I'm a Nutritionist, I'm Curvy, and My Labs Are Optimal

The scale read 103kg this morning.

I stood in my bathroom and looked at that number with something close to neutrality. Not indifference, because I'm human and I have days that are harder than others, but a genuine understanding that what I was looking at was data, and that data tells only part of a story.

The fuller picture: my blood work is textbook optimal by functional medicine standards. My heart rate variability sits between 50 and 80. My Oura recovery scores consistently come in above 90. My inflammatory markers are low, my blood glucose regulation is excellent, my lipid profile is strong, and my insulin sensitivity is optimal. I run ultramarathons. I'm currently training for a 92km gravel cycling event. I'm 180cm tall, I wear a size 16 to 18, and I am the nutritional scientist you'd be trusting with your metabolic health.

I think it's worth sitting with that for a moment, because the wellness industry has spent decades telling women that credibility looks a certain way, and it doesn't look like me.

I want to offer a different account.

What my blood work tells us

Every six months I run comprehensive blood panels: fasting glucose, insulin sensitivity, lipid panels, inflammatory markers, hormone levels. The results are consistently optimal across every measure. This is not something I say to reassure you that I'm fine despite my size. I say it because it is clinically relevant, and because it points to something the research has been demonstrating for years.

Metabolic health and body size are not the same variable. The Health at Every Size research base, now spanning more than two decades of peer-reviewed evidence, shows that metabolic markers can be excellent across a wide range of body sizes, and that focusing on health behaviours rather than weight loss produces better metabolic and psychological outcomes over time (Ulian et al., Obesity Reviews, 2018). My labs are a lived example of that finding, not an exception to it.

What my body cannot tell you about is my history. And that context matters considerably.

When I was lighter

I have been about 15kg lighter than I am now. I want to be straightforward about what that period actually looked like.

My hair fell out. I lost muscle mass despite consistent training. My menstrual cycle disappeared. I was cold constantly. My energy collapsed and my athletic performance went with it. My hunger signals shut down so completely that I was eating around 1,500 calories while expending close to 3,000 through training, and I felt almost nothing in the way of appetite.

That was not a fixed or healthy relationship with food. That was a metabolism in serious suppression. Research on adaptive thermogenesis documents this clearly: when body weight is maintained significantly below an individual's biological set point, metabolic rate can suppress by 300 to 500 calories per day beyond what would be predicted for that body size alone (Rosenbaum and Leibel, International Journal of Obesity, 2010). My lips were blue. My body was doing what bodies do when they have been under-resourced for long enough: it was shutting down everything it could afford to lose.

I was thinner. I was objectively less healthy. And it took me time to fully understand why, which is where the genetics come in.

What my genetic testing showed

I've had comprehensive genetic testing through SelfDecode. Understanding my results changed the way I think about appetite, structure, and what health actually requires for a body like mine.

I carry the FTO AA genotype combined with LEPR GG variants. For context: the FTO gene variant is associated with higher circulating ghrelin levels (the hormone that drives hunger) and reduced dopamine signalling in response to food (Frayling et al., Science, 2007). The LEPR gene affects leptin receptor function. Leptin is the hormone your fat cells use to signal satiety to the brain. With LEPR variants, that signal is significantly blunted: even when my body has adequate energy stores, my brain is not receiving the message clearly (Wauters et al., Journal of Clinical Endocrinology and Metabolism, 2001).

Studies show that people with these genetic variants consume 125 to 280 more calories per day when eating freely compared to those without them (Haupt et al., Obesity, 2009). The hunger signals are real. They are not a failure of discipline. They are a feature of the biology.

For years I interpreted this as something being wrong with me. How could I, a nutritional scientist with an honours degree, not manage my own appetite without significant effort? The answer, once I understood it properly, was straightforward: I was fighting a biological reality with willpower, and willpower is not a match for genetics over the long term. Nobody's is.

Why I track, and why I probably always will

II know that macro tracking sits uncomfortably in a wellness space that has spent recent years, rightly, pushing back against diet culture and the harm it has caused. I want to be precise about what tracking means for me and why it is not the same thing as restriction.

My internal hunger and satiety signals are not reliable guides. This is not a psychological problem. It is a physiological one, rooted in the genetic variants I've described. A 2019 study found that individuals with multiple genetic variants affecting appetite regulation, including the FTO and LEPR combination I carry, consumed up to 30% more calories before reporting fullness compared to those without these variants (Livingstone et al., BMJ, 2019). That is biology, not a character flaw.

Intuitive eating is genuinely healing for many women, particularly those working to repair a relationship with food that restriction has damaged. It assumes, though, that hunger and satiety signals are fundamentally intact. For some of us, they are not, and pretending otherwise does not serve our health.

What tracking gives me is not control in the diet-culture sense. It gives me information that my physiology cannot reliably provide. I know my protein requirements for the training I'm doing. I understand my carbohydrate needs relative to training volume. I have a calorie range that supports metabolic health without suppression. This structure is not a cage. It is the scaffolding that allows me to eat well, train hard, recover properly, and feel good in my body without constantly overriding signals that would, left unstructured, drive me consistently toward more than my body needs.

Research supports self-monitoring as one of the strongest predictors of long-term weight management, not because restriction produces health, but because awareness allows people to make choices that align with their actual needs rather than dysregulated hunger signals (Burke, Wang and Sevick, Journal of the American Dietetic Association, 2011).

I have made peace with the fact that this is likely permanent. My genetics will not change. My leptin receptors will not begin working differently. My biological set point is where it is, and it is higher than what diet culture has decided is acceptable. This is not a defeat. It is simply accurate information about the body I live in, and it is far more useful to work with that information than against it.

What set point theory actually means for women like me

We all have a biological weight range our bodies actively defend, shaped by genetics, hormonal history, and metabolic experience rather than by any aesthetic standard (Müller et al., Current Obesity Reports, 2016). My genetic variants mean my natural set point sits higher. When I was 15kg lighter, I was living well below that range, and my body made its position on that very clear.

At 103kg, with adequate nutrition supporting my training and a structure around eating that works with my genetics, I am carrying the best metabolic health of my life. I've gained significant muscle, my performance is strong, my recovery is good, and my labs reflect all of that. I have also gained some fat alongside the muscle, and I want to be honest that I am still in the process, as I described in my recent post on reverse dieting, of finding the full equilibrium of that.

The point is not that 103kg is a magic number or a destination. The point is that when I stopped trying to maintain a weight my body could not sustain without significant physiological cost, and started working with my actual biology, everything that matters about health improved.

I would rather be curvy, strong, and metabolically well than thin, depleted, and fighting my own physiology every day. That is not a consolation. That is a genuine preference based on understanding what health actually feels like.

What I want you to take from this

I'm sharing all of this because I think the wellness space has created a particular kind of shame that doesn't get named often enough: the shame of needing structure, the shame of not thriving on intuitive eating, the shame of being in a larger body even when your health markers are excellent.

Some of us have genetics that mean we cannot rely on internal hunger cues. Some of us have biological set points that are higher than what our culture has decided is acceptable. Many of us have spent years in restriction and are now working to repair what that cost us metabolically. These are not personal failings. Genetic variants affecting appetite regulation and metabolism are extraordinarily common. A genome-wide association study identified 97 genetic loci associated with body mass index (Locke et al., Nature, 2015). The odds are reasonable that some of what I've described here resonates with your own experience.

If you've tried eating freely and found it consistently moved you away from feeling well, it may not be because you're doing it wrong. It may be because your particular biology requires a different kind of support.

My body does not diminish my expertise. In many ways, it has deepened it. I understand metabolic complexity, appetite dysregulation, genetic variants, and the long-term consequences of restriction not just from the research, but from living all of it. That combination of clinical knowledge and personal experience is what I bring to the women I work with through Sérenité, and it is why I am not willing to pretend my body is something other than what it is in order to appear more credible.

Strong, fuelled, and metabolically well: that is the standard worth working toward. In whatever body that looks like for you.

References:

Bacon, L., & Aphramor, L. (2011). Weight science: evaluating the evidence for a paradigm shift. Nutrition Journal, 10(1), 9.

Burke, L. E., Wang, J., & Sevick, M. A. (2011). Self-monitoring in weight loss: a systematic review of the literature. Journal of the American Dietetic Association, 111(1), 92-102.

Frayling, T. M., et al. (2007). A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science, 316(5826), 889-894.

Haupt, A., et al. (2009). Impact of variation in the FTO gene on whole body fat distribution, ectopic fat, and weight loss. Obesity, 17(10), 1942-1945.

Livingstone, K. M., et al. (2019). FTO genotype and weight loss: systematic review and meta-analysis of 9563 individual participant data from eight randomised controlled trials. BMJ, 354, i4707.

Locke, A. E., et al. (2015). Genetic studies of body mass index yield new insights for obesity biology. Nature, 518(7538), 197-206.

Mensinger, J. L., et al. (2020). Diet-free interventions and health outcomes: a systematic review and meta-analysis. Nutrition Research Reviews, 1-19.

Müller, M. J., et al. (2010). Changes in energy expenditure with weight gain and weight loss in humans. Current Obesity Reports, 5(4), 413-423.

Phillips, S. M., & Van Loon, L. J. (2011). Dietary protein for athletes: from requirements to optimum adaptation. Journal of Sports Sciences, 29(sup1), S29-S38.

Rosenbaum, M., & Leibel, R. L. (2010). Adaptive thermogenesis in humans. International Journal of Obesity, 34(S1), S47-S55.

Stice, E., et al. (2008). Relation of obesity to consummatory and anticipatory food reward. Physiology & Behavior, 97(5), 551-560.

Ulian, M. D., et al. (2018). Effects of health at every size® interventions on health-related outcomes of people with overweight and obesity: a systematic review. Obesity Reviews, 19(12), 1659-1666.

Wauters, M., et al. (2001). Leptin receptor gene polymorphisms are associated with insulin in obese women with impaired glucose tolerance. The Journal of Clinical Endocrinology & Metabolism, 86(7), 3227-3232.

If you're a woman in perimenopause struggling with metabolic health despite doing "all the right things," the missing piece might be understanding your unique internal landscape. My Sérenité Women's Wellness Program uses blood pathology analysis to create truly personalized nutrition protocols that work with your specific metabolism. Learn more about working together