Considering taking Wegovy to lose weight? Here are the risks and benefits – and how it differs from Ozempic
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The weight-loss drug Wegovy is now available in Australia.
Wegovy is administered as a once-weekly injection and is approved specifically for weight management. It’s intended to be used in combination with a reduced-energy diet and increased physical activity.
So how does Wegovy work and how much weight can you expect to lose while taking it? And what are the potential risks – and costs – for those who use it?
Let’s look at what the science says.
What is Wegovy?
Wegovy is a brand name for the medication semaglutide. Semaglutide is a glucagon-like peptide-1 receptor agonist (GLP-1RA). This means it makes your body’s own glucagon-like peptide-1 hormone, called GLP-1 for short, work better.
Normally when you eat, the body releases the GLP-1 hormone which helps signal to your brain that you are full. Semaglutides enhance this effect, leading to a feeling of fullness, even when you haven’t eaten.
Another role of GLP-1 is to stimulate the body to produce more insulin, a hormone which helps lower the level of glucose (sugar) in the blood. That’s why semaglutides have been used for several years to treat type 2 diabetes.
How does Wegovy differ from Ozempic?
Like Wegovy, Ozempic is a semaglutide. The way Wegovy and Ozempic work in the body are essentially the same. They’re made by the same pharmaceutical company, Novo Nordisk.
But there are two differences:
1) They are approved for two different (but related) reasons.
In Australia (and the United States), Ozempic is approved for use to improve blood glucose levels in adults with type 2 diabetes. By managing blood glucose levels effectively, the medication aims to reduce the risk of major complications, such as heart disease.
Wegovy is approved for use alongside diet and exercise for people with a body mass index (BMI) of 30 or greater, or 27 or greater but with other conditions such as high blood pressure.
Wegovy can also be used in people aged 12 years and older. Like Ozempic, Wegovy aims to reduce the risk of future health complications, including heart disease.
2) They are both injected but come in different strengths.
Ozempic is available in pre-loaded single-dose pens with varying dosages of 0.25 mg, 0.5 mg, 1 mg, or 2 mg per injection. The dose can be slowly increased, up to a maximum of 2 mg per week, if needed.
Wegovy is available in prefilled single-dose pens with doses of 0.25 mg, 0.5 mg, 1 mg, 1.7 mg, or 2.4 mg. The treatment starts with a dose of 0.25 mg once weekly for four weeks, after which the dose is gradually increased until reaching a maintenance dose of 2.4 mg weekly.
While it’s unknown what the impact of Wegovy’s introduction will be on Ozempic’s availability, Ozempic is still anticipated to be in low supply for the remainder of 2024.
Is Wegovy effective for weight loss?
Given Wegovy is a semaglutide, there is very strong evidence it can help people lose weight and maintain this weight loss.
A recent study found that over four years, participants taking Wevovy as indicated experienced an average weight loss of 10.2% body weight and a reduction in waist circumference of 7.7cm.
For those who stop taking the medication, analyses have shown that about two-thirds of weight lost is regained.
What are the side effects of Wegovy?
The most common side effects are nausea and vomiting.
However, other serious side effects are also possible because of the whole-of-body impact of the medication. Thyroid tumours and cancer have been detected as a risk in animal studies, yet are rarely seen in human scientific literature.
In the four-year Wegovy trial, 16.6% of participants who received Wegovy (1,461 people) experienced an adverse event that led to them permanently discontinuing their use of the medication. This was higher than the 8.2% of participants (718 people) who received the placebo (with no active ingredient).
Side effects included gastrointestinal disorders (including nausea and vomiting), which affected 10% of people who used Wegovy compared to 2% of people who used the placebo.
Gallbladder-related disorders occurred in 2.8% of people who used Wegovy, and 2.3% of people who received the placebo.
Recently, concerns about suicidal thoughts and behaviours have been raised, after a global analysis reviewed more than 36 million reports of adverse events from semaglutide (Ozempic or Wegovy) since 2000.
There were 107 reports of suicidal thoughts and self-harm among people taking semaglutide, sadly including six actual deaths. When people stopped the medication, 62.5% found the thoughts went away. What we don’t know is whether dose, weight loss, or previous mental health status or use of antidepressants had a role to play.
Finally, concerns are growing about the negative effect of semaglutides on our social and emotional connection with food. Anecdotal and scientific evidence suggests people who use semaglutides significantly reduce their daily dietary intake (as anticipated) by skipping meals and avoiding social occasions – not very enjoyable for people and their loved ones.
How can people access Wegovy?
Wegovy is available for purchase at pharmacists with a prescription from a doctor.
But there is a hefty price tag. Wegovy is not currently subsidised through the Pharmaceutical Benefits Scheme, leaving patients to cover the cost. The current cost is estimated at around A$460 per month dose.
If you’re considering Wegovy, make an appointment with your doctor for individual advice.
Lauren Ball, Professor of Community Health and Wellbeing, The University of Queensland and Emily Burch, Accredited Practising Dietitian and Lecturer, Southern Cross University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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What I Wish People Knew About Dementia – by Dr. Wendy Mitchell
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We hear a lot from doctors who work with dementia patients; sometimes we hear from carers too. In this case, the author spent 20 years working for the NHS, before being diagnosed with young-onset dementia, at the age of 58. Like many health industry workers who got a life-changing diagnosis, she quickly found it wasn’t fun being on the other side of things, and vowed to spend her time researching, and raising awareness about, dementia.
Many people assume that once a person has dementia, they’re basically “gone before they’re gone”, which can rapidly become a self-fulfilling prophecy as that person finds themself isolated and—though this word isn’t usually used—objectified. Talked over, viewed (and treated) more as a problem than a person. Cared for hopefully, but again, often more as a patient than a person. If doctors struggle to find the time for the human side of things with most patients most of the time, this is only accentuated when someone needs more time and patience than average.
Instead, Dr. Mitchell—an honorary doctorate, by the way, awarded for her research—writes about what it’s actually like to be a human with dementia. Everything from her senses, how she eats, the experience of eating in care homes, the process of boiling an egg… To relationships, how care changes them, to the challenges of living alone. And communication, confusion, criticism, the language used by professionals, or how things are misrepresented in popular media. She also talks about the shifting sense of self, and brings it all together with gritty optimism.
The style is deeply personal, yet lucid and clear. While dementia is most strongly associated with memory loss and communication problems, this hasn’t affected her ability to write well (7 years into her diagnosis, in case you were wondering).
Bottom line: if you’d like to read a first-person view of dementia, then this is an excellent opportunity to understand it from the view of, as the subtitle goes, someone who knows.
Click here to check out What I Wish People Knew About Dementia, and then know those things!
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The Emperor’s New Klotho, Or Something More?
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Unzipping The Genes Of Aging?
Klotho is an enzyme encoded in humans’ genes—specifically, in the KL gene.
It’s found throughout all living parts of the human body (and can even circulate about in its hormonal form, or come to rest in its membranaceous form), and its subgroups are especially found:
- α-klotho: in the brain
- β-klotho: in the liver
- γ-klotho: in the kidneys
Great! Why do we care?
Klotho, its varieties and variants, its presence or absence, are very important in aging.
Almost every biological manifestation of aging in humans has some klotho-related indicator; usually the decrease or mutation of some kind of klotho.
Which way around the cause and effect go has been the subject of much debate and research: do we get old because we don’t have enough klotho, or do we make less klotho because we’re getting old?
Of course, everything has to be tested per variant and per system, so that can take a while (punctuated by research scientists begging for more grants to do the next one). Given that it’s about aging, testing in humans would take an incredibly long while, so most studies so far have been rodent studies.
The general gist of the results of rodent studies is “reduced klotho hastens aging; increased klotho slows it”.
(this can be known by artificially increasing or decreasing the level of klotho expression, again something easier in mice as it is harder to arrange transgenic humans for the studies)
Here’s one example of many, of that vast set of rodent studies:
Suppression of Aging in Mice by the Hormone Klotho
Relevance for Alzheimer’s, and a science-based advice
A few years ago (2020), an Alzheimer’s study was undertaken; they noted that the famous apolipoprotein E4 (apoE4) allele is the strongest genetic risk factor for Alzheimer’s, and that klotho may be another. FGF21 (secreted by the liver, mostly during fasting) binds to its own receptor (FGFR1) and its co-receptor β-klotho. Since this is a known neuroprotective factor, they wondered whether klotho itself may interact with β-amyloid (Aβ), and found:
❝Aβ can enhance the ability of klotho to draw FGF21 to regions of incipient neurodegeneration in AD❞
In other words: β-amyloid, the substance whose accumulation is associated with neurodegeneration in Alzheimer’s disease, is a mediator in klotho bringing a known neuroprotective factor, FGF21, to the areas of neurodegeneration
In fewer words: klotho calls the firefighters to the scene of the fire
Read more: Alignment of Alzheimer’s disease amyloid β-peptide and klotho
The advice based on this? Consider practicing intermittent fasting, if that is viable for you, as it will give your liver more FGF21-secreting time, and the more FGF21, the more firefighters arrive when klotho sounds the alarm.
See also: Intermittent Fasting: What’s the truth?
…and while you’re at it:
Does intermittent fasting have benefits for our brain?
A more recent (2023) study with a slightly different (but connected) purpose, found results consistent with this:
Longevity factor klotho enhances cognition in aged nonhuman primates
…and, for that matter this (2023) study that found:
Associations between klotho and telomere biology in high stress caregivers
…which looks promising, but we’d like to see it repeated with a sounder method (they sorted caregiving into “high-stress” and “low-stress” depending on whether a child was diagnosed with ASD or not, which is by no means a reliable way of sorting this). They did ask for reported subjective stress levels, but to be more objective, we’d like to see clinical markers of stress (e.g. cortisol levels, blood pressure, heart rate changes, etc).
A very recent (April 2024) study found that it has implications for more aspects of aging—and this time, in humans (but using a population-based cohort study, rather than lab conditions):
Can I get it as a supplement?
Not with today’s technology and today’s paucity of clinical trials, you can’t. Maybe in the future!
However… The presence of senescent (old, badly copied, stumbling and staggering onwards when they should have been killed and eaten and recycled already) cells actively reduces klotho levels, which means that taking supplements that are senolytic (i.e., that kill those senescent cells) can increase serum klotho levels:
Orally-active, clinically-translatable senolytics restore α-Klotho in mice and humans
Ok, what can I take for that?
We wrote about a senolytic supplement that you might enjoy, recently:
Fisetin: The Anti-Aging Assassin
Want to know more?
If you have the time, Dr. Peter Attia interviews Dr. Dena Dubal (researcher in several of the above studies) here:
Click Here If The Embedded Video Doesn’t Load Automatically
Enjoy!
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MSG vs. Salt: Sodium Comparison
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It’s Q&A Day at 10almonds!
Q: Is MSG healthier than salt in terms of sodium content or is it the same or worse?
Great question, and for that matter, MSG itself is a great topic for another day. But your actual question, we can readily answer here and now:
- Firstly, by “salt” we’re assuming from context that you mean sodium chloride.
- Both salt and MSG do contain sodium. However…
- MSG contains only about a third of the sodium that salt does, gram-for-gram.
- It’s still wise to be mindful of it, though. Same with sodium in other ingredients!
- Baking soda contains about twice as much sodium, gram for gram, as MSG.
Wondering why this happens?
Salt (sodium chloride, NaCl) is equal parts sodium and chlorine, by atom count, but sodium’s atomic mass is lower than chlorine’s, so 100g of salt contains only 39.34g of sodium.
Baking soda (sodium bicarbonate, NaHCO₃) is one part sodium for one part hydrogen, one part carbon, and three parts oxygen. Taking each of their diverse atomic masses into account, we see that 100g of baking soda contains 27.4g sodium.
MSG (monosodium glutamate, C₅H₈NO₄Na) is only one part sodium for 5 parts carbon, 8 parts hydrogen, 1 part nitrogen, and 4 parts oxygen… And all those other atoms put together weigh a lot (comparatively), so 100g of MSG contains only 12.28g sodium.
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Prolonged Grief: A New Mental Disorder?
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The issue is not whether certain mental conditions are real—they are. It is how we conceptualize them and what we think treating them requires.
The latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) features a new diagnosis: prolonged grief disorder—used for those who, a year after a loss, still remain incapacitated by it. This addition follows more than a decade of debate. Supporters argued that the addition enables clinicians to provide much-needed help to those afflicted by what one might simply consider a too much of grief, whereas opponents insisted that one mustn’t unduly pathologize grief and reject an increasingly medicalized approach to a condition that they considered part of a normal process of dealing with loss—a process which in some simply takes longer than in others.
By including a condition in a professional classification system, we collectively recognize it as real. Recognizing hitherto unnamed conditions can help remove certain kinds of disadvantages. Miranda Fricker emphasizes this in her discussion of what she dubs hermeneutic injustice: a specific sort of epistemic injustice that affects persons in their capacity as knowers1. Creating terms like ‘post-natal depression’ and ‘sexual harassment’, Fricker argues, filled lacunae in the collectively available hermeneutic resources that existed where names for distinctive kinds of social experience should have been. The absence of such resources, Fricker holds, put those who suffered from such experiences at an epistemic disadvantage: they lacked the words to talk about them, understand them, and articulate how they were wronged. Simultaneously, such absences prevented wrong-doers from properly understanding and facing the harm they were inflicting—e.g. those who would ridicule or scold mothers of newborns for not being happier or those who would either actively engage in sexual harassment or (knowingly or not) support the societal structures that helped make it seem as if it was something women just had to put up with.
For Fricker, the hermeneutical disadvantage faced by those who suffer from an as-of-yet ill-understood and largely undiagnosed medical condition is not an epistemic injustice. Those so disadvantaged are not excluded from full participation in hermeneutic practices, or at least not through mechanisms of social coercion that arise due to some structural identity prejudice. They are not, in other words, hermeneutically marginalized, which for Fricker, is an essential characteristic of epistemic injustice. Instead, their situation is simply one of “circumstantial epistemic bad luck”2. Still, Fricker, too, can agree that providing labels for ill-understood conditions is valuable. Naming a condition helps raise awareness of it, makes it discursively available and, thus, a possible object of knowledge and understanding. This, in turn, can enable those afflicted by it to understand their experience and give those who care about them another way of nudging them into seeking help.
Surely, if adding prolonged grief disorder to the DSM-5 were merely a matter of recognizing the condition and of facilitating assistance, nobody should have any qualms with it. However, the addition also turns intense grief into a mental disorder—something for whose treatment insurance companies can be billed. With this, significant forces of interest enter the scene. The DSM-5, recall, is mainly consulted by psychiatrists. In contrast to talk-therapists like psychotherapists or psychoanalysts, psychiatrists constitute a highly medicalized profession, in which symptoms—clustered together as syndromes or disorders—are frequently taken to require drugs to treat them. Adding prolonged grief disorder thus heralds the advent of research into various drug-based grief therapies. Ellen Barry of the New York Times confirms this: “naltrexone, a drug used to help treat addiction,” she reports, “is currently in clinical trials as a form of grief therapy”, and we are likely to see a “competition for approval of medicines by the Food and Drug Administration.”3
Adding diagnoses to the DSM-5 creates financial incentives for players in the pharmaceutical industry to develop drugs advertised as providing relief to those so diagnosed. Surely, for various conditions, providing drug-induced relief from severe symptoms is useful, even necessary to enable patients to return to normal levels of functioning. But while drugs may help suppress feelings associated with intense grief, they cannot remove the grief. If all mental illnesses were brain diseases, they might be removed by adhering to some drug regimen or other. Note, however, that ‘mental illness’ is a metaphor that carries the implicit suggestion that just like physical illnesses, mental afflictions, too, are curable by providing the right kind of physical treatment. Unsurprisingly, this metaphor is embraced by those who stand to massively benefit from what profits they may reap from selling a plethora of drugs to those diagnosed with any of what seems like an ever-increasing number of mental disorders. But metaphors have limits. Lou Marinoff, a proponent of philosophical counselling, puts the point aptly:
Those who are dysfunctional by reason of physical illness entirely beyond their control—such as manic-depressives—are helped by medication. For handling that kind of problem, make your first stop a psychiatrist’s office. But if your problem is about identity or values or ethics, your worst bet is to let someone reify a mental illness and write a prescription. There is no pill that will make you find yourself, achieve your goals, or do the right thing.
Much more could be said about the differences between psychotherapy, psychiatry, and the newcomer in the field: philosophical counselling. Interested readers may benefit from consulting Marinoff’s work. Written in a provocative, sometimes alarmist style, it is both entertaining and—if taken with a substantial grain of salt—frequently insightful. My own view is this: from Fricker’s work, we can extract reasons to side with the proponents of adding prolonged grief disorder to the DSM-5. Creating hermeneutic resources that allow us to help raise awareness, promote understanding, and facilitate assistance is commendable. If the addition achieves that, we should welcome it. And yet, one may indeed worry that practitioners are too eager to move from the recognition of a mental condition to the implementation of therapeutic interventions that are based on the assumption that such afflictions must be understood on the model of physical disease. The issue is not whether certain mental conditions are real—they are. It is how we conceptualize them and what we think treating them requires.
No doubt, grief manifests physically. It is, however, not primarily a physical condition—let alone a brain disease. Grief is a distinctive mental condition. Apart from bouts of sadness, its symptoms typically include the loss of orientation or a sense of meaning. To overcome grief, we must come to terms with who we are or can be without the loved one’s physical presence in our life. We may need to reinvent ourselves, figure out how to be better again and whence to derive a new purpose. What is at stake is our sense of identity, our self-worth, and, ultimately, our happiness. Thinking that such issues are best addressed by popping pills puts us on a dangerous path, leading perhaps towards the kind of dystopian society Aldous Huxley imagined in his 1932 novel Brave New World. It does little to help us understand, let alone address, the moral and broader philosophical issues that trouble the bereaved and that lie at the root not just of prolonged grief but, arguably, of many so-called mental illnesses.
Footnotes:
1 For this and the following, cf. Fricker 2007, chapter 7.
2 Fricker 2007: 152
3 Barry 2022
References:
Barry, E. (2022). “How Long Should It Take to Grieve? Psychiatry Has Come Up With an Answer.” The New York Times, 03/18/2022, URL = https://www.nytimes.com/2022/03/18/health/prolonged-grief-
disorder.html [last access: 04/05/2022])
Fricker, M. (2007). Epistemic Injustice. Power & the Ethics of knowing. Oxford/New York: Oxford University Press.
Huxley, A. (1932). Brave New World. New York: Harper Brothers.
Marinoff, L. (1999). Plato, not Prozac! New York: HarperCollins Publishers.Professor Raja Rosenhagen is currently serving as Assistant Professor of Philosophy, Head of Department, and Associate Dean of Academic Affairs at Ashoka University. He earned his PhD in Philosophy from the University of Pittsburgh and has a broad range of philosophical interests (see here). He wrote this article a) because he was invited to do so and b) because he is currently nurturing a growing interest in philosophical counselling.
This article is republished from OpenAxis under a Creative Commons license. Read the original article.
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Neuroaffirming care values the strengths and differences of autistic people, those with ADHD or other profiles. Here’s how
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We’ve come a long way in terms of understanding that everyone thinks, interacts and experiences the world differently. In the past, autistic people, people with attention deficit hyperactive disorder (ADHD) and other profiles were categorised by what they struggled with or couldn’t do.
The concept of neurodiversity, developed by autistic activists in the 1990s, is an emerging area. It promotes the idea that different brains (“neurotypes”) are part of the natural variation of being human – just like “biodiversity” – and they are vital for our survival.
This idea is now being applied to research and to care. At the heart of the National Autism Strategy, currently in development, is neurodiversity-affirming (neuroaffirming) care and practice. But what does this look like?
Reframing differences
Neurodiversity challenges the traditional medical model of disability, which views neurological differences solely through a lens of deficits and disorders to be treated or cured.
Instead, it reframes it as a different, and equally valuable, way of experiencing and navigating the world. It emphasises the need for brains that are different from what society considers “neurotypical”, based on averages and expectations. The term “neurodivergent” is applied to Autistic people, those with ADHD, dyslexia and other profiles.
Neuroaffirming care can take many forms depending on each person’s needs and context. It involves accepting and valuing different ways of thinking, learning and experiencing the world. Rather than trying to “fix” or change neurodivergent people to fit into a narrow idea of what’s considered “normal” or “better”, neuroaffirming care takes a person-centered, strengths-based approach. It aims to empower and support unique needs and strengths.
Adaptation and strengths
Drawing on the social model of disability, neuroaffirming care acknowledges there is often disability associated with being different, especially in a world not designed for neurodivergent people. This shift focuses away from the person having to adapt towards improving the person-environment fit.
This can include providing accommodations and adapting environments to make them more accessible. More importantly, it promotes “thriving” through greater participation in society and meaningful activities.
At school, at work, in clinic
In educational settings, this might involve using universal design for learning that benefits all learners.
For example, using systematic synthetic phonics to teach reading and spelling for students with dyslexia can benefit all students. It also could mean incorporating augmentative and alternative communication, such as speech-generating devices, into the classroom.
Teachers might allow extra time for tasks, or allow stimming (repetitive movements or noises) for self-regulation and breaks when needed.
In therapy settings, neuroaffirming care may mean a therapist grows their understanding of autistic culture and learns about how positive social identity can impact self-esteem and wellbeing.
They may make efforts to bridge the gap in communication between different neurotypes, known as the double empathy problem. For example, the therapist may avoid relying on body language or facial expressions (often different in autistic people) to interpret how a client is feeling, instead of listening carefully to what the client says.
Affirming therapy approaches with children involve “tuning into” their preferred way of communicating, playing and engaging. This can bring meaningful connection rather than compliance to “neurotypical” ways of playing and relating.
In workplaces, it can involve flexible working arrangements (hours, patterns and locations), allowing different modes of communication (such as written rather than phone calls) and low-sensory workspaces (for example, low-lighting, low-noise office spaces).
In public spaces, it can look like providing a “sensory space”, such as at large concerts, where neurodivergent people can take a break and self-regulate if needed. And staff can be trained to recognise, better understand and assist with hidden disabilities.
Combining lived experience and good practice
Care is neuroaffirmative when it centres “lived experience” in its design and delivery, and positions people with disability as experts.
As a result of being “different”, people in the neurodivergent community experience high rates of bullying and abuse. So neuroaffirming care should be combined with a trauma-informed approach, which acknowledges the need to understand a person’s life experiences to provide effective care.
Culturally responsive care acknowledges limited access to support for culturally and racially marginalised Autistic people and higher rates of LGBTQIA+ identification in the neurodivergent community.
Authentic selves
The draft National Autism Strategy promotes awareness that our population is neurodiverse. It hopes to foster a more inclusive and understanding society.
It emphasises the societal and public health responsibilities for supporting neurodivergent people via public education, training, policy and legislation. By providing spaces and places where neurodivergent people can be their authentic, unmasked selves, we are laying the foundations for feeling seen, valued, safe and, ultimately, happy and thriving.
The author would like to acknowledge the assistance of psychologist Victoria Gottliebsen in drafting this article. Victoria is a member of the Oversight Council for the National Autism Strategy.
Josephine Barbaro, Associate Professor, Principal Research Fellow, Psychologist, La Trobe University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Everything You Need To Know About The Menopause – by Kate Muir
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Kate Muir has made a career out of fighting for peri-menopausal health to be taken seriously. Because… it’s actually far more serious than most people know.
What people usually know:
- No more periods
- Hot flushes
- “I dunno, some annoying facial hairs maybe”
The reality encompasses a lot more, and Muir covers topics including:
- Workplace struggles (completely unnecessary ones)
- Changes to our sex life (not usually good ones, by default!)
- Relationship between menopause and breast cancer
- Relationship between menopause and Alzheimer’s
“Wait”, you say, “correlation is not causation, that last one’s just an age thing”, and that’d be true if it weren’t for the fact that receiving Hormone Replacement Therapy (HRT) or not is strongly correlated with avoiding Alzheimer’s or not.
The breast cancer thing is not to be downplayed either. Taking estrogen comes with a stated risk of breast cancer… But what they don’t tell you, is that for many people, not taking it comes with a higher risk of breast cancer (but that’s not the doctor’s problem, in that case). It’s one of those situations where fear of litigation can easily overrule good science.
This kind of thing, and much more, makes up a lot of the meat of this book.
Hormonal treatment for the menopause is often framed in the wider world as a whimsical luxury, not a serious matter of health…. If you’ve ever wondered whether you might want something different, something better, as part of your general menopause plan (you have a plan for this important stage of your life, right?), this is a powerful handbook for you.
Additionally, if (like many!) you justifiably fear your doctor may brush you off (or in the case of mood disorders, may try to satisfy you with antidepressants to treat the symptom, rather than HRT to treat the cause), this book will arm you as necessary to help you get what you need.
Grab your copy of “Everything You Need To Know About The Menopause” from Amazon today!
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