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Why Your Body Responds to Food the Way It Does: A Genetic Deep Dive into Carbs, Hunger and Weight Regulation

Why Your Body Responds to Food the Way It Does: A Genetic Deep Dive into Carbs, Hunger and Weight Regulation

December 13, 2025
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If you’ve ever wondered why some people feel full after a small meal, why others constantly crave sweets, or why weight loss feels harder for you than it “should,” your genetics may hold important clues.


A personalised nutrigenetic functional test can help identify metabolic tendencies and guide a tailored nutrition plan based on your unique biology. With this information, you can shape a nutrition plan that works with your biology instead of against it.


How DNA Is Measured in Genetic Testing


Genetic tests don’t read your whole genome. Instead, they scan specific locations called SNPs (single nucleotide polymorphisms). Here’s how it works:


• A saliva or cheek-swab sample is collected.

• Your DNA is broken into small fragments.

• A microarray chip checks thousands of SNP sites.

• At each site, the machine identifies which two bases you carry (A, T, C or G).

• If the SNP changes a protein, the result is also shown as amino acids (e.g., Thr/Ile).

• For some older SNPs, historical labels (A1/A2) are used.


The final report tells you which versions of each SNP you have. SNPs can influence how enzymes work, how receptors respond to hormones and how effectively your body performs metabolic tasks. Some SNPs change the shape of a protein (shown as amino acids like Pro, Ala, Gly). Others simply affect regulation (shown as A/T/C/G). A few still use historical names like A1/A2. Each SNP below affects a different aspect of metabolism or appetite regulation.


ADRB2 (Adrenergic Beta-2 Receptor)— How Efficiently You Mobilise Stored Energy


SNPs: rs1042713 (Arg16Gly), rs1042714 (Gln27Glu)


ADRB2 affects how your fat cells respond to adrenaline — which determines how easily you burn stored fat, how quickly you mobilise glucose and how metabolically “flexible” you are.


rs1042713 (Arg16Gly)


  • AA (Arg/Arg): slower fat mobilisation; may feel sluggish with high carb intake

  • AG (Arg/Gly): moderate response

  • GG (Gly/Gly): sustained fat oxidation; better carb tolerance


rs1042714 (Gln27Glu)


  • CC (Gln/Gln): receptors desensitise quickly

  • CG (Gln/Glu): average response

  • GG (Glu/Glu): stable receptors; improved metabolic flexibility


What this means for you

If your receptors down-regulate easily, high-sugar foods may lead to energy crashes and easier fat gain. You may feel your best with steady meals built around lean protein, fibre and controlled carbohydrates.


MC4R (Melanocortin 4 Receptor) — The Gene That Sets Your Appetite “Volume”


SNP: rs17782313


MC4R influences your natural hunger signals and how satisfied you feel after eating.


Genotypes


  • TT: typical satiety

  • TC: slightly increased hunger

  • CC: reduced fullness → large portions, snacking, emotional eating


What this means

If you carry the C allele, hunger is not “your fault” — your brain’s satiety signals simply reset more slowly. You may thrive with structured eating, high-protein breakfasts and high-volume meals that stretch the stomach without adding calories.


PPARG (Peroxisome Proliferator-Activated Receptor Gamma) — Your Insulin-Sensitivity Master Switch


SNP: rs1805192 (Pro12Ala)


PPARG is essential for glucose metabolism and how efficiently your body stores and releases energy.


Genotypes


  • CC (Pro/Pro): higher risk of insulin resistance

  • CG (Pro/Ala): improved insulin response

  • GG (Ala/Ala): most insulin-sensitive profile


What this means

If you are Pro/Pro, your body may struggle with large carb-heavy meals. A Mediterranean dietary pattern (olive oil, legumes, vegetables, fish) is especially beneficial for this genotype.


AGER / RAGE (Advanced Glycation Endproduct Receptor) — Glycation, Inflammation and Metabolic Ageing


SNP: rs2070600 (Gly82Ser)


AGER controls how strongly your cells react to AGEs — inflammatory compounds produced from sugar and high-temperature cooking.


Genotypes


  • GG (Gly/Gly): typical AGE signalling

  • GA (Gly/Ser): higher inflammatory response

  • AA (Ser/Ser): highest AGE accumulation


What this means

If you carry the Ser allele, charred foods, fried foods and sugary products can have a bigger impact on inflammation, skin ageing and metabolic health. Antioxidant-rich foods (berries, herbs, turmeric) and gentle cooking methods are protective.


TCF7L2 (Transcription Factor 7-Like 2) — Insulin Release and Diabetes Risk


SNP: rs12255372


This gene affects how effectively your pancreas releases insulin.


Genotypes


  • GG: normal insulin secretion

  • GT: reduced β-cell performance

  • TT: significantly reduced insulin output


What this means

If you have the T allele, your body may struggle with blood sugar spikes. Balanced meals (protein + fibre + healthy fats) and lower-GI carbohydrates help keep glucose stable.


KCNJ11 (Potassium Inwardly-Rectifying Channel Subfamily J Member 11) — First-Phase Insulin Release


SNP: rs5219 (E23K)


Controls the potassium channel that triggers early insulin release after meals.


Genotypes

  • GG (E/E): strong early insulin response

  • GA (E/K): reduced insulin release

  • AA (K/K): weakest response


What this means

If your early insulin release is impaired, you may experience post-meal fatigue or cravings. Magnesium intake, balanced meals and regular movement can support glucose control.


GLUT2 (Glucose Transporter Type 2) — Sugar Transport and Sweet Preference


SNP: rs5400 (Thr110Ile)


Influences how efficiently you transport glucose/fructose and how sensitive you are to sweetness.


Genotypes


  • CC: typical sugar sensitivity

  • CT: increased sugar preference

  • TT: strongest sweet cravings and altered glucose sensing


What this means

If you have the Ile allele, managing sugar cravings becomes essential. Natural sweeteners (allulose, erythritol), fruit-based snacks and removing sugary foods from the home environment can help.


FTO (Fat Mass and Obesity-Associated Gene) — Appetite, Satiety and Weight-Gain Risk


SNP: rs9939609


FTO does not change protein structure but shifts the way your brain regulates hunger.


Genotypes


  • TT: typical appetite

  • AT: increased appetite and snacking

  • AA: highest hunger drive


What this means

The A allele is strongly linked with grazing, portion size and preference for calorie-dense foods. Protein-rich meals and planned eating strategies reduce its impact.


DRD2 / ANKK1 (Dopamine Receptor D2 / Ankyrin Repeat And Kinase Domain Containing 1) — Reward, Cravings and Emotional Eating


SNP: rs1800497 (Taq1A)


This variant reduces dopamine receptor density, changing how rewarding food feels.


Genotypes


  • GG (A2/A2): normal reward processing

  • GA (A1/A2): mild reward deficiency

  • AA (A1/A1): strong reward deficiency → cravings and emotional eating


What this means

If you carry the A1 allele, your brain compensates by seeking more stimulation — often from high-calorie foods. Supporting dopamine through protein, exercise and non-food rewards is key.


Summary Table


Gene

SNP

Role

Genotype Effects

Practical Focus

ADRB2

rs1042713 / rs1042714

Fat oxidation, adrenaline response

Arg/Gly and Gln/Glu variants alter metabolic flexibility

Reduce refined carbs; exercise

MC4R

rs17782313

Appetite, satiety

C allele → increased hunger

High-protein, structured meals

PPARG

rs1805192

Insulin sensitivity

Pro allele → insulin resistance

Mediterranean diet; limit saturated fat

AGER

rs2070600

Glycation, inflammation

Ser allele → higher inflammation

Avoid sugar, fried foods

TCF7L2

rs12255372

Insulin secretion

T allele → impaired β-cell response

Low-GI diet; balanced meals

KCNJ11

rs5219

Early insulin release

K allele → reduced insulin signalling

Balanced plates; magnesium

GLUT2

rs5400

Sugar transport, sweet taste

Ile allele → sugar preference

Substitute sweeteners; manage cravings

FTO

rs9939609

Appetite regulation

A allele → increased hunger

Protein-rich meals; planning

DRD2

rs1800497

Reward pathways

A1 allele → emotional eating

Exercise; dopamine support


Are Your Genes Contributing to Weight-Loss Resistance?


If you feel like you’re doing “everything right” but still struggle with appetite, cravings, carb intolerance or stubborn weight, your genetics may offer missing insights.


If you’d like support with testing or interpretation, you can book a consultation or contact me to order a test.


Reference list:

Zhang, H., Wu, J. and Yu, L. (2014) ‘Association of Gln27Glu and Arg16Gly polymorphisms in β2-adrenergic receptor gene with obesity susceptibility: A meta-analysis’, PLoS ONE, 9(6), p. e100489. Available at: https://doi.org/10.1371/journal.pone.0100489

Vesnina, A., Prosekov, A., Kozlova, O. and Atuchin, V. (2020) ‘Genes and eating preferences, their roles in personalized nutrition’, Genes, 11(4), p. 357. Available at: https://doi.org/10.3390/genes11040357

Álvarez-Martín, C., Caballero, F.F., de la Iglesia, R. and Alonso-Aperte, E. (2025) ‘Association of MC4R rs17782313 genotype with energy intake and appetite: A systematic review and meta-analysis’, Nutrition Reviews, 83(3), pp. e931–e946. Available at: https://doi.org/10.1093/nutrit/nuae075

Deeb, S.S. et al. (1998) ‘A Pro12Ala substitution in PPARγ2 associated with decreased receptor activity, lower body mass index and improved insulin sensitivity’, Nature Genetics, 20(3), pp. 284–287. Available at: https://doi.org/10.1038/3099

Stumvoll, M. et al. (2002) ‘The peroxisome proliferator-activated receptor-γ2 Pro12Ala polymorphism determines diabetes risk in obesity’, Diabetes, 51(8), pp. 242–247. Available at: https://pubmed.ncbi.nlm.nih.gov/12145143/

Larsen, H.G. et al. (2024) ‘The Gly82Ser polymorphism in the receptor for advanced glycation endproducts increases the risk for coronary events in the general population’, Scientific Reports, 14, p. 11567. Available at: https://doi.org/10.1038/s41598-024-62385-5

Grant, S.F. et al. (2006) ‘Variant of transcription factor 7-like 2 (TCF7L2) gene confers risk of type 2 diabetes’, Nature Genetics, 38(3), pp. 320–323. Available at: https://doi.org/10.1038/ng1732

Lyssenko, V. et al. (2007) ‘Mechanisms by which common variants in the TCF7L2 gene increase risk of type 2 diabetes’, Journal of Clinical Investigation, 117(8), pp. 2155–2163. Available at: https://doi.org/10.1172/JCI30706

Eny, K.M. et al. (2008) ‘Genetic variant in the glucose transporter type 2 is associated with higher intakes of sugars in two distinct populations’, Physiological Genomics, 33(3), pp. 355–360. Available at: https://doi.org/10.1152/physiolgenomics.00148.2007

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), pp. 889–894. Available at: https://doi.org/10.1126/science.1141634

Wardle, J. et al. (2008) ‘Obesity-associated genetic variation in FTO is associated with diminished satiety’, Journal of Clinical Endocrinology & Metabolism, 93(9), pp. 3640–3643. Available at: https://doi.org/10.1210/jc.2008-0472

Sun, X., Luquet, S. and Small, D.M. (2017) ‘DRD2: Bridging the genome and ingestive behavior’, Trends in Cognitive Sciences, 21(5), pp. 372–384. Available at: https://doi.org/10.1016/j.tics.2017.03.004

Blum, K., Thanos, P.K. and Gold, M.S. (2014) ‘Dopamine and glucose, obesity, and reward deficiency syndrome’, Frontiers in Psychology, 5, p. 919. Available at: https://doi.org/10.3389/fpsyg.2014.00919

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