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Prof. Dr. Mustafa Özdoğan · Medical Oncologist

A different perspective on nutrition: DNA-based diets & Nutrigenomics

A different perspective on nutrition: DNA-based diets & Nutrigenomics
In this article

Diet according to DNA: personalized nutrition or fortune-telling?

Why does one of two people following the same diet lose weight quickly while the other struggles? Why does the same meal send one person's blood sugar soaring while having a milder effect on another? "DNA-based diets", which seek answers to these questions in our genes, have become a large market in recent years. Tests claiming to identify "the best diet for you" from a saliva sample are also widely sold in Türkiye. But what does science say? The short answer: Personalized nutrition is a real and important goal; however, there is no evidence that this goal can be achieved with a DNA test alone. In this article, we discuss what nutrigenomics is, what randomized studies actually show, which genetic tests are truly useful in nutrition, and why different types of data need to be evaluated together.

Update · September 2026
  • The article has been completely revised; randomized studies, professional organizations' views, genuinely useful genetic tests, the market, data privacy and the situation in Türkiye have been added.
  • Corrections: The CYP1A2 example about caffeine was reversed: in this variant, the AA genotype belongs to the group that breaks down caffeine quickly ; moreover, there is no "G" genotype for this variant. The 200 and 400 mg caffeine limits were established for the general population, rather than according to genotype.
  • The MTHFR C677T example was corrected: with adequate folate intake, the TT genotype was associated with a lower risk of colorectal cancer. The interaction between red meat and the NAT2 genotype was not confirmed in a large pooled analysis.
  • The FTO example was placed in context: according to a meta-analysis of randomized studies, carriers of the FTO risk genotype respond to weight-loss programs just as well as others.
  • The statement "DNA-based diets are particularly preferred by professional athletes" was removed because it was not supported by a source.
Briefly
  • Differences between people are real: Blood lipid and blood sugar responses to the same meal vary greatly from person to person.
  • But genetics plays a small part: In the PREDICT study of 1.002 people, genetic variants explained approximately %10 of the differences in post-meal blood sugar responses and only %1 of the differences in blood lipid responses. Meal timing, sleep, exercise and gut microbiota are at least as important.
  • Randomized studies: In the study of 1.607 people, Food4Me, personalized dietary advice was more effective than general advice; however, adding genetic information provided no additional benefit. In the DIETFITS study of 609 people, genotype also failed to predict who would lose more weight on a low-fat or low-carbohydrate diet.
  • Expert opinion: The United States Academy of Nutrition and Dietetics states that there is insufficient evidence to determine the contribution of genetic testing to nutrition practice.
  • There are genuinely useful tests too: Genetic tests addressing specific medical questions, such as lactose intolerance and celiac disease, can guide care in the right patient.

Terms: nutrigenetics, nutrigenomics and epigenetics

  • Nutrigenetics: Studies how our genetic differences affect our responses to foods. For example, "Does a person with this genotype break down caffeine more slowly?"
  • Nutrigenomics: Studies how foods affect gene activity. In everyday language, all "DNA-based diet" tests are marketed under this heading, but most are actually nutrigenetic tests.
  • Epigenetics: Studies the mechanisms determining when and how much genes function without changing the DNA sequence. One striking example is the Dutch Hunger Winter: people who were in the womb during the famine of 1944-45 had chemical marks on the growth-related IGF2 gene that differed from their siblings even six decades later. We explained the measurement of epigenetic age in this article .

Different responses to the same meal: real, but genetics is a small part

It is now well established that people respond differently to the same foods. In 2020, Nature Medicinepublished the PREDICT study, in which 1.002 people (including twins) received the same standardized meals. Differences between individuals in post-meal responses were very large: variability of %103 for blood lipids (triglycerides), %68 for blood sugar and %59 for insulin.

However, the picture changes when we ask how much of these differences is genetic:

The share explained by genetic variants
PREDICT study, percentage of variation in post-meal responses.
Blood sugar
%9,5
Blood lipids (triglycerides)
%0,8
C-peptide (insulin secretion)
%0,2
How to read this: Genetic variants added to the prediction model explained approximately one tenth of the differences in blood sugar responses and only one percent of the differences in blood lipid responses. In contrast, gut microbiota explained %7,1 of the differences in blood lipid responses; the contribution of meal context, such as timing, exercise and sleep, was as large as that of meal composition. Twin comparisons found heritability of %48 for blood sugar responses and %0 for blood lipid responses. The bars are drawn relative to %100 of the total variation; the remainder consists of non-genetic factors.

Thus, "different responses to the same meal" are real; however, most of this variation comes from our gut bacteria, when and under what conditions we eat, our sleep and our activity, rather than our genes. We discussed meal timing in detail in our chrono-nutrition article .

Figure 1 · Same meal, different response: why?

Factors determining post-meal responses and the contribution of genetics.

same meal, different responsedifferences between people in blood lipid responses are very large meal timing,sleep, exercise(meal context) gutmicrobiota meal compositioncarbohydrate, fat,fiber, protein genetic variantsblood sugar ~%10,blood lipids ~%1 conclusionfor personalized nutrition, a standaloneDNA test is insufficient; multiple data are needed
How to read this: Responses to the same meal differ greatly between people; these differences are particularly large for blood lipids. Meal context, including timing, sleep and exercise, gut microbiota, meal composition and genetic variants jointly determine these differences. Genetic variants explain approximately 10 percent of variation in blood sugar responses and approximately 1 percent of variation in blood lipid responses. Thus, a DNA test alone is insufficient for personalized nutrition; multiple types of data must be evaluated together.

Do diets based on DNA work? Randomized studies

The most reliable way to establish whether an approach actually works is to assign people randomly to groups and compare them. The key studies of DNA-based diets are as follows:

Study Question Result
Food4Me
7 European countries, 1.607 people, 6 months
General advice or personalized advice? Does adding blood values and genetics to personalized advice make a difference? Personalized advice was more effective (less salt, saturated fat and red meat). Adding genetic information provided no additional benefit.
DIETFITS
United States, 609 people, 12 months
Can a "genotype pattern" consisting of three genes predict whether a low-fat or low-carbohydrate diet will work better? Weight loss was similar with both diets (5,3 and 6,0 kg). The genotype pattern did not predict who would lose more weight with which diet.
FTO meta-analysis
8 studies, 9.563 people
Do carriers of the obesity-associated FTO risk genotype respond less well to weight-loss programs? No. Carriers of the risk genotype responded to programs involving diet, exercise and medication just as well as others.
United States Academy of Nutrition and Dietetics review
12 randomized studies
Does adding genetic testing to nutritional counseling improve outcomes? There is insufficient scientific evidence to answer this question.

The Food4Me result is particularly instructive: personalized nutrition works, but this effect largely comes from reviewing a person's current diet and providing specific feedback accordingly; genetic information adds nothing to this effect. We also discussed the place of genetic testing in nutrition in our article on DNA-based genetic tests for nutrition .

Where do the examples in the old article stand today?

The FTO gene and weight

FTO is the gene whose association with obesity is best known. In a study involving 38 thousand people in 2007, those carrying two copies of the risk genotype (AA), approximately %16 of adults, weighed an average of 3 kg more and had 1,67 times higher odds of obesity than people without this variant. The finding mentioned in the old article, "AA carriers gain more weight when eating a high-fat, low-carbohydrate diet", comes from an observational study conducted at a single time point in Sweden; it measured body mass index at that moment rather than weight gain. A meta-analysis of randomized studies, however, shows that FTO genotype does not affect weight-loss success. Thus, healthy eating and physical activity work regardless of your FTO gene. For more information on obesity and the healthiest diets, see this article .

Caffeine and CYP1A2

The CYP1A2 enzyme breaks down caffeine in the liver. For the variant called rs762551, people with the AA genotype break down caffeine quickly, while carriers of the C allele (AC and CC) do so more slowly. In a Costa Rican study of 2.014 heart attack patients and 2.014 healthy people, among slow caffeine metabolizers, drinking 2-3 cups of coffee daily was associated with a %36 increase in heart attack risk, and 4 or more cups daily with a %64 increase; no such increase was observed among fast metabolizers. This association was more pronounced below age 59. However, this is a case-control study, and genotype-based coffee advice has not yet entered guidelines. The European Food Safety Authority (EFSA) recommendations, regardless of genotype, are as follows: up to 200 mg at once and 400 mg daily for healthy adults, and up to 200 mg of caffeine daily for pregnant and breastfeeding women are safe.

MTHFR, folate, alcohol and colorectal cancer

MTHFR is an enzyme involved in folate metabolism. The old article stated that the C677T variant increased colorectal cancer risk; however, the evidence shows a different picture. In a meta-analysis of 77 studies, the TT genotype, compared with CC, was associated with a slightly lower risk (odds ratio 0,88). This protective effect is particularly seen in people with adequate folate intake; the advantage disappears with folate deficiency and excessive alcohol consumption. Regardless of genotype, a folate-rich diet was associated with lower risk in both groups.

NAT2, well-done red meat and cancer

Some carcinogens formed in meat cooked at high temperatures are processed by the NAT2 enzyme. Small studies had reported increased risk among smokers with the "rapid acetylator" genotype who preferred well-done red meat. However, in a pooled analysis of 11 studies and more than 17 thousand people, high red meat intake was associated with a similar increase in colorectal cancer risk (%38-43) in both slow and rapid acetylators; genotype did not modify the effect. Thus, the message is the same for everyone: limit red and processed meat. We discussed foods that reduce colorectal cancer risk in this article, and the impact of lifestyle on this cancer in this article .

Genetic tests that are genuinely useful for nutrition

Genetic tests cannot be said to have no place in nutrition. Tests that address a specific medical question and whose result changes treatment are useful:

  • Lactose intolerance: The LCT -13910 variant near the lactase gene determines whether the lactase enzyme persists in adulthood. It can be used in diagnosis alongside methods such as breath testing.
  • Celiac disease: If both HLA-DQ2 and DQ8 genotypes are absent, celiac disease is practically excluded. This test is particularly useful in people who have already started a gluten-free diet or whose blood tests and biopsy results disagree. However, carrying these genotypes does not mean having celiac disease; a substantial proportion of the population carries these genes.
  • Inherited diseases: In conditions such as metabolic diseases identified by newborn screening, including phenylketonuria, hereditary iron accumulation (hemochromatosis) and familial high cholesterol, genetic diagnosis directly determines the dietary and treatment plan.

Figure 2 · Medical genetic testing versus DNA diet testing

The fundamental differences between the two types of test.

medical genetic testfor a specific questionlactose intolerance,celiac disease (HLA-DQ2/DQ8),inherited diseasesordered by a physicianthe result changesmanagement DNA diet testa package for everyoneweight, caffeine, vitamin"predispositions"direct salesin randomized studiesadditional benefitwas not demonstrated the test's purpose, evidence and what its resultwill change should be asked at the outset
How to read this: A medical genetic test addresses a specific question, such as lactose intolerance, celiac disease (HLA-DQ2/DQ8) or inherited diseases. It is ordered by a physician and its result changes patient management. A DNA diet test, by contrast, resembles a package prepared for everyone; it reports predispositions related to weight, caffeine and vitamins and is sold directly to consumers. Randomized studies have not demonstrated an additional benefit over dietary advice. For every test, ask at the outset about its purpose, evidence and what its result will change.

Personalized nutrition: multiple data rather than a single test

The idea of personalized nutrition is sound; the mistaken assumption is that it can be achieved with a single DNA test. Today's most promising approaches combine multiple types of data:

  • Personalized blood sugar prediction: A study of 800 people in Israel, published in 2015 in Cell, showed that an algorithm combining blood values, diet, body measurements, physical activity and gut microbiota could predict post-meal blood sugar responses, and that a diet prepared accordingly reduced blood sugar fluctuations.
  • The ZOE METHOD study: In a randomized study published in 2024 that followed 347 people for 18 weeks, a personalized nutrition program based on blood lipid, blood sugar and microbiota data reduced triglycerides more than standard dietary advice (0,13 mmol/L) and produced approximately 2,5 kg more weight loss; there was no difference in LDL cholesterol. It should also be noted that the study was conducted by a commercial company, %86 of participants were women, and the findings have been criticized.
  • Continuous glucose monitors: Their use in people without diabetes is becoming more widespread, but evidence that they improve health outcomes remains limited.

Figure 3 · Levels of evidence in personalized nutrition

From strongest to weakest evidence.

strong evidencehealthy eating principles for everyone:vegetables, fruit, fiber, minimally processed food individual adaptationbased on the person's current dietfeedback; effective in Food4Me multiple datablood values, glucose responses,microbiota: promising, limited evidence a diet based solely on a DNA testin randomized studiesno additional benefit demonstrated
How to read this: The strongest evidence supports healthy eating principles applicable to everyone: vegetables, fruit, fiber and minimally processed food. Feedback tailored to the person's current diet was also effective in the Food4Me study. Personalization using multiple data, such as blood values, blood sugar responses and microbiota, is promising but supported by limited evidence. Diets based solely on DNA testing have not demonstrated additional benefits in randomized studies.

The market, regulation and data privacy

  • The market: Commercial reports suggest that the nutrigenomics market is growing rapidly; estimates range for 2023 from approximately 450 million dollars to estimates for 2025 of approximately 610 million dollars, and for 2035 of approximately 3 billion dollars. Estimates vary between reports and are not independent scientific sources.
  • Regulation: The United States Food and Drug Administration (FDA) does not review non-medical, "general wellness" direct-to-consumer tests before they enter the market, and advises consumers to consult a healthcare professional before making dietary or health decisions based on these tests. An international consensus report published in 2017 also emphasizes that nutrigenetic tests are unregulated and lack defined standards.
  • Advertising oversight: In 2021, the United Kingdom Advertising Standards Authority ruled that an advertisement for a DNA diet test claiming to "unlock the secret of your ideal diet" was unsupported by evidence.
  • Data privacy: Genetic data are permanent and concern your relatives as well as you. The company 23andMe, which holds the genetic data of millions of people, filed for bankruptcy in March 2025 and was sold to a nonprofit research organization in July 2025. This process raised the question of what happens to genetic data when companies change hands.
The situation in Türkiye
  • Tests are widespread: Many laboratories in Türkiye offer tests called "DNA diet", "genetic diet test" or "nutrigenetic test". Prices are, for example, around 199 dollars for a test from an international company and 249 euros for a domestic package including a dietitian consultation. Some promotions contain unsupported promises such as "permanent weight loss".
  • Genetic data are sensitive: The Personal Data Protection Law (KVKK) classifies genetic data as "special-category personal data". Before taking a test, obtain written information on where and for how long your data will be stored and with whom they may be shared.
  • Professional organization views: We could not find a published opinion from dietitian or nutrition organizations in Türkiye regarding DNA diet tests.

What should you do in practice?

  • Start with the basics: A balanced diet rich in vegetables, fruit, legumes and whole grains, with little processed food, applies to everyone. We compiled the basic tips for healthy eating in a separate article.
  • Start personalization with your current diet: Reviewing your current diet with a dietitian and receiving specific feedback is more useful than a DNA test.
  • If you have a specific medical question (lactose intolerance, suspected celiac disease, a family history of high cholesterol), consult your physician; medical genetic testing may be ordered if necessary.
  • If you are considering a DNA diet test: Ask which genes are examined, what scientific evidence supports each recommendation and how your data will be protected.
  • Observe your own response: Your own experience, such as how coffee affects your sleep or palpitations, is often more informative than your genotype.

Frequently asked questions

Can a DNA diet test tell me the best diet for me?
Not with current evidence. Randomized studies have not shown that advice based on genetic information provides additional benefits over general advice or advice tailored to a person's current diet. Nor can your genotype predict whether a low-fat or low-carbohydrate diet will suit you better.
I carry a risk variant in the FTO gene; is losing weight impossible?
No. The FTO risk variant is associated with an average of a few extra kilograms; however, carriers respond to weight-loss programs involving diet, exercise and medication just as well as others.
If I have a slow caffeine-metabolizing genotype, should I stop drinking coffee?
There is no definitive genotype-based recommendation on this issue. General advice is that healthy adults should not exceed 400 mg daily (approximately 3-4 cups of filter coffee). Observing how coffee affects your sleep, palpitations or blood pressure, and consulting your physician if you have heart disease, is more informative.
How do my genes affect my cancer risk and diet?
Apart from some inherited cancer syndromes, findings that genetic differences interact with diet to alter cancer risk are limited and inconsistent. Risk factors such as red and processed meat, alcohol and excess weight matter for everyone, regardless of genotype. We discussed the relationship between nutrition, genetics and cancer in this article previously.
When is nutrition-related genetic testing truly necessary?
For specific medical questions, such as suspected lactose intolerance or celiac disease, familial inherited high cholesterol or iron accumulation disease, genetic tests performed after a physician's assessment are useful.
Are my genetic data safe?
Everyone having a test should ask this question. Genetic data are permanent and also concern your relatives. Under the KVKK, genetic data are special-category personal data; before testing, find out how your data will be stored, with whom they may be shared and whether you can request deletion.

Glossary

Nutrigenetics
The field studying how genetic differences affect responses to foods.
Nutrigenomics
The field studying how foods affect gene activity.
Epigenetics
Mechanisms determining when and how much genes function without changing the DNA sequence.
Polymorphism
Common small differences in DNA sequences between individuals.
Genotype
The combination of the two copies a person carries at a particular gene region (for example, AA, AC or CC).
Microbiota
All the bacteria and other microorganisms living in the gut.
Randomized controlled trial
A type of study that randomly assigns participants to groups and most reliably demonstrates the effect of an approach.

DROZDOGAN Academy Commentary

We are all unique; that is true. But the part of our uniqueness reflected in nutrition is not written only in our genes. Our gut bacteria, sleep, when and how we eat, activity and habits are at least as influential as our genes.

⚡ Why it matters

DNA diet tests are a rapidly growing market and are often sold with promises beyond the scientific evidence. A false sense of confidence can lead people away from proven healthy eating principles. Genetic data privacy is also becoming increasingly important.

✅ Solid findings

Randomized studies have shown that people respond differently to the same foods and that personalized dietary advice can be more effective than general advice. Genetic tests have a clear role in specific conditions such as lactose intolerance and celiac disease.

⚠️ Limitations

Genetic information has not been shown to provide additional benefits to dietary advice. The effects of individual genes are small; most findings on gene-diet interactions are observational and have not been replicated. Evidence for approaches based on multiple data is promising but still limited and comes mostly from commercial companies.

🩺 What to do in practice
  1. First, proven healthy eating principles should be applied.
  2. Start personalization with an assessment of your current diet .
  3. For a specific medical question , consult your physician if genetic testing is needed.
  4. If you are going to have a DNA diet test, the evidence and data privacy should be questioned.
❓ Open questions

Will approaches combining genetic, microbiota, blood value and lifestyle data prevent disease more effectively than general advice in the long term? Can polygenic risk scores make a meaningful contribution to dietary advice? Will independent quality standards be established for DNA diet tests?

Our brief verdict: Personalized nutrition is a scientifically meaningful goal; however, it cannot currently be achieved with a saliva test. There is no approved "DNA diet" supported by high-level evidence. The most reliable route to personalization is to adapt proven nutrition principles to a person's current diet, health, blood values and living conditions.

Transparency note
  • This article was updated in September 2026. Sources used include Food4Me (2017), DIETFITS (2018), the FTO meta-analysis (2016), the Frayling (2007) and Sonestedt (2009) studies, the Cornelis (2006) CYP1A2 study, the EFSA 2015 caffeine opinion, the MTHFR meta-analysis (2012), the NAT2 pooled analysis (2014) and Le Marchand (2002) study, PREDICT (2020), Zeevi (2015) and ZOE METHOD (2024), Dutch Hunger Winter studies, the United States Academy of Nutrition and Dietetics 2014 position paper and 2021 consensus report, the consensus report by Grimaldi and colleagues from 2017, FDA statements, the United Kingdom Advertising Standards Authority ruling, sources on lactose and celiac genetics, and laboratory pages in Türkiye.
  • Corrections: The previous version stated for CYP1A2 that "GA and AA variants have difficulty tolerating caffeine; up to 400 mg can be consumed with GG". This is an A/C variant, the AA genotype is the fast-metabolizing group, and the 200/400 mg limits were established for the general population rather than by genotype. The statement that MTHFR C677T increases colorectal cancer risk was corrected according to meta-analyses. The interaction between NAT2 and well-done red meat was softened because it was not confirmed in a large pooled analysis. The finding in the FTO example was identified as observational and unsupported by randomized studies. The statement "particularly preferred by professional athletes" was removed because it lacked source support.
  • Reported from secondary sources: Some findings on MTHFR and folate come from a review; the 23andMe bankruptcy and sale process from company statements and review sources; market size from commercial reports; prices in Türkiye from company pages; and the KVKK definition of genetic data from a summary of a Board decision.
  • Unverified: The views of dietitian or nutrition organizations in Türkiye on DNA diet tests; current test prices in Turkish lira in Türkiye; results of systematic reviews on continuous glucose monitor use in people without diabetes; and the numerical methylation difference in the Dutch Hunger Winter study's 2008 publication.
  • Based on general knowledge: The use of breath tests for lactose intolerance, the prevalence of HLA-DQ2/DQ8 carriage in the population, the role of genetic diagnosis in phenylketonuria, hemochromatosis and familial hypercholesterolemia, the equivalence of 400 mg caffeine to approximately 3-4 cups of filter coffee, and general healthy eating advice are presented as established knowledge.
  • The evidence levels, diagrams and Academy commentary are our own. The diagrams derive from verified statements in the text; they contain no new data.
  • This article is not personal medical advice. We have no conflict of interest involving any company or product.

References

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  5. Sonestedt E et al. Fat and carbohydrate intake modify the association between genetic variation in the FTO genotype and obesity. Am J Clin Nutr. 2009.
  6. Cornelis MC et al. Coffee, CYP1A2 genotype, and risk of myocardial infarction. JAMA. 2006.
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  13. Heijmans BT et al. Persistent epigenetic differences associated with prenatal exposure to famine in humans. PNAS. 2008.
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