Monthly Archives: December 2019
DHEA for Urogenital Atrophy and Sexual Function
DHEA for Urogenital Atrophy and Sexual Function
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
DHEA for Urogenital Atrophy and Sexual Function
Susan R. Davis, MBBS, FRACP, PhD
January 15, 2015
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
Jan 5, 2016 12:01 AM By Susan Scutti
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.
Posted by Dr Colin HollowayMayo Clin Proc. 2010 January; 85(1): 87–94. doi: 10.4065/mcp.2009.0413 PMCID: PMC2800285
Maire B. Mac Bride, MBBCh, Deborah J. Rhodes, MD, and Lynne T. Shuster, MD Author information ►Copyright and License information ► This article has been cited by other articles in PMC. Go to:
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.
TABLE 3. Vaginal Estrogen Products Go to:
SYSTEMIC ESTROGEN AGENTS AND VVA
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.
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As pharmaceutical use continues to rise, side effects are becoming a costly health issue
As pharmaceutical use continues to rise, side effects are becoming a costly health issue
February 21, 2019 3.36pm AEDT If doctors questions evidence-based medicine guidelines, they are often viewed as incompetent practitioners. from http://www.shutterstock.com, CC BY-ND
- Kevin Dew Professor of Sociology, Victoria University of Wellington
Kevin Dew receives funding from the New Zealand Health Research Council. the Marsden Fund and the Faculty of Humanities and Social Sciences of Victoria University of Wellington..
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The use of pharmaceuticals is on the rise and, globally, the expenses for drugs are projected to reach US$1.5 trillion by 2021.
The ageing of populations is one of the drivers of this upward trend, but another important influence is our growing tendency to treat conditions and circumstances we didn’t use to medicalise.
Read more: Medicines to treat side effects of other medicines? Sometimes less is more beneficial
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.
Proto diseases 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.
Read more: Randomised control trials: what makes them the gold standard in medical research?
This particular type of trial was designed to assess the efficacy of medications. The first such trial assessed the use of streptomycin in the treatment of pulmonary tuberculosis.
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 evidence-based.
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.
For many people their sense of identity is shaped by their relationship to medications. At times they may be reliant on drugs for some quality of life, but they often have to trade off what is gained against at times debilitating side effects.
Read more: We’re all at risk from scary medicine side effects, but we have to weigh the risks with the benefits
Remedies and poisons
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 methodologies work.
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 health care.
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 monitoring agencies.
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.
The Kronos Early Estrogen Prevention Study (KEEPS): what have we learned?
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.
Menopause. 2019 Sep;26(9):1071-1084. doi: 10.1097/GME.0000000000001326.
The Kronos Early Estrogen Prevention Study (KEEPS): what have we learned?
Miller VM1, Naftolin F2, Asthana S3, Black DM4, Brinton EA5, Budoff MJ6, Cedars MI7, Dowling NM8, Gleason CE9, Hodis HN10, Jayachandran M11, Kantarci K12, Lobo RA13, Manson JE14, Pal L15, Santoro NF16, Taylor HS15, Harman SM17.
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 the use 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.
Menopausal hormone therapy and breast cancer: what is the evidence from randomized trials?
Climacteric. 2018 Dec;21(6):521-528. doi: 10.1080/13697137.2018.1514008. Epub 2018 Oct 9.
Menopausal hormone therapy and breast cancer: what is the evidence from randomized trials?
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.
5 big changes to medicine in the past few decades
Featured Articles in Internal Medicine In the News
5 big changes to medicine in the past few decades
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.”
- See Also: 10 years of life-changing FDA approvals
Prostate-specific antigen blood tests
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.
Here’s the conclusion of a Cochrane study on the topic:
“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.
Time to end drug company distortion of medical evidence
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.
Doctors’ prescribing habits are influenced by drug reps and other industry marketing. Monkey Business Images/Shutterstock
Time to end drug company distortion of medical evidence
December 4, 2019 5.35am AEDT
- Ray Moynihan Assistant Professor, Bond University
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.
Bond University provides funding as a member of The Conversation AU.
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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.
Read more: Antidepressants may not be as effective as we thought, and shouldn’t be the only treatment for depression
Widespread industry influence is jeopardising the integrity of research and medical education, and threatening the quality of patient care.
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.
Read more: Vaginal mesh controversy shows collective failure of the TGA and Australia’s specialists
Those same companies then sponsor the “education” of your doctor, often with the evidence they’ve funded, and good food and wine.
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.
Read more: Who’s paying for lunch? Here’s exactly how drug companies wine and dine our doctors
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.
In Britain, Labour is proposing the government funds clinical trials and creates state-owned pharmaceutical makers.
More needs to be done
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.
Read more: We need new rules for defining who is sick. Step 1: remove vested interests
If weight loss is your only goal for exercise, it’s time to rethink your priorities
Choose an activity you enjoy so it’s easier to stick to. Shutterstock
If weight loss is your only goal for exercise, it’s time to rethink your priorities
November 20, 2019 6.23am AEDT
- Evelyn Parr Research Fellow in Exercise Metabolism and Nutrition, Mary MacKillop Institute for Health Research, Australian Catholic University
Evelyn Parr does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.
Australian Catholic University provides funding as a member of The Conversation AU.
As an aesthetic society, we often demonise body fat and stigmatise people with lots of it. There’s often an assumption that people carrying excess weight don’t exercise and must be unhealthy.
But that’s not true: you can be fat and fit. In fact, as we age, low levels of fitness can be more harmful to our health than high amounts of fat.
Read more: Interactive body map: physical inactivity and the risks to your health
For those considering starting exercise, try looking beyond weight loss for motivation. No matter how much you weigh, there are always benefits to exercise.
Exercise actually does a pretty poor job of getting us to expend enough excess energy to lose weight. This is partly due to a compensatory effect of our appetite, which increases after we exercise.
Exercise changes our body composition – how much fat we have as a ratio to how much lean (muscle) tissue we have – but this doesn’t always cause big changes on the scales.
Here are just five ways exercise improves our health, no matter how much we weigh.
1. Better cardiorespiratory fitness
Cardiorespiratory fitness is a measure of how far and hard you can run without needing to stop, or how many stairs you can climb without being out of breath. Running for longer, or climbing more stairs, means you have a higher absolute cardiorespiratory fitness which cannot be improved with weight loss alone.
Having a high body mass index (BMI) may reduce the absolute intensity you can exercise but it doesn’t mean it is less effective.
You may be able to jog between every third lamppost, for example, but not run consistently for 1 km. While it may seem the periodic jogging is not as impressive, it’s all relative to your baseline and any exercise is better than none.
If you’re carrying a lot of excess weight, you might prefer non-weight bearing exercise such as swimming or cycling indoors to minimise stress on your joints – but this will depend on you and what you like doing. After all, you’re more likely to continue exercising if you enjoy it.
If you’re thinking “but I hate running/swimming/cycling/dancing and I’d rather lift weights”, then lift weights! Although lifting weights doesn’t have the same effects as cardio training, the benefits are still as important for mobility, joint function and maintaining muscle mass as we age.
Read more: Don’t have time to exercise? Here’s a regimen everyone can squeeze in
2. Lowered risk of heart disease and stroke
Exercise reduces the risk of heart disease and stroke, even in those with a chronic disease such as diabetes, irrespective of body fatness.
Regular exercise helps lower blood pressure, improves delivery of blood throughout the body, and reduces inflammation, even in those with a high body mass index.
3. Reducing the ‘bad’ fat
Exercise improves our body’s ability to use energy. We store large amounts of energy as fat, which is quite hard to break down, as it costs a lot of oxygen compared to “cheaper” fuels for the body to use like glucose.
But when we exercise regularly, we increase our body’s ability to use fat as a fuel source as well as requiring more energy at rest.
This doesn’t necessarily mean more exercise equals more fat loss, but it does mean more fat turnover, and typically less fat stored in and around the organs (the “bad” visceral fat).
Read more: Belly fat is the most dangerous, but losing it from anywhere helps
4. Mental health benefits
Research has consistently shown that people who exercise (regardless of body size and shape) have better mental health and lower levels of stress, depression and emotional problems.
It does this via blood flow to the brain, increased release of endorphins that make us feel happy, and by helping to moderate the brain’s response to stress.
Often, the hardest part is getting started with exercise or going to perform the exercise, but once you are moving the mental health benefits begin.
5. Preventing weight gain
While exercise may not help us lose a lot of weight on the scales, it’s a good way to keep weight off and prevent weight regain.
Regular exercise continues to encourage the body to use stored fuels and remodel tissues (such as muscle) to grow healthier and stronger.
But preventing weight regain is tough. People who have lost weight may need greater amounts of exercise to counteract the physiological drive to return to the heavier body weight.
Read more: Genes, joules or gut bugs: which one is most to blame when it comes to weight gain?
If you need some extra help getting started or finding a routine that suits you, talk to your GP or consider seeing an accredited exercise physiologist.
Heres why you are always tired even though you are healthy
Featured Articles in Internal Medicine In the News
Here’s why you’re always tired even though you’re healthy
Physician Sense, for MDLinx | November 26, 2019
You know that it’s vital to get between 7-8 hours of sleep (or possibly more) nightly. You might even advise your patients to do the same. Additionally, you may have cultivated a healthy sleep routine. Why then are you, or your patients, always tired? You won’t need to tattoo the words “always tired” on your face because your caffeine consumption, bags under your eyes, and struggle to stay awake during all-hands meetings speak for themselves. Here’s what could be amiss.
You might have all of the outward indications of a healthy person. But why are you always tired? Here are some possibilities.
Poor sleep quality
Seven to 8 hours of sleep are useless if those hours are of poor quality. This could be why you’re always tired. Maybe you have a partner who snores, or a pet who needs to be on top of you in order to feel secure in the night. If you’re waking up repeatedly, you might not be getting the restorative sleep that you need. While sleep researchers are just beginning to scratch the surface of what these sleep stages do, it appears we might need REM sleep for memory consolidation and deeper, slow brain wave sleep for tissue repair. These sleep stages take place in cycles. Disruptions to the cycles might thwart the restorative effects of sleep.
Is there any disease state that isn’t worsened by or connected to stress? Well, we know excessive fatigue is. Circumstances have improved for us humans over millennia. While most of us don’t have to scan the savanna for lions, we still have the same fight-flight-freeze response that helped our ancestors survive predatory beasts. It’s the same system that kicks in when your hardcase CMO casts his predatory gaze your way. It’s not a life-or-death situation, but try reasoning with your amygdala. Every time this or other stressful situations arise, your amygdala pumps out epinephrine and norepinephrine depending on perceived needs. That can get pretty taxing and could be why you’re always tired.
Disrupted circadian rhythm
This is a common one for any physician doing shift work. Sleep-regulating hormones and neurons respond in part to sunlight exposure. If you’re sleeping during the day and working at night, you’re not receiving typical amounts of natural light. This, in turn, might be disrupting normal sleep-regulating hormone secretion. Also, studies have shown that exposure to the blue light emitted from electronic devices is disruptive to sleep. Spending evening hours glued to your smartphone or laptop could be sabotaging your circadian rhythm.
Over-reliance on carbohydrates
The American diet is very carb-heavy, and in some ways it creates a vicious cycle. Fast-burning carbs provide use with quick hits of energy, prompting spikes in insulin to transfer glucose into our cells. We get a short energetic lift, and a precipitous crash follows that leaves us craving more carbs. The cycle repeats itself. Slower-digesting macronutrients, such as fats and proteins, provide more stable sources of energy.
In Defense of Progesterone: A Review of the Literature
Alter therapy Health Med., 23 (6), 24-32 Nov 2017
In Defense of Progesterone: A Review of the Literature
- PMID: 29055286
Context • The medical literature on the use of progesterone in postmenopausal women is often confusing and contradictory. Some physicians implicate natural progesterone in an increase in the risk of breast cancer. The chemical structure of natural progesterone (P4) is quite different from chemically altered, synthetic chemicals called progestins, which results in different actions at the cell level. Objective • The research team intended to review the literature to examine the benefits and safety of natural progesterone and determine whether it can cause an increase or decrease in breast cancer risk. Design • A review of the medical literature to examine the benefits and safety of natural progesterone as compared with synthetic progestins. Intervention • Studies examined compared controls not receiving hormone therapy with women receiving estrogen alone and in combination with natural progesterone and with various synthetic progestins, such as medroxyprogesterone acetate-the most commonly used synthetic progestin. Outcome Measures • Outcome measures included factors such as progression and survival of breast and other cancers and other epidemiological and laboratory data. Results • A meta-analysis of 3 studies involving 86 881 postmenopausal women reported that the use of natural progesterone was associated with a significantly lower risk of breast cancer compared with synthetic progestins. Anovulation and low levels of serum progesterone have been associated with a significantly higher risk of breast cancer in premenopausal women. Use of progesterone has been linked to lower rates of uterine and colon cancers and may also be useful in treating other cancers such as ovarian, melanoma, mesothelioma, and prostate. Progesterone may also be helpful in preventing cardiovascular disease and preventing and treating neurodegenerative conditions such a stroke and traumatic brain injury. Conclusions • Physicians should have no hesitation prescribing natural progesterone. The evidence is clear that progesterone does not cause breast cancer. Indeed, progesterone is protective and preventative of breast cancer.