Monthly Archives: July 2021
We Need to Know How Menopause Changes Women’s Brains
We Need to Know How Menopause Changes Women’s Brains
This might turn out to be a crucial window to try to prevent Alzheimer’s and other chronic diseases that often accompany older age.
By Kim TingleyPublished July 21, 2021Updated July 22, 2021
During menopause, which marks the end of a woman’s menstrual cycles, her ovaries stop producing the hormones estrogen and progesterone, bringing an end to her natural childbearing years. But those hormones also regulate how the brain functions, and the brain governs their release — meaning that menopause is a neurological process as well. “Many of the symptoms of menopause cannot possibly be directly produced by the ovaries, if you think about the hot flashes, the night sweats, the anxiety, the depression, the insomnia, the brain fog,” says Lisa Mosconi, an associate professor of neurology at Weill Cornell Medicine and director of its Women’s Brain Initiative. “Those are brain symptoms, and we should look at the brain as something that is impacted by menopause at least as much as your ovaries are.”
In June, Mosconi and her colleagues published in the journal Scientific Reports one of the few studies to observe in detail what happens to the brain throughout the menopause transition, not just before and after. Using various neuroimaging techniques, they scanned the brains of more than 160 women between the ages of 40 and 65 who were in different stages of the transition to examine the organ’s structure, blood flow, metabolism and function; they did many of the same scans two years later. They also imaged the brains of men in the same age range. “What we found in women and not in men is that the brain changes quite a lot,” Mosconi says. “The transition of menopause really leads to a whole remodeling.”
On average, women in the United States enter the menopause transition — defined as the first 12 consecutive months without a period — at around 50; once diagnosed, they are in postmenopause. But they may begin to have hormonal fluctuations in their 40s. (For some women, this happens in their 30s, and surgical removal of the ovaries causes immediate menopause, as do some cancer treatments.) Those fluctuations cause irregular periods and potentially a wide variety of symptoms, including hot flashes, insomnia, mood swings, trouble concentrating and changes in sexual arousal. During this phase, known as perimenopause, which averages four years in length (but can last from several months to a decade), Mosconi and colleagues observed that their female subjects experienced a loss of both gray matter (the brain cells that process information) and white matter (the fibers that connect those cells). Postmenopause, however, that loss stopped, and in some cases brain volume increased, though not to its premenopausal size. The researchers also detected corresponding shifts in how the brain metabolized energy, but these did not affect performance on tests of memory, higher-order processing and language. This suggests that the female brain “goes through this process, and it recoups,” says Jill M. Goldstein, a professor of psychiatry and medicine at Harvard Medical School and founder and executive director of the Innovation Center on Sex Differences in Medicine at Massachusetts General Hospital. “It adapts to a new normal.”
Understanding what happens in the brain around the time of the menopause transition could inform when and how doctors treat a given woman’s symptoms. Hormone therapy — whether estrogen alone or in combination with a progestogen — is not ordinarily prescribed until postmenopause, and carries risks; on the other hand, it can help treat hot flashes, bone loss or undesirable urinary or vaginal changes for women under 60 (or who have begun menopause within the past 10 years), according to the North American Menopause Society. Some women who receive hormone therapy might also gain cognitive benefits, but more evidence is needed to identify who should be treated. Randomized control trials of postmenopausal women have tried to assess whether hormone therapy decreased the risk of Alzheimer’s disease or other cognitive declines, but these have returned mixed results so far.
Yet Mosconi and colleagues found that women in their study who had a particular genetic risk factor for Alzheimer’s disease began to develop amyloid plaques, which are linked to the disease, during perimenopause in their late 40s and early 50s — earlier than previously thought. If the brain changes significantly during perimenopause, that might turn out to be a crucial window during which to try to prevent Alzheimer’s and other chronic diseases that often accompany older age. (Because hormone therapy is not generally prescribed for perimenopausal women, clinical trials on its potential cognitive benefits have not been done for them.)
Several major chronic diseases, including Alzheimer’s, appear to afflict women disproportionately. As Goldstein and her colleagues noted in a January opinion column in JAMA Psychiatry, more than two-thirds of those diagnosed with Alzheimer’s are women (only in part because they live longer, and older people are at greater risk). Women, too, are at twice the risk of developing a major depressive disorder, and they do so in tandem with cardiovascular disease at twice the rate men do — a combination, the authors point out, that increases their risk of death from cardiovascular causes as much as fivefold. Heart disease is also a risk factor for Alzheimer’s.
Figuring out why those health disparities exist and what to do about them will require researchers to consider sex and gender specifically as variables, which science has been slow to do. Over the past 30 years, for example, researchers hoping to understand age-related cognitive decline have generally analyzed data from men and women collectively, obscuring differences between the sexes as far as when deficits tend to appear and how to diagnose them. “We need to think about designing studies from the outset in a way that’s relevant for women and men,” says Janine Austin Clayton, director of the Office of Research on Women’s Health at the National Institutes of Health. “Men and women both undergo chronological aging and reproductive aging, but in distinct ways,” she says. “Not looking at those separately masks findings and is a missed opportunity.”
Another challenge is separating the impacts on health caused by aging versus those caused by the hormonal changes that accompany menopause. Ideally, you would compare a large number of women who are experiencing them to women of the same age who are not. But by their 50s, most women have reached perimenopause; by their 60s, almost all are postmenopausal. Mosconi and her colleagues accounted for this by comparing women with age-matched men. But, as Stephanie Faubion, director of the Mayo Clinic Center for Women’s Health and medical director of the NAMS, points out, “Men’s brains are going to be different than women’s.”
The fact that women can experience significant brain changes around menopause also raises questions about how commonly this happens and the extent to which it affects women’s daily lives, says Pauline Maki, a professor of psychiatry, psychology and obstetrics & gynecology at the University of Illinois at Chicago College of Medicine. It’s crucial to note, she says, that women frequently report cognitive deficits around menopause, and that such symptoms are usually temporary. But her work has shown that they are more likely to have a lasting impact on low-income women of color — probably, she says, because those women have higher rates of stress, disrupted sleep and other mental-health burdens that “make the brain more vulnerable.”
Conversely, there are a number of possible preventive measures to protect cognitive health before and after the menopause transition. Abstaining from tobacco, being physically active, eating a plant-rich diet, reducing stress and getting enough sleep — these are all ways to support brain function. “Menopause is a critical window, when a woman might begin to develop the first signs of chronic disease,” Clayton says. As such, it’s an important time for her to check in with her health care provider and discuss her reproductive history and menopause status, each of which can influence her disease risk and treatment options. In turn, providers of all kinds need to be prepared to care for women throughout their transition: “It’s not just in the realm of gynecology,” Faubion says, “and we have to stop thinking of it that way.”
Lifting Weights? Your Fat Cells Would Like to Have a Word.
Lifting Weights? Your Fat Cells Would Like to Have a Word.
A cellular chat after your workout may explain in part why weight training burns fat.
By Gretchen ReynoldsPublished July 21, 2021Updated July 22, 2021
We all know that lifting weights can build up our muscles. But by changing the inner workings of cells, weight training may also shrink fat, according to an enlightening new study of the molecular underpinnings of resistance exercise. The study, which involved mice and people, found that after weight training, muscles create and release little bubbles of genetic material that can flow to fat cells, jump-starting processes there related to fat burning.
The results add to mounting scientific evidence that resistance exercise has unique benefits for fat loss. They also underscore how extensive and interconnected the internal effects of exercise can be.
Many of us pigeonhole resistance training as muscle building, and with good reason. Lifting weights — or working against our body weight as we bob through push-ups, squats or chair dips — will noticeably boost our muscles’ size and strength. But a growing number of studies suggest weight training also reshapes our metabolisms and waistlines. In recent experiments, weight workouts goosed energy expenditure and fat burning for at least 24 hours afterward in young women, overweight men and athletes. Likewise, in a study I covered earlier this month, people who occasionally lifted weights were far less likely to become obese than those who never lifted.
But how weight training revamps body fat remains murky. Part of the effect occurs because muscle is metabolically active and burns calories, so adding muscle mass by lifting should increase energy expenditure and resting metabolic rates. After six months of heavy lifting, for example, muscles will burn more calories just because they are larger. But that doesn’t fully explain the effect, because adding muscle mass requires time and repetition, while some of the metabolic effects of weight training on fat stores seem to occur immediately after exercise.
Perhaps, then, something happens at a molecular level right after resistance workouts that targets fat cells, a hypothesis that a group of scientists at the University of Kentucky in Lexington, the University of Nebraska-Lincoln and other institutions recently decided to investigate. The researchers had been studying muscle health for years, but had grown increasingly interested in other tissues, especially fat. Maybe, they speculated, muscles and fat chatted together amiably after a workout.
In the past decade, the idea that cells and tissues communicate across the expanse of our bodies has become widely accepted, though the complexity of the interactions remains boggling. Sophisticated experiments show that muscles, for instance, release a cascade of hormones and other proteins after exercise that enter the bloodstream, course along to various organs and trigger biochemical reactions there, in a process known as cellular crosstalk.
Our tissues also may pump out tiny bubbles, known as vesicles, during crosstalk. Once considered microscopic trash bags, stuffed with cellular debris, vesicles now are known to contain active, healthy genetic material and other substances. Released into the bloodstream, they relay this biological matter from one tissue to another, like minuscule messages in bottles.
Intriguingly, some experiments indicate that aerobic exercise prompts muscles to release such vesicles, conveying a variety of messages. But few studies had looked into whether resistance exercise might also result in vesicle formation and inter-tissue chatter.
So, for the new study, which was published in May in The FASEB Journal, from the Federation of American Societies for Experimental Biology, the researchers decided to examine the cells of bodybuilding mice. They first experimentally incapacitated several of the leg muscles in healthy adult mice, leaving a single muscle to carry all the physical demands of movement. That muscle swiftly hypertrophied, or bulked up, providing an accelerated version of resistance training.
Before and after that process, the researchers drew blood, biopsied tissues, centrifuged fluids and microscopically searched for vesicles and other molecular changes in the tissues.Sign up for the Well Newsletter Get the best of Well, with the latest on health, fitness and nutrition. .
They noted plenty. Before their improvised weight training, the rodents’ leg muscles had teemed with a particular snippet of genetic material, known as miR-1, that modulates muscle growth. In normal, untrained muscles, miR-1, one of a group of tiny strands of genetic material known as microRNA, keeps a brake on muscle building.
After the rodents’ resistance exercise, which consisted of walking around, though, the animals’ leg muscles appeared depleted of miR-1. At the same time, the vesicles in their bloodstream now thronged with the stuff, as did nearby fat tissue. It seems, the scientists concluded, that the animals’ muscle cells somehow packed those bits of microRNA that retard hypertrophy into vesicles and posted them to neighboring fat cells, which then allowed the muscles immediately to grow.
But what was the miR-1 doing to the fat once it arrived, the scientist wondered? To find out, they marked vesicles from weight-trained mice with a fluorescent dye, injected them into untrained animals, and tracked the glowing bubbles’ paths. The vesicles homed in on fat, the scientists saw, then dissolved and deposited their miR-1 cargo there.
Soon after, some of the genes in the fat cells went into overdrive. These genes help direct the breakdown of fat into fatty acids, which other cells then can use as fuel, reducing fat stores. In effect, weight training was shrinking fat in mice by creating vesicles in muscles that, through genetic signals, told the fat it was time to break itself apart.
“The process was just remarkable,” said John J. McCarthy, a professor of physiology at the University of Kentucky, who was an author of the study with his then graduate student Ivan J. Vechetti Jr. and other colleagues.
Mice are not people, though. So, as a final facet of the study, the scientists gathered blood and tissue from healthy men and women who had performed a single, fatiguing lower-body weight workout and confirmed that, as in mice, miR-1 levels in the volunteers’ muscles dropped after their lifting, while the quantity of miR-1-containing vesicles in their bloodstreams soared.
Of course, the study mostly involved mice and was not designed to tell us how often or intensely we should lift to maximize vesicle output and fat burn. But, even so, the results serve as a bracing reminder that “muscle mass is vitally important for metabolic health,” Dr. McCarthy said, and that we start building that mass and getting our tissues talking every time we hoist a weight.
Ovarian cancer screening persists despite advice against it
Australian Doctor Group
Staff AusDoc Article
Ovarian cancer screening persists despite advice against it: survey
Many women, including those at only average risk, are undergoing screening for ovarian cancer despite Australian guidelines advising against it, a study suggests.
Researchers, led by the Peter MacCallum Cancer Centre in Melbourne, surveyed more than 800 patients and 250 doctors to investigate attitudes to ovarian cancer screening.
Randomised controlled trials have failed to demonstrate that annual screening via transvaginal ultrasound and/or CA125 improves survival rates among women, the researchers said.
And some studies show false positive results from screening leads to harm, including unnecessary surgery and cancer-specific distress.
Despite this, among a cohort of 832 women from families with multiple cases of breast cancer, the research team found 15% had undergone ovarian cancer screening in the past two years.
Only 4% of the entire cohort (ages 25-70) were BRCA1/2 mutation carriers. The women’s cancer risk ranged from average to high based on family history and germline mutation status.
Almost 80% said they would continue with screening even if their doctor told them it was ineffective, because they wanted to ‘stay healthy for family’ and for ‘peace of mind’.
Meanwhile, most of the 192 GPs surveyed agreed there was no reliable way to detect ovarian cancer early and screening could lead to unnecessary investigation.
Nevertheless, more than 40% said they still thought screening could be useful and a similar proportion had actually ordered ultrasound or CA125 testing in the past two years.
Their reasons included patient request (21%), a chance of early detection (16%), patient peace of mind (14%) and no other available screening options (11%).
Better education and possibly restricted access to screening should be considered, the authors said.
What should you eat after you’ve been on antibiotics? And can probiotics and prebiotics get your gut back to normal?
What should you eat after you’ve been on antibiotics? And can probiotics and prebiotics get your gut back to normal?
July 19, 2021 11.13am AEST
- Clare Collins Laureate Professor in Nutrition and Dietetics, University of Newcastle
Clare Collins is affiliated with the Priority Research Centre for Physical Activity and Nutrition, the University of Newcastle, NSW. She has received research grants from NHMRC, ARC, MRFF, Hunter Medical Research Institute, Diabetes Australia, Heart Foundation, Bill and Melinda Gates Foundation, nib foundation, Rijk Zwaan Australia, WA Dept. Health, Meat and Livestock Australia, and Greater Charitable Foundation. She has consulted to SHINE Australia, Novo Nordisk, Quality Bakers, the Sax Institute and the ABC. She was a team member conducting systematic reviews to inform the Australian Dietary Guidelines update and the Heart Foundation evidence reviews on meat and dietary patterns.
University of Newcastle provides funding as a member of The Conversation AU.
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Antibiotics treat infections caused by bacteria. But they can also destroy the good bacteria in your gut. For some people, this results in an upset stomach and diarrhoea.
One UK review of the research looked at changes in gut bacteria after antibiotics commonly prescribed for respiratory and urinary tract infections found that after treatment, the numbers and diversity in bacteria types rapidly declines.
It also found some types of “bad” microorganisms increased while some “good” ones decreased.
For most people, once antibiotic treatment was stopped, the gut bacteria recover to some degree. But other studies suggest some antibiotics can have long-lasting effects on the balance of microorganisms.
It’s important to use antibiotics only when needed, and definitely not for viral infections, because antibiotics can’t kill viruses such as the common cold or COVID-19.
So what should you eat after a course of antibiotics? You might have heard of probiotics and prebiotics, but what are they, and what evidence is there to show they’re beneficial?
Probioitcs contain ‘good gut bacteria’
Probiotics are foods, typically yoghurts and yoghurt drinks, that contain “good gut bacteria”: live microorganisms that can recolonise the gut or improve your gut health.
To be called a probiotic, they must be able to resist stomach acid and digestive processes, and then be able adhere to the gut walls and grow, while not causing any issues for the gut wall. They must also be tested for safety and efficacy in controlled trials.
Read more: Plain, Greek, low-fat? How to choose a healthy yoghurt
To be called a probiotic, the dose of microorganisms needs to be sufficient to help restore the “good” bacteria, by elbowing out the “bad bacteria”.
Most yoghurts contain “good bacteria” but not all can survive the acidity of the stomach acid or the bacteria won’t grow in the bowel, so there is no probiotic benefit.
For probiotics to exert these beneficial effects, they not only have to make it to the large bowel, but once there they need the right fuel to help them grow well. That’s where prebiotics come into play – but more on them shortly.
What does the science say about probiotics?
Probiotics are widely promoted as being good for your overall health. The science on that has been mixed, but it does suggest people who are likely to get diarrhoea after antibiotics may benefit from consuming them.
One review of the evidence found probiotics may be useful for those at high risk of antibiotic-associated diarrhoea, such as the elderly and people in hospital.
The review found side effects were common when taking antibiotics and include taste disturbances, nausea, abdominal cramping, soft stools, fever and flatulence.
But people taking probiotics reported fewer side effects, suggesting they may be helpful in countering some of the side effects.
So what are prebiotics?
Prebiotics are compounds that help beneficial gut microorganisms grow and survive.
Prebiotic foods contain complex carbohydrates that can’t be digested and dietary fibres that resist digestive processes in the stomach and small intestine.
They pass undigested into the large bowel where they are fermented by the healthy “good” bacteria.
Read more: Gut feeling: how your microbiota affects your mood, sleep and stress levels
To be called a prebiotic, they need to undergo the processes above, and be shown in clinical trials to selectively improve the microorganism composition in the gut.
Not all dietary fibres are prebiotic. Common ones include complex carbohydrates called fructo-oligosaccharides, inulin and resistant starch.
You can find foods at the supermarket with added prebiotics, but non-digestible carbohydrates occur naturally in many everyday foods, including:
- grains: barley, rye bread, rye crackers, pasta, gnocchi, couscous, wheat bran, wheat bread, oats
- legumes: chickpeas, lentils, red kidney beans, baked beans, soybeans
- vegetables: artichokes, asparagus, beetroot, chicory, fennel bulb, garlic, green peas, leek, onion, shallots, spring onion, snow peas, sweetcorn, savoy cabbage
- fruit: nectarines, white peaches, persimmon, tamarillo, watermelon, rambutan, grapefruit, pomegranate, dates, figs
- nuts: cashews, pistachios.
Additional sources of resistant starch include under-ripe bananas, cooked and cooled rice, cornflour, cooked and cooled potatoes.
For babies, breast milk is naturally rich in oligosaccharides.
So who should have them?
Prebiotic foods are good for everyone, contain a range of nutrients and help promote a healthy bacterial gut environment.
The benefits of probiotics for a range of health conditions are unclear – they’re likely to be small, and depend on what is being taken and the underlying health issues.
But people at high risk of diarrhoea after antibiotics may benefit from consuming probiotic – as well as prebiotic – foods daily.
There is also emerging evidence that combining specific probiotics and prebiotics can increase the beneficial effects of both. Both the pro- and prebiotics could be added to the one food, termed a “synbiotic”, or they could be from separate sources but eaten together.
When it comes to antibiotics, the bottom line is only take them when prescribed for bacterial infections. Take them according to instructions from the manufacturer, your pharmacist and your doctor.
Vaginal oestrogen for vaginal dryness
A systematic review of the efficacy and safety of vaginal estrogen products for the treatment of genitourinary syndrome of menopause
Biehl, Colton, BS; Plotsker, Olivia; Mirkin, Sebastian, MDMenopause: April 2019 – Volume 26 – Issue 4 – p 431–453 doi: 10.1097/GME.0000000000001221 Review Article Buy
Objective: We updated a systematic review to evaluate the totality of evidence available for the efficacy and safety of vaginal estrogen products for the treatment of genitourinary syndrome of menopause (GSM) based on published randomized controlled trials.
Methods: We searched the Cochrane Library, Ovid, PubMed, Medline, Embase, and Clinicaltrials.gov for English-language articles from database inception to June 2018. Our search consolidated 2,086 potential sources to 53 full-text articles that were reviewed and found relevant to our systematic review.
Results: We identified 53 studies that met the inclusion criteria that evaluated the efficacy and safety of vaginal estrogen versus placebo or other hormone and nonhormone controls. Compared with placebo, all vaginal estrogens demonstrated superiority in objective endpoints and subjective endpoints of GSM, whereas some trials demonstrated superiority versus placebo in urogenital symptoms. No significant difference was observed between various dosages and dosage forms of vaginal estrogen products. Vaginal estrogen showed superiority over vaginal lubricants and moisturizers for the improvement of objective clinical endpoints of vulvovaginal atrophy but not for subjective endpoints. Unopposed vaginal estrogens seemed safe, although studies were not powered to detect a long-term estrogenic side effect.
Conclusion: Estrogen products were found to be clinically effective for the treatment of GSM with doses as low as 4 μg. Vaginal estrogen products seem to be safe with few adverse effects, although there is a lack of long-term controlled clinical trial safety data. This review supports the use of commercially available vaginal estrogen therapies as an effective and safe first-line therapy for the treatment of moderate-to-severe GSM.
Hormone therapy shown to reduce effects of nocturia in postmenopausal women
Hormone therapy shown to reduce effects of nocturia in postmenopausal women
Study suggests that various types of hormone therapy are effective in reducing the number of times during the night that postmenopausal women are woken up by the need to urinate
As women age, they are more likely to wake up in the middle of the night to pass urine. The loss of estrogen during the menopause transition accelerates this problem, which is known as nocturia. A new study evaluated the effectiveness of different hormone therapies in managing the frequency of nocturia. Study results are published online today in Menopause, the journal of The North American Menopause Society (NAMS).
The loss of estrogen during menopause has been shown to create bladder dysfunction, sleep disorders, hot flashes, and alterations in renal water and salt handling, all of which result in higher diuresis overnight. To date, there has been little research done regarding the effect of hormone therapy on nocturia, even though hormone therapy has been proven to improve the causative factors of postmenopausal nocturia such as sleep disorders, obstructive sleep apnea, and hot flashes.
Vaginal estrogen has already been shown to help manage the various symptoms of the genitourinary syndrome of menopause, especially with regard to improving urinary function. However, little was known about the effect of systemic treatment. In addition, there is some limited evidence suggesting significant benefits of using oral estrogen in combination with oral progesterone, but nothing is known about the effects of other hormone combinations or the newer tissue-selective estrogen complex (TSEC) on nocturia.
In this new study involving nearly 250 women, participants were divided into four treatment groups: estrogen and progesterone (E+P); estrogen only in patients with prior hysterectomies; TSEC; and no treatment. The study concluded that systemic treatment with either E+P or TSEC led to a significant reduction in nocturia prevalence and significant improvement of bothersome symptoms in women with two or more nocturnal voids. The use of estrogen only resulted in a significant reduction in urgency prevalence.
Researchers believe that additional research should be conducted to better understand the underlying pathophysiologic triggers.
Objective: To observe the impact of different hormonal treatment options on nocturia, its causative factors and bother in postmenopausal women.
Methods: This prospective study recruited 245 postmenopausal women and divided them into four treatment groups based on patient’s choice: Estrogen + Progesterone (E+P), Estrogen-only in patients with a prior hysterectomy, tissue-selective estrogen complex (TSEC) and no treatment. Nocturia and its causative factors were observed using two standardized questionnaires before and after treatment: the International Consultation on Incontinence Questionnaire Nocturia Module and the Targeting the individual’s Aetiology of Nocturia to Guide Outcomes (TANGO). The results of the Targeting the individual’s Aetiology of Nocturia to Guide Outcomes were divided in four influencing topics of which the sum score was calculated.
Results: A significant reduction in prevalence of nocturia ≥ twice per night was seen after treatment, as the prevalence decreased from 27.7% (59/213) to 16.4% (35/213). Specified per therapy, a significant reduction in nocturnal voiding frequency was observed in patients treated with E+P and TSEC (P = 0.018 and P = 0.018, respectively). This improvement could be explained by a significant reduction in SLEEP sum score in patients treated with E+P and TSEC (P < 0.001, P = 0.013, respectively). Estrogen-only led to a significant change in URINARY TRACT sum score, which is the result of a reduction in urgency prevalence (P = 0.039).
Conclusions: E+P and TSEC treatment led to a significant reduction in nocturia prevalence and bother in women with ≥ 2 nocturnal voids. This effect is mainly the result of improvement in sleep disorders, however an improvement in bladder disorders can be suggested as well. More research is necessary to confirm these findings.
Kim Pauwaert, An-Sofie Goessaert, Lynn Ghijselings, Wendy Bower, An Mariman, Dirk Vogelaers, Herman Depypere, Karel Everaert. Menopause 2021 Mar 15. doi: 10.1097/GME.0000000000001741. Online ahead of print. Hormone therapy as a possible solution for postmenopausal women with nocturia: results of a pilot trial
I have closed my books for nearly a year now, as I had become too busy and overloaded with patients wanting my help. I am now in a position to being able to start taking in new patients again, but am restricting myself to menopausal women and patients needing LDN. These are the patients I feel can benefit most from my help. I intend working for as long as possible, as I enjoy the work I do, and am in good health. I know that many of you have been disappointed in not being able to see me, so have made this decision with that in mind.
Thinking of getting a minor cosmetic procedure like botox or fillers? Here’s what to consider first
Thinking of getting a minor cosmetic procedure like botox or fillers? Here’s what to consider first
July 6, 2021 2.53pm AEST
- Simone Buzwell Senior Lecturer in Psychology, Swinburne University of Technology
- Gemma Sharp NHMRC Early Career Senior Research Fellow, Monash University
- Susan Rossell Professorial Research Fellow at Brain and Psychological Sciences Research Centre, Swinburne University of Technology
- Toni Pikoos Sessional tutor, Swinburne University of Technology
Gemma Sharp receives funding from an NHMRC Early Career Research Fellowship (Health Professional Category).
Susan Rossell receives funding from an NHMRC Senior Research Fellowship.
Toni Pikoos received funding from the Australian government.
Simone Buzwell 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.
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At a dinner party recently, my friend Kaity whispered, “I’ve been staring at my face in Zoom meetings and I look tired. I’m considering Botox. What are the risks?”
I shouldn’t have been surprised; Kaity isn’t alone in thinking cosmetic procedures could fix Zoom-face-fatigue. Our new research shows one in three Australians have new concerns about their appearance since the pandemic began.
What’s more, Kaity is in the primary demographic: 35-50 year old women. And she lives in Australia, where we have the highest cosmetic procedure rates per capita. We spend A$350 million to A$1 billion on cosmetic procedures per year – a figure expected to increase.
For most people, cosmetic procedures lead to improved self-esteem, confidence and body image. I never thought Kaity was shy, or had self-esteem issues, but she told me she’s different at work and after the last year she craves some self-care.
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However, for a significant minority, there are negative outcomes. So before deciding if it was right for Kaity, she needed to consider a few things:
1. What type of cosmetic procedure?
First, the type of cosmetic procedure is important. There are two forms: major and minor.
Major cosmetic procedures (“cosmetic surgery”) involve cutting the skin, such as for facelifts or breast augmentation. These are conducted under anaesthetic by medical doctors bound by Medical Board of Australia guidelines.
Minor cosmetic procedures, such as fillers and botox, are different. There is no anaesthetic, or cutting the skin, although they may involve piercing the skin. Fillers involve injecting subtances under the surface of the skin to add volume, while botox is a drug that relaxes the muscle to reduce wrinkles.
The category of minor cosmetic procedures also includes microdermabrasion, which removes superficial layers of dead skin cells to “polish” the skin.
Read more: Will microdermabrasion or skin needling give me better skin?
2. What provider do you choose?
Minor cosmetic procedures aren’t regulated in Australia and can be administered by doctors, nurses, dentists or beauticians. They aren’t funded by Medicare, so the outcomes are not monitored.
Concern about shonky operators prompted a warning from NSW Health Commission about unsafe and illegal practices, with a number of women experiencing significant harm.
So it’s essential to choose a reputable practitioner. But how do you find one?
Providers of minor cosmetic procedures don’t require registration. But if you choose someone registered with the Australian Health Practitioner Regulation Agency (AHPRA), you know you’re being treated by a practitioner who is bound to minimum professional standards of safety and patient care.
If you’re unsure, you can always ask your GP and check for verified reviews of your preferred cosmetic practitioner.
3. How much does it cost?
The cost of minor cosmetic procedures range up to thousands of dollars per session. One session lasts for about four months so must be repeated, making them an ongoing cost.
Luckily Kaity could afford it, but there are reports of cosmetic customers going without food to pay for procedures, and feeling the need to go back for more and more.
Minor cosmetic procedures shouldn’t cause financial strain. If it would cause Kaity financial pressure, she should not go ahead.
4. What are the side effects?
The possible side effects vary depending on the procedure and may include:
- swelling or bruising at the injection site
- dry eyes or throat
- headaches or flu-like symptoms
- muscle stiffness.
They’re usually not long-lasting.
Read more: Cosmetic facial procedures are not risk free – here are some of the most popular
5. What could go wrong?
Botox and dermal fillers can be administered incorrectly, resulting in “droopy eyelid”, “cockeyed eyebrows”, odd lumps or scarring.
Rashes or bleeding are possible, as is necrosis, where skin cells die. There are also reports of blurred vision and even blindness.
It’s assumed these are rare, but given the lack of data, rates are unknown.
6. Could it cause psychological distress?
The psychological consequences of minor cosmetic procedures are often ignored. For most people, they are positive.
However, some people rely on cosmetic treatments to self-manage psychological disorders or stress.
Minor cosmetic procedures don’t solve psychological problems and may exacerbate underlying emotional difficulties and relationship strain. Indeed for some patients, cosmetic procedures have contributed to self-harm, even suicide.
Importantly, some psychological factors predispose people to negative outcomes and in turn are exacerbated by cosmetic procedures. These include body dysmorphic disorder (BDD) – which has long been a contraindication for cosmetic work, meaning people with BDD shouldn’t have cosmetic procedures.
BDD involves preoccupation with appearance flaws, with some spending hours checking their appearance, with negative impacts on employment and relationships.
BDD symptoms usually worsen after cosmetic procedures, or concern shifts to a new body part. Other psychological and social factors, as well as identity concerns, are also linked to negative outcomes.
Read more: Body dysmorphic disorder and cosmetic surgery: are surgeons too quick to nip and tuck?
Customers of minor cosmetic procedures are more likely than average to have psychological disorders. We found more than 25% of minor cosmetic procedure customers had potential BDD and high numbers reported psychological distress, including anxiety, stress and/or depression. But some providers fail to adequately screen for these conditions, putting their customers at risk.
During lockdowns and COVID restrictions, people with BDD struggled because they couldn’t access beauty treatments, which fuelled their desire for future therapies.
7. Are your expectations realistic?
A final risk factor involves the motivations for procedures. Previously, only external motivations were considered unhealthy: having minor cosmetic procedures to please others, or believing the procedures would lead to friends and career success.
We did find this in our research, but in addition, we discovered unrealistic internal motivations – such as believing minor cosmetic procedures would change your personality – are similarly problematic.
Read more: New year, new you? Why we think a better body will be a better self
Essentially, your expectations must be realistic because if they’re not, it’s likely the procedures will result in distress.
These red flags can indicate if cosmetic procedures are a safe choice – and ethical cosmetic providers will screen customers for these before proceeding.
Can eating certain foods make you smarter?
Health check: can eating certain foods make you smarter?
March 25, 2019 5.57pm AEDT
Green vegetables, nuts and berries are among the foods that could improve our brain function.
- Margaret Morris Professor of Pharmacology, Head of Pharmacology, UNSW
- Michael Kendig Postdoctoral Research Fellow, UNSW
Margaret Morris receives funding from the National Health and Medical Research Council, Australia and Australian Research Council and she is affiliated with Nutrition Australia.
Michael Kendig has received funding from the Ian Potter Foundation.
UNSW Australia provides funding as a member of The Conversation AU.
Trying to keep up with what constitutes a “healthy” diet can be exhausting. With unending options at the supermarket, and diet advice coming from all directions, filling your shopping trolley with the right things can seem an overwhelming task.
For a long time we’ve known diet is key to maintaining physical health.
But emerging evidence indicates diet quality also plays a critical role in our cognitive function.
We’re learning some of the best things to eat in this regard include vegetables, nuts and berries, foods containing “good fats” and, possibly, fermented foods.
As well as potentially improving our brain function, eating these sorts of foods could improve our mental well-being – and could even help the planet, too.
Read more: Research Check: does eating chocolate improve your brain function?
Diet and brain function
In the face of rising obesity rates, over the past couple of decades, researchers have questioned whether increased weight, or poor diet, could influence cognition. They have since looked at what sorts of diets might impair or improve the function of our brains.
Long term follow-up studies show obesity is associated with mild impairments in several domains of cognitive function, including short-term memory, attention and decision-making.
Research has also shown short-term memory is poorer in people who report eating more saturated fat and sugar.
Conversely, the Mediterranean diet has been associated with better brain health and maintenance of cognitive abilities into older age. A Mediterranean diet is based on vegetables, whole grains, legumes and nuts, with healthy fats such as olive oil. Intake of red meat, saturated fats and sugar is limited.
A healthy diet has many elements, so let’s look at what particular foods might explain these benefits.
Vegetables, nuts and berries
Evidence indicates eating more vegetables slows the gradual decline in cognitive abilities that occurs naturally as we age.
While all veggies are likely to contribute, those in the cruciferous (Brassicaceae) family may confer particular benefits through their high fibre, folate, potassium and vitamin content. Vegetables in this family include broccoli, cauliflower, brussels sprouts, and fad favourites kale and rocket.
Interestingly, while there’s good evidence for the protective role of vegetables, there’s less evidence when it comes to fruit.
Berries, though, contain high levels of antioxidants. These compounds protect the body by scavenging harmful free radicals and reducing inflammation. Together these functions are likely to protect our cognitive ability.
Studies in rats, and in older people with mild cognitive impairment, indicate supplementing diets with berries improves performance in various memory tasks.
Nuts, meanwhile, are excellent sources of monounsaturated and polyunsaturated fats, minerals and vitamins. Studies in animals have shown the addition of nuts improves learning and memory. Emerging evidence in humans suggests consuming nuts within a Mediterranean-style diet improves measures of cognition, such as the capacity for verbal reasoning.
Healthy diets such as the Mediterranean diet are also characterised by foods such as oily fish, avocados, olive oil and small amounts of animal-derived fats (such as from red meat).
One of our experiments in rats showed diets high in saturated fat from lard or high in sugar led to memory impairments, whereas an oil-based diet high in polyunsaturated fats didn’t.
Read more: Food as medicine: your brain really does want you to eat more veggies
Importantly, rats fed these different diets did not differ in their total energy intake – only the type of fat and sugar varied.
While we can’t comment directly on the effects in humans, these findings suggest eating excess sugar, or animal-based fats, may negatively impact cognition.
For thousands of years humans have prolonged the life of foods through fermentation, which increases the proportion of Lactobacillus and other healthy gut bacteria.
Kombucha and kefir are trendy right now, but other popular fermented foods include kimchi, miso, yoghurt and sauerkraut. Intake of these foods is thought to maintain the diversity of the gut microbiome.
Read more: Health check: will eating nuts make you gain weight?
Interest in the potential cognitive effects of fermented foods stems from emerging evidence for the importance of the gut microbiota in cognition and health.
It’s well known that a poor diet can reduce the diversity of the gut microbiome. Our work in rats has shown the cognitive impairments produced by exposure to an unhealthy “cafeteria” diet – a Western-style diet high in saturated fat and sugar – are linked to changes in the gut microbiome.
It’s not possible to attribute “miracle” properties to one food group alone. We suggest a balanced, varied diet is the best approach to sustain not only brain health, but heart health too.
And there may be other reasons to seek out these foods. A newly published study showed eating fruit and vegetables improved mental well-being. Subjects tended to feel happier, less worried, and reported higher levels of overall life satisfaction.
The link between diet quality and better mental health is now well-established.
The recently published EAT-Lancet report adds a further compelling reason to eat healthily: the environment. This commission argued for a “planetary health” diet – akin to the Mediterranean diet – consisting of whole grains, vegetables, fruits, nuts and dairy, healthy fats, with low animal protein and few processed foods.
It is thought that shifting to such a diet, together with reducing food waste and adopting more sustainable food production systems, will minimise environmental damage and safeguard individual health.
The central message is the health of individuals and of the planet are inextricably linked, and this requires a rethink of global food systems.
Read more: Want to improve your mood? It’s time to ditch the junk food
Overhauling food systems – and individual food habits – will not be simple while foods high in fat and sugar are so readily available and relatively cheap.
Nonetheless, recognising that eating well might benefit the planet, as well as the body and brain, might motivate people to change their dietary habits
LDN has some remarkable properties for a range of medical problems. It is safe, effective for most of the conditions listed below, and is becoming more of interest to doctors, the more we know about it.https://ldnresearchtrust.org/ldn-documentaries
Brain & Nervous SystemMultiple SclerosisTreatment
Low-Dose Naltrexone for Treating MS Symptoms
What evidence says about using this opioid addiction drug off-label
By Julie Stachowiak, PhD Medically reviewed by Shaheen Lakhan, MD, PhD on January 05, 2020 Table of Contents
Low-dose naltrexone (LDN), a drug used to treat opioid addiction, is getting a lot of attention as an off-label treatment for multiple sclerosis (MS)—namely, for the reduction of symptoms and relapses. It’s a popular treatment among MS patients, but scientific evidence supporting its use is just beginning to take shape. https://0b8d31a303aaac1e37a3482792ce9746.safeframe.googlesyndication.com/safeframe/1-0-38/html/container.html
That’s not because early results haven’t been promising—they have. Instead, it’s because this is an inexpensive medicine that’s been on the market for decades, meaning pharmaceutical companies have little financial interest in researching it.
In spite of that obstacle, scientists have learned a fair amount about LDN in recent years, and its use as an MS drug has now got a fairly compelling, although still preliminary, body of evidence behind it.
Naltrexone was approved by the U.S. Food and Drug Administration (FDA) in 1984 for the treatment of opioid addiction, and in 1994 to treat alcohol use disorder (AUD). At the full recommended dose—50 to 100 milligram (mg) per day—naltrexone blocks the effect of opioids and reduces a person’s desire to drink.
While these are the only two FDA-approved uses for the drug, it is used for several other health issues in an off-label capacity.
At the time naltrexone was first developed, researchers at the Penn State College of Medicine began studying its use in treating autoimmune disorders (where the immune system mistakenly attacks the body’s own cells). Multiple sclerosis is believed to be an autoimmune disease, with the immune system attacking and destroying the myelin coating of nerve fibers, impeding nerve functioning. https://0b8d31a303aaac1e37a3482792ce9746.safeframe.googlesyndication.com/safeframe/1-0-38/html/container.html
Some research supports the use of LDN for reducing the severity and frequency of MS symptoms. This drug is not considered a disease-modifying therapy. https://0b8d31a303aaac1e37a3482792ce9746.safeframe.googlesyndication.com/safeframe/1-0-38/html/container.html
The suspected effect of LDN is similar to what occurs during pregnancy, in which increased endorphin levels lead to extended MS remissions.
LDN is also being used off-label and/or researched as a treatment for:
- Complex regional pain syndrome
- Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)
- Inflammatory bowel disease (Crohn’s disease, ulcerative colitis)
- Amyotrophic lateral sclerosis (ALS)
- Diabetic neuropathy
- Mesenteric panniculitis
- Postural orthostatic tachycardia syndrome (POTS)
- Mast cell activation syndrome
In addition, it’s been proposed as a treatment for multiple other conditions, including: https://0b8d31a303aaac1e37a3482792ce9746.safeframe.googlesyndication.com/safeframe/1-0-38/html/container.html
- Hashimoto’s thyroiditis
- Parkinson’s disease
- Alzheimer’s disease
- Rheumatoid arthritis
- Sjögren’s syndrome
- Celiac disease
- Restless legs syndrome
Effectiveness in MS
Researchers are beginning to understand the mechanisms of action in LDN, which are significantly different from that of full-strength naltrexone.
LDN is made up of two molecules. One of the molecules, dextro-naltrexone, binds to immune cells. The other, levo-naltrexone, attaches itself to opioid receptors. These actions are dose-dependent, meaning they happen in low doses but not higher ones.
The result of those molecular attachments includes several mechanisms that may lead to improvements in MS symptoms, including:
- Alterations in immune function, including suppression of T cells and B cells, due to increasing endorphin, enkephalin, and opioid growth factor levels
- Lowered neuroinflammation due to the altering of glial cell action in the central nervous system and down-regulating of TH17
- Lowered inflammation in the rest of the body due to the inhibition of proinflammatory immune cells (including cytokines, TNF-a, NF-kB, and TH17)
A review of LDN research published in 2018 noted several beneficial outcomes from peer-reviewed studies using the drug to treat MS, including:
- Safe and well-tolerated
- Significantly reduced spasticity
- Significant benefits for mental health
- Improvement in quality of life
- Reduced fatigue
- Use as a single therapy resulted in stable disease state
However, not all results have been positive or consistent. The review cited:
- One study showing LDN treatment resulted in no significant differences in quality of life, which conflicts with a later study
- One study reporting side effects of insomnia and nightmares in a minority of cases
- A survey that found treatment with LDN didn’t reduce the amount of disease-modifying therapies people were prescribed
LDN is most commonly taken in pill form. Liquid sublingual (under the tongue) and transdermal (through the skin) forms are also available.
The dosages commonly prescribed in people with MS range from 1.5 milligrams (mg) to 4.5 mg per day. It is advised that people with any form of spasticity take no more than 3 mg daily, as it may contribute to muscle stiffness.
Typically, when prescribing doses higher than 1.5 mg, doctors recommend starting at 1.5 mg and gradually increasing the dosage. Be sure to follow your doctor’s instructions and note any increase in side effects when you increase the dose.
Not Available at Standard Pharmacies
Low doses of naltrexone aren’t available from standard pharmacies. You’ll have to get it through a compounding pharmacy where it’s specially made. Some local options may be available, depending on where you live, or you can try a trusted online option.
LDN can be taken with or without food. Some doctors recommend taking it between 9:00 p.m. and midnight to correspond with the body’s natural peak endorphin release. https://0b8d31a303aaac1e37a3482792ce9746.safeframe.googlesyndication.com/safeframe/1-0-38/html/container.html
Naltrexone side effects are infrequent at low doses. The most common side effects include:
- Vivid dreams
- Sleep disturbance/insomnia
- Nausea (typically subsides after about two weeks)
- Constipation or diarrhea
- Morning stiffness
- Dry mouth
Ask your doctor about the sublingual or transdermal forms of LDN if intestinal problems persist; these forms don’t pass through the intestinal tract.
If sleep-related side effects are a problem for you, your doctor may adjust the timing of your dosage.
In rare cases—less than 10 percent—symptoms may temporarily increase. This increase may last for a few weeks or, rarely, up to three months. If this happens to you, talk to your doctor. You may be advised to lower your dosage temporarily.
Considerations and Contraindications
One of the main issues with using LDN is its interaction with many of the disease-modifying drugs used to treat MS. Based on the pharmacokinetic action of the drugs, LDN may interact with interferon drugs, including Avonex, Rebif, or Betaseron. By contrast, there appear to be no conflicts with Copaxone.
Because it is excreted from the body through the liver, LDN is not recommended for people with hepatitis, liver disease, or cirrhosis.
Studies haven’t been done on the use of LDN and opioid medications together. Because of regular-strength naltrexone’s effect on opioid receptors, it’s recommended that you don’t combine LDN with opioid drugs such as OxyContin (oxycodone), Vicodin (hydrocodone-acetaminophen), Ultram (tramadol), or codeine-based cough syrups.
So far, very little data exists on LDN during pregnancy or breastfeeding. Be sure to talk to your doctor if you become pregnant or want to become pregnant while taking this drug.
LDN costs range from about $45 to $100 dollars for a month’s supply, depending on which compounding pharmacy you go through. Because it’s off-label for MS and considered an experimental treatment, your insurance may not cover it. Be sure to check with your carrier.
The pharmacy may make this drug to order rather than keeping it in stock, so you may need to call in refills earlier than you’re used to.