Why Everything Hurts in Menopause
If you have reached your mid-forties or beyond and found that your body has started to ache in ways it never used to, your knees, your back, or an old injury you thought had healed years ago, you are describing something a great many women experience, and something that can often be explained by the biology of the menopause transition. The aches may be widespread, they move around, and they rarely point to a single thing a scan can find, and that combination is what makes this kind of pain so easy to dismiss, both by the women living with it and sometimes by the clinicians they see. What follows is what the evidence shows about why it happens, how strong that evidence is, and what helps.
Oestrogen changes how your body handles pain
Oestrogen has a role in pain, and the clearest human evidence comes from brain-imaging research at the University of Michigan. Researchers scanned healthy women twice, once when their oestrogen was low and once when it was high, while a steady, controlled muscle pain was maintained, and measured the brain's own pain-relieving system as they did.[1] When oestrogen was high, the women's brains released more of their own natural painkillers during the pain, the endogenous opioid system that quietly dampens everyday aches. When oestrogen was low, that same system went quiet in the deep brain regions that handle pain, and the women rated the identical pain as worse.
This was a small study of only eight women whose oestrogen was adjusted with a patch rather than women moving through menopause, but it demonstrates the mechanisms involved in pain perception. What it helps show is that oestrogen influences how much pain relief your own brain can generate, and that when oestrogen falls, some of that built-in relief reduces with it. Oestrogen receptors sit all the way along the pain pathway, from the nerves in your skin through your spinal cord to your brain, which is why a change in oestrogen can be felt at so many points at once.[2]
When the pain system itself becomes more sensitive
Not all pain comes from damage in the tissue. Sometimes the problem lies in the volume of the signal rather than its source, and this is one of the most useful ideas in modern pain science for understanding midlife pain. When the nervous system becomes sensitised, it amplifies pain signals and keeps the volume turned up even when there is little or no remaining damage to the tissue itself.[3] This is part of why light pressure can hurt, why pain spreads to areas that are perfectly healthy, why old injuries seem to reawaken, and why your scans can come back clear while your pain remains entirely real.
Pain that is widespread, that moves around, and that is out of proportion to anything an image can explain has a name in current pain science, nociplastic pain, where the pain response has itself become more sensitive. Recognising that pattern matters because it can change the treatment approach, though it is worth being clear that widespread pain with a normal scan does not by itself establish nociplastic pain, which needs a compatible clinical pattern rather than the absence of a finding.
What turns the volume up further
Three things sit alongside the hormonal change and add to the load.
The evidence is strongest for sleep. In experimental studies, depriving healthy people of sleep lowers their pain threshold, and even modest night-to-night dips in sleep quality predict more pain the following day.[4] Broken sleep is one of the most common features of the menopause transition, and while research looking specifically at sleep and pain in postmenopausal women is still limited, the wider evidence that poor sleep worsens pain is strong and consistent, so addressing the causes and triggers of broken sleep can make a real difference to how much you hurt.
The evidence for mood is also good. Pain and low mood draw on overlapping circuits in the brain, so anxiety and low spirits can raise how much pain reaches you, and that shared wiring helps explain why pain tolerance shifts when mood does.
The evidence on inflammation is more nuanced, and worth stating carefully. The strongest menopause-specific data comes from a study that followed women over many years and reported inflammatory markers rising around the final menstrual period in a large majority of them, clustering around that time rather than simply tracking age.[5] What is less clear is oestrogen's role, because oestrogen is not straightforwardly anti-inflammatory, and its effect depends on the dose and the tissue, which is part of why MHT settles joint symptoms for some women and not others.[6]
Why women carry more of this than men
Women live with more chronic pain conditions than men, from migraine and fibromyalgia to irritable bowel syndrome and most autoimmune pain conditions, and that pattern is clear in large population data across countries.[7] In 2015 researchers reported that in mice, male and female bodies used different immune cells to produce the same pain, so blocking the cell driving pain in males stopped the pain in males but not in females, because the female nervous system was running the pain through a different pathway entirely.[8] The difference between women and men in pain is not only how much, it is partly the machinery itself.
These findings come from pain research broadly rather than from menopause specifically, so applying them to midlife is a reasonable extension rather than a tested claim, and it should be read that way. The reasonable reading, supported by the Michigan evidence that oestrogen shapes the brain's own pain relief, is that women may not gain a new pain signal at menopause so much as lose a protection they have carried for decades. In that study, when the women's oestrogen was high their brains released as much of their own pain relief during pain as the men's did and the difference between the sexes disappeared, and when their oestrogen was low that relief dropped below the men's and their pain ratings rose.
What the evidence says helps
The encouraging part is that several of the things that turn this pain up are things you can influence.
Sleep comes first, because on current evidence it does the most, and a regular bedtime and a cooler, darker room can influence how much you hurt the next day.[4]
Movement matters next, and the principle is little and often rather than heroic. Loading your muscles and joints gently keeps them strong and signals to a sensitised nervous system that movement is safe, and as a Clinical Myotherapist it is where I most often see women begin to turn a corner.
Your stress load and your mood come alongside it, because pain and low mood share the same wiring, so anything that settles your nervous system, whether that is slower breathing, time outdoors, or proper support for your mental health, tends to take some of the edge off the pain as well.
For some women, increasing oestrogen with MHT is part of the answer, particularly when pain sits alongside other menopause symptoms. The evidence here is mixed rather than settled, with a large 2026 review finding no significant overall effect of MHT on general muscle and joint pain, which is why this is best approached as a conversation with your GP built around your own history rather than as a guaranteed fix.[9]
What to say at your GP appointment
Walking in able to describe the pattern changes the conversation, so it helps to say something like this: my pain is widespread, it shifts around, it is worse when I sleep badly, and it began to line up with my other menopause symptoms. From there you can ask directly whether your symptoms could be part of the transition, and whether anything on your list, from sleep to MHT, is worth trying, and it is reasonable to ask for a longer appointment if you have several things to cover. If you feel dismissed, treat that as information rather than a verdict on you, because it is reasonable to look for a GP with an interest in menopause, and bringing a couple of weeks of notes makes a real difference, since a clear pattern on paper is far harder to wave away than a tired description at the end of a busy appointment.
In simple terms
Falling oestrogen reduces how much of its own pain relief your brain can generate.
When the pain system itself becomes more sensitised, pain can be widespread and real even when every scan is clear.
Sleep, mood and inflammation each add to the load, and of the three, sleep has the strongest evidence.
Women carry more chronic pain partly through different biology, not weaker tolerance, and MHT is worth discussing with your GP when pain sits alongside other menopause symptoms.
Medical terms,
Endogenous opioid system: the brain's own natural pain-relief chemistry.
Central sensitisation: increased responsiveness of pain-processing neurons in the spinal cord and brain, turning the volume up on pain.
Nociplastic pain: pain from altered processing that is not fully explained by tissue damage or nerve disease.
Inflammatory markers: blood signals that indicate inflammation somewhere in the body.
References
[1] Smith YR, Stohler CS, Nichols TE, Bueller JA, Koeppe RA, Zubieta JK. Pronociceptive and antinociceptive effects of estradiol through endogenous opioid neurotransmission in women. Journal of Neuroscience. 2006;26(21):5777–5785. (n=8; oestradiol adjusted by patch; mechanistic.)
[2] Chen Q, Zhang W, Sadana N, Chen X. Estrogen receptors in pain modulation: cellular signaling. Biology of Sex Differences. 2021;12:22.
[3] Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain. 2011;152(3 Suppl):S2–S15.
[4] Krause AJ, Prather AA, Wager TD, Lindquist MA, Walker MP. The pain of sleep loss: a brain characterization in humans. Journal of Neuroscience. 2019;39(12):2291–2300. (Experimental sleep loss lowers pain threshold.)
[5] El Khoudary SR, Chen X, Qi M, Matthews KA, Karlamangla AS, Gold EB, Harlow SD, Thurston RC, Joffe H, Pavlovic J, Greendale GA. The relation between systemic inflammation and the menopause transition: the Study of Women's Health Across the Nation. J Clin Endocrinol Metab. 2025 Oct 16;110(11):e3566–e3576. doi:10.1210/clinem/dgaf175. PMID:40123296; PMCID:PMC12527447.
[6] Straub RH. The complex role of estrogens in inflammation. Endocrine Reviews. 2007;28(5):521–574.
[7] Mogil JS. Qualitative sex differences in pain processing. Nature Reviews Neuroscience. 2020;21(7):353–365; Bartley EJ, Fillingim RB. Sex differences in pain. British Journal of Anaesthesia. 2013;111(1):52–58.
[8] Sorge RE, Mapplebeck JCS, Rosen S, et al. Different immune cells mediate mechanical pain hypersensitivity in male and female mice. Nature Neuroscience. 2015;18(8):1081–1083.
[9] Overton R, et al. The effect of menopausal hormone therapy on musculoskeletal pain: a systematic review and meta-analysis. Post Reproductive Health. 2026;32(1):52–68.
This information is educational only and does not constitute personal medical advice. Always consult a qualified health professional about your individual circumstances.
© Menopause Hub 2026.
Anna Pattison. Former Registered Nurse, Clinical Myotherapist, Menopause Mentor.
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