The setpoint hypothesis revisited

The homeostasis 

(hō’mē-ō-stā’sĭs): The ability or tendency of an organism or cell to maintain internal equilibrium by adjusting its physiological processes.

Humans are warm blooded and the enzymes that make us, require a certain temperature to operate optimally. The water and ion concentration of cells must remain at a certain level to allow for normal cellular processes to occur. Homeostatic processes make us able to adapt to environmental changes. Feedback mechanisms are responsible for maintaining particular levels of processes. Most processes allow for some variation, but if pushed too far in one direction the process may break down.

Body temperature is maintained by thermoreceptors communicating with our hypothalamus, by sweating, vasoconstriction and dilation, hairs standing on end, shivering, shifts in metabolism and other. All of these factors work in unison and affect each other and by doing so maintain our body temperature at around a rough mean.

During energy restriction we get hungry, our thyroid hormone levels decrease, non essential processes like that of reproduction is down regulated, and energy expenditure goes down. It is difficult to make people gain weight by overfeeding and it is difficult to make people lose weight by underfeeding. The feeding always affects energy expenditure. Thus body weight or some level of cellular mass is required for survival and the body is self regulating to make sure sufficient tissue mass is present for survival and eventually reproduction.

None of this justifies the use of the term “setpoint” in body weight regulation.

The set point 

“Again, this supports the idea that the body has a body fat mass ‘set point’ that it attempts to defend against changes in either direction. It’s one of many systems in the body that attempt to maintain homeostasis.” 

Stephan Guyenet 

Although I have much respect for Stephan Guyenet and appreciate his very fine blog, I don’t understand his focus on the body fat setpoint. I don’t understand anyones focus on body fat setpoint for that matter. I’ve never felt comfortable using the “setpoint” word when it comes to body weight regulation. It makes me think of a glowing red number etched into my hypothalamus. “15 kg fat” NO MORE, NO LESS. It does not feel very “organic” to have a set point and I’m pretty sure I am organic. But of course, no one is claiming there is a number etched in my brain.

When it comes to the body fat setpoint, I rather like the lake comparison. A lake can for those less informed seem to have a set point of water level. Despite rather large fluctuations in temperature, evaporation and water going into and out of the lake, the lake maintains it water level because the factors mostly responsible for the level influence each other. This does not mean that it is difficult to change the level, nor does it mean the lake «attempts to defend against change.» Build a damn dam and the water level will go up. Drain it, and the level goes down. It’s not very hard, you just have to push the right buttons.

If our fat mass changes through life and in various situations and in fact is not that difficult to change, then why the hell say it’s a set point? It’s obviously not very set, is it? Most of the time we are gaining and losing fat at pretty much equal speeds, although with constant variations around the mean. The fact that the fat storing and fat using process does not spiral out of control either way, that most of us don’t get very lean or very obese, would mean that there is a control mechanism, a feedback loop or a set point. But all the body’s processes are regulated. We are self regulated and all processes work best around a given mean determined by the nature of the very process and the processes it affects or is affected by.

A homeostatic process must have a level to operate on. It’s the way the world works. The level can usually be changed by modifying the factors that make the process.

Stephan Guyenet claims that one criterion for the cause of modern fat gain is that it “…has to cause leptin resistance or otherwise disturb the setpoint.”

What I don’t understand is, why can’t we say disturb the “regulation of body weight”, “the metabolism” or “the process.” Why “disturb the setpoint”?

The language

“..the body doesn’t want to lose weight. It’s extremely difficult to fight the fat mass setpoint, and the body will use every tool it has to maintain its preferred level of fat: hunger, reduced body temperature, higher muscle efficiency (i.e., less energy is expended for the same movement), lethargy, lowered immune function, et cetera.” 

Stephan Guyenet 

Whenever body fat setpoint is discussed it seems the body is at war with one of its processes. Why turn it into fight? Obviously it is not that difficult to “fight the fat mass set point”. I’ve asked people who’ve lost weight who said it was easy. What’s more is that they have stayed lean with ease. The setpoint hypothesis was invented mostly because people didn’t lose weight by eating low fat and that they often regained lost weight. Now, I could try to change the water level of a lake by drinking the water through a straw, and when failing I could conclude that the water level is “extremely difficult to fight”, but it wouldn’t be a very good conclusion.

I believe firmly that our language is a great obstacle for scientific progress. The main reason is that it is very hard to imagine things that cannot be put into preexisting words. Also our minds operate within the boundaries of our language and language will limit the things we can imagine. I think quantum physics is a good example of an area in which the language simply is not sufficient. The electrons can be in several places in the same time. Some things are both particles and waves. Matter consists mostly of empty space and so on. On top of it all, once words are set, once something is described in a particular way, it usually stays that way.

In Guyenets posts about the body fat setpoint, the word setpoint is often given with quotation marks, like in the above quote. I can only assume that this means that the word setpoint is not an accurate description of what he is talking about, that it is not actually a set point, but that it is used for the lack of a better word.

Guyenet also writes extensively about leptin. Leptin is an interesting protein, but it is just one of those signaling molecules involved in the homeostatic regulation. Of course weight will change if we or nature messes with leptin, its receptors in the hypothalamus or any other involved part. But the existence of leptin does not justify the use of the setpoint term.

Body fat mass can be quite easy to change so why the hell do we need the setpoint? I feel the word contributes nothing to our understanding and if anything just complicates the matter more than necessary. How about adding a muscle mass setpoint and a bone mass setpoint? How about a hair growing speed setpoint or a saliva setpoint? Does it help our understanding?

I do not think the use of the word setpoint is neutral. It affects out thinking and I am afraid its existence is a net negative contributor to the science of body weight.

On the website of one of the leading obesity clinics in Norway we are told that the clinic bases its work on the setpoint theory. They call it theory, but talk about it as an undeniable fact. This is a problem because the hypothesis rests on the assumption that weight loss is inherently difficult and that the body (in the words of Guynet) “will fight” that weight loss. It is not a very positive attitude. Remember that the setpoint hypothesis saw light of day partly because losing weight through traditional (eating less) methods did not give the expected (based on thermodynamics) results and that people constantly regained lost weight. The clinic thus operates on the assumption that it may take years of hard work to change the setpoint downwards and that it takes a very short time to change the setpoint upward (that the body «gets used» to a new higher level of fat mass).

What if the obesity clinic, instead of basing its treatment on setpoint theory (forcing overweight people to starve and doing insane amounts of exercise), said that weight loss does not have to be difficult and lasting weight loss is possible? What if they read some real science, pushed the right buttons and stopped torturing people? The studies are out there. It really does not have to be difficult. The metabolism must be altered, mostly through changing the hormonal milieu and reducing inflammation thus achieving a homeostatic regulation at a lower amount of body fat mass. And there is little evidence it has to take years to do so.

The conclusion

«When something seems ‘the most obvious thing in the world’ it means that any attempt to understand the world has been given up.» 

 Bertolt Brecht 

If the point of this rambling is lost on you, let me try to sum it up.

The body fat “setpoint” is just a word used to describe a level of a self regulating biological process.

To call a certain mean level of a homeostatic regulation a set point is unproblematic. As far as I can see, this is how Stephan Guyenet uses the term. But when medical professionals use the setpoint hypothesis to argue that body weight loss by nature is difficult and near impossible, we have a problem. The continued use of the expression seems to affect both medical professionals and researchers in a negative way, because it closes their mind for other possibilities, among them that weight loss from a physiological point of view is easy if you just push the right buttons. That we do not always know what these buttons are does not mean weight loss must be difficult, only that we are ignorant. Many aspects of metabolic regulation are under our control. Most important of all is that the level of homeostatic regulation of body fat called the setpoint, seems to be determined by what we eat.

Kurt Harris, the messiah, the hype and the throwing of scales

I think Kurt Harris is a smart man and makes some very good points now and then, not to mention his reading list resembles my own. But reading his blog recently I keep thinking of Monty Pythons Life of Brian. For those less versed in the film (shame on you!), Brian is mistaken for the messiah and tries his best to convince a rapidly growing crowd that he’s not. But whatever he does, it is taken as a sign and further confirmation that he is the messiah and he can do nothing wrong.

Dr. Harris stopped blogging for a while, which somehow seemed to increase his blogging status. He disabled his comments section and I bet that also increased his standing. In a recent post he talks about the important fact that people are focusing too much on stupid details and forgetting about true science, the bigger picture and how to relax and enjoy life. According to Harris in the “do no harm” post: “I’ve had more laudatory emails and fresh donations (Thank you all!) as a result of this post than any I’ve written in a long time.

Kurt is the new Brian. “Therapy versus Life,” has an important message and despite how obvious it is, it needs to be repeated. Worrying about the lectins in the beans you just ate or whether or not you should add an extra t-spoon of coconut oil to your daily diet will only take down a road you really don’t want to go. It will not make you live longer or happier!

Sure, a good diet can make life better, you might lose weight and be more toned. But life’s there to be lived. I advocate a diet mostly free of modern foods and I am really interested in finding answers about what foods affect the body in what way and what exercise is the most effective and so on. But I’m constantly working hard not to lose my head (and perhaps overcompensating a bit) and under no circumstance am I willing to give up beans with my bacon, beer or ice-cream or sugar (yeah that’s right, glucose AND fructose) in my daily cup of earl gray tea. Oh, and I’ve been exercising regularly once a week for about the last six months. Why? Because it doesn’t matter.

I’m not saying it’s easy to be happy. I’m saying we will definitely not get any happier by focusing on minor and insignificant details relating to diet or exercise.

Paleo is fad (fad = a temporary fashion; a craze, interest or activity that (some) people follow enthusiastically, but lasts for a short period of time). Sure it’s a good idea to not eat modern foods, but we must not start suggesting that a food is bad because it is modern. And we must not forget that a paleo diet is not actually a defined diet, but rather a some general guidelines based on not so strong evidence about what our ancestors ate.

Paleo is likely a fad because humans are crazy about inventing new words, labeling everything and grouping things together. The world is to complex not to make subgroups of everything and we’re so bloody good at it. Don’t get me wrong, I actually like the word paleo, but I bet a new craze will take over; the paleo group feel will dilute and hopefully integrate more into standard dietary advice.

But what about the throwing of scales? Talking to more and more people trying to lose weight just further convinces me that weighing is an obstacle for success. The first thing you should do if you want to lose weight is to chuck the old measuring tool in the trash. As I said, humans get to caught up in details and especially numbers on a scale. Have patience, in time you’ll know if you are losing fat. You were clothes, don’t you? Your clothes are the only reference you need. If you can’t get in or out of them, you’ve gained weight. Oh, and perhaps some getting to know your body and how you actually feel might help to.

And as for me? I feel an overpowering urge to tackle the “set-point” hypothesis issue. Something smells fishy about the standard theory which Harris and Guyenet, amongst others, find the most fitting.

Hva er egentlig problemet med rødt kjøtt? (In Norwegian)


Mandag 31. januar la Nasjonalt råd for ernæring frem rapporten, ”Kostråd for å fremme folkehelsen og forebygge kroniske sykdommer.” Rapporten er en vitenskapelig gjennomgang av kostens påvirkning på en rekke sykdommer og helsetilstander, og gir konkrete råd om forebygging. Blant rådene er en anbefaling om restriksjon i inntaket av rødt kjøtt. Begrunnelsen er at rødt kjøtt øker risikoen for tykk- og endetarmskreft. Så sikre er rådet i saken at de sier det er en ”overbevisende” årsakssammenheng mellom de to faktorene. Det vil si, det er egentlig ikke Nasjonalt råd for ernæring som er sikre. De gjengir bare konklusjonen fra en rapport fra World Cancer Research Fund (WCRF) fra 2007 [1]. Det var denne rapporten som konkluderte med en overbevisende sammenheng mellom inntak av rødt kjøtt og kreft i tykk- og endetarm og det er denne rapporten de norske anbefalingene hviler tungt på.

Sentralt i den delen av vitenskapen som dreier seg om kostholdsfaktorers påvirkning på helse er spørsmålet om kausalitet, d.v.s. hvilken faktor som direkte forårsaker en helseeffekt. Det er kun en type vitenskapelige studier som med god sikkerhet kan vise kausale årsakssammenhenger. I tilfellet med rødt kjøtt ville en slik type studie bestå av minst to grupper med mennesker som er like på alle måter bortsett fra i inntaket av rødt kjøtt. Om en gruppe spiser mye kjøtt og en annen lite, kan vi følge gruppene over tid og etter hvert registrere hvor mange i hver av gruppene som får tykktarmskreft. Om gruppen som spiste mye kjøtt fikk så mye mer kreft enn gruppen som spiste lite at det ikke kan anses å være tilfeldig, kunne vi anta at kjøtt fører til kreft. Det vil si, selv da hadde vi ikke bevist noe, for selv et slikt resultat betyr lite inntil noen gjør akkurat den samme studien om igjen og får et tilsvarende resultat. Kausalitet, det at kjøtt faktisk fører til kreft, krever at resultater i slike studier er reproduserbare. En slik studie har aldri og vil aldri bli gjort. Selv om det kunne gitt oss et endelig svar en gang for alle, er slike studier altfor dyre og resurskrevende å gjøre over lang tid på mange mennesker. I stedet gjør man det som av mange regnes som det nest beste – epidemiologiske eller observasjonelle studier. Slike studier deler gjerne ut spørreskjemaer til en stor gruppe mennesker med spørsmål om hva og hvor mye de spiser. Disse menneskene følges så opp over mange år og man registrerer sykdommer etter hvert som de oppstår. Deretter kan man gjennom statistiske metoder se om det er en sammenheng mellom inntak av rødt kjøtt og kreft. Det viktigste å huske på med slike studier, og gjerne det første man lærer i metodefag på skolen, er at de ikke sier noen ting om kausalitet. De kan ikke under noen omstendigheter fortelle oss om kjøttspising fører kreft, kun at de to faktorene kan opptre sammen i en befolkning. Man kan finne at rødt kjøtt korrelerer (opptrer sammen med) med kreftforekomst, men det kan godt tenkes at de som spiser mest rødt kjøtt også røyker mer eller er mer utsatt for en miljøfaktor som kan gi kreft. Dermed er det en annen faktor som er sannsynlig årsak til kreften, selv om kjøtt og kreft korrelerer. Man kan for eksempel, gjennom å bruke en slik studie, finne at det er en sammenheng mellom fotstørrelse og intelligens. Man bør likevel være forsiktig med å kirurgisk øke fotstørrelsen for å få økt intelligens, fordi korrelasjonen mest sannsynlig kommer av at voksne med store føtter skårer høyere på tester enn barn med små føtter.

I et merkelig sitat fra den nye norske rapporten skrives det at det tyske Bundesinstitut für Risikobewertung, ” …konkluderer at de epidemiologiske studiene ikke dokumenterer entydig at sammenhengen er kausal.” Grunnen til at setningen er rar er som nevnt over at epidemiologiske studier ikke kan dokumentere kausalitet. Dette er vitenskapelig metode for nybegynnere.

Ettersom alle studier som finnes om sammenhengen mellom inntak av rødt kjøtt og tykktarmskreft er i gruppen epidemiologiske studier, kan vi ikke si at rødt kjøtt fører til kreft. Men om alle våre data, selv om de som er epidemiologiske, tyder på at det finnes en sammenheng og vi i tilegg har svært sannsynlige årsaksforklaringer fra for eksempel dyrestudier eller cellestudier, så kan man si at det er overbevisende sannsynlig at høyt inntak av rødt kjøtt fører til tykk- og endetarmskreft.

Så hva er egentlig grunnlaget for konklusjonen i den norske repporten?

I hovedsak er den norske anbefalingen basert på rapporten fra World Cancer Research Fund fra 2007. Denne rapporten hevder også at det er en overbevisende sammenheng mellom rødt kjøtt og tykk- og endetarmskreft. Stewart Truswell skrev i 2009 en sterk kritikk av rapporten til WCRF i American Journal of Clinical Nutrition [2]. Truswell stiller seg undrende til at rødt kjøtt ble flyttet fra å ha en sannsynlig (probable) sammenheng med tykk- og endetarmskreft i rapporten fra 2002, til å ha en overbevisende (convincing) sammenheng i 2007.

Truswell trekker blant annet frem at WCRF har utelukket 13 studier med til sammen 1.578.970 deltakere, hvorav kun to av disse fant en positiv sammenheng mellom rødt kjøtt og kreft. Michael Marmot og Martin Wiseman som medforfattet WCRF-rapporten hevder at flere av disse studiene ikke så på rødt kjøtt direkte, men at noen så på bearbeidet kjøtt og rødt kjøtt sammen og andre på kjøtt generelt [3]. WCRF tok heller ikke med en oppfølgingsstudie av 5 grupper vegetarianere som var sammenlignet med sosialt like altetere. Denne fant ingen forskjell i dødelighet fra tykk- og endetarmskreft [2]. I et tilfelle rapporterte WCRF direkte feil, da de hevdet at i en finsk studie av Pietinen og kolleger, var den relative risikoen for tykk- og endetarmskreft for storfe, svin og lam 1.2, når den i virkeligheten var 0.9 eller 0.8. Marmot og Wiseman innrømmet dette, men unnskyldte seg med at de ikke hadde tatt så mye hensyn til denne studien likevel.

WCRF valgte bort én stor studie som viste en lav risiko for kreft, til fordel for en metodisk dårligere studie som vist langt høyere risiko, fordi den sistnevnte passet bedre inn i den statistiske metoden de brukte. I tilegg til feilmerking av en studie og andre mer eller mindre grove feil fra forfatterne av WCRF-rapporten, minner Truswell oss på at i CD-en som fulgte med rapporten ble det hevdet at ”…mechanisms for involvement of meat in colorectal cancer are far from plausible.

I tilegg til WCRF refereres det i kostholdsanbefalingene til en metaanalyse (analyse av analyser) av 15 prospektive studier som fant en positiv sammenheng mellom risiko for tykk- og endetarmskreft og inntak av rødt kjøtt. Relativ risiko var 1.28 for høyt mot lavt inntak av rødt kjøtt – et tall som er alt for lavt for å vekke oppmerksomheten til forskere som ikke allerede har et forutinntatt forhold til rødt kjøtt.

Den norske rapporten viser også til en ny og svært stor studie av Amanda Cross og medarbeidere [4]. Denne studien undersøkte hele 494036 deltagere over 6.8 år (Rapporten fra Nasjonal råd for ernæring sier at studien hadde 545653 deltakere og kikk over 10år, men dette er misvisende). Denne studien er et godt eksempel på datagrunnlaget for kostholdsanbefalinger ettersom den brukte en svært vanlig epidemiologisk metode. Studien baserte sine funn på spørreskjemaer som ble delt ut i oppstarten av studien. Spørreskjemaene innholdt spørsmål om hva deltakerne vanligvis spiste. Etter ca 7år sjekket man om det var en sammenheng mellom sykdom og det som ble oppgitt i disse skjemaene. Denne metoden tar ikke hensyn til kostholds- og livsstilsfaktorer som endrer seg i løpet av studien, men dette er dessverre likevel en helt vanlig metode å bruke. De i studien som spiste mest kjøtt hadde mindre utdannelse, var yngre, røykte mer og var generelt mer overvektige. Disse faktorene ble kontrollert for i analysen, men faktorer som sukkerinntak som er nært knyttet til overvekt, brydde ingen seg om. Næringsstoffgruppen som kalles karbohydrater er spesielt interessant og burde kontrolleres for, fordi man vet at senkning av blodsukkeret reduserer vekst og utvikling av tykktarmskreft [5]. Uansett, forskerne fant at høyt inntak av rødt kjøtt var forbundet med økt risiko for tykk- og endetarmskreft (Hazard Ratio=1.24, for de som er interessert.)

Truswell er ikke den eneste som er kritisk til hvor mye som tolkes inn i dataene som finnes. I “Red meat and colorectal cancer: a critical summary of prospective epidemiologic studies”, fra 2010 [6] fremmer Alexander og Cushing en viktig innvending. Det at andre faktorer enn rødt kjøtt, for eksempel vestlig livsstil og et høy inntak av raffinert sukker, også korrelerer med kreft, begrenser muligheten til å isolere effekten av rødt kjøtt. I sitt grundige review konkluderer Alexander og Cushing med at de tilgjengelige epidemiologiske bevis ikke er nok til å støtte en uavhengig positiv sammenheng mellom rødt kjøtt og tykk- og endetarmskreft.

Hvis rødt kjøtt forårsaker kreft i tykktarmen, vil man forvente å finne at økende inntak av kjøtt gir økende forekomst av kreft. Altså jo mer kjøtt, jo mer sykdom, en såkalt dose-respons sammenheng. Nasjonalt råd for ernæring sier i rapporten sin at en slik dose-respons sammenheng finnes, men de oppgir ingen kilde med uttalelsen. Jeg sjekket, og fant at noen studier har et dose-respons forhold mens andre ikke har det.

Den norske rapporten fremhever flere ganger at de epidemiologiske studiene støttes av mekanistiske studier. Problemet er bare at de mekanistiske studiene omhandler teorier som er svært dårlige, så dårlige at de ikke kan brukes til å støtte noe som helst. I rapporten står det, ”Mekanismer for utvikling av kreft og de mulige kostfaktorer som kan påvirke risiko for kreftutvikling er grundig diskutert i rapporten fra World Cancer Research Fund rapporten (1) og den medfølgende CD.” Jeg synes konklusjonen angående mekanismer som gis på denne CD-en er verdt å gjenta, ”…far from plausible.”

Så de vitenskapelige ”bevisene” som finnes for sammenhengen mellom rødt kjøtt og tykk- og endetarmskreft er kun fra studier som ikke egentlig kan si noe om årsaken til kreft. Noen av disse studiene viser ingen sammenheng, mens noen finner en sammenheng og ofte er sammenhengen svak. Epidemiologiske studier har en mengde svakheter, kanskje først og fremst det man kaller ”confounding factors.” For at ikke andre faktorer enn kjøtt, for eksempel røyking eller fysisk aktivitet, skal være årsaken til en eventuell sammenheng, kontrollerer man for disse faktorene i de statistiske utregningene. Men hvilke faktorer man kontrollerer for er fullstendig opp til de respektive forskere. Det er for eksempel vanlig å kontrollere for inntak av mettet fett, fordi man har en oppfatning om at mettet fett er farlig. Andre faktorer som godt kan tenkes å være den egentlige årsaken til en positiv sammenheng kan bli oversett, enten på grunn av forutinntatthet eller på grunn av manglende kunnskap, og det er ikke usannsynlig at rødt kjøtt blir uskyldig dømt. Disse studiene blir sett i sammenheng med dyre- og cellestudier som heller ikke kan si noe om årsaken til kreft, og som er basert på relativt dårlige biologiske hypoteser.

Man skulle kanskje tro at for å kunne si at det er en overbevisende sammenheng mellom to faktorer, måtte man ha flere gode randomiserte kontrollerte studier som er gullstandarden når det kommer til å peke på årsaker. Men slik er det ikke. Ingen slike studier finnes og vi må nøye oss med det nest beste.

Interessant nok står det i ”Kostråd for å fremme folkehelsen og forebygge kroniske sykdommer” at ”Ut fra en helhetlig vurdering av forskningsfeltet, inklusive manglene på klare mekanismer, kan man reise spørsmål ved om sammenhengen heller burde kategoriseres som sannsynlig.” Rådet kommer dermed med selv med en innvending reist av mange andre, men unnlater å ta hensyn til den.

Samtidig med de norske anbefalingene kom det også ut nye kostholdsanbefalinger i USA. I USA valgte de en mer moderat tilnærming til kjøtt og kreft og skriver, “…moderate evidence suggests an association between the increased intake of processed meats (e.g., franks, sausage, and bacon) and increased risk of colorectal cancer and cardiovascular disease.” Rødt kjøtt gis tilnærmet ingen oppmerksomhet.

Til syvende og sist er bevisene for en sammenheng mellom rødt kjøtt og kreft i tykktarm og endetarm dårlige. Dette betyr ikke at sammenhengen ikke finnes, og det er fortsatt mulig at kjøtt faktisk gir oss kreft. Så valget må bli opp til den enkelte av oss. Jeg kommer til å fortsette med å spise kjøtt, mye kjøtt og aller helst rødt kjøtt. Mitt eneste håp er at myndighetenes ensidige fokusering på korn, frukt og grønt gjør at kjøttprisene går ned så jeg kan fortsette å nyte min dagelige porsjon rødt kjøtt.


1. Food, nutrition, physical activity, and the prevention ofcancer: a global perspective. Washington DC: American Institute for Cancer Research; 2007.

2. Truswell AS: Problems with red meat in the WCRF2. Am J Clin Nutr 2009, 89: 1274-1275.

3. Marmot M, Wiseman M: Reply to AS Truswell. The American Journal of Clinical Nutrition 2009, 89: 1275-1276.

4. Cross AJ, Leitzmann MF, Gail MH, Hollenbeck AR, Schatzkin A, Sinha R: A prospective study of red and processed meat intake in relation to cancer risk. PLoS Med 2007, 4: e325.

5. Seyfried TN, Shelton LM: Cancer as a metabolic disease. Nutr Metab (Lond) 2010, 7: 7.

6. Alexander DD, Cushing CA: Red meat and colorectal cancer: a critical summary of prospective epidemiologic studies. Obes Rev 2010.

New dietary guidelines – the fairies are rejoicing

Nonsense, n; That which is not sense; spoken or written words which make no sense or convey absurd ideas; also, absurd or senseless action.

I am writing nonsense, but it is because no sense within my mind will answer the purpose. 

Hawthorne (1871) 

All around are heated discussions and angry tweeters, heads are being slammed on desks, palms being slammed on faces (preferably ones one) and Einstein’s definition of madness is being quoted frequently.

Ladies and gentlemen, I give you the new and updated dietary guidelines.

Someone once said that science pretends to be more reasonable than it is, and so ends up being more unreasonable as a consequence. I am more inclined to replace science with scientists.

There is so much to be said about dietary guidelines and I am sure much will be said in the near future. I will not go into details and argue what statements are sound and supported by science and which are not. But I do find the entire process very interesting and I wonder if a time comes when people will look back at this while giving themselves a good facepalm and thinking, “What the hell were they thinking?” I can’t wait till the future gets here.

I was at the Norwegian Health Directorate yesterday to get a copy of the new national guidelines and to hear what the perpetrators had to say. As expected, they served fruit and bad coffee. It was interesting to hear how the authors boasted about the foolproof methodology they had used. How only the best information from the best sources, like the World Health Organization and the World Cancer Research Fund, was used. It got me thinking how remarkable it is that in some peoples mind, as long as the methodology is good the conclusion is equally good. But good methodology does not translate into good science. It might help, but in the case of WCRF report, for example, it clearly did not. I checked, and it is full of arbitrary mess ups like translating correlation directly into causation, not to mention its use of thermodynamics and its cherry picking articles and miss referencing.

The Norwegian guidelines were neatly divided into 13 simple, easy to follow points (loosely translated):

1: Diet should be primarily plant based and contain lots of vegetables, fruit, berries, whole grain and fish, and contain limited amounts of red meat, salt, added sugar and energy dense foods.

2: It is recommended to maintain a balance between energy intake and energy expenditure.

3: Eat 5 portions of vegetables, fruit and berries a day.

4: Eat minimum 4 portions of whole grain products each day.

5: Eat the equivalent of 2-3 dinner portions of fish per week.

6: It is recommended that low fat dairy products be a constituent of the daily diet.

7: It is recommended that one chooses lean meat and meat products and limit the intake of red and processed meat.

8: It is recommended that one choose plant oils and margarines.

9: Drink water.

10: Limit intake of added sugar.

11: Limit intake of salt.

12: Supplements might be necessary to ensure nutrient intake for parts of the population.

13: A minimum of 30 min of physical activity per day is recommended.

There you have it. The recipe for good and healthy living. The diet should be plant based. I know there are humans in the world and even small societies that do live on a primarily plant based diet and who seemingly are in good health. But in no way does this imply that a plant based diet is healthier than one animal based. It doesn’t even prove that a plant based diet is healthy, just that it might be possible. Of course the guidelines are not based on anthropologic evidence, but on a fear of animal fat and meat. It is not based on scientific data supporting a link between the intake of animal fats and disease, but on a completely irrational fear that fat might be deleterious to health, a fear created by a wonderful combination of a scientific field consisting of people who have forgotten what science is but who are still constantly cheering each other on in close cooperation with media and marketing interests.

The one vital part missing in the dietary guideline picture is what we do when the brilliant foolproof methodology gives us a conclusion. This is not when we rest on our laurels, but the time for some actual science to take place. This is when we have to check if the conclusion makes sense in light of what we know from all the different areas of science.

There is no evidence of this last part taking place in the guideline process. But the guidelines are not worthless. In fact a good and scientifically sound way to base your diet and lifestyle would be to use the guidelines in the following way:

Mind the advice about cutting sugar as well as the advice about exercising. Don’t mind the fish and the water and the vegetables, do the complete opposite of the rest:

– Diet should be animal based.

– Grain intake should be minimal

– Butter and animal fats should be substituted for plant oils and margarine.

– Do not pay attention to energy intake and expenditure,

and remember to get enough salt.