Blood sugar is designed to rise and fall across the day. It’s shaped by what we eat, how we move, how we sleep, and even how stressed we feel. And because these inputs impact our hormonal outputs, glucose swings don’t stay confined to energy: they ripple through the endocrine system and influence metabolism, appetite, mood, and reproductive signalling. When glycaemic control is consistently poor, the downstream effects can show up as fatigue, easier weight gain, irregular cycles and disrupted fertility markers, and higher cardiometabolic risk, even in people who don’t meet the criteria for diabetes. By contrast, steadier blood sugar creates a calmer internal environment and supports more predictable hormonal messaging, more stable energy, and better long-term regulation throughout the body. Before we dive into hormones, here’s a quick crash course on blood sugar.
A Quick 101 on Blood Sugar
Blood glucose refers to the concentration of glucose (sugar) circulating in the bloodstream. It’s the body’s primary fuel, particularly for the brain, and comes from three different sources: dietary carbohydrates, stored glycogen in the muscles and liver, and via gluconeogenesis (the production of glucose from non-carbohydrate substrates). After we eat , glucose rises and triggers the release of insulin to facilitate uptake of glucose into the cells to either use or store. In between meals and once insulin levels have dropped, another regulatory hormone called glucagon promotes the release of glucose stores to use as energy. These natural ‘spikes’ and falls are normal, and in healthy individuals, produce a controlled post-meal rise followed by a gradual return to baseline. When we eat sugar in excess, this balance can be thrown off. A high-sugar meal tends to raise blood glucose rapidly and prompts a larger insulin response to move glucose out of the bloodstream.
The result is often a steep rise followed by an equally steep drop, which leaves us light-headed, shaky, and suddenly ravenous, even if we've just eaten. In some cases, the body also recruits cortisol to help stabilise blood sugar, effectively treating the swing as a physiological stressor. This is why keeping blood glucose steady is one of the most impactful levers for consistent energy: when the system is repeatedly destabilised, we rely more heavily on counter-regulatory hormones and metabolic “workarounds” to restore balance. (1) Now, let’s move on to how this impacts our hormones.
Blood Sugar + Sex Hormones
Insulin sensitivity naturally fluctuates across the menstrual cycle - meaning our bodies don’t handle the same meal in the same way each week. Oestrogen generally supports insulin sensitivity and helps our cells take up and use glucose more efficiently. Progesterone, which is dominant in the luteal phase (after ovulation), shifts the body in the opposite direction: our cells become less responsive to insulin and our energy needs rise. In practical terms, the same meals can lead to bigger blood sugar swings, and we may notice more cravings, less stable energy, or feeling hungrier more quickly. In men, insulin resistance over time is associated with lower testosterone levels, and in women, it can stimulate ovarian androgen production, contributing to acne, hirsutism, and metabolic dysfunction - patterns commonly observed in PCOS. (2,3 4)
Blood Sugar, Hunger Hormones + Weight Regulation
Blood sugar dynamics directly influence the hormones that regulate our appetite. Leptin is a hormone that switches hunger off, but chronic high insulin/sugar impairs leptin signalling – which makes it more difficult for us to feel full. On the other side we have Ghrelin, the main hunger hormone, which rises when blood sugar falls to switch hunger on. When the input (food) is balanced, these hormones rise and fall naturally and gradually, but, rapid sugar spikes followed by sharp declines, typical after high-glycaemic meals, trigger rebound hunger and increases calorie intake.
Controlled feeding studies demonstrate that high-glycaemic meals increase hunger and later energy intake compared with lower-glycaemic alternatives. (5,6) In real life, this often looks like sudden hunger and sweet cravings as early as an hour or two - despite having had a “proper” meal. In the luteal phase, this is amplified by the reasons we’ve already touched on.
Blood Sugar + Thyroid Function
Our thyroid is often ignored, but it’s incredibly important to every aspect of our metabolism. The relationship between sugar regulation and thyroid function is bidirectional. In simple terms, Thyroid hormones help set our metabolic “speed,” which influencers our basal metabolic rate and how efficiently we use glucose for energy. But when blood sugar becomes unstable, the body switches on stress pathways which affect thyroid hormone activity. Low blood sugar triggers stress hormones - cortisol and adrenaline - which reduces the conversion of T4 into active T3 and increases production of reverse T3 (an inactive form that competes with T3). Over time, chronic under-fuelling or erratic intake can create a cycle of more volatile blood sugar and more symptoms linked with lower thyroid output; think flatter energy, feeling colder, slower digestion, and stubborn fatigue. (7,8)
Across the menstrual cycle, the thyroid–blood sugar link often becomes more noticeable because ovarian hormones shift insulin sensitivity and stress reactivity. In the follicular phase, higher oestrogen supports better glucose handling, so blood sugar stays steadier and we have less of a reliance on cortisol and adrenaline. In the luteal phase, progesterone rises, insulin sensitivity duces, and energy needs increase - so missed meals, longer gaps between eating, or high-glycaemic choices more easily produce dips and spikes. Those swings trigger more counter-regulatory hormones, which reduces T4-to-T3 conversion and increases reverse T3, making thyroid signalling less effective when many of us already feel more tired, hungry, or prone to cravings.
In perimenopause, fluctuating and overall declining oestrogen can amplify this pattern. With less consistent oestrogen support, glucose control becomes less predictable, sleep disruption is common, and stress is higher - all of which increases reliance on cortisol and adrenaline to stabilise blood sugar. That hormonal backup system feeds into thyroid hormone conversion, so symptoms can overlap and reinforce each other: energy crashes, stronger cravings, feeling wired-and-tired, poorer tolerance to fasting or under-eating, and a general sense that metabolism feels less resilient than it used to.
Using blood sugar as an example, it’s easy to see that hormonal systems don't operate in isolation and instead, are an interconnected system that react to energy availability and metabolic signalling. Blood sugar stability underpins the function of reproductive, thyroid, appetite, and stress hormones alike and while individual responses can vary, consistent daily habits - balanced meals, adequate energy intake, sleep, and stress management – will compound over time and build a more resilient baseline. In many cases, addressing glycaemic stability is a foundational step toward broader hormonal health.
References
Nakrani MN, Wineland RH, Anjum F. Physiology, Glucose Metabolism. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560599/
MacGregor KA, Gallagher IJ, Moran CN. Relationship Between Insulin Sensitivity and Menstrual Cycle Is Modified by BMI, Fitness, and Physical Activity in NHANES. J Clin Endocrinol Metab. 2021 Sep 27;106(10):2979-2990. doi: 10.1210/clinem/dgab415. PMID: 34111293; PMCID: PMC8475204.
Yeung EH, Zhang C, Mumford SL, Ye A, Trevisan M, Chen L, Browne RW, Wactawski-Wende J, Schisterman EF. Longitudinal study of insulin resistance and sex hormones over the menstrual cycle: the BioCycle Study. J Clin Endocrinol Metab. 2010 Dec;95(12):5435-42. doi: 10.1210/jc.2010-0702. Epub 2010 Sep 15. PMID: 20843950; PMCID: PMC2999972.
Zarei S, Mosalanejad L, Ghobadifar MA. Blood glucose levels, insulin concentrations, and insulin resistance in healthy women and women with premenstrual syndrome: a comparative study. Clin Exp Reprod Med. 2013 Jun;40(2):76-82. doi: 10.5653/cerm.2013.40.2.76. Epub 2013 Jun 30. Erratum in: Clin Exp Reprod Med. 2013 Sep;40(3):141. PMID: 23875163; PMCID: PMC3714432.
Kellerer M, Lammers R, Fritsche A, Strack V, Machicao F, Borboni P, Ullrich A, Häring HU. Insulin inhibits leptin receptor signalling in HEK293 cells at the level of janus kinase-2: a potential mechanism for hyperinsulinaemia-associated leptin resistance. Diabetologia. 2001 Sep;44(9):1125-32. doi: 10.1007/s001250100614. PMID: 11596667.
Mirza NM, Klein CJ, Palmer MG, McCarter R, He J, Ebbeling CB, Ludwig DS, Yanovski JA. Effects of high and low glycemic load meals on energy intake, satiety and hunger in obese Hispanic-American youth. Int J Pediatr Obes. 2011 Jun;6(2-2):e523-31. doi: 10.3109/17477166.2010.544740. Epub 2011 Feb 10. PMID: 21309658; PMCID: PMC3128645.
Eom YS, Wilson JR, Bernet VJ. Links between Thyroid Disorders and Glucose Homeostasis. Diabetes Metab J. 2022 Mar;46(2):239-256. doi: 10.4093/dmj.2022.0013. Epub 2022 Mar 24. PMID: 35385635; PMCID: PMC8987680.
Brenta G. Why can insulin resistance be a natural consequence of thyroid dysfunction? J Thyroid Res. 2011;2011:152850. doi: 10.4061/2011/152850. Epub 2011 Sep 19. PMID: 21941681; PMCID: PMC3175696.
Disclaimer: The information presented in this article is for educational purposes only and is not intended to diagnose, prevent, or treat any medical or psychological conditions. The information is not intended as medical advice, nor should it replace the advice from a doctor or qualified healthcare professional. Please do not stop, adjust, or modify your dose of any prescribed medications without the direct supervision of your healthcare practitioner.
