Are My Genes Making Me Hungry?

What Nutrigenomics Taught Me About Appetite, Willpower and Self Compassion

For much of my life, I have been very interested in food, particularly sweet food.

I enjoy food. I think about food (a lot) and have a pretty big appetite. I can find it difficult to stop eating sometimes, particularly when it’s sweet or savoury things. Like many people, I have sometimes interpreted this through a moral lens.

Am I just greedy?

Why haven’t I got better willpower?

Why can’t I simply be more disciplined?

Studying nutrition has increasingly made me question these assumptions. More recently, looking at my own nutrigenomics results has given me another perspective altogether. My genes are not an excuse for my choices, and certainly not a prediction of my future, but they provide context.

What is nutrigenomics?

Nutrigenomics and nutrigenetics explore the relationship between our genes, nutrients, and metabolism. We all carry genetic variations called single nucleotide polymorphisms, or SNPs. Most are common variations rather than disease causing mutations. Some may subtly influence the way proteins, receptors, enzymes or signalling pathways function.

My Lifecode Gx Metabolics report looks at six interconnected areas: appetite regulation, nutrient sensing, sugar metabolism, fat metabolism, cholesterol and bile, and mitochondrial function and inflammation. Importantly, our genes do not work in isolation.

That interconnectedness is important because metabolic health is not simply genetic. Diet, movement, sleep, stress, ageing and our wider environment all interact with genetic susceptibility. A recent systematic review of personalised nutrition also highlights this complexity. Gene and diet interactions are emerging, but findings remain mixed and researchers continue to call for better designed genotype specific trials.

In other words, DNA may influence the ingredients we have to hand , but it does not determine the specific cake we bake.

What did my own results tell me about hunger?

This was the part that really caught my attention. Several of my results sit within pathways involved in hunger, food seeking and satiety.

My FTO rs9939609 result is AT. Lifecode interprets the A allele as being associated with greater FTO expression, increased ghrelin signalling, increased hunger, reduced satiety (fullness) after meals and a greater preference for calorie dense foods.

FTO is one of the better studied obesity associated genes. Research has linked the rs9939609 risk allele with appetite related behaviours, and experimental research has also identified relationships between FTO and ghrelin, although genetics is only one part of the picture.

My LEPR result was also interesting. LEPR codes for the leptin receptor. Leptin is one of the signals involved in communicating energy sufficiency to the brain. My report interprets my rs1137101 GG genotype as potentially reducing leptin sensitivity and therefore weakening fullness (satiety0 signalling, with more hunger and slower metabolism.

Then there is MC4R, (part of the brain’s melanocortin system) which also helps regulate appetite and energy balance. My result at rs17782313 is interpreted in the report as potentially producing weaker satiety signalling and a tendency towards larger meals. I thought” tick”. I often out-eat my husband!

However, this is where caution matters. MC4R rs17782313 has been associated with obesity risk, but the evidence about exactly how this particular common variant influences appetite and energy intake is less consistent. I have also never been obese, although I was overweight around both my pregnancies.

A recent systematic review found some evidence of increased appetite, but the findings were sensitive to the statistical model used and there was not a clear association with measured energy intake.

I also carry variants in NPY and FAAH which my report interprets as potentially influencing food seeking, appetite and endocannabinoid signalling. Lifecode Gx interpret this as a likelihood to forage (food seeking and snacking) and preferentially for fat rich foods.

The report however does not say:

“Always hungry, never full, prone to snacking especially on sweet, fat rich foods, with slow metabolism and prone to being overweight.”

However, it can feel like this sometimes, particularly if I’m tired, stressed and haven’t exercised. The report collectively they made me consider:

Perhaps I experience hunger and satiety differently from someone who finds it easy to eat half a meal, decline a biscuit when offered, and seems at peace with their answer?

That thought was surprisingly liberating.

From judgement to curiosity

The most useful outcome of my nutrigenomics testing has not been discovering a special diet dictated by my DNA. It has been self-compassion.

For years, behaviours such as wanting another portion, thinking about food or struggling with my wobbly bits could easily be translated into character judgements. I have been my greatest critic:

• Greedy

• Poor motivation

• Lacking willpower

Understanding more about appetite biology doesn’t absolve me of responsibility for my choices. Quite the opposite. It gives me more information with which to make them.

It changes the question from:

“What’s wrong with me?”

to:

“What can I put in place that makes this easier for my biology?”

This is a very different conversation. It’s about partnering with my body, being curious about how best to support not just my SNPs but my lived experience and my daily habits.

Hunger is only half the story

The other part of my report that fascinated me was nutrient sensing.

Our cells constantly respond to whether energy and nutrients are plentiful or scarce. Pathways involving AMPK, mTOR, sirtuins, PGC1A and PPARs help coordinate that response. Together, they help cells respond to food availability, fasting, exercise and stress by adjusting how energy is produced, stored and used.

My report describes this broadly as movement between a fed state, where building and storage are prioritised, and a lower energy state in which pathways supporting fuel mobilisation and cellular adaptation become more active. This is a concept known as metabolic flexibility where we can adapt our fuel use according to availability and demand, rather than relying continuously on incoming food. My nutrient sensing SNPs suggest that I should be able to move into fat burning as my insulin response is effective.

I don’t interpret my genetic results as saying that I need to fast. There isn’t enough evidence to make that type of SNP specific prescription, however it encouraged me to think about the pattern of my eating, what I eat and how often, and how quickly.

Time restricted eating

One strategy I personally use is time restricted eating (TRE), creating a defined eight hour period in which I eat and a longer fast period in which I don’t. For me, the biggest benefit may actually be behavioural. TRE creates a clear difference between eating and not eating. I am not thinking about food until midday and I stop eating at 8pm.

In this pattern, I am less likely to graze or forage. My body has adapted and I am more aware of whether I am genuinely hungry or simply responding to habit, boredom, Haribo availability or the sight of food!

There is growing evidence that time restricted eating can improve some cardiometabolic outcomes. A 2026 systematic review and meta-analysis found that TRE overall improved several measures of metabolic health compared with usual eating patterns, with earlier eating windows generally performing better than later ones. However, the ideal length of the eating window was much less clear, and TRE is not safe or effective for everyone.

For me it is simply a way of leaning into metabolic flexibility rather than being in a continuously fed state.

What I eat less of and how I eat

Within my TRE window food quality matters. I eat protein with each meal, plenty of low glycaemic fibre including vegetables, salads, some fruit and berries, healthy fats including 2-3 portions of oily fish weekly.

I avoid ultra processed foods and refined foods which is helpful for a myriad of reasons, but for me, over-eating is more likely to be associated with UPFs. Chewing and eating mindfully support ghrelin and feelings of satiety, so this really helps. Avoiding eating at the computer or while watching TV helps me. I also find sweet non-sugar drinks like Coke Zero drive my foraging tendencies and I can crave sweets after drinking, so I try and drink infrequently. I drink gut friendly, low sugar kombucha if I want the fizz.

I know what foods are linked to over-eating and I know when I’m most vulnerable to them. I rarely eat bread and when I do it’s rye bread or sourdough, or homemade keto bread. I know that refined carbohydrates like pastries, scones and sweets especially Haribo, and crisps are hard for me to control, so I don’t buy them and maybe have once or twice a week. If I have sweets, dessert or crisps, I enjoy them. I no longer label food good or bad but know what less helpful to my biology. I don't beat myself up, if I have a sweet day; no moralising or judgement.

These are my personalised adaptations and are not a prescription for anyone else and they also don’t work all the time. Tiredness due to poor sleep, lack of exercise, and feeling a bit burnt-out can disrupt my best laid supports. But in general, 80% of the time they support my biology.

Genes are information, not destiny

As a certified nutrigenomics practitioner, I am curious about what our SNPs can teach us, and I remain cautious about applying nutrigenomics. A genetic report can look impressively precise. There are gene names, SNP numbers, biochemical pathways and beautifully coloured results. The reports are not definitive and include words like "may" and “can” increase. SNPs are not a prediction.

For me, nutrigenomics works best as one layer of information and sits alongside any symptoms, health history, blood results, dietary intake, movement, sleep, stress, preferences and, most importantly, lived experience.

“What is it like to be living in this body with this biology?”

My genes haven’t told me exactly what to eat.

They haven’t removed my personal responsibility.

And they certainly haven’t condemned me to a particular weight or metabolic future.

What they have given me is another way of understanding myself.

Perhaps the greatest change has been moving away from asking:

“Why haven’t I got more willpower?”

and towards asking: "Knowing a little more about my biology, what can I do to make the choices that support me easier?”

"When I am feeling at a low ebb, I need self compassion and more self-care, not judgement or harsh words."

That feels to me like a much more useful application of personalised nutrition.

And a much kinder one too.

A note about nutrigenomics testing

Nutrigenomics testing identifies genetic variants and possible associations. It does not diagnose disease or predict with certainty how an individual will respond to a particular food or diet. Many SNP effects are small, and evidence differs between variants. Genes interact continually with lifestyle and environment and the genes tested in relation to appetite; for example, additional untested genes influencing appetite.

Testing is therefore best interpreted within the wider clinical assessment and your lived experience, rather than used in isolation.

This article describes my own experience and is for educational purposes only. Time restricted eating and other dietary approaches may not be appropriate for everyone. Individual health circumstances should always be considered.

References

Bossowska M, Bossowski F, Adamska Patruno E, Maliszewska K, Krętowski A. (2026). Personalised nutrition in obesity and prediabetes: Do genotypes matter? Nutrients, 18(5), 815. https://doi.org/10.3390/nu18050815

Chen YE et al. (2026). Effects of timing and eating duration of time restricted eating on metabolic outcomes: systematic review and network meta-analysis.

Karra E et al. (2013). A link between FTO, ghrelin, and impaired brain food cue responsivity. Journal of Clinical Investigation.

Álvarez Martín, et al. (2025). Association of MC4R rs17782313 genotype with energy intake and appetite: a systematic review and meta-analysis.

Lifecode Gx. (2025). Personalised Metabolics Report and references within.