Fries or banana: the same calorie, a different message
Two hundred calories is a number from a combustion chamber. Your immune system reads something else: composition, heat, processing, and everything that comes along with it.
More texts from the nutrition cluster
The calorie measures how much heat a food gives off when you burn it. It says not one word about the message that arrives in your immune system. Food is not only fuel. It is information.
Lunch break. Two plates. On one of them a small portion of fries, on the other two bananas. Both carry roughly the same amount of energy. On any nutrition calculator they look identical.
And still, something very different happens afterwards in these two bodies.
I hear this question often in my practice: if I eat the same number of calories by the end of the day, surely it makes no difference where they come from. On the scale that is sometimes roughly true. For your immune system it is not.
What to expect here
- Why the calorie is a price tag without an ingredient list
- What happens in the immune system in the hours after eating
- Why bacterial signalling material rises in the blood after fatty meals
- How inflammation is measured, and where hs-CRP reaches its limits
- AGEs, acrylamide and the controlled trial that found nothing
- Repeatedly heated frying oil: rat data and human observation
- Emulsifiers between mouse data and a mild human study
- What the banana brings biochemically, beyond vitamins
- The Dietary Inflammatory Index and its weaknesses
Two plates, the same number, two different messages
The calorie comes from a device called a bomb calorimeter. You burn a sample and measure the heat. A clean physical measurement. But it answers only one question: how much energy is in there.
What it does not measure: how fast that energy arrives. Which messengers get released along the way. Whether your gut bacteria get anything at all. Whether your immune system briefly stands up and takes a look.
The calorie is a price tag. It tells you what something costs, but nothing about what is inside the bag. The thermodynamic side is covered in the calorie myth. Here it is about what your immune system reads out of a meal.
Fries from the deep fryer
- Starch, quickly available, together with plenty of fat
- High temperature, and with it Maillard products and acrylamide
- Oil with a history, depending on the fryer heated many times over
- Very little fibre per calorie
- In processed versions often emulsifiers
Two bananas
- Sugar, but packaged in cell structure and fibre
- No heat, barely any newly formed glycation products
- Resistant starch depending on ripeness, food for bacteria
- Potassium in a relevant amount
- Polyphenols as companions
This is not a moral verdict, it is a list of variables that the calorie number leaves out. Those are exactly the ones that make the difference in the studies.
You are not imagining things when your body responds differently to two portions of the same size. You ate two different signals. The question is rarely whether something is allowed, but which message you send how often.
And now you know why the same number on two plates does not have to mean the same thing.
The hours after eating: your immune system briefly stands up
Do you know that feeling after a heavy lunch? Heavy, sluggish, as if someone had turned the volume down in your head. In the background, something measurable is running during those hours.
Specialists call it the postprandial phase. Picture a security desk: a delivery arrives, someone stands up and checks it. Not an alarm, simply the job. What matters is how large the delivery is and how often someone has to stand up.
A group around Ghanim gave twenty healthy people 910 calories each, one half as a meal of fat and fast carbohydrates, the other half rich in fibre and fruit.
After the meal high in fat and carbohydrates, plasma lipopolysaccharide, SOCS-3, Toll-like receptors 2 and 4 and NF-kappaB binding activity rose significantly. After the calorie-matched meal, all of these rises stayed away.
For you that means: same person, same calorie count, two different immune responses.
Ghanim et al., Diabetes Care 2009. DOI: 10.2337/dc09-0979 [RCT, n=20]Herieka and Erridge evaluated 57 such studies. The markers floating freely in plasma rose inconsistently, while those on the white blood cells rose almost every time. The response is real, it is simply often looked for in the wrong place.
A second level surprises many people. After a fatty meal, bacterial signalling material rises in the blood, even in healthy people. The technical term for it is metabolic endotoxaemia. The gut lining is a row of doormen: nutrients may pass, bacterial fragments may not.
Erridge and colleagues put twelve healthy men through four conditions: fasting, three cigarettes, a high fat meal, and both together.
From a baseline of 8.2 pg per millilitre, endotoxin rose by about 50 percent after the high fat meal. Without a meal, or after smoking alone, that did not happen.
For you that means: not a sign of illness, but a normal process. The question is how high the wave is and how often it comes.
Erridge et al., Am J Clin Nutr 2007. DOI: 10.1093/ajcn/86.5.1286 [RCT, n=12] · Herieka & Erridge, Mol Nutr Food Res 2014. DOI: 10.1002/mnfr.201300104 [Systematic Review]The term comes from animal research. Cani and colleagues fed mice a high fat diet for four weeks and saw plasma endotoxin rise to two to three times the baseline. In humans, only the short term rise has been documented so far.
If these waves come often and high, the baseline level can shift. That also has to do with weight regulation: silent inflammation and weight.
The inflammatory response after eating is not a fault in your body, it belongs to the work of digestion. It becomes interesting through two questions: how high does the wave rise, and how often does it come. Both can be influenced, without prohibitions.
And now you know why a single meal leaves measurable traces.
How do you measure inflammation at all? hs-CRP and its limits
Many people come into my practice with a blood panel and say: my inflammation value was normal, so it cannot be that. I understand the conclusion. It is simply not as solid as it sounds.
What is usually meant is C-reactive protein. It is produced in the liver when interleukin-6 arrives there, and it shoots up during pneumonia. For low grade inflammation, the more sensitive variant is used, high sensitivity CRP.
In the SEASONS study from Massachusetts, a more inflammatory dietary pattern was associated with an hs-CRP above 3 mg per litre, with an odds ratio of 1.08 and 1.10 respectively. So the association exists, but per point it is small.
The limit becomes even clearer in an analysis of 2,567 postmenopausal women. There, interleukin-6 and TNF-alpha receptor 2 tracked with the dietary pattern, while hs-CRP did not.
That is not a contradiction, it is a hint about the tool. CRP is unspecific. It rises with a trivial infection and after hard training. And the short wave after a meal is usually not captured by it at all.
An unremarkable hs-CRP is good news, but it is not proof that low grade inflammation is absent. Conversely, an elevated value proves no dietary cause, because a trivial infection can produce a similar swing. A trend over time says more, and putting it in context belongs in a conversation with your physician.
Not every inflammation is visible, and not every visible value is inflammation. A lab value is a window, not an X-ray.
And now you know why a normal inflammation value does not settle the nutrition question.
Heat, browning, aroma: AGEs and acrylamide
The smell when fries come out of the hot fat is no accident. It comes from the Maillard reaction, the same one that gives bread its crust. It has a side effect: advanced glycation end products form, AGEs for short, meaning protein structures that have become sticky.
The group around Uribarri at Mount Sinai built a large AGE database and systematically compared methods of preparation.
Dry heat raised AGE formation ten to a hundred fold across all categories. Vegetables, fruit, whole grains and milk contain little even after cooking. Moist heat, short cooking times and acidic ingredients lowered it considerably.
For you that means: the same potato steamed and deep fried are two different things.
Uribarri et al., J Am Diet Assoc 2010. DOI: 10.1016/j.jada.2010.03.018 [Mechanism Review]With starchy foods a second compound joins in: acrylamide. It forms from asparagine and reducing sugars as soon as the temperature climbs above roughly 120 degrees Celsius.
The panel on contaminants of the European Food Safety Authority assessed the evidence on acrylamide in 2015.
It chose a reference point of 0.17 mg per kilogram of body weight per day for neoplastic effects in mice and 0.43 mg for nerve damage in rats. Potato products, coffee and baked goods contribute most to intake.
For you that means: this is about years, not about one portion. Golden rather than dark brown.
EFSA CONTAM Panel, EFSA Journal 2015. DOI: 10.2903/j.efsa.2015.4104 [Systematic Review]Mechanistically the story is described. AGEs dock onto a receptor called RAGE, and through it NF-kappaB can be activated. And this is where I place things differently from many advice articles. The methodologically strongest human trial on it found no difference.
Linkens and colleagues randomised 73 abdominally overweight but otherwise healthy people, double blind, to four weeks of a low AGE or a high AGE diet. Insulin sensitivity, vascular function, inflammation and lipid profile were measured.
Intake of the individual AGE compounds differed by 2.7, 5.3 and 3.7 fold, verifiable in urine and plasma. No target value showed a difference. Anyone who presents AGEs as the main culprit would have to account for this trial too.
Linkens et al., JCI Insight 2022. DOI: 10.1172/jci.insight.156950 [RCT, n=73] · Ribeiro et al., Nutr Rev 2019. DOI: 10.1093/nutrit/nuz034 [Systematic Review]
The more interesting question is not whether AGEs are evil. It is this: why does the same substance stand out in observational data and not in the controlled experiment. Perhaps the association is measuring the processed, high fat pattern around it.
And now you know why heat plays a role, but probably not the leading one.
The oil that has already been hot twenty times
Hardly anyone thinks about the ingredient list at a takeaway, and even less about the fryer. Yet the history of the oil is measurable. Oil oxidises when heated, and the more often it gets hot, the further that runs.
Ng and colleagues fed rats for six months with fresh soybean oil, or oil heated five or ten times.
Blood pressure rose by 20 and 33 percent respectively with heated oil, while it stayed stable with fresh oil. The vessel wall thickened, VCAM-1 and ICAM-1 went up.
For you that means: a rat experiment, not numbers you can transfer to humans. What stays: fresh oil was unremarkable, heated oil was not.
Ng et al., Int J Exp Pathol 2012. DOI: 10.1111/j.1365-2613.2012.00839.x [In vivo, rat]A group around Qin pooled the observational studies on the consumption of fried food.
Highest versus lowest intake produced a relative risk of 1.28 for major cardiovascular events and 1.37 for heart failure, rising linearly. For mortality there was no association, and heterogeneity was high.
For you that means: more fried food goes along with more events. Recall bias and spread are named by the authors themselves as weaknesses.
Qin et al., Heart 2021. DOI: 10.1136/heartjnl-2020-317883 [Meta-analysis, k=17]When cardiovascular risk comes up, cholesterol almost always enters the conversation. My take on that is in the cholesterol myth.
The point is not the oil in itself, but its history. Fresh fat and fat heated twenty times are chemically not the same thing. That is the difference between oven potatoes and fries from a fryer that has been running for days.
And now you know why the question about preparation is sometimes more important than the one about the food itself.
Emulsifiers: the detergents on the ingredient list
Many packages carry numbers with an E in front of them. E 466 is carboxymethylcellulose, E 433 is polysorbate-80. Both are emulsifiers, chemically related to what sits in your dish soap.
Your gut lining carries a mucus layer whose inner part is normally almost free of bacteria. A safety zone between microbiome and cells. What happens if you regularly eat mild detergents along with your food?
Chassaing and colleagues gave mice low concentrations of both emulsifiers and used germ free animals and faecal transplants to separate cause from effect.
Both produced low grade inflammation, excess weight and metabolic syndrome in the mice, and in susceptible animals a pronounced gut inflammation. The microbiome moved closer to the mucosa, and that change was necessary and sufficient.
For you that means: a mouse study, which in the first place says something about mice. It explains why researchers then looked in humans.
Chassaing et al., Nature 2015. DOI: 10.1038/nature14232 [In vivo, mouse] · Viennois et al., Cancer Res 2017. DOI: 10.1158/0008-5472.CAN-16-1359 [In vivo, mouse]A follow up paper additionally described increased tumour development in the colon in the mouse model. That too is animal research, and I do not scale it up. Seven years later the first human study arrived. It is called FRESH and it is small.
Healthy adults received an emulsifier free diet for eleven days, or the same diet with 15 grams of carboxymethylcellulose per day, double blind. Nine versus seven people.
More abdominal complaints occurred, microbiome diversity was lower, short chain fatty acids in stool went down. In two of seven, the microbiome advanced into the otherwise largely bacteria free mucus layer.
For you that means: the effect in humans is real, but far milder than in the mouse. What stands out is the spread.
Chassaing et al., Gastroenterology 2022. DOI: 10.1053/j.gastro.2021.11.006 [RCT, n=16]The gap in size between mouse and human is not the fine print here, it is the message. Anyone who turns the Nature paper into a supermarket alarm skips the human trial. Anyone who reads it as an all clear skips the two out of seven.
From the perspective of Clinical Psychoneuroimmunology, the point is not whether an additive should be banned. The interesting question is: why do some people react clearly and others not at all. That is unresolved, and it is not an established way of typing people.
And now you know why an ingredient list tells you more than a nutrition table.
The fatty acid ratio: which tone your immune system strikes
Fat is not only energy. From certain fatty acids your body builds messengers that either fuel inflammation or dial it down. They are called eicosanoids, and their raw material comes from what you eat.
Omega-6 fatty acids tend to yield the fuelling variants, omega-3 fatty acids the calming ones. Both are essential for life. It is about proportions. Frying oils often consist largely of plant oils rich in omega-6.
In 2002 Simopoulos gathered studies on the ratio of omega-6 to omega-3 in a review article.
Human dietary history, according to that work, rested on a ratio around 1 to 1, while western diets sit at roughly 15 to 1 up to 16.7 to 1. In the individual studies, 4 to 1 was favourable in secondary prevention. The favourable ratio appears to depend on the condition.
For you that means: a useful tool for thinking, no more than that. A review from 2002, not a meta-analysis, and its significance is still being debated.
Simopoulos, Biomed Pharmacother 2002. DOI: 10.1016/s0753-3322(02)00253-6 [Mechanism Review]I consider the ratio idea a good picture and a poor target. Good, because it explains why fat quality counts. Poor, because hardly anyone can steer that number. More on this under omega-3 from plants, animals or algae and ALA, EPA and DHA.
You do not have to calculate a ratio. It is enough to know which material your body builds its messengers from. If you rarely eat fried food and regularly have omega-3 sources on your plate, you can shift that material slowly.
And now you know why the type of fat means more than its amount in grams.
The other side: what the banana brings biochemically
So far it has been about what might be unfavourable. A banana delivers sugar, that is true. But packaged: in cell structure, in fibre, with potassium, polyphenols and, depending on ripeness, resistant starch.
Reynolds and colleagues produced systematic reviews on carbohydrate quality for a series co-funded by the WHO.
At highest versus lowest fibre intake, all-cause mortality, coronary heart disease, stroke, type 2 diabetes and colorectal cancer were 15 to 30 percent lower, most favourable between 25 and 29 grams per day. For the glycaemic index, effects were small and the evidence was low.
For you that means: the amount of fibre carries the evidence, not the glycaemic index.
Reynolds et al., Lancet 2019. DOI: 10.1016/S0140-6736(18)31809-9 [Meta-analysis, k=185 cohorts]Fibre is not filler material, it is food. Bacteria in the colon break it down and form short chain fatty acids. One of the most important is called butyrate, the preferred fuel of the colon lining. With unripe bananas, resistant starch comes on top.
In a crossover study with twelve people, the breakdown of resistant starch fed the butyrate producers. Seven showed the pattern fully, four a mixed picture, one person not at all. More on this under L-glutamine and butyrate.
Then there is potassium. In a WHO meta-analysis of 22 randomised trials, a higher potassium intake lowered systolic blood pressure by 3.49 mmHg. The effect showed up in high blood pressure, not in normal blood pressure.
The 2021 international tables classify fruit as a group as low glycaemic, while most potato varieties rank high. That does not answer your personal curve, and there is a separate text on blood sugar spikes.
| What is measured | Portion of fries | Two bananas |
|---|---|---|
| Energy | comparable | comparable |
| Postprandial immune response | clearly pronounced with fat plus fast carbohydrates | not detectable in the same experiment |
| Glycation products | high through dry heat | low, no heat treatment |
| Acrylamide | relevant contribution per the authority | no contribution |
| State of the fat | depends on how often the oil was hot | not applicable |
| Fibre per calorie | low | higher, plus resistant starch |
| Food for butyrate producers | hardly any | yes, individually different |
| Potassium | low | relevant everyday source |
| Glycaemic classification | mostly high | fruit as a group low |
One lever is missing from almost every advice article: the postprandial wave can also be influenced by combining.
Three groups of ten healthy people each drank either water, a glucose solution or orange juice with the same calorie count alongside a 900 calorie meal of fat and fast carbohydrates.
After water or glucose, several inflammatory signals rose, among them Toll-like receptors 2 and 4 and plasma endotoxin. In the orange juice group they stayed away. A second group found a similar pattern with 18 people.
For you that means: it is not only about removing things, it is also about combining them.
Ghanim et al., Am J Clin Nutr 2010. DOI: 10.3945/ajcn.2009.28584 [RCT, n=30] · Cerletti et al., Thromb Res 2015. DOI: 10.1016/j.thromres.2014.11.038 [RCT, n=18]On the plant side there is a much discussed candidate: turmeric and inflammation. Why unprocessed foods fill you up differently is covered in the text on unprocessed food.
A banana is not medicine. It is fruit. Three bananas a day make nobody healthier on their own, and a single portion of fries decides nothing. Your body receives thousands of meals over the years. The sum is what counts.
And now you know why the second side of this comparison is not made of vitamins, but of structure, bacterial food and companion compounds.
The Dietary Inflammatory Index: a tool, not a verdict
Is there a number for the overall inflammatory effect of a diet? There is one. It is called the Dietary Inflammatory Index, DII for short, and it shows nicely how a research tool can be used well and badly.
A team at the University of South Carolina screened around 6,500 papers on the effect of dietary parameters on six inflammatory markers. 1,943 of them were computed into a score across 45 parameters.
The maximally pro-inflammatory diet reaches plus 7.98, the maximally anti-inflammatory one minus 8.87, and the global median sits at plus 0.23.
For you that means: the scale judges no single food, it judges a pattern over time.
Shivappa et al., Public Health Nutr 2014. DOI: 10.1017/S1368980013002115 [Mechanism Review] · Tabung et al., J Nutr 2016. DOI: 10.3945/jn.115.228718 [Cohort, n=5,230 plus n=3,634]The index has been tested against blood values several times. A Harvard group found the same association with CRP and adiponectin using its own, empirically built index.
A Spanish group examined two large cohorts for DII and all-cause mortality, then pooled twelve cohorts.
In the extreme quartile comparison the hazard ratio was 1.85 and 1.42 respectively, and in the meta-analysis the highest DII range was associated with 23 percent higher all-cause mortality.
For you that means: consistent across many countries, and still an association rather than proof of cause and effect.
Garcia-Arellano et al., Clin Nutr 2019. DOI: 10.1016/j.clnu.2018.05.003 [Meta-analysis, k=12 cohorts]It rests on memory. In questionnaires people systematically underestimate what they eat and overestimate what sounds good.
The effect sizes are small. In SEASONS the odds ratio per point was 1.08 to 1.10. Statistically demonstrable, unremarkable for a single person.
It was built for populations, not for you. As a diagnostic for an individual it is not validated.
Observational data show no causality. People who eat in a less inflammatory way also move more, smoke less often and sleep better. You can correct for that confounding statistically, but never completely.
The same holds for the processing data. An umbrella review of 45 pooled analyses covering nearly 9.9 million people found associations with ultra processed foods for 32 of 45 parameters. Under GRADE, 41 of them are of low quality.
Twenty weight stable adults lived in a research centre for four weeks, two weeks each on an ultra processed and on an unprocessed diet, matched for calories, macronutrients, sugar, sodium and fibre.
In the ultra processed phase they ate 508 calories more per day, weight went up by 0.9 kilograms and came down by the same amount in the other phase.
For you that means: with the same nutrient balance on paper, the degree of processing can change eating behaviour.
Hall et al., Cell Metab 2019. DOI: 10.1016/j.cmet.2019.05.008 [RCT, n=20] · Lane et al., BMJ 2024. DOI: 10.1136/bmj-2023-077310 [Systematic Review]Conversely, the baseline level also moves in the other direction. In the PREDIMED sub-studies, C-reactive protein, interleukin-6 and adhesion molecules fell on a Mediterranean diet, while they rose on a low fat diet.
Directions instead of prohibitions
- Proportion before purity. It is not the one portion that counts, but how often in the week a meal is heavily processed, high in fat and low in fibre.
- Watch the temperature. Moist heat, shorter cooking times and an acidic ingredient can lower the new formation of glycation products.
- Fibre as the foundation. The evidence is steadier here than for the glycaemic index. 25 to 29 grams per day was the most favourable range.
- Combine instead of only removing. In two small studies the postprandial response stayed away when something rich in polyphenols was drunk alongside.
- Pay attention to your own spread. In the small studies not everyone reacted the same way. What happens in you is something only you can observe.
For the body, food is not only fuel. It is information. And information can be dosed, without being forbidden.
If you want to do more than read, and would like your own values and your own pattern put in context: below this article you will find the option to book an appointment.
The Dietary Inflammatory Index is not a list of prohibitions, it is an attempt at order for researchers. What you can take away is not a number but a question: in my life, what is the proportion between the meals that wake my immune system up and the ones that leave it in peace?
And now you know why there is no list of forbidden foods in this article.
Frequently asked questions about inflammatory foods
Are fries really that unhealthy, or is that exaggerated?
Neither. A single portion on its own decides nothing. What stands out is the sum over years. A meta-analysis of 17 observational studies found a 28 percent higher relative risk of major cardiovascular events at the highest intake of fried food. For all-cause mortality there was no association, and the spread between studies was wide. These are observational data, not proof of cause and effect. The useful question is one of frequency, not of prohibition.
How many calories does a banana have, and why is that the wrong question?
The calorie count only describes how much heat is released when a food is burned in a laboratory. It says nothing about how fast the energy arrives, what your gut bacteria get out of it, and whether your immune system reacts. A banana brings fibre, potassium, resistant starch depending on ripeness, and polyphenols along with it. Those companions are exactly what the number leaves out.
What is postprandial inflammation, and would I even notice it?
Postprandial means: after eating. Inflammatory signals rise briefly afterwards, and that belongs to the work of digestion. In one controlled study, Toll-like receptors 2 and 4, SOCS-3 and plasma lipopolysaccharide rose clearly after a meal of fat and fast carbohydrates. After a calorie-matched meal rich in fibre and fruit, those rises did not appear. Most of the time you feel nothing of it.
Is feeling tired after a meal a sign of inflammation?
That cannot be said that way. Tiredness after eating has many possible reasons: portion size, the distribution of blood flow, the blood sugar curve, the sleep of the night before. The postprandial immune response runs in parallel, but it is not established as the cause of that feeling. It is still a signal worth looking at.
What are AGEs, and which foods contain the most of them?
AGEs are advanced glycation end products. They form when sugar and protein react under heat, in the same Maillard reaction that gives bread its crust. A large database project found that dry heat can raise the AGE content ten to a hundred fold across all food groups. Animal foods rich in fat and protein rank highest. Moist heat, shorter cooking times and acidic ingredients lowered new formation considerably.
Is acrylamide in fries dangerous, and from what amount?
The European Food Safety Authority assessed acrylamide in 2015 and set a reference point of 0.17 mg per kilogram of body weight per day for neoplastic effects in mice, and 0.43 mg for peripheral nerve damage in rats. Acrylamide forms when starchy foods are heated above roughly 120 degrees Celsius. Potato products, coffee and baked goods contribute most to intake. In practice that means: golden rather than dark brown.
Are emulsifiers such as E 466 harmful to the gut?
In mice the data are clear. Carboxymethylcellulose and polysorbate-80 produced low grade inflammation there and let bacteria move closer to the mucosa. In humans there is so far a single controlled study: 16 people, eleven days, 15 grams daily. The effects were milder. In two of seven participants bacteria approached the inner mucus layer. A signal worth taking seriously, not proof of harm at everyday amounts.
Which foods promote inflammation the most?
There is no clean ranking, and lists of that kind usually mislead. What does emerge is a pattern: heavily processed products, plenty of fast carbohydrates and fat in the same meal, high cooking temperatures, repeatedly heated frying oils, little fibre. An umbrella review of 45 pooled analyses found associations with ultra processed foods for 32 of 45 health parameters, while rating the data quality as mostly low.
How long does it take for inflammatory markers to change through diet?
Very fast in the short term, slow in the long term. The response to a single meal is measurable within one to five hours. Shifting a baseline level takes longer. In the PREDIMED sub-studies, C-reactive protein, interleukin-6 and adhesion molecules fell on a Mediterranean diet within months, while they rose on a low fat diet.
Which blood value shows silent inflammation, and when is it abnormal?
High sensitivity CRP is measured most often. In the SEASONS analysis a value above 3 mg per litre counted as the threshold for an elevated level. The value has limits though. It rises with a trivial infection and often does not capture the short wave after a meal at all. In an analysis of 2,567 women, interleukin-6 and TNF-alpha receptor 2 tracked with the dietary pattern, while a dichotomised hs-CRP did not.
Does a banana have too much sugar if I watch my blood sugar?
The 2021 international tables for the glycaemic index classify fruit as a group as low glycaemic, meaning 55 or below on the glucose scale. Most potato varieties, by contrast, rank high. With bananas the value also depends on ripeness, because unripe fruit contains more resistant starch. Your individual answer is shown more precisely by a glucose sensor worn over two weeks than by any table.
Do I now have to give up fried food completely?
No, that would not be the message of this article. What the data suggest is a question of frequency and proportion. One detail from the animal work is interesting: fresh oil was unremarkable there, repeatedly heated oil was not. And two small human studies point to a second lever. In people who drank something rich in polyphenols with a high fat meal, several inflammatory signals did not appear.
Where this topic leads next
The question of what message a meal sends does not end at the plate. It leads on into the gut, into cellular energy, and into the question of what can be measured at all. From here, several paths lead into other areas.
Fries or banana
The same calorie, two messages to your immune system
this articleGut barrier and zonulin
What the evidence on intestinal permeability actually shows
Butyrate and mucosa
Where the colon cells get their preferred fuel from
Measuring the omega-3 index
The blood value that reflects the fat quality of your membranes
And if you are looking for the systems perspective, meaning the link between gut, inflammation and cellular energy, you will find it in the article on burnout, gut, inflammation and mitochondria.
Scientific sources
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- Shivappa et al. A population-based dietary inflammatory index predicts levels of C-reactive protein in the Seasonal Variation of Blood Cholesterol Study (SEASONS). Public Health Nutr. 2014;17(8):1825-33. DOI: 10.1017/S1368980013002565 PMID: 24107546 [Cohort, n=495 to 559]
- Tabung et al. Construct validation of the dietary inflammatory index among postmenopausal women. Ann Epidemiol. 2015;25(6):398-405. DOI: 10.1016/j.annepidem.2015.03.009 PMID: 25900255 [Cohort, n=2,567]
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