Er proteiner mettende?

«The mechanisms by which protein may affect satiety remain elusive.» 

Halton and Hu 2004 [1] 

Although the immediate satiating effect of dietary fat may be comparatively weak, there is no doubt that ingested fat does inhibit feeding.” 

Leonhardt 2004 [2] 

«Protein er bra både fordi det gjør at du blir mett og fordi det hjelper deg til å holde på muskelmassen når du slanker deg, sier Cathrine Borchsenius» 

For dem som følger med på kostholdsinformasjon i media og kostholdsdebatter generelt er det vanskelig å ikke få med seg at proteiner metter. ”Ekspert” på ”ekspert” fastslår at proteiner metter mer enn karbohydrater og fett og at et sunt kosthold helst inneholder fiberrike karbohydrater og mye proteiner.

Sunnhet og slanke kropper er nærmest blitt ensbetydende med hvitt kjøtt, kyllingfiléter, mager fisk, egg og magre meieriprodukter som cottage cheese. Dette er et ultramoderne kosthold, ettersom verken mennesker eller dyr i naturen bevisst ville forsøke å innta mye proteiner til fordel for fett eller karbohydrater. Det ville vært et evolusjonært feilspor og mennesker som lever på tradisjonelle kosthold vet at for mye proteiner ikke er lurt.

Proteiner egner seg ikke særlig som energisubstrat for kroppen. Derfor vil et kosthold med mye proteiner, i fravær av nok fett eller karbohydrater, gjøre oss slappe og uopplagte. Inuittene hadde et eget ord for dette: ”kaninsyken,” oppkalt etter hvordan man følte seg hvis man lot seg friste til å spise mye kaninkjøtt (i fraværet av fett) tidlig på våren når kaninene var tynne og inneholdt lite fett. 
Kosthold med lite karbohydrater virker positivt ved alle livsstilsykdommer og er den mest effektive slankemetoden vi kjenner til. Men om du ikke samtidig er villig til å spise mye fett er ikke dette en holdbar strategi. Kun de med en velfungerende metabolisme kan basere kosten på proteiner og karbohydrater med et lavt inntak av fett, og likevel ha god helse. Men det er da en selvfølge at man ikke inntar korn, sukker eller raffinerte planteoljer.

At proteiner er sunt og mettende blir gjerne trukket frem som en av de få tingene de ulike kostholdsleirene kan eniges om. Men, de samme som hevder at proteiner er mettende hevder gjerne at fett er lite mettende. Men den påstanden passer dårlig med vitenskapelige resultater. For hvis man gjør en kostholdsstudie (og mange slike har blitt gjort) der man ber folk spise mindre karbohydrater og mye fett, så går disse langt mer ned i vekt enn de som spiser lite fett. Ikke nok med det, i disse studiene kan de som spiser mye fett spise så mye de vil, det vil si når de er sultne og til de er mette, mens i gruppene som spiser mindre fett må man begrense det totale matinntaket for å gå ned i vekt.

Det hender at jeg, mer eller mindre ufrivillig, får et proteinbasert kosthold. Spesielt i perioder med mye jobb og da jeg ikke orker å lage god nok niste. Da ender det noen ganger opp med egg og kjøtt med lite fett eller liknende proteinrike matvarer. Dette fører over tid alltid til lavt energinivå og litt lavt blodsukker. Jeg blir trøtt, uopplagt, sliter med å konsentrere meg og ikke minst får jeg veldig lyst på karbohydrater. Det er i slike situasjoner, når man er skikkelig sugen på karbohydrater at man bør vente med å gå å handle mat.

Heldigvis vet jeg at om jeg bare spiser noe fettrikt, f.eks. kokosfett, vil jeg få tilbake energien og suget etter søtt vil forsvinne. Jeg kunne også følt meg bedre om jeg spiste noe karbohydratrikt, men jeg vet også at dette er en dårlig langsiktig strategi og noe jeg fort får lide for senere.

Er da egentlig proteiner så mettende som folk vil ha det til?

David Weigle og kolleger [3] satte 19 personer på 3 ulike etterfølgende dietter: Først en diett med nok energi til å holde kroppsvekten til deltakerne uendret, som inneholdt 15% protein, 35% fett og 50% karbohydrater. Denne ble fulgt i to uker. Deretter fulgte de en diett som inneholdt like mye energi, men med 30% protein, 20% fett og 50% karbohydrat. Denne ble også fulgt i to uker. Til slutt fulgte de et likt kosthold (30% protein, 20% fett og 50% karbohydrat), men nå kunne deltakerne spise så mye de ville. Dette ble fulgt i 12 uker. Underveis ble blant annet sult, metthet og kroppsvekt målt.

Desverre er ikke Weigle blant de mest opplyste forskere og skrev blant annet i innledningen

Both low-fat diets (2– 4) and low-carbohydrate diets that are high in fat and protein have been shown to cause a decrease in ad libitum caloric intake and significant weight loss in humans. Thus, it appears that diets with fat contents at opposite extremes have the same therapeutic result, despite evidence that excessive dietary fat intake promotes obesity.” 

Forskerne forstår ikke hvordan noen kan gå ned i vekt bade ved å spise mindre fett og mindre karbohydrater når de tross alt vet at fett er fetende, men de foreslår at dette kan forklares ut ifra proteininnholdet i maten:

This paradox could be explained if it is the high protein content rather than the lower carbohydrate content of low-carbohydrate diets that offsets the deleterious effect of high fat intakes and results in weight loss.” 

I de fleste studier med lavkarbodietter er ikke proteininntaket særlig høyt. Det er derfor ikke sannsynlig at proteinene har skylden for vekttapet, men for å vite dette må man lese studiene, noe Weigle ikke hadde gjort.

Studien til Weigle og kolleger blir ofte brukt for å hevde at proteiner er mettende. Målinger underveis viste at sultfølelse hos deltakerne ble redusert da de etter to uker startet dietten med 30% protein.

Konklusjonen i studien var slik

An increase in dietary protein from 15% to 30% of energy at a constant carbohydrate intake produces a sustained decrease in ad libitum caloric intake that may be mediated by increased central nervous system leptin sensitivity and results in significant weight loss. This anorexic effect of protein may contribute to the weight loss produced by low-carbohydrate diets.” 

Denne konklusjonen er problematisk av flere grunner. For det første gikk både sult og metthet hos utøverne tilbake til utgangspunktet så fort de igjen kunne spise så mye de ville, selv om de hele tiden inntok lik mengde protein. 

Fra Weigle et al: Figuren viser at sult (rundinger) gikk ned helt i fra starten, men spesiellt da deltakerne  startet med 30% protein (CRC1). Men sultfølelse gikk tilbake til utgangspunktet uten at proteininntaket endret seg.
For det andre var det, i denne studien som i alle slike studier, langt mer enn bare proteinmengden som varierte i de ulike diettene. Under er et eksempel på fra en dagsmeny i studien: 
Grunnen til at studien blir brukt til fordel for høyere proteininntak, er både at deltakerne rapporterte at de var mindre sultne i starten av studien, men også fordi energiinntaket gikk ned når proteininntaket gikk opp.

Kan man så konkludere fra en slik studie at sultfølelse hos deltakerne gikk ned (midlertidig) på grunn av det økte proteininntaket? Selvfølgelig ikke. Endringene kan være på grunn av proteinene, men de kan også være på grunn av en hvilken som helst annen kostholdsfaktor som endret seg.

Forfatterne er klar over dette og skriver om én av disse endringene at

It is likely that a reduction in dietary fat by 15% of total energy contributed to weight loss in the present study.” 

Annebeth Skov og kolleger [4] fordelte 65 personer på to forskjellige kosthold med seks måneders varighet. Begge innholdt 30% fett. Det ene kostholdet hadde 12% energi fra protein og det andre 25%. Etter seks måneder hadde lavproteingruppen gått ned 5.1kg mens høyproteingruppen gikk ned 8.9kg. Også denne studien brukes for å hevde at proteiner er mettende. Men også her var det mer enn bare proteinmengden som endret seg.

I denne studien blir kostholdet med 12% protein kalt et høykarbohydratkosthold mens 25% protein blir kalt et høyproteinkosthold. Dette får oss automatisk til å fokusere på proteinene. Men dette kostholdet inneholdt også en god del mindre karbohydrater slik at de to intervensjonene like gjerne kunne kalles lavkarbohydrat og høykarbohydrat. Dette er et gjennomgående problem i slike studier: Hva skal man kalle diettene? Egentlig er det akkurat det samme hva man kaller de, så lenge man husker å diskutere alle sider av saken. Dette blir dessverre ikke gjort, verken av forfatterne av slike studier eller fagpersoner som tolker dem. Når en diett i en studie kalles høyproteindiett, fokuseres det ofte alt for mye på proteinene og andre, like sannsynlige årsaksfaktorer, faller i skyggen.

Skov og hennes danske kolleger skrev senere at

The mechanisms responsible for the larger weight loss caused by an HP [high protein] diet may be attributed to a greater satiety and fullness, and also the thermogenic effect of protein.” 

Og tross alt, det kan være de har rett. Det kan godt være proteiner som er mettende. Men vi må også undersøke om det kan være andre faktorer. En rekke studier har målt metthet de første timene etter et inntatt måltid, og mange av disse har målt høyest metthet med måltider med mye proteiner. Men selv om det, basert på disse studiene, er riktig å si at proteiner er mer mettende enn karbohydrater og fett, er det fortsatt ikke hele sannheten og ikke den viktige delen av sannheten.

Det som betyr noe er hvor sultne vi er over tid, ikke hvordan vi har det rett etter et måltid. Studiene som sammenligner enkeltmåltider er som regel dårlig kontrollert, dvs man tar ikke hensyn til andre kostholdsfaktorer eller hva slags kosthold deltakerne har før testen. De er også ofte unaturlige måltider med proteininnhold på 40 – 75%. Dessuten er de gjort på svært få individer.

Én av disse studiene ble gjort av James Stubbs og kolleger [5]. De fant at et måltid med mye protein (60%) førte til størst metthet. Men de fant også at det ikke var noen forskjell i matinntaket ved neste måltid. Dette var også en av de bedre studiene av enkeltmåltider.

Thomas Holton [1] er klar over hvor usikre slike studier er og skriver

There are, however, some methodological issues concerning this type of research. Satiety appears to be influenced by a wide variety of factors including palatability, food mass, energy density, fiber and glycemic index. When using real foods, it is difficult if not impossible to control for all of these influences at the same time while still delivering different amounts of protein.” 

Fett blir ofte ansett å være det minst mettende næringsstoffet. Det er det helt garantert ikke. Som nevnt tidligere, vil mennesker som reduserer karbohydratinntaket til fordel for fett automatisk spise mindre og bli mindre sultne.

Som jeg skrev i den forrige posten, er det viktige at det er nok energi tilgjengelig for leverceller. En foreslått effekt av proteinindusert metthet er nettopp at proteinene blir omgjort til glukose som deretter kan forbrennes. Et kosthold med mye fett og lite karbohydrater sørger for konstant god energitilgjenglighet for lever og lite sult.

Troen på at proteiner er spesielt mettende ser ut til å være ubegrunnet. Den stammer blant annet fra virkelighetsfjerne forsøk av enkeltmåltider, som gir helt andre resultater enn kostholdsforsøk med reelle kosthold. En annen grunn til denne troen er at lavkarbo ofte blir ansett å være høyproteinkosthold, selv om det vanligvis ikke er det.

I en studie av Samaha og kolleger [8], fulgte deltakerne et lavkarbokosthold med 1630kcal, 22% protein, 41% fett og 37% karbohydrat, eller et lavfettkosthold med 1576kcal, 16% protein, 51% karbohydrat og 33% fett. Lavkarbogruppen gikk ned mest i vekt. I ettertid har lavkarbokostholdet i denne studien blitt omtalt som et høyproteinkosthold, til tross for at proteininntaket var godt under 1 gram per kilo kroppsvekt. Det er ganske enkelt usannsynlig at vekttapet her var på grunn av et høyt proteininntak.

Det kan også se ut til at det store fokuset på proteiner delvis kommer fordi stadig mer vitenskap viser at karbohydrater er spesielt fetende. Når så mange fortsatt tror at fett er fetende, sitter man igjen med proteiner.

At nok proteiner er bra, betyr ikke at mer er bedre. Endrer man proteinmengden så gjør man det alltid på bekostning av andre næringsstoffer og en eventuell effekt kan ikke i seg selv tilskrives endring i proteinmengde alene, men må sees i lys av annen kunnskap som sier noe om hvor sannsynlig det er at nettopp proteiner er årsaken. Det er ikke sannsynlig at et kosthold med mye protein til fordel for fett eller karbohydrater er verken mettende eller mulg å følge over tid.

Referanser

1. Halton TL, Hu FB: The effects of high protein diets on thermogenesis, satiety and weight loss: a critical review. J Am Coll Nutr 2004, 23: 373-385.

2. Leonhardt M, Langhans W: Fatty acid oxidation and control of food intake. Physiol Behav 2004, 83: 645-651.

3. Weigle DS, Breen PA, Matthys CC, Callahan HS, Meeuws KE, Burden VR, Purnell JQ: A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations. Am J Clin Nutr 2005, 82: 41-48.

4. Skov AR, Toubro S, Ronn B, Holm L, Astrup A: Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity. Int J Obes Relat Metab Disord 1999, 23: 528-536.

5. Stubbs RJ, van Wyk MC, Johnstone AM, Harbron CG: Breakfasts high in protein, fat or carbohydrate: effect on within-day appetite and energy balance. Eur J Clin Nutr 1996, 50: 409-417.

6. Friedman MI: Control of energy intake by energy metabolism. Am J Clin Nutr 1995, 62: 1096S-1100S.

7. Bessesen DH: Update on obesity. J Clin Endocrinol Metab 2008, 93: 2027-2034.

8. Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams T, Williams M, Gracely EJ, Stern L: A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med 2003, 348: 2074-2081.

Food reward, a factor in obesity

 “I think food reward offers the most compelling explanation for the US/global obesity epidemic.” 

Stephan Guynet 
In studies where the food intake and energy expenditure of subjects are carefully monitored over a period of weeks to months (which tends to average out day-to-day fluctuations) a remarkable balance between calories consumed and calories burned was observed. When various mammals, from mice to monkeys, are either overfed or starved for a few weeks, their weight soon returns to normal levels when free access to food is resumed. Crucially, our mammalian bodies seem to be able to regulate feeding based on the amount of energy available in the food we consume, not just on the volume of that food.

The above quote David Linden, suggests the body controls body weight by registering the amount of energy in food. This theorizing usually leads to the white adipose tissue derived hormone leptin and particularly its effect on the hypothalamus. Leptin, in general, correlate with adipose tissue mass. But the energy the body needs comes from two places: food and stored energy. Increasing use of stored energy will make animals and human eat less. Any energy-sensing control system must register the total amount of energy available, both from foods and from fat and glycogen stores. From this point of view, obesity could to be caused by the body not having access to its own stored energy and so continues to signal for food intake. Alternatively, the stored energy is readily available, but somehow an obese person experience feelings of hunger and craving that overpower any signal telling the brain that there is enough energy available. This scenario makes it likely that obesity is caused by a malfunctioning control system.

Stephan Guyenet has created quite a stir lately with his posts about food reward. Several of the posts have over 100 comments, some more rational than others, but people clearly have strong feelings about this. I think one of the reasons some people feel personally offended by his writing, is that they feel food reward lends support to overweight being caused by lack of willpower. This is definitely not Stephan’s intent, nor does his reasoning indicate willpower as a major factor. Nevertheless, willpower is a major part of food reward, as one of the opposing forces to a physiological drive to consume rewarding foods.

The theory of food reward is a theory of how foods affect our feelings, stimulate our behavior and how some foods appear addictive and promote addictive behavior. This seems lost on many. Food reward does not and cannot explain how we fatten. To find the answer to this we need to look at the physiology of the fat cells. Basic biochemistry still applies and some foods are more fattening than others, although as it seems, Stephan does not think so and he even uses his belief that macronutrients doesn’t matter as an argument in favor of the food reward theory. But the theory itself is a theory of why we (over)eat, not a theory of how we gain fat.

Even though the theory of food reward is not about willpower, willpower invariably enters into the equation. Many physiological drives can be affected by conscious thought. Stick your hand in ice water and your head tells you to pull it out (or your spine), but you can keep it submerged by willpower, some longer than others. Highly rewarding foods do, according to Guyenet, cause obesity in susceptible people, just like drugs may make addicts of some (often the same people). Still, I cannot see that food reward argues more strongly for willpower as a part of obesity, than other rational theories.

The theory of food reward is actually mostly about carbohydrates as most of the data relating to it is from the studying of sweet foods. As Hans-Rudolf Berthoud put it 

For nonsweet palatable foods (typically high-fat foods), there is less convincing evidence for development of dependence…” [1]
So it seems the key questions are:

– do sweet foods cause addiction and increased energy intake with subsequent obesity?

or
– do sweet foods cause obesity (fat storage) with following addiction or addiction like behavior possibly caused by metabolic clues?

As we undoubtedly fatten differently and not everyone becomes obese despite similar obesogenic environments, we can conclude that addiction to high palatability foods is 1) genetic and that preexisting differences in reward functions cause obesity; 2) intake of palatable foods is in itself addictive and leads to obesity; or 3) obesity (the excess storage of energy in fat tissue) cause changes in reward functions thus further accelerating obesity.

As many lean people also eat large amounts of highly rewarding foods, it seems unlikely that the food itself can be to blame. So, either food reward is secondary to the harmful effects of sugars/grains (sweet food not found in hunter gatherers): these foods create excessive fat storage in obesity prone people and this cause addictive behavior towards the very same foods; or it is the primary cause of obesity: people prone to weight gain have physiological measurable differences in parts of the brain that cause an addictive intake of fattening foods.

Although I enjoyed the posts about food reward I was left with very many unanswered questions after reading:

The reasoning 
Stephan uses the fact that hunter-gatherers are lean in support of rewarding foods causing obesity in non HG societies, arguing that one of the reasons hunter gatherers are lean is because their diets are bland (although I think many HG’s would disapprove of their diets being called bland). This argument could go both ways. Because if the foods that drive fat gain also promote addictive intake of the same foods, then traditional diets can be as tasty as any, just as long as they do not contain these particular foods. As long as they don’t, there is no reason to think blandness is the cause of leanness.

Although lean traditional people’s diets are more unrewarding then say a SAD diet, this does not mean that we in the west become obese because our foods are not.

Also we have to ask: if obese people remove fattening foods, which are the same as those considered highly rewarding, will the addictive behavior/strong cravings for the fattening foods subside? I know from experience that many who struggle with strong cravings, lose their cravings when switching to a LCHF diet. The fact that some feel cravings even after some time on low carb diets, does not favor a set-point hypothesis. It could just indicate a dietary insufficiency, like the lack of salts or some fatty acids. As the cravings usually disappear before a considerable weight is lost, it is unlikely that the cravings were caused by the obesity itself. Often, it seems that cravings disappear when people regain the ability to burn fat.

Burning fat, or having a functional metabolism will make us eat less. The oxidation of fat in the liver offers a strong satiety signal [2]. So, even if lipolysis is high in obese, hunger will not go down if somehow the burning of fat in the liver is restricted. This is sort of a “metabolism argument”: One of the things that separate those prone to obesity and insulin resistance from the rest, is a poor and broken metabolism. They rely on glucose (glycogen) for fuel and have poor fatty acid oxidation in combination with blood sugar fluctuations and cravings, so fat is stored rather than burned as it should. Resolving the metabolism issues will in many reduce the cravings and rewarding foods are no longer an issue.

Another important question to ask is: how often during the day and how much hyperpalatable, highly rewarding foods do people who become obese actually eat?

If people become obese without consuming highly rewarding foods (something I consider very possible) then the theory of food reward argues strongly that this type of obesity is mostly due to lack of willpower, as there is no addiction to blame.

The “bland food” study from 1965 Stephan writes of can be used to support a “food reward” theory, but there are many other ways of explaining why the overweight people lost weight while the lean did, not. If the obese ate high sugar/grain and franken-fat diets, that also happen to be palatable once you get used to it, then of course they lost weight on the liquid diet.

The first volunteer continued eating bland food from the machine for a total of 70 days, losing approximately 70 pounds. After that, he was sent home with the formula and instructed to drink 400 calories of it per day, which he did for an additional 185 days, after which his total weight loss was 200 lbs. The investigators remarked that «during all this time weight was steadily lost and the patient never complained of hunger or gastrointestinal discomfort.» This is truly a starvation-level calorie intake, and to eat it continually for 255 days without hunger suggests that something rather interesting was happening in this man’s body.

This isn’t really that interesting. With all likelihood the man could have lost an equal amount of weight eating real foods that are far more rewarding but not fattening. It has been known to happen.

I think decreased fasting insulin occurs as a result of weight loss…

Stephan Guyenet 

Another important point is that the body fat “setpoint” is still a theoretical point, and any theory based on the setpoint hypothesis is equally hypothetical. 

As one would expect if food reward influences the body fat setpoint, lean volunteers maintained starting weight and a normal calorie intake, while their obese counterparts rapidly lost a massive amount of fat and reduced calorie intake dramatically without hunger. This suggests that obesity is not entirely due to a «broken» metabolism (although that may still contribute), but also at least in part to a heightened sensitivity to food reward in susceptible people. This also implies that obesity may not be a disorder, but rather a normal response to the prevailing dietary environment in affluent nations.

Lean people have good access to their own body fat and high fat oxidation rates. They have a better working liver than obese, and they definitely had a better pre experiment diet than the obese. The above results can be explained exclusively by a broken metabolism theory. There is no need to involve food reward.

Some people may be inclined to think «well, if food tastes bad, you eat less of it; so what!» Although that may be true to some extent, I don’t think it can explain the fact that bland diets affect the calorie intake of lean and obese people differently.

Most diets affect lean and obese differently. These people are per definition quite different metabolism wise, and foods affect metabolism. Once again, the fact that one of the many diets that affect lean and obese differently are bland, does not lend much evidence for palatability playing a major part in obesity.

Although the rewarding abilities of different foods might explain some of the reason we overeat on fattening foods there are very many other ways you are likely to gain weight. As David Pier points out in the comments section:

Excess fructose? Too high an omega-6/omega-3 ratio? Too much omega-6? Too little omega-3? Too much polyunsaturated fat in general? Too little saturated fat? Micronutrient (choline, minerals, etc.) deficiencies? Excess total carbohydrate? Superstimulating hyperpalatibility? Over-availability? Excess insulin (cause and/or effect)? Gut flora (cause and/or effect)? Lack of fiber (insoluble and/or soluble)? Multi-generational epigenetic changes? Artificial sweeteners? Endocrine disruptors? Sleep disturbances? Psychological causes essentially independent of all hormonal homeostatic mechanisms?

In his third post, Guyenet writes about the review of low fat non energy restricted diets where overweight lost more weight than lean:

In other words, low-fat groups reduced their calorie intake by an average of 271 calories per day, and lost 7.5 pounds (3.2 kg). When they considered only people who started off overweight, they lost 12.8 pounds (5.8 kg). The investigators noted that the results were similar no matter what the duration of the trial, because weight loss plateaued fairly quickly.

Then he writes

This is all without any instruction to reduce calorie intake, therefore we can assume these dieters were eating to fullness.

No you can’t assume that. These are participants included in non blinded weight loss trials. I would say it’s a safer bet that they were in fact restricting their food intake.

The best low-carbohydrate diet study I’ve seen was published in 2008 in the New England Journal of Medicine (3). 322 «moderately obese» participants were placed on a low-carbohydrate diet, a calorie-restricted low-fat diet, or a Mediterranean diet, for two years. The low-carbohydrate group’s carbohydrate intake decreased by 130 grams per day, which is about half of a typical person’s total intake, and neatly corresponds to the reduction in calories of 561 per day, despite not being instructed to reduce calorie intake.

At two years, the low-carbohydrate group had lost 10.4 lbs (4.7 kg), which is very similar to the average weight loss seen in low-fat diet trials.

There are two major issues here. 1) The study by Shai et al is a horrible study: The Atkins based diet came with recommendations of getting fat from vegetable sources; By 24 months, carbohydrates constituted 40% in the low carb group and 50% in the low fat group. The low fat diet went from baseline fat intake of 31,4% to 30% (no reduction at all); the aurhors left out baseline energy intakes and only reported reductions; The study also used intention to treat analyses. The weight loss in the low carb group for the 272 who completed the study was 5.5kg in the “low carb” and 3.3kg in the “low fat” group. After 6 months the study diets were not very dissimilar.

If this is the best low-carbohydrate study Guyenet has read, he needs to read the other studies. Low-carbohydrate diets usually outperform low fat diets, as long as carbohydrate intake is kept restricted. This outperformance is despite low fat groups having caloric restrictions while low carb groups can stuff themselves as much as they want. His reasoning that low carb and low fat perform equally is flawed in so many ways, and he uses this reasoning to support a food reward hypothesis.

I think the reason very low-carb ketogenic diets cause fat loss is the same reason extreme low-fat diets cause it: they have a greatly reduced reward value.” 

Stephan Guyenet 

The fact that participants in the Lindberg study lost weight without caloric restrictions does not mean food reward had anything to do with it. Once again, if certain foods themselves cause fattening, and we restrict these foods, weight loss is likely to occur. There is no need to blame blandness.

Messing about with dopamine signaling can cause obesity in animal models, and there are differences in dopamine receptors between «normal» people and those prone to addictive behavior. It is not strange that messing about with the brain will cause all sorts of things, but it does not mean obesity is caused by food reward.

There is more reasoning to discuss, but this post is getting way to long. Is there really enough available evidence to justify calling food reward a dominant factor in obesity? If there is, I can’t say I found evidence of this in Stephan’s posts.

And as Paul Jaminet pointed out:

Likewise, we’re all familiar with young people who eat massive quantities of junk food and remain slender. The high food reward diets, even toxic and malnourishing diets, seem not to cause weight gain until some kind of metabolic damage occurs.

It seems that metabolic damage – the disease of obesity – is a prerequisite for food reward to matter.

Obese people should eat boring diets
Guyenet even offers tips on how to make food less palatable and more bland. But does this mean that there are people out there who have tried all the obvious ways to lose weight, like reducing inflammation and cutting back on carbs, who have not succeeded and are left with trying to make food not taste good?

The most palatable foods are those packed with fat and sugar. These foods are the first to go on any dietary strategy. Do we need to make the rest of the diet bland?

Guyenet offers a range of advice for losing weight based on food reward theory. For example:

Don’t snack. In France and many other countries with strong food traditions, snacks are for children. Adults eat at mealtime, in a deliberate manner.

And yet, if snack in itself do not seem to cause obesity, why not snack?

Don’t add fat to your food. That doesn’t mean don’t eat fat, it just means keep it separate from your cooking. If you want to eat butter, eat it separately rather than mixing it in with your dish.

…I don’t know what to say about this…but I know I don’t like it.

Some of his advices are meant mostly for those who struggle to lose weight, but I fear if anyone would follow them, they would die of boredom instead:

Eat only single ingredients with no flavorings added. No spices, herbs, salt, added sweeteners, added fats, etc. If you eat a potato, eat it plain. If you eat a piece of chicken, eat it plain. It can be in the same meal as other foods, but don’t mix anything together. If you would like to keep salt in your diet, dissolve it in water and drink it separately.

There are more of course. Most make sense, but they also make sense without considering food reward.

Importantly, all the studies used to support the award theory can also be used to support different theories. While they do no not falsify a reward theory they do not provide strong supportive evidence. But this is how science works. Stephan is right in offering the theory and he might turn out to be spot on. It will be interesting to see what future studies will reveal. We need some RCT’s to enlighten the causation between food and dopamine response and function, well any kind of RCT in this field would be important. I would like to make foods that are highly rewarding (measured by dopamine response or something fancy, that make people crave them, and that does not contain anything inherently fattening. Then I would give people free access to it to see if they got fat. Wonder what it could be?

«Some people have lost fat simply by avoiding carbohydrate or fat. I’ve heard people say that a low-carbohydrate diet in particular curbs their cravings and allow them to have a healthy relationship with food again (although others have developed strong cravings on low-carbohydrate diets). I believe this is mostly, if not exclusively, driven by the fact that carbohydrate and fat are major reward factors.»

Stephan Guyenet

References

1. Berthoud HR, Lenard NR, Shin AC: Food reward, hyperphagia, and obesity. Am J Physiol Regul Integr Comp Physiol 2011, 300: R1266-R1277.

2. Friedman MI, Harris RB, Ji H, Ramirez I, Tordoff MG: Fatty acid oxidation affects food intake by altering hepatic energy status. Am J Physiol 1999, 276: R1046-R1053.