians ask their patients with cancer about physical activity, and if inadequate, recommend more.
“Even if that is all providers have time to do, it demonstrates to patients that physical activity is an important part of managing their health and lays out the expectation that being physically active is healthier than being sedentary,” said Dr. Schmitz. “This is true even for patients with advanced disease and those experiencing limitations, although those cancer patients will need a medically supervised program.”
Physicians are busy professionals. Unpacking the benefit of exercise for your patients will take precious minutes. However, many patients with cancer enjoy exercise programs greatly, and appreciate the guidance in retrospect. Focusing on exercise can be a productive and empowering portion of the clinical encounter.
In interested in learning more, the Moving Through Cancer initiative’s website provides ample information on high-quality exercise programs and answers to frequently asked questions. Keep in mind that physicians need to refer patients to exercise programs, with most exercise programs requiring physician approval.
The hormone progesterone is often associated with pregnancy, but did you know that it has many other amazing benefits for your body? A woman’s progesterone levels gradually decline with age, which allows estrogen to dominate, causing many unwanted negative health symptoms. By restoring your progesterone levels back to normal, you can alleviate your symptoms.
10 Amazing Benefits of Progesterone
1. PMS – Progesterone regulates the menstrual cycle and relieves the symptoms of premenstrual syndrome.
2. Anxiety, Depression and Low Moods – Progesterone acts as a natural antidepressant, relieves anxiety and improves moods. It also relieves postpartum depression which is caused by the drastic drop in progesterone after childbirth.
3. Migraines and Headaches – Progesterone is helpful in relieving migraines and headaches.
4. Fertility and Pregnancy – Progesterone promotes the survival of the embryo and fetus throughout a pregnancy.
5. Fluid Retention and Weight Gain – Progesterone relieves fluid retention and weight gain caused by estrogen dominance.
6. Sleep – Progesterone has a calming effect that helps promote sound sleep.
7. Bone Health – Progesterone promotes bone building and helps reverse osteoporosis.
8. Thyroid Function – Progesterone helps the thyroid hormones be used by the cells of your body which allows for optimal thyroid function and energy.
9. Cancer Prevention – Progesterone protects you against endometrial and breast cancer.
10. Brain Healing – Progesterone reduces swelling and improves mental clarity after a traumatic brain injury.
Bioidentical Progesterone: The Real Thing By replenishing your progesterone with bioidentical progesterone, you can relieve your symptoms. Bioidentical progesterone is identical to the progesterone made by your body. Progesterone is the natural female hormone that promotes pregnancy by preparing the body for conception, regulating the menstrual cycle and maintaining the pregnancy. It also balances the estrogen in your body and plays an important role in your overall well-being.
Progestins are NOT Progesterone It’s important to make the distinction between progestin and progesterone, because they are not the same. Progestins (such as Provera) are synthetic chemicals with a different molecular structure than progesterone, which makes them patentable by the pharmaceutical companies, but they do not have the same beneficial effects as your body’s naturally occurring progesterone. In fact, progestins are used in hormonal contraceptives and in the “morning after pills” to prevent pregnancy. The Women’s Health Initiative showed that progestins cause bleeding problems, blood clots, and even cancer.
Mainstream medicine still erroneously uses these two terms interchangeably today. If you’re still in doubt, just ask your doctor if you can take progestin while you’re pregnant. You’ll hear a resounding “no”!
Research Fellow in Brain Plasticity and Rehabilitation, Western Sydney University
Siobhan Schabrun receives funding from The National Health and Medical Research Council (NHMRC)
This is part of our series on Changing the Brain, about what’s happening in our brain in various mental states and how we can change it for the better and worse.
Demand for drugs and devices that can enhance brain functions such as memory, creativity, attention and intelligence, is on the rise. But could the long-term side-effects outweigh the benefits of being “smarter”?
Known as “smart drugs” or “neuroenhancers”, the field of nootropics (literally translated as mind-bending) is one of the most debated topics in neuroscience. Healthy people of all ages are seeking cognitive enhancement for personal improvement, athletic performance, academic success, professional advantage and to maintain function into old age.
Demand is driven by a changing work environment that increasingly requires use of the mind and not the muscles, heavier workloads, pressure to succeed and an ageing population seeking to reduce the risk of dementia.
Strategies for cognitive enhancement are diverse, ranging from brain training programs to physical activity, drugs and brain stimulation devices. It’s well known neuroenhancers such as lifelong learning, brain training and physical activity have positive effects on memory and attention. These strategies are also safe and inexpensive. The downside? They require substantial time and effort.
Most of us already use brain stimulation
Neuroenhancers that can be swallowed (pills, liquids) or devices that can be worn, are appealing because they require much less effort. In fact, most of us already use a daily smart drug to improve alertness and attention: coffee.
The effects of caffeine on mental function have been known for centuries, and high levels of caffeine consumption (equivalent to five to six cups of coffee per day) were once banned in Olympic competition. Studies have shown alertness and attentiveness are increased and reaction times shortened, when caffeine is consumed.
These effects are greater in people who are sleep-deprived. With approximately 1.6 billion cups of coffee consumed worldwide every day, it’s clear cognitive enhancement is something most of us welcome.
The case in favour of smart drugs becomes murkier as the level of risk becomes greater. Methylphenidate (MPH, also called Ritalin) is commonly prescribed for adolescents with attention deficit-hyperactivity disorder (ADHD). However, MPH can also improve working memory, attention, alertness and reaction times in healthy individuals.
The drug is sold on the black market to high school and university students as a study and examination aid. Students report taking the drug for its performance enhancing effects and not for recreational or medicinal use.
The use of MPH, a prescription-only drug, in healthy individuals is not without risk. At high doses, MPH can interfere with cognition and produce side effects that impair athletic performance.
Other possible side-effects include anxiety, irritability, nausea, abdominal pain, heart palpitations and blurred vision. Concerns have also been raised about the potential for MPH to disrupt the development of the adolescent brain, with lasting behavioural consequences.
The risks associated with smart drugs raise an important ethical question. What level of risk should people who are otherwise healthy be willing to accept in pursuit of cognitive enhancement?
All drugs have side-effects. But when a drug is medically indicated, there is generally agreement the benefits outweigh the risks. Making this judgement in healthy individuals is much more complex. Where do we draw the line between the desire for improved cognition (and potentially greater productivity and success) and health? As the field of nootropics grows, this is a question we’ll need to ponder.
Non-invasive brain stimulation, where magnetic fields or electrical currents are applied to the brain using a device worn on the head, is another potential method of cognitive enhancement. These currents are thought to alter the activity of brain cells but, high quality evidence is lacking and long-term safety studies are yet to be completed.
Despite this, the simplicity of the technology (you can build a device with a 9V battery and a handful of cords) makes it difficult to regulate. There is a growing market for DIY brain stimulation and devices are available for purchase via the internet.
You can even find online instructions on how to build a brain stimulation device of your own. A key concern is healthy individuals using these devices could produce detrimental, long-lasting brain effects that are difficult to reverse.
There is no denying neuroenhancers exist and are widely used: the question is to what extent we will be able to make ourselves smarter in future, and at what cost?
I posted an article about vaginal dryness and pain yesterday. This is a followup on that, where the use of DHEA suits some women much better. This needs to be done by a compounding chemist, which I can arrange for those that need this. Posted by Dr Colin Holloway
What is the current evidence on the use of intravaginal dehydroepiandrosterone (DHEA) in urogenital atrophy and sexual function?
Commentary from Susan R. Davis, MBBS, FRACP, PhD
Sex steroids are vital for the integrity of the urogenital tract (vagina, vulva, lower urinary tract, and supporting pelvic structures). These tissues are rich in estrogen and androgen receptors. In addition, estrogen and testosterone enhance blood flow to the genital tract, which is fundamental for genital sexual arousal and lubrication.
;The fall in estrogen at menopause and the gradual decline in androgen levels with age result in what is now described as genitourinary syndrome of menopause (GSM). This includes vulvovaginal atrophy (VVA) and an increase in vaginal pH. At a cellular level, there is a reduction in healthy vaginal epithelial superficial cells and an increase in parabasal cells. The increase in vaginal pH changes the vaginal microflora. Lactobacilli disappear, and as a consequence there is increased vulnerability to vaginal infection. Symptoms of VVA include vaginal dryness, irritation, itching, infection, and dyspareunia. This in turn leads to diminished sexual desire, arousal difficulties, diminished physical and emotional sexual satisfaction, and relationship issues.
Most postmenopausal women will experience some GSM symptoms. Symptoms of VVA can be effectively treated with either vaginal or systemic estrogen therapy. Estrogenization will thicken and revascularize the vaginal epithelium, lower vaginal pH, and normalize vaginal flora. The number of vaginal epithelial superficial cells will increase.[8,9] Although data show that vaginal estrogen acts locally, thus minimizing systemic exposure to estrogen, some studies have shown blood estradiol levels increase with vaginal application.[10,11,12] A two- to fivefold increase in serum estradiol has been reported after one week of vaginal administration of a 25 µg estradiol vaginal tablet or 1g of 0.625 mg conjugated estrogen cream. After 24 weeks of treatment, only 2% of women have estradiol levels outside the postmenopausal range.
Researchers have looked for alternative approaches for GSM management. In postmenopausal women, adrenal dehydro-epiandrosterone (DHEA) is an important precursor for extra-gonadal biosynthesis of estrone (by aromatization) and testosterone (by 5-alpha reduction). Casson and colleagues first studied the effects of a vaginal DHEA 150 mg pessary versus placebo in five premenopausal women as a mode of hormone delivery and reported an increase in blood levels of DHEA with this approach. The daily vaginal application of three different doses of DHEA cream (6.5 mg, 13 mg, and 23.5 mg) was studied for one week in postmenopausal women. Labrie and colleagues reported a decrease in vaginal pH, an improvement in the vaginal cell maturation index, and restoration of DHEA levels to the range for premenopausal women at the highest dose. The circulating levels of other sex steroids remained within the normal range for postmenopausal women.
A randomized controlled trial of the daily application of three different doses of vaginal DHEA ovules (3.25 mg, 6.5 mg, or 13 mg) was studied over 12 weeks in 218 postmenopausal women who met the entry criterion of dyspareunia. This single study has resulted in a number of publications to support the efficacy of this treatment for VVA.[16,17,18,19,20,21] In these various publications, the investigators have reported an improvement in vaginal cytology and a reduction in pH. An analysis restricted to the women who fulfilled investigational criteria for a low percentage of vaginal epithelial cells and vaginal pH greater than 5 reported an increase in superficial cells and a reduction in pH with an associated improvement in dyspareunia compared with placebo. Sexual function was assessed by three questions in the Menopause Quality of Life Questionnaire (sexual desire, vaginal dryness during intercourse, or avoiding intimacy) and by the Abbreviated Sexual Function Questionnaire. At 12 weeks the total Menopause Quality of Life Questionnaire sexual domain score showed a significantly greater response for each treatment group versus placebo, with more mixed findings in the Abbreviated Sexual Function Question-naire.Vitality
DHEA Benefits Include Helping To Relieve Vaginal Pain Caused By Menopausal Dryness, Atrophy
New research suggests a DHEA vaginal suppository for treating vaginal dryness may be one step closer to government approval. The DHEA formulation could provide an effective alternative for women hoping to ease their symptoms of menopause — without resorting to estrogen.
During perimenopause, vaginal tissues begin to atrophy, the lining thins and secretes less and less fluid, and the pH becomes more alkaline, explain the researchers. Not only do these signs of age lead to discomfort during sex, they also increase a woman’s susceptibility to infections and urinary problems. While hormonal treatments may help alleviate such symptoms, many women have a past history of cancer or higher genetic risk for reproductive cancers rendering such medicines unsafe.
As an alternatives to estrogen treatments, some women resort to non-hormonal lubricants. While these products may temporarily provide moisture and even ease sexual pains, they do not correct the physical problems producing the symptoms. By comparison, DHEA (dehydroepiandrosterone) is a precursor of estrogens and androgens and so can induce physical changes that protect the vagina, according to the researchers. That said, the DHEA product in this study is still considered “hormonal” by regulatory authorities, such as the Food and Drug Administration.
Safety Testing a New Product
For the study, a research team from EndoCeutics, a private bio-pharm company, recruited nearly 500 women to participate in a randomized, double-blind, placebo-controlled trial of its DHEA suppository product. The majority of the women, 84 percent, complained of moderate to severe vaginal dryness. The researchers divided the women, ranging in age from 40 to 80, into two groups: 325 women in the DHEA-treatment group and 157 in a placebo group. After a baseline gynecological test, the women used a daily suppository of either the DHEA or placebo, depending on their group, for 12 weeks.
Compared with the women using a placebo, the women who used the DHEA ovules experienced improvements. Their scores on a scale of 0 to 3 for pain during sex dropped 0.36 points more than the women using placebo and their scores improved by 0.27 points with regard to vaginal dryness. Importantly, the gynecologists who examined them saw 86 percent to 121 percent better improvements in vaginal secretions, integrity of the vaginal lining, lining thickness, and tissue color in the women who used DHEA, while their vaginal pH shifted 0.66 points toward acidity (a positive direction).
“The only side effect reasonably related to treatment is vaginal discharge due to melting of the vehicle at body temperature and this was reported in about 6 percent of the participants,” noted the researchers in their study.
Importantly, this therapy has not been tested in patient at risk or with a history of breast cancer.
“Although this medication is considered ‘hormonal,’ the mechanism appears to be primarily local with minimal side effects beyond vaginal discharge from the suppository,” Dr. JoAnn V. Pinkerton, executive director of North American Menopause Society, stated in a press release.
Source: Efficacy of intravaginal dehydroepiandrosterone (DHEA) on moderate to severe dyspareunia and vaginal dryness, symptoms of vulvovaginal atrophy, and of the genitourinary syndrome of menopause. Menopause. 2016.
I was asked by a patient to do an article on vaginal atrophy. This is common condition, and not reported by our patients, and doctors forget to ask. There is so much to cover in a consultation some important issues get overlooked. Some of the reasons patients don’t mention this may be embarrassment, or stoicism (Just meant to be). Please mention this at your next consultation, if this is a problem for you. I will make an effort to ask the question about vaginal dryness and painful sex more frequently during consultations. This is on my to do list for next year.
Vulvovaginal atrophy (VVA) is a common and underreported condition associated with decreased estrogenization of the vaginal tissue. Symptoms include dryness, irritation, soreness, and dyspareunia with urinary frequency, urgency, and urge incontinence. It can occur at any time in a woman’s life cycle, although more commonly in the postmenopausal phase, during which the prevalence is close to 50%.
Clinical findings include the presence of pale and dry vulvovaginal mucosa with petechiae. Vaginal rugae disappear, and the cervix may become flush with the vaginal wall. A vaginal pH of 4.6 or more supports the diagnosis of VVA. Even while taking systemic estrogen, 10% to 20% of women may still have residual VVA symptoms. Breast cancer treatment increases the prevalence of VVA because the surgical, endocrine, and chemotherapeutic agents used in its treatment can cause or exacerbate VVA. Local estrogen treatment for this group of women remains controversial.
Vulvovaginal atrophy (VVA) is a common condition, especially in postmenopausal women. Vaginal atrophy, atrophic vaginitis, and urogenital atrophy are other terms used to describe this constellation of symptoms associated with decreased estrogenization of the vulvovaginal tissue.
Although treatment with topical estrogen is effective in alleviating symptoms, women frequently do not report symptoms and thus go untreated.1,2
Common symptoms include vaginal dryness, irritation, postcoital bleeding, and soreness. These symptoms may be associated with vaginal discharge and dyspareunia. Urinary symptoms associated with VVA include frequency, urgency, and urge incontinence.Go to:
Vulvovaginal atrophy can occur at any time in a woman’s life cycle, although it is more common in the postmenopausal phase, a time of hypoestrogenism. Other causes of a hypoestrogenic state include lactation, various breast cancer treatments, and use of certain medications. In situations other than menopause, VVA may resolve spontaneously when estrogen levels are restored.
Numerous retrospective studies have evaluated the prevalence of symptoms of VVA (Table 1).3–10Although these studies differ in type of symptoms elicited, study design, and study population, they provide a range of estimates of VVA prevalence. They all used self-reported symptoms of vaginal dryness to determine the prevalence of VVA. In general, the prevalence ranged from about 4% in the early premenopausal groups to 47% in the late postmenopausal group.
TABLE 1. Studies Assessing Prevalence of Vaginal Dryness
The prevalence of VVA in some subgroups of women can be much higher. In a cohort of breast cancer survivors, vaginal dryness was present in 23.4% of the premenopausal patients and in 61.5% of the postmenopausal patients.8Go to:
Vulvovaginal atrophy occurs under conditions of hypoestrogenism. In the premenopausal state, estradiol levels fluctuate from 10 to 800 pg/mL (to convert to pmol/L, multiply by 3.671),11 depending on when measured during the cycle. In the postmenopausal state, estradiol levels are typically less than 30 pg/mL. After menopause, circulating estradiol derives from estrone, which is peripherally converted in adipose tissue from adrenal androstenedione.
The vaginal epithelium is a stratified squamous epithelium, which until menopause is moist and thick with rugae. At menopause, with declining levels of estrogen, the vaginal epithelium thins. Fewer epithelial cells result in less exfoliation of cells into the vagina. As epithelial cells exfoliate and die, they release glycogen, which is hydrolyzed to glucose. Glucose, in turn, is broken down into lactic acid by the action of lactobacillus, a normal vaginal commensal organism. Without this cascade, the pH in the vagina rises, resulting in a loss of lactobacilli and an overgrowth of other bacteria, including group B streptococcus, staphylococci, coliforms, and diphtheroids12 (Figure 1). These bacteria can cause symptomatic vaginal infections and inflammation. After menopause, the elasticity of the vagina is reduced and connective tissue increases.13 A decline in estrogen level causes a decrease in vaginal blood flow and a decrease in vaginal lubrication. These changes can be reversed by the use of estrogens.14,15
FIGURE 1. Proposed cascade-of-effects mechanism for vulvovaginal atrophy.
The effects of endogenous estrogens on vulvovaginal tissues are mediated through estrogen receptors (ERs) α and β, found at sites throughout the urogenital area, including the vagina, vulva, labia, urethra, and bladder trigone. These sites, in turn, regulate transcription at specific areas on the DNA.16Go to:
The initial symptom is often lack of lubrication during intercourse. Eventually, persistent vaginal dryness may occur. Thinning of the epithelial lining may also cause pruritus, soreness, and a stinging pain in the vaginal and vulvar area, which, in turn, may further contribute to dyspareunia. Vaginal spotting, due to small tears in the vaginal epithelium, may also occur. Women with VVA may report a thin yellow or grey watery discharge secondary to the rise in pH that accompanies VVA.17
Women with VVA often report symptoms such as urgency, frequency, nocturia, and urge incontinence. Urinalysis may show microscopic hematuria. Recurrent urinary tract infections can also result. Stress incontinence is commonly found in this age group of women, but current evidence suggests it is not directly attributable to VVA.18
Women do not always report their symptoms of VVA. They are more likely to report vaginal discharge and urinary urgency but are less likely to report vaginal itching, soreness, or dyspareunia. Women may not report symptoms because they are self-treating, feel the symptoms are not important enough, or are embarassed.19Go to:
Clinical findings include atrophy of the labia majora and vaginal introitus. The labia minora may recede. Vulvar and vaginal mucosae may appear pale, shiny, and dry; if there is inflammation, they may appear reddened or pale with petechiae. Vaginal rugae disappear, and the cervix may become flush with the vaginal wall. Vaginal shortening and narrowing tend to occur.20
A thin watery yellow vaginal discharge may be observed. A urethral caruncle, a small, soft, smooth friable red outgrowth along the edge of the urethra, may develop.Go to:
The diagnosis of VVA is a clinical one. However, 2 tests may be used to support the diagnosis: a vaginal pH and a vaginal maturation index (VMI). To assess pH, a piece of litmus paper is placed on the lateral vaginal wall until moistened. A pH of 4.6 or greater indicates VVA, assuming the patient does not have bacterial vaginosis. Premenopausal women without VVA typically have a pH of 4.5 or less.12
The VMI (Figure 2) is the criterion standard for VVA confirmation but is generally not used or needed in clinical practice. This test assesses the relative proportion of parabasal, intermediate, and superficial vaginal epithelial cell types. In premenopausal women, greater than 15% superficial cells would be considered normal; however, in postmenopausal women with VVA, the typical proportion would be less than 5%.
FIGURE 2. Photomicrographs of superficial and intermediate cells (top) and atrophic cells (bottom). (Papanicolaou stain; original magnification x20). Courtesy of the Mayo Cytopathology Laboratory. Go to:
The differential diagnosis includes other conditions that cause chronic vaginal and vulvar itching, discharge, or pain (eg, vaginal infections, irritants, and vulvovaginal dermatoses). Vaginal infections can be caused by bacteria, viruses, protozoa, and fungi. The 3 most common vaginal infections are Candidavulvovaginitis, bacterial vaginosis, and trichomoniasis. Bacterial vaginosis may result from atrophic changes in the vagina. Irritants that can cause chronic vaginal itch include perfumes, any locally applied lubricant or moisturizer, and soaps. Vulvovaginal dermatoses, including lichen sclerosus, lichen planus, and lichen simplex chronicus, may cause similar symptoms.21 Cancer and precancerous lesions, including vulvar intraepithelial neoplasm, vulvar cancer, and extramammary Paget disease, are in the differential diagnosis of any localized areas of redness, thickening, or ulceration (Table 2). Biopsy should be performed if a malignancy is suspected or if the diagnosis is unclear.
TABLE 2. Differential Diagnosis for Symptoms of Vulvovaginal Atrophy Go to:
Current over-the-counter treatments include nonhormonal vaginal moisturizers for VVA symptoms and lubricants for dyspareunia. Vaginal moisturizers, which are water based, are available as liquids, gels, or ovules inserted every few days. Vaginal moisturizers can be safely used long term, but they need to be used regularly for optimal effect.
Vaginal lubricants are shorter acting than moisturizers and are applied at the time of sexual activity to reduce dyspareunia. They can be either water or silicone based, with the water-based products being the most widely available. They are applied to the vaginal opening and/or to the penis and often require repeated application during sexual activity. Silicone-based lubricants require application of only a very small amount and last longer; however, they can interfere with erectile function in male partners. The choice of lubricant may depend on individual preferences and product availability.
On the basis of an evidence-based review of clinical trials examining available low-dose vaginal estrogen preparations for the treatment of VVA in postmenopausal women, The North American Menopause Society (NAMS) 2007 position statement noted that “the choice of therapy should be guided by clinical experience and patient preference.”22 NAMS also stated it is generally unnecessary to prescribe a progestogen in combination with low-dose vaginal estrogen to prevent endometrial hyperplasia or cancer.
On the basis of a meta-analysis of 19 randomized clinical trials involving 4162 postmenopausal women, the 2006 Cochrane Database of Systematic Reviews concluded that vaginal estrogen is an effective treatment for VVA23 and that all forms, whether cream, ring, or tablet, appeared to relieve symptoms more effectively than nonhormonal gels and placebo. Differences observed between the treatments were in participant preferences.
SYSTEMIC ABSORPTION OF VAGINAL HORMONAL PREPARATIONS
Therefore, for symptomatic vaginal atrophy that does not respond to self–care measures, estrogen treatment is the standard of care, typically with vaginally administered local estrogens. Prescription vaginal estrogens are available as either estradiol or conjugated estrogens. In some countries outside the United States, vaginal estriol is also available.Go to:
An important concern about treatment safety relates to the extent of systemic absorption of vaginal estrogens. The conclusion from several studies comparing different doses of estradiol vaginal tablets24,25 or different vaginal estrogen preparations (conjugated estrogens and estradiol vaginal tablets)26 is that systemic absorption occurs, but to a limited extent. Labrie et al26 showed that levels of estradiol increased on average from a baseline (pretreatment) level of 3 pg/mL to 17 pg/mL on day 7 of treatment for both estradiol vaginal tablets (25 μg) and conjugated estrogen cream (0.625 mg). Nilsson and Heimer24 showed that, although plasma estradiol concentration diminished by the 14th day of daily treatment with 10 or 25 μg of vaginal estradiol, it was still statistically significantly higher than pretreatment levels. Some evidence shows that estradiol levels diminish over time when vaginal estrogens are used consistently.24,25
Although vaginal estrogens applied as a cream, vaginal tablets, or a low-dose vaginal ring are systemically absorbed, the rise in serum estrogen levels appears to remain well below premenopausal levels. Nonetheless, this may be of concern to women with a history of breast or other hormonally sensitive cancersGo to:
Because all low-dose vaginal estrogens appear comparable in efficacy for the treatment of VVA, the choice of estrogen formulation is determined by the clinician and by each woman’s preferences. Estrogen creams are currently the least costly and most widely used but require commitment to regular use for sustained effect. Dosing vaginal creams can be confusing because the dose of active estrogen cream is specified in milligrams, the dose of base cream in grams, and applicator volume in proportions. A simplified approach to dosing is provided in Table 3. The estradiol tablet is preferred by some to avoid the messiness of cream. The estradiol ring is long acting and requires less sustained effort to use; however, it requires dexterity to insert and remove and needs to be replaced every 3 months. The presence of a cystocele or rectocele may cause ring displacement.
Systemic estrogen therapy, in the form of patches, oral agents, or a higher-dose vaginal ring, is sometimes used for VVA, especially when the patient also has hot flashes. However, 10% to 20% of women may have residual VVA symptoms even while taking systemic estrogen.27 These women will require administration of local vaginal estrogens alone or along with systemic therapy for relief of VVA symptoms.
Two studies have shown that oral hormone therapy (HT) may worsen symptoms of urinary incontinence. The Heart and Estrogen-Progestin Replacement Study found a higher risk of both urge (odds ratio, 1.5; 95% confidence interval [CI], 1.2-1.8; P<.001) and stress incontinence (odds ratio, 1.7; 95% CI, 1.5-2.1; P<.001) in the hormone-treated group vs the placebo group throughout the treatment period.28
It has been suggested that urge incontinence worsened with HT because progesterone was a component. However, in the Women’s Health Initiative, 3 treatment groups were evaluated for urge incontinence (conjugated estrogens alone, conjugated estrogens with progesterone, and placebo). Women given conjugated estrogens alone were at increased risk of developing urge incontinence compared with those receiving placebo (relative risk, 1.32; 95% CI, 1.10-1.58), whereas the women given combination conjugated estrogens with progesterone were not (relative risk, 1.15; 95% CI, 0.99-1.34).29 Thus, whether oral HT adversely affects urge urinary incontinence remains unclear.Go to:
BREAST CANCER AND VVA
Currently, more than 2 million women in the United States have a history of breast cancer. In breast cancer survivors, the estimated prevalence of vaginal atrophy, by symptom report, ranges from 23% to 61%.8 Prescribing even very low-dose localized estrogen treatments for these patients can cause concern because of the potential for systemic absorption.
Concern about the provision of any form of estrogen, either systemic or local, to breast cancer survivors contributes to the high incidence of VVA in women with breast cancer. Discontinuation of HT may trigger the onset of VVA symptoms.
Many surgical, endocrine, and chemotherapeutic treatments for breast cancer can cause or exacerbate VVA.10,30–37 Tamoxifen acts as an estrogen antagonist or agonist depending on the target organ and menopausal status. In premenopausal women, tamoxifen may cause VVA by acting as an estrogen antagonist and blocking the naturally high levels of endogenous estrogen. In postmenopausal women, however, it acts as an estrogen agonist on the urogenital tract.38
Raloxifene does not appear to have an effect on the urogenital area in either premenopausal or postmenopausal women. Davies et al35 found no significant differences in incidence of VVA when comparing databases of postmenopausal women treated with raloxifene vs placebo.
Aromatase inhibitors (AIs) are prescribed as adjuvant systemic therapy to women with ER+ breast cancer. In the ATAC (Arimidex, Tamoxifen, Alone or in Combination) study, designed to compare outcomes in postmenopausal breast cancer survivors taking tamoxifen, anastrozole (an AI), or a combination of both, Cella et al10 demonstrated that vaginal dryness was more common in the group taking anastrozole than in the group taking tamoxifen (18.5% vs 9.1%). Dyspareunia was also more common in the anastrozole group (17.3% vs 8.1%).10
Chemotherapy itself can result in vaginal dryness and dyspareunia. In a randomized clinical trial comparing high-dose chemotherapy with standard-dose chemotherapy for breast cancer survivors, followed by radiotherapy and tamoxifen in all patients, more patients in the high-dose chemotherapy group experienced persistent vaginal dryness.37
Chemotherapeutic agents used in the treatment of breast cancer can also cause VVA because of chemotherapy-induced ovarian failure. Premenopausal women account for 25% of all diagnosed breast cancer cases and are more likely to need systemic chemotherapy. The risk of permanent chemotherapy-induced ovarian failure is more common in women older than 40 years (49%-100%) than in those younger than 40 years (21%-71%).39
Premenopausal women with hormone-sensitive (ER+) advanced breast cancer may be offered gonadotropin-releasing hormone agonists to induce a temporary menopause through suppression of ovarian function, with VVA as a potential adverse effect.40 High-risk premenopausal women who areBRCA1/2+ sometimes choose bilateral oophorectomy, which in turn increases their likelihood of developing VVA.
Whether breast cancer survivors with VVA can be safely treated with low-dose vaginal estrogens remains controversial. Kendall et al41 addressed this question when they followed up 7 breast cancer survivors taking AIs to suppress estrogen levels. These women took 25-μg vaginal tablets of estradiol daily for 2 weeks and then twice weekly for severe symptoms of VVA. After 2 weeks of treatment, mean serum estradiol levels increased from a pretreatment value of 1.4 pg/mL or less to 19.6 pg/mL. The estrogen levels had decreased to less than 9.5 pg/mL by 4 weeks of therapy in most women, but only 2 women had pretreatment estradiol levels at week 7. If third-generation AIs decrease the levels of circulating estrogens more than earlier-generation AIs and at the same time improve survival, Kendall et al41 hypothesized that a small increase in circulating estradiol could worsen survival outcomes.Go to:
COMPLEMENTARY AND ALTERNATIVE MEDICINE
Complementary and alternative medicine products have been extensively studied in the treatment of hot flashes, but less information is available on their use in VVA. One study found that Vitamin E and phytoestrogen applied locally as a gel improved the symptoms of VVA.42 An evaluation of VVA was undertaken in a cross-sectional study of 60 women, half of whom had taken 1,25-dihydroxyvitamin D (0.5 μg/d of calcitriol) orally for at least 1 year and half of whom had not. The prevalence of vaginal atrophy was significantly higher in the group who did not use vitamin D, as measured by VMI and symptoms.43
In a separate study, soy supplementation for the treatment of VVA was investigated. Phytoestrogens such as soy bind to ERs in the vagina and bladder. A randomized controlled trial evaluating dietary supplementation with 12 to 20 mg/d of soy showed no improvement in VMI.44
Currently, well-established effective complementary and alternative medicine treatments for VVA are lacking.Go to:
Future studies will continue to explore the use of even lower doses of vaginal estrogens. The efficacy and safety of 10-μg vaginal tablets of low-dose estradiol for the treatment of VVA were evaluated in a 2009 study; after 12 weeks of therapy, significant improvements in symptoms, pH, and VMI were observed, with no adverse effects.45 In a recent study comparing treatment with 25 μg of estradiol, 10 μg of estradiol, and placebo, Bachmann et al46 found that both active groups experienced improvement in vaginal atrophy symptoms, vaginal pH, and VMI, with greater improvements seen for the higher dose.
Interest in vaginal estriol products is strong because of the inverse relationship with breast cancer risk at a population level. Studies have shown that estriol improves symptoms of VVA and reduces the incidence of urinary tract infection. Exogenous estriol administration does not alter serum estradiol or follicle-stimulating hormone levels.47–50
Studies are currently under way to evaluate newer selective ER modulators (SERMs), which specifically target urovaginal health without compromising breast health.51
Because moisturizers and lubricants also play a role in the treatment of VVA, better delivery systems for these nonhormonal vaginal treatments will likely be developed in the future.Go to:
Vulvovaginal atrophy, a common and often underreported condition, occurs in women who experience hypoestrogenic states. Systemic treatment, when prescribed for menopausal symptoms, may not be sufficient to control VVA. Local estrogens include creams, tablets, and rings, all of which are equally effective. Thus, patient preference will guide the choice. A growing number of women are at risk of developing VVA because of decreased use of systemic HT and increased use of SERMs, AIs, and chemotherapy in women with a history of breast cancer, for whom the safety of even low-dose vaginal estrogens has not been established.
Future research on VVA will likely explore the use of much lower doses of vaginal estrogens, seek to develop newer delivery systems for nonhormonal therapy, and develop SERMs that preferentially target urogenital tissues.
One reason for this medicalisation is the creation of new conditions.
The goal of preventing future disability and early death has fashioned
new disorders – including high cholesterol and blood pressure. Such
proto diseases are based on a person’s risk profile at a time when
disease is not present and symptoms are not felt.
can be identified in an ever growing proportion of the population. The
belief that treating these conditions will lead to future cost savings
drives up drug consumption, aimed at bringing cholesterol, blood
pressure and glucose levels into line.
A simple shift towards lowering the threshold that determines when
someone should be taking such drugs can lead to a substantial expansion
in the number of people who are offered them by health professionals.
While these medicines can indeed prevent future disease for individuals,
if one takes a population health approach, it is not a given that cost
savings will outweigh costs incurred.
Another driver is the dominance of evidence-based medicine (EBM). The
idea of basing medicine on evidence would seem to be common sense.
However, sitting at the top of the hierarchy of evidence-based medicine
is the evaluation procedure of the double-blind, placebo-controlled trial.
Following the fallout from the thalidomide tragedy in the 1950s and 1960s, there was an increased impetus to put in place rigorous procedures for the assessment of potentially toxic pharmaceuticals
by clinical trials. This effort to prevent lethal and dangerous drugs
getting on to the market was transformed from a test for new drugs to a
standard that all therapeutic interventions were expected to meet.
This remains the case even though many therapeutic interventions –
surgery, counselling, public health advice – do not work like drugs and
are not as easy to assess. As a consequence, medications are about the
only form of therapeutic intervention that can successfully become
Since the development of the evidence-based medicine movement, there
has been a trend where health professionals are required to follow
evidence-based protocols and guidelines. These guidelines are an
effective way of promoting the expansion of medication use. If health
professionals do not follow standards and guidelines – for example don’t
ask you to take a cholesterol test when you reach a certain age and
recommend the cholesterol-lowering drug – they are in danger of being viewed as incompetent practitioners.
Some pharmaceuticals work very well. They can help prolong life and
ameliorate symptoms. Many people will recall situations where they were
glad a drug was readily available.
But the Greek term pharmakon refers to both remedy and poison.
Pharmaceuticals are well known for their toxic effects, which is one
reason why access to many drugs is carefully controlled, requiring a
medical doctor’s prescription. But research shows that even with doctors
overseeing these drugs, side effects occur on a large scale and we have
woefully inadequate means of reporting side effects and adverse reactions.
The costs of responding to adverse drug reactions and the disease and
premature death they can cause makes side effects an important public
health problem. Yet only around 10% of serious adverse drug reactions are reported to agencies that monitor drug safety.
To deal with this issue, we need to consider trends in drug
consumption, regulation and policy. We need to understand how decisions
about drug use are made in clinical consultations and in homes, and how
drug monitoring agencies, drug subsidising agencies and drug trial
There is little resistance to the ever expanding use of
pharmaceuticals. Individuals, health professionals and health care
institutions, nation states and international health agencies are
increasingly governed by the dominance of pharmaceutical approaches to
But there are interventions that we could be putting in place to
ameliorate this expansion. We need to develop more rigorous vigilance
procedures so that when drugs come on the market, they are carefully
monitored for adverse reactions, and both patients and health
practitioners are actively encouraged to report any concerns to drug
We also need to regulate the advertising of prescription medicines
more tightly, particularly in New Zealand where drug companies can
advertise their products and only have to make fleeting reference to
possible side effects.
This is a major study which has been ongoing for many years, from the Mayo Clinic. Their conclusions show the safety and benefits from HRT given after the menopause, and no increase in blood clots. This is just further evidence of what I have been saying for many years.
1Departments of Surgery and Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN.2Department of Obstetrics and Gynecology, New York University School of Medicine, New York, NY.3Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, University of Wisconsin School of Medicine and Public Health and the Geriatric Research, Madison, WI.4Department of Epidemiology and Biostatistics, School of Medicine, University of California, San Francisco, CA.5Utah Lipid Center, Salt Lake City, UT.6Department of Medicine, Los Angeles Biomedical Research Institute at Harbor-University of California Los Angeles, Torrance, CA.7Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, San Francisco, CA.8Departments of Acute and Chronic Care, Epidemiology and Biostatistics, George Washington University School of Nursing and Milken Institute School of Public Health, Washington, DC.9Division of Geriatrics, Department of Medicine, University of Wisconsin School of Medicine and Public Health and the William S. Middleton Memorial VA, Geriatric Research, Education and Clinical Center, Madison, WI.10Atherosclerosis Research Unit, University of Southern California, Los Angeles, CA.11Department of Physiology and Biomedical Engineering, Division of Nephrology and Hypertension, Division of Hematology Research, Mayo Clinic, Rochester, MN.12Department of Radiology, Mayo Clinic, Rochester, MN.13Department of Obstetrics and Gynecology, Columbia University, New York, NY.14Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA.15Department of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, New Haven, CT.16Department of Obstetrics and Gynecology, University of Colorado School of Medicine, Aurora, CO.17Phoenix Veterans Administration Health Care System, Phoenix, AZ.
The Kronos Early Estrogen Prevention Study (KEEPS) was designed to address gaps in understanding the effects of timely menopausal hormone treatments (HT) on cardiovascular health and other effects of menopause after the premature termination of the Women’s Health Initiative.
The KEEPS was a randomized, double-blinded, placebo-controlled trial to test the hypothesis that initiation of HT (oral conjugated equine estrogens [o-CEE] or transdermal 17β-estradiol [t-E2]) in healthy, recently postmenopausal women (n = 727) would slow the progression of atherosclerosis as measured by changes in carotid artery intima-media thickness (CIMT).
After 4 years, neither HT affected the rate of increase in CIMT. There was a trend for reduced accumulation of coronary artery calcium with o-CEE. There were no severe adverse effects, including venous thrombosis. Several ancillary studies demonstrated a positive effect on mood with o-CEE, and reduced hot flashes, improved sleep, and maintenance of bone mineral density with both treatments. Sexual function improved with t-E2. There were no significant effects of either treatment on cognition, breast pain, or skin wrinkling. Variants of genes associated with estrogen metabolism influenced the age of menopause and variability in effects of the HT on CIMT. Platelet activation associated with the development of white matter hyperintensities in the brain.
KEEPS and its ancillary studies have supported the value and safety of theuse of HT in recently postmenopausal women and provide a perspective for future research to optimize HT and health of postmenopausal women. The KEEPS continuation study continues to pursue these issues.
1a Atherosclerosis Research Unit, Departments of Medicine and Preventive Medicine, Keck School of Medicine , University of Southern California , Los Angeles , CA , USA.2b Department of Obstetrics, Gynecology, and Reproductive Sciences , Yale University School of Medicine , New Haven , CT , USA.3c Department of Psychiatry , Yale University School of Medicine , New Haven , CT , USA.
The relationship between menopausal hormone therapy (HT) and breast cancer is complex and further complicated by misinformation, perception, and overgeneralization of data.
These issues are addressed in this mini-review through the lens of the Women’s Health Initiative (WHI) that has colored the view of HT and breast cancer. In the WHI, unopposed conjugated equine estrogen (CEE) reduced breast cancer risk and mortality. In the WHI CEE plus continuously combined medroxyprogesterone acetate (MPA) trial, although the hazard ratio (HR) was elevated it was statistically non-significant for an association between CEE + MPA and breast cancer. In fact, the increased HR was not due to an increased breast cancer incidence rate in women randomized to CEE + MPA therapy but rather due to a decreased and unexpectedly low breast cancer rate in the subgroup of women with prior HT use randomized to placebo. For women who were HT naïve when randomized to the WHI, the breast cancer incidence rate was not affected by CEE + MPA therapy relative to placebo for up to 11 years of follow-up. The current state of science indicates that HT may or may not cause breast cancer but the totality of data neither establish nor refute this possibility.
Further, any association that may exist between HT and breast cancer appears to be rare and no greater than other medications commonly used in clinical medicine.
Naveed Saleh, MD, MS, for MDLinx | November 26, 2019
Sometimes even the most ensconced medical knowledge is subject to contention, revision, and even derision. For instance, who would have thought that mouth-to-mouth resuscitation—a life-saving technique formally recognized in 1740 that has since been practiced for centuries—would no longer be necessary during CPR?
Medicine has changed greatly, not just over the past few years, but over the centuries.
Let’s take a look at five areas where medicine has changed over the past several years.
CT scans in kids
Once upon a time, physicians were less concerned about the radiation exposure inherent in CT scans. This all changed, however, in 2007, when debate over the safety of pediatric CT came to the fore, in part because of the publication of a review article in the New England Journal of Medicine (NEJM), in which the authors wrote:
“The number of computed tomographic (CT) studies performed is increasing rapidly. Because CT scans involve much higher doses of radiation than plain films, we are seeing a marked increase in radiation exposure in the general population. Epidemiologic studies indicate that the radiation dose from even two or three CT scans results in a detectable increase in the risk of cancer, especially in children.”
Results from a more recent high-powered systematic review published in Otolaryngology—Head and Neck Surgery supported the findings from the 2007 NEJM publication. Although data were limited, the researchers found that there was a marginal significant increase in the risk of all combined cancers in children receiving facial CT. Specifically, one case of excess malignancy resulted from 4,000 brain CTs. Furthermore, the risk of malignancy during the 10 years following CT exposure was 1 brain tumor per 10,000 patients exposed to a 10 mGy scan at age < 10 years.
Antibiotic prophylaxis for dental procedures
“Compared with previous recommendations, there are currently relatively few patient subpopulations for whom antibiotic prophylaxis may be indicated prior to certain dental procedures,” according to the American Dental Association.
More specifically, only a subset of patients with joint replacement or heart conditions should receive prophylactic antibiotics, and in these cases it’s best to consult with an orthopedic surgeon or cardiologist, respectively.
Lipid management guidelines
In case you missed it, there’s been another war. And no, we’re not talking about some conflict that played out in a far-flung theater. Instead, we’re talking about the statin wars that played out in the pages of top medical journals, with editors acting as generals.
Here’s a version of what happened.
In 2013, a review published in BMJ undermined the value of giving statins as primary prevention to patients at low-risk of heart attack or stroke. In these patients, the risk of adverse effects such as myopathy and myositis outweighed any potential benefit. Importantly, a joint task force of the American College of Cardiology (ACC) and the American Heart Association (AHA) convened in 2013 de-emphasized the importance of lipid levels when treating those at risk of heart disease, and recommended focusing on the risks of heart attack and stroke instead.
In 2016, the Lancet cast serious shade on the BMJ review article, claiming that the absolute benefits of statins as primary prevention far outweigh any risk of adverse effects. Soon editors at both the BMJ and Lancet were accusing one another of endangering public health.
In 2018, the ACC/AHA joint task force reconvened and, in a reversal, once again stressed the importance of lipid management.
Rescue breathing guidelines
Although CPR saves lives, it is not performed nearly enough when a person drops to the ground in public. One reason could be the “ick” factor associated with rescue breathing.
In 2015, the AHA updated its guidelines to make compression-only CPR an alternative to the rule of 30 compressions followed by 2 rescue breaths among lay rescuers.
Here is the AHA’s calculus:
“Evidence comparing layperson compression-only CPR with conventional CPR is derived from RCTs of dispatcher-guided CPR and observational studies. There were no short-term survival differences in any of the 3 individual randomized trials comparing the 2 types of dispatcher instructions. Based on meta-analysis of the 2 largest randomized trials (total n = 2,496), dispatcher instruction in compression-only CPR was associated with long-term survival benefit compared with instruction in chest compressions and rescue breathing. Among the observational studies, survival outcomes were not different when comparing the two types of CPR.”
The American Red Cross, on the other hand, still includes rescue breathing in its CPR guidelines. The organization suggests to “push fast” and “push hard,” with compressions at least 2 inches deep and at a rate of 100 per hour. After compressions, rescue breathing should be performed.
One pivotal randomized trial, however, reined in the importance of chest compressions for select populations. Researchers assessed 1,941 patients who experienced out-of-hospital cardiac arrest, among whom 981 received chest compressions and 960 received both chest compression and rescue breathing. They concluded the following:
“In this multicenter, randomized trial, CPR instructions consisting of chest compression alone did not increase survival to hospital discharge overall, as compared with instructions consisting of chest compression plus rescue breathing. However, the results suggest that chest compression alone may increase survival among certain subgroups of patients—those with a cardiac cause of arrest and those with ventricular fibrillation.”
The prostate-specific antigen (PSA) blood test was once considered a very important diagnostic tool for men of a certain age to receive. For years, men received the test even though the benefit was unclear.
In 2009, however, based on the results of a US trial, the US Preventive Services Task Force (USPSTF) recommended against its use. In 2017, the USPSTF updated its recommendations, suggesting that providers engage in shared-decision making to discuss the benefits and drawbacks of PSA testing with their patients. The USPSTF also recommended against using the PSA test in men aged 70 years and older.
As a biomarker, PSA has several limitations. Conditions other than cancer can raise PSA levels. These conditions include benign prostatic hyperplasia and prostatitis. Furthermore, PSA levels go up with age. Conversely, drugs, chemotherapy, and obesity can lower PSA levels.
Furthermore, results from PSA blood tests aren’t always accurate, and higher levels don’t necessarily mean cancer. Thus, many men with normal PSA levels may end up receiving a diagnosis of prostate cancer. In fact, between 23% and 42% of men with prostate cancer detected by PSA test results have tumors that would not affect their health if left otherwise untreated. And while you may be tempted to think “better safe than sorry,” consider that overdiagnosis comes with risks of its own, including risk of sepsis from repeat biopsies, increased costs, and anxiety.
“Any reduction in prostate cancer-specific mortality may take up to 10 years to accrue; therefore, men who have a life expectancy less than 10 to 15 years should be informed that screening for prostate cancer is unlikely to be beneficial. No studies examined the independent role of screening by DRE.”
Let’s consider a quotation taken from Dr. Atul Gawande that sheds some light on the ever-changing field of medicine, and how even our most entrenched beliefs can be dispatched:
“We look for medicine to be an orderly field of knowledge and procedure. But it is not. It is an imperfect science, an enterprise of constantly changing knowledge, uncertain information, fallible individuals, and at the same time lives on the line. There is science in what we do, yes, but also habit, intuition, and sometimes plain old guessing. The gap between what we know and what we aim for persists. And this gap complicates everything we do.”
Medicine has changed greatly, not just over the past few years, but over the centuries. But, without change, there would be no progress. We are grateful for this and look forward to whatever changes the future will bring.
You are all aware of the issues I have had with attacks on doctors who prescribe natural hormones from many in the medical profession. My patients often bare the brunt of this hostility, which is very unfair. One of the reasons for this web site is to try and put the record straight regarding what I do, and give patients the information they need to know it is safe and has research to back it up as well.
Ray Moynihan receives research funding from the National Health and Medical Research Council. He is co-chair of the scientific committee for the Preventing Overdiagnosis international scientific conference, co-sponsored by the World Health Organization, Sydney, December 5-7.
Republish our articles for free, online or in print, under Creative Commons licence.
While there’s much to celebrate in medicine, it’s now beyond doubt that we have too much of it. Too many tests, diagnoses, pills and procedures are wasting resources that could be better spent meeting genuine need.
As a recent OECD report concluded, up to one-fifth of health spending may be wasted, and many patients “unnecessarily harmed” by treatments they didn’t need.
Antidepressants, for example, can be life-savers for some people. But drug company-funded studies have overplayed their benefits and downplayed their harms, contributing to overuse and unnecessary side effects.
Today in The BMJ a global group of researchers, doctors, editors, regulators and advocates outline key strategies to reduce the financial entanglement with industry. The first step is ensuring the evaluation of any new tests, treatments and technologies are free from industry influence.
Distorted research, education and clinical practice
A huge proportion of medical research is currently funded by industry – in the United States almost 60%. Yet there’s a mountain of evidence that company-sponsored studies tend to overstate product benefits and playdown harms.
One example is cholesterol-lowering drugs, or statins. A review analysing almost 200 studies of statins found that company-sponsored studies were much more likely to find results favourable to the sponsors’ drug.
There’s similar distortion with devices, like pelvic mesh, used to treat pelvic organ prolapse. In this case, poor testing meant many women received the mesh without knowing the risks of horrendous harms, including severe pain, infection, and repeated surgery.
As a study of 280,000 doctors reveals, accepting just one sponsored meal is associated with higher prescribing of the sponsor’s products: a 20% increase in statins, and a doubling of antidepressants.
Industry argues it’s information helps patients, but a systematic review found differently. Doctors who accept marketing, including sales representatives, tend to prescribe more, at higher cost, and lower quality, such as prescribing an inappropriate drug, or prescribing that is not in line with guidelines.
Just look at the opioid epidemic in the United States. One study found the amount of marketing, including payments to doctors, was associated with small but significant increases in both prescriptions and deaths from overdose.
How to end commercial influence
Evidence of the dangers of financial relationships with industry has caused many groups to seek more freedom. As we show in today’s BMJ Analysis, there are signs of change.
In Norway, industry-supported education can no longer be used formally by doctors, and the government funds independent drug information.
Some medical journals no longer accept drug company advertising. Citizen groups like the US National Women’s Health Network accept no funds from companies selling healthcare products.
The biggest challenge is working out ways to evaluate tests and treatments, free from the influence of companies developing them. But radical reform is in the wind in many places.
In Italy, the promotional budgets of drug companies are taxed to create a pool for independent research.
Our proposals are from a team with expertise across medicine, law, and philosophy and includes people from The BMJ and the World Organisation of Family Doctors.
We argue the pathway to independence includes three key reforms:
government policies ensuring the evaluation of tests, treatments and technologies is free from sponsor influence
reforms to ensure medical education is free from industry support and on-going professional accreditation can’t be gained from company-sponsored events
new rules to end marketing interactions between industry and prescribing doctors, such as sales representatives’ visits.
In our view, tackling the current epidemic of medical excess can only work if decision-makers within health care seek much more independence from those profiting from that excess. And if you want to help develop more detailed recommendations for reform, and support the campaign launched in BMJ today, you can do so here.