Food and Drug Reward: Overlapping Circuits in Human Obesity and Addiction
Common Cellular and Molecular Mechanisms in Obesity and Drug Addiction
Is Fast Food Addictive?
Metabolic and Hedonic Drives in the Neural Control of Appetite: Who is the Boss?
The truth of the matter is, obesity researchers have been converging on the food reward hypothesis for years now-- and I'm a relative latecomer. I recently came across an outstanding 2008 review paper by several leaders in the field titled "Mechanisms of Leptin Action and Leptin resistance" (1). I highly recommend this review to anyone with a background in the biological sciences who wants to understand how leptin works in both the lean and obese state. Here's a passage from the end of the paper:
Some evidence exists for developmental alterations in neural and other systems that may underlie some propensity to obesity, but the ready availability of palatable, calorically dense food (the basis for [diet-induced obesity] in experimental animals) clearly plays a dominant role. Indeed, the obesity and cellular leptin resistance of [diet-induced obese] animals are reversed by replacing the palatable calorie-dense chow used to promote obesity with standard chow. Although some of the obesogenic effects of tasty foods may be due to their nutrient content, the hedonic or rewarding properties of these foods also contribute...
How then is the action of leptin to regulate the perception of food reward overwhelmed to promote obesity in the face of plentiful tasty food? Leptin is only one of many inputs into the mesolimbic [dopamine] system and other neural pathways that regulate the perception of food reward, and physiological leptin levels may not be able to suppress the myriad other signals that compel us to consume tasty food. Although leptin may reasonably inhibit the drive to overeat foods with only modestly rewarding properties, leptin may be insufficient to effectively compete with the rewarding properties of more palatable treats because these more-rewarding foods engage powerful neural responses that oppose leptin within the mesolimbic [dopamine] system and elsewhere.Basically, what they're saying is pretty simple: the brain's hard-wired mechanisms for regulating food intake and fat mass in a natural environment are not sufficient to protect against modern hyper-palatable and hyper-rewarding food. These are researchers who primarily study the mechanisms of leptin resistance in the brain. If anything, they have an incentive to de-emphasize the food reward hypothesis as it potentially takes the spotlight off their own research (the same applies to me). The fact that they nevertheless place such a strong emphasis on the idea speaks volumes.
The journal Cell just published a review paper by Drs. Karen Ryan, Randy Seeley and Stephen Woods-- Drs. Seeley and Woods are leaders in obesity research (2). Here's what they had to say about food reward:
When a [high-fat diet] is suddenly made available to an individual, sensory properties of the food (e.g., odor, taste, mouth feel) are intrinsically pleasant and lead to more food being consumed. As this continues, excess calories accumulate as increased adiposity, and increased circulating fatty acids lead to increased lipid flux into the brain, insulin/leptin resistance, an inflammatory condition, and so on. Stated another way, the increased palatability of the diet initiates a vicious cycle in which hedonics cause more food to be eaten than is necessary to meet energy needs, and the increased calories in turn initiate events that lead to insulin/leptin resistance and a consequent tendency to eat even more food (Figure 4).It's worth noting that they're referring specifically to insulin and leptin resistance in the brain in that passage. I do differ with them somewhat on the role of fat per se.
Dr. Robert Lustig just published an editorial in the journal Nature titled "Public Health: the Toxic Truth About Fructose" (3). First of all, congratulations to Dr. Lustig for publishing his letter in such a high-impact journal. He argues that sugar consumption should be regulated by the government because in excess, it's a threat to public health. One section of the article describes sugar's effects on the reward and pleasure systems in the brain:
Sugar also has clear potential for abuse. Like tobacco and alcohol, it acts on the brain to encourage subsequent intake. There are now numerous studies examining the dependence-producing properties of sugar in humans6. Specifically, sugar dampens the suppression of the hormone ghrelin, which signals hunger to the brain. It also interferes with the normal transport and signalling of the hormone leptin, which helps to produce the feeling of satiety. And it reduces dopamine signalling in the brain's reward centre, thereby decreasing the pleasure derived from food and compelling the individual to consume more1, 6.Another nice food reward review paper (4), hot off the presses, had this to say:
Food reward, not hunger, is the main driving force behind eating in the modern obesogenic [obesity-promoting] environment. Palatable foods, generally calorie-dense and rich in sugar/fat, are thus readily overconsumed despite the resulting health consequences.Last but not least, my own recent review paper on obesity, published in the Journal of Clinical Endocrinology and Metabolism (5). I don't claim to be a leader in the obesity research field, but my mentor Dr. Michael W. Schwartz, senior author on the paper, is. Here's what we had to say:
These findings collectively suggest that obesity can arise when animals or humans are confronted with foods whose palatability/reward value greatly exceeds that to which they are genetically adapted, and hence that interventions that inhibit food reward can prevent fat gain and promote fat loss.These latter four review papers were all published in the last couple of months.
Approaching a Consensus
There are many different research groups approaching obesity from many different angles, but most of the review papers being published today acknowledge the central role of food reward in the development of obesity. The reason is simple: the idea is strongly supported by the scientific literature, but it's also just common sense. In any scientific discipline, there will always be some disagreement, but the evidence at this point is strong enough that the field as a whole seems to be reaching a consensus.
* Reward. The brain contains a "reward" system, whose job it is to gauge the desirability of food (among other things) and reinforce and motivate behaviors that favor the acquisition of desirable food. For example, if you eat a strong cheese for the first time, maybe it won't taste very good to you. As it's digested, your reward system gets wind that it's full of calories however, and the next few times you eat it, it tastes better and better until you like the flavor. This is called an acquired taste, and the reward system is what does the acquiring, motivating you to obtain a food it has deemed safe and desirable. Eventually, you may go out of your way to purchase the cheese or beer at the grocery store because you like it so much, and maybe you'll consume cheese or beer even if you aren't hungry or thirsty. This is an example of the reward system reinforcing and motivating behaviors related to foods that it considers desirable. Processed "junk foods" such as ice cream, fast food, sweetened soda, cookies, cake, candy and deep fried foods are all archetypal hyper-rewarding foods.
Palatability is a related concept-- it is simply the pleasantness of a food; how much a person enjoys eating it. Palatability is determined in part by inborn preferences (e.g., a taste for sugar and energy dense foods), and in part by the reward system (acquired tastes). Palatability is governed by the hedonic system in the brain, which is closely integrated with the reward system.
The reward system is what motivates you to get food and put it to your lips, every time you eat. When scientists shut it down in mice, they completely cease eating (6). The hedonic system influences how much you eat once you begin a meal-- highly palatable food generally increases food intake by activating this system (7). Together, reward and hedonic circuitry in the brain determine in large part how often you eat, what you eat, and how much you eat, and this is influenced by the attributes of the food that's available.
I haven't seen you mention it before (search came up with nothing), so I was wondering how, if at all, the breakdown of people as supertasters/normal/nontasters with respect to bitter flavors factors into the food reward hypothesis.
This is good news, I think. Although a total consensus is probably impossible, something approximating one will allow people to focus on what ought to be done about the problem. That, of course, is probably even a trickier issue.
Thanks again Stephan. They've been using vagus nerve cutting and/or blocking near the intestines for years as an obesity cure. Now they're combining it with gastric bypass for increased weight loss in overweight patients.
I understand that meditation and controlled breathing can help improve vagus nerve tone, with possible implications for ghrelin and leptin signalling. Any thoughts about that?
Actually I'd like more info on vagus nerve and it's involvement in eating in general if you have any. I think this area needs to be explored alongside the hypothalamus. It seems the entire nervous system is intimately involved in eating.
I spend a lot of time in France with friends. Last week we drove down to the Alps to ski. On stopping at a motorway services for a break we walked through the door and were faced with an amazing array of beautiful, creamy delicious desserts and pastries. We tried a couple and they were mouthwateringly delicious, very, very high food reward. Walk along most French town streets and you will see plenty of patisseries full of pastries, cakes and sweets that are delicious and high calorie. Yet you just don't see many fat people in France.
It would seem strange that the country that invented high reward, high calorie food and has been eating it for hundreds of years doesn't have much of an obesity problem.
Consensus Science and the Peer Review... http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719747/
I don't think anyone disagrees that pleasure (including food) reward occurs. The disagreement is whether it's the *primary cause* of obesity.
There's a contradiction in your cites. Some say food reward makes people eat more of the rewarding food. Lustig says reducing food reward makes people eat more of the unrewarding food.
And it's not just the palatability of food. Example: many people are raised to believe wasting food is a sin. As children, they're praised for cleaning their plates. Praise by parents is rewarding. So cleaning plates persists as a rewarding activity.
When presented with enough food for 3 meals, even if it's tastelss pap, they'll still clean their plates.
Cause of obesity is complex, different in different people, and no one factor can explain it all.
The psychosocial (something that tends to get left out in the paleo and low carb blogaspheres with favor given to the physiologic aspects) aspects of obesity are huge, I think, and tie in very closely to the food reward theories. The psychosocial and cultural variables also may help explain why the french are able to stay relatively lean (decreasingly so in the modern world, btw) in the face of such rewarding foods. Yet it'll likely never be understood (anything, for that matter) with linear thinking.
@Frank G-your argument, while I get it, is also one of the defense mechanisms people use to hold onto beliefs that become increasingly untenable in the face of mounting evidence. You have to be careful calling all consensus science "extremely pernicious."
No primary cause, just more or less influential variables that tend to be individual, with some variables dominating more or less across the board (does that make sense). As you alluded, the psychosocial variables (such as cleaning you plate) are also huge.
Also, at first look (I haven't read his paper) Lustig's argument doesn't seem to contradict food reward at all, especially if he argues that increasing intake is what is required to keep reward high (kind of a "reward resistance" taking place).
oh no, "scientific consensus" is an oxymoron. There is nothing scientific about consensus. It is a political term. It means science be dammed, we know the answer. Look what it did for the lipid hypothesis, climate science, USDA guidelines, etc.
@Thomas: Good science will stand on its own two feet, without any need to call on consensus, or appeal to authority, or attempts at cutting short any debate with phrases such as "The truth of the matter is..." or trying to undermine my comments with pop-psychology such as attributing it to a defense mechanism ;-)
As it says in the review I posted above...
>> “...consensus is invoked only in situations where the science is not solid enough. Nobody says the consensus of scientists agrees that E = mc2. Nobody says the consensus is that the sun is 93 million miles away. It would never occur to anyone to speak that way” (M. Crichton). <<
What I read above is a self-affirming consensus among researchers who focus their study on the brain, that (guess what) the brain is the key to everything.
I feel no threat to any "beliefs that become increasingly untenable in the face of mounting evidence" because I do not base my decisions on beliefs. And I have not been convinced to change my position, by any of the evidence so far presented. I remain open to change my position but it will not be because "everybody else has".
"What I read above is a self-affirming consensus among researchers who focus their study on the brain, that (guess what) the brain is the key to everything."
Substitute "insulin" for brain, and it sounds like what you're doing too. This includes the whole low carb mania that seems to be going around now. Are you sure you're being entirely objective?
"because I do not base my decisions on beliefs."
You hold no opinion or take no action unless the science is super solid (no consensus required, I guess)? This seems to be a rather black and white way to live/think and, in reality, is somewhat self delusion IMO (you think you don't base your decisions on beliefs but you really do-we all do) and worse than simple ignorance (or at least equivalent to it).
I got this from Wikipedia:
"Consensus decision-making is a group decision making process that seeks the consent, not necessarily the agreement, of participants and the resolution of objections."
"Consensus should not be confused with unanimity."
If this is true, I'm not sure what's wrong with it. The problem lies when consensus is confused with established fact, which it isn't, and treated as such, with the attempt to squash any alternative ideas.
Consensus decision making happens all of the time, everywhere. What is the alternative?
Yes thank-you gunther gatherer... I am sure that I am being as objective as the next person.
I do not subscribe to any "mania" nor do I blindly follow some "guru" or whatever other derogatory term you care to throw out.
Why do you think I am even here reading this blog if I did not think that Stephan has something to add to the discussion? The brain-focused studies are valuable and help to answer questions... I am just not so quick to dismiss the effect of the rest of the body.
I thought of some examples of defining causes of obesity. Imagine 3 scenarios.
Subject A is leptin deficient. Someone offers him a bowl of gruel, no salt, sugar, or butter. He wolfs it down.
Subject B ate 2 hours ago. You offer her a bowl of gruel, and she says no thanks. Then you offer her a chocolate croissant, and she eats it.
Subject C is in high school. All the cool kids are vegans. They're sitting at the vegan table eating spinach and tofu casserole. C hates spinach and she hates tofu, but she gets some and joins the cool kids. She eats it all so they won't think she's not really a vegan.
Ask what makes people eat, and A says it's hunger, B says it's delicious taste, and C says it's social cues. Like the blind men and the elephant.
Here are a couple of articles that might be of interest.
I don't have access to full text, so I don't know if they decided brain insulin was clinically relevant or not. If someone finds out, I'd be interested in knowing.
@Thomas: more pop-psychology and now with added slurs against my character? "...self delusion ... and worse than simple ignorance"
I guess it would be OK for me to ask, who is being defensive now?
I need to be convinced by evidence-based proof and interpretations of that evidence which stand up to scrutiny -- in this case my own scrutiny has the final say when I make decision about my own life. Obviously this can change as new evidence is forthcoming.
What I detest is being told what to think by others... when I read that the CIH is dead and buried and then hear talk of coffins and final nails etc... these are all just words until I see some evidence. I came looking for the evidence but have yet to see anything convincing BUT I will keep looking and reading.
The "consensus science" debate is one of semantics and most importantly in what context the term is being used. Michael Crichton & company appear to be opposed to the term when used in a political context: codifying consensus science as public policy. As with all bureaucracies, once you codify something it becomes resistant to change. The way Dr Guyenet appears to be using the term would better be stated as "Here's the CURRENT consensus most scientists studying the issue have come to. We would love to see any evidence you have contradicting these claims to further our understanding."
At least that's my take.
Well Hugh, you certainly read a great deal more into that than I did... especially the bit about "We would love to see any evidence you have contradicting these claims to further our understanding"
It is indeed a reasonable stance for a scientist to take but to be frank (hah!) most of what I read above were attempts to close any doors to further discussion of alternatives.
As a lone researcher I don't know that Dr Guyenet has the power to truly shut any doors with regards to obesity research, except maybe on his blog, but as far as I can tell he leaves the comments section wide open for people to debate and disagree to their hearts content. And by so doing, he is leaving open the possibility for someone to come here and point to evidence that blows a hole in the current consensus. And knowing this community, were somebody to do that, even if Dr Guyenet ignored someone else would be certain to pick up the flag.
Apologies; “self delusion” may have been a bit harsh. But your own scrutiny (just like everyone else’s) is subject to your beliefs, biases, and past experiences). You are not exempt and I don’t think that is mere pop-psychology. I’m not sure you occupy the scientific high ground you think you do.
“Obviously this can change as new evidence is forthcoming.”
Yes, I agree. Me too.
“What I detest is being told what to think by others...”
Me too (we do have some commonalities). While I think the CIH is limited and believe there is ample evidence to prove it, you shouldn’t necessarily change your thinking unless you believe the same, which you obviously don’t. I don’t have any problem with that. The “nails in the coffin” stuff is hyperbole used by both sides of the argument.
I agree with Hugh. I’ll give Stephen the benefit of the doubt on “trying to close the doors” on alternative hypothesis.
There is a consensus that obesity is multi-factorial, yes? Which factors dominate in the general population and what can be done to tackle them?
I believe that something needs to be done a.s.a.p. about the aggressive marketing of manufactured foods, some targeted at children. Once a child is hooked on Crap-in-a-bag®, it's hard to break the addiction, in a similar way to class-A drugs, which are also extremely "moreish".
In the US, you appear to have much more aggressive marketing than what we have in the UK. Over here, TV ad breaks occur only every 15 minutes approx and last only 2 minutes approx.
I still don't see why so many consider the food reward theory and the carbs>insulin>fat theory to be mutually exclusive. They seem perfectly complementary and mutually re-enforcing to me.
We are approaching agreement on food reward in the research community because the evidence at this point is overwhelming, plain and simple. There is no conspiracy, no good old boys' club, no herd mentality, and I find those insinuations to be a rather lazy way of arguing against the idea. Again, recall that some of the people writing these reviews acknowledge the importance of food reward despite the fact that it potentially takes the spotlight off their own research.
Regarding the carb-insulin hypothesis, I have yet to see a single shred of compelling evidence demonstrating that it's relevant in a normal human (rather than a diabetic getting lumps of fat from injecting mega-doses of insulin into the same place day after day-- that is not evidence). The animal, and human, research as it stands today almost unanimously indicates that elevated insulin plays little or no role in the fattening process. Remember that when I first read GCBC, before I knew anything about insulin biology, I believed Taubes-- it wasn't until I took it upon myself to look into his claims and think about them more deeply that I realized they crumble under the most cursory examination. That's why the people who actually study insulin physiology and body fat mass regulation don't take Taubes's idea seriously-- they see right through him.
I eagerly await the evidence that insulin causes fat accumulation in a normal, intact animal or human, particularly in the context of all the other hormones that normally regulate energy metabolism. Until that evidence appears, I'll remain baffled that people continue to cling so tightly to the idea.
@Stephan writes "...in a normal, intact animal or human..."
Are you limiting the scope to only healthy, intact, presumably lean individuals with fully functioning metabolisms? Doesn't that then become circular, as in "healthy and intact" = "healthy and intact"..?
Are we supposed to ignore the Type 1 Diabetic: as an example of an almost complete absence of insulin in an otherwise (typically) young, lean, healthy person; and the fact that unless treated with insulin they are unable to store any body fat?
Or at the other extreme the stereo-typical Type 2 who is decidedly not healthy nor lean by the time they are finally diagnosed? And in their case they have been running with chronically high levels of insulin, and IR for many years (or decades) prior to diagnosis... by which time a large percentage of beta cell function is already lost to glucotoxicity and beta cell exhaustion?
Or the person with Metabolic Syndrome. Or the overweight, or morbidly obese?
Are you suggesting that obesity research does not apply to these people? We should only look at the healthy ones?
It is an interesting idea and we do need to establish how we get from point A to point B... but short term studies (like the trial you cited previously of injecting rodents with insulin for 7 days) don't really compare with the real life of humans and the long term effects (years or decades) of raised insulin.
You can't inject mice for a week and expect to use that as an effective model of chronically high insulin in humans with IR.
For the rest please re-read my comment above. I said nothing about "conspiracy", "good old boys' club", or "herd mentality". My point is that in a research world where there are specializations and sub-specializations, I don't find it surprising when researchers tend to reinforce the one narrow area that they are focusing on, without stepping back to see if, or how it might fit into the bigger picture... losing the wood for the trees as it were. As I recall, Gary Taubes wrote about this in GCBC; and how having the editor's backing he was then able to spend time (rarely available to full-time researchers) examining the research from the multiple fields related to obesity.
I am glad that you feel comfortable speaking on behalf of the research community -- you certainly have more claim to that position than I -- but I also wonder to what extent the research community speaks with the same voice?
As I recall, Dr Lustig talks about a difference between the short term of effects of insulin vs. the long term. He also seemed pretty convinced that insulin is a major player in obesity. This was in an interview posted November 2011. Isn't he part of the same research community?
I think the reason people cling to the idea that insulin causes weight gain is because they've experienced it themselves. People who have never had weight problems really can't understand the situation in those who have.
It's like those "controlled trials" in which they claim scientific evidence that potatoes are more satiating than fat. Yet most people who go on LC diets find they're not as hungry, and they eat less as a result.
This effect is most pronounced in people with metablic syndrome or insulin resistance. Thin, young, insulin-sensitive people can often eat a lot of carbs without gaining weight.
If you want to say people with metabolic syndrome or insulin resistance are not normal, well then, OK. But these are the very people who need help with diets. These are the people Taubes is speaking to.
“I still don't see why so many consider the food reward theory and the carbs>insulin>fat theory to be mutually exclusive.”
CIH really serves no purpose other than to lend credence to “carbs are bad” and “eat all you want as long as you avoid carbs.” A hypothesis that doesn’t fit most of the world’s population should have been stillborn. All these years later, Taubes’s “answer” to all the people in the world that eat high carb diets is the (false) statement that Asians really eat brown rice instead of white rice (“healthy” whole grains FTW). Other people say it is because Asians don’t eat as much and they have more active lifestyles (eat less, move more FTW).
CIH also just isn’t logical the way it is routinely described. If the evil hormone insulin drives glucose into fat cells and forces abnormal fat accumulation (like the picture on Taubes’ blog), why do low-carbers try to minimize blood glucose spikes? Glucose spikes should be good – it means that insulin is unable to force the blood sugar into the fat cells thus avoiding fat accumulation. Eating protein with carbs decreases the blood glucose spike largely because the protein is insulinogenic and boosts the production of the evil hormone. This larger boost of insulin forces the glucose into cells even more effectively.
Isn’t this what CIH says you should avoid – big, effective insulin spikes? Even if you eat protein by itself, glucagon forces the liver to give up its own stored glucose, so you get the same situation – insulin spike forcing blood glucose (liberated from the liver) into fat cells and leading to abnormal fat accumulation. According to CIH logic, insulin resistance should be good. Type II diabetics should be the leanest people because all that glucose stays in their blood instead of being forced into the fat cells.
Maybe instead of theories based upon simplistic single hormone mechanisms that fail to account for most of the world’s population, the answer is that Americans just started to eating more food because of various sociological and convenience factors which directed them towards crap-in-a-box, cheap and convenient but high profit food with a long shelf-life where a few cents of flour, rancid seed oil, sugar and/or salt has been engineered to be highly rewarding.
"Are we supposed to ignore the Type 1 Diabetic: as an example of an almost complete absence of insulin in an otherwise (typically) young, lean, healthy person; and the fact that unless treated with insulin they are unable to store any body fat?"
People with virtually zero serum insulin (untreated type 1 diabetics) represent about 0.1% of the total population. So yes Frank. We do ignore them.
Blogger Gretchen said...
"This effect is most pronounced in people with metablic syndrome or insulin resistance. Thin, young, insulin-sensitive people can often eat a lot of carbs without gaining weight."
Top priority should be
tackling metabolic syndrome/IR using a low-carb diet (to reduce calories eaten and increase calories burned), sensible exercise, Vitamin D3, Magnesium, Metformin etc.
Once metabolic syndrome/IR has been tackled, safe carbs can be eaten.
You missed the point completely Nigel -- was that deliberate?
You simply focused on the number of Type 1s in the general population when I quite clearly suggested accepting them as "...as an example of an almost complete absence of insulin in an otherwise (typically) young, lean, healthy person; and the fact that unless treated with insulin they are unable to store any body fat".
Rodent studies have some role to play but when it comes to real humans there are limits (practical and ethical) to what can be tested. Here we have an otherwise healthy, lean person who is characterised by a singular lack of the hormone in question -- why are you willing to dismiss anything that can be learned from this?
Dr Lustig in the presentation I posted above also touches on Type 1 and how especially teenage girls know full well how to use their insulin as an effective method of weight control.
I've explained previously why the effects of insulin on some diabetics is not relevant to the question of whether or not insulin plays a physiological role in the fattening process in non-diabetics. Briefly, 1) insulin stops glycosuria, so you stop peeing out calories; 2) many diabetics experience hypoglycemic episodes, which are a potent trigger for food intake and fat gain (Jenny Ruhl remarks that in her experience, insulin doesn't typically cause fat gain if you use it carefully and don't cause hypos); 3) in the case of diabetes, insulin is administered without the other hormones that are typically co-secreted with it by the pancreas (e.g. amylin; if you give diabetics insulin plus amylin they actually lose weight) and 4) insulin is required for fat storage in fat cells, so you get uncontrolled lipolysis.
At this point, some people would say "aha, #4 means insulin is fattening!". Nope-- not in a physiological context. Insulin secretion rises in parallel with fat cell insulin resistance, such that total insulin action on fat cells remains the same or is even reduced over the course of fat gain. This is apparent because circulating fatty acids are normal or even increased at all stages of obesity-- there is nothing keeping fatty acids from exiting the fat cell. This fact alone is fatal to the CIH, at least Taubes's version of it.
I've considered Lustig's position in great detail. He and I have communicated, and I've asked him for the references he uses to support his position, and read them. I continue to respectfully disagree with his position because nothing I read supported the idea that the effects of insulin on the brain are different between the short and long-term, in fact nothing he provided me even really addressed the question. He uses the results of his octreotide study to support the idea that suppressing insulin causes fat loss. I encourage you to look up what octreotide does and come to your own conclusions about how solid that line of reasoning is.
There is no evidence whatsoever that insulin plays a causal role in the development of common obesity, and there's ample evidence to suggest that it does not, and that it is in fact the result of obesity rather than the cause.
I think you hit the nail on the head. The main reason some people believe the CIH is because they've had a good experience with low-carb. Low-carb lowers insulin, and low-carb helped me lose weight, therefore lowering insulin is what caused me to lose weight. As Gary Taubes would say, correlation doesn't equal causation.
There is plenty of evidence that contradict the food reward hypothesis. Children eating sweetened breakfast cereals are leaner than those eating plain cereals. One 6-week trial found that increasing intake of cereals and cereal bars made dieters more satiated than increasing vegetable intake. People of all ages who report consuming more candy and chocolate are leaner than non-consumers. Decades of studies have consistently shown sugar intake to be negatively associated with BMI. The french and italian typical diets are unarguably among the most palatable, yet they remain among the most obesity-resistant. (and if you think these populations don't actually regularly eat the delicious foods we associate with their culture, you need to go live here. Just take Nutella which has been a breakfast staple in both these countries for nearly 40 years).
To my knowledge there is no evidence that food reward directly impacts body fat set point negatively, as no experiment has been done that can discern the effect of the food reward from the effects of the rewarding food used.
The fact that populations that have historically eaten more palatable diets are now more obesity-resistant while populations that historically ate less palatable diets (such as most traditional populations) are by far the most obesity-susceptible in modern society, indicates that the relationship between food reward and weight regulation is more complex than just ,more reward = more obesity. Declaring a scientific consensus while we still have a pretty simplistic understanding of how food reward relates to weight regulation just seems like a bad idea to me, completely analogous with earlier blunders like the diet-heart hypothesis.
Thank-you Stephan. I wasn't asking you to agree with Dr Lustig's position but just to acknowledge that the research community clearly has not reached consensus or agreement on this issue.
You say that [chronically high insulin] is "the result of obesity rather than the cause." and I know we have discussed this chicken vs. egg before. Perhaps your focus starts from before there is any metabolic disorder, while my personal experience/experiment started from the other end of the continuum, working backwards. At some stage we both reach the point of the "big bang" where a person goes from being normal and intact to a trajectory, that if unchecked, ultimately leads to Metabolic Syndrome -- abdominal obesity, IR, dyslipidemia, Glucose intolerance etc...
As I see it there is a vicious cycle involving (in no specific order):
1) High levels of insulin fed by a diet rich in sugars and refined starches
2) Insulin Resistance (IR) that requires ever higher levels of insulin to overcome
3) Excess fat mass that increases the IR
4) Increased hunger and fat storage due to the action of high levels of insulin
I said "in no specific order" because each of these processes feeds back into the others.
So at your point of study there may be no significant chronically raised insulin but rather you do see some excess fat mass. Then on a later date the chronically raised insulin and IR is now evident so you observe a chronology of events... when it may be that it was all happening simultaneously.
So what starts the whole ball rolling? My bet is on the "Western" diet -- rich in sugars an refined starches (I accept that foods have been manipulated to be hyper-rewarding but I'm still waiting for examples that do not contain sugar and/or refined starches) -- either as eaten over decades by the individual and/or perhaps even their mother when they were still in the womb.
As for insulin requiring hypos to increase hunger I suggest you try it. Hypos are not required.
I'm going to guess that by the time I post this, others will have already said something similar: there seems to be something oxymoronic about the phrase "scientific consensus." And for those who cry it out as an argument, congratulations, your fanbase now has a lower average intelligence.
As someone who has a French father and who has spent years in France, eating in the homes of my family and friends, I can tell you that French food is often misunderstood by people who have only experienced it as tourists or out of a cookbook. I suspect this is also the case for the other countries you mentioned.
On a day-to-day basis, French people tend to eat relatively simple, home-cooked food. Typical lunch at my grandparents' house would start with fresh melon, then small portions of grilled fish or sausage on the BBQ, plus green beans cooked in a pan with tomato paste and a little olive oil. White bread is eaten with every meal, as well as wine. There was cheese at the end of the meal for those who were still hungry. Dessert was almost always fruit and/or plain yogurt (sugar bowl provided). Dinner was usually quite modest. The food was good, but certainly not hyperpalatable by any stretch of the imagination, and that was typical of nearly all the families I stayed with.
Traditionally, the French rarely eat at restaurants, and don't eat much processed food in general. Everyday French food is not the parade of hyperpalatable items that some people think it is. French people do eat food that is hyperpalatable, like fine restaurant food and pastries, but not all the time.
The fact that people who eat more sugar or more sweetened breakfast cereals are leaner in observational studies is interesting, but it's hardly a convincing argument against the FRH in my opinion.
You said that no experiment has been done that distinguishes between the reward value of food and the properties of the food itself. That is not true-- there are many experiments in which food quality is kept identical or very similar and food intake and/or body fat mass changes are measured between different palatability/reward conditions. I've previously referenced those on my blog. Keep in mind that in those experiments, the hypothesis has two arms and a leg tied behind its back, because the most potent reward factors, energy density, fat, sugar and starch, cannot be changed without changing the diet's composition.
I continue to maintain that the FRH is overwhelmingly supported by the scientific literature, and by simple common sense.
Re Reward: I find that the tastier the food, the less I eat. I even at one time considered coming up with a High-Taste Diet, on the theory that given free choice, we all have a daily taste requirement, and we'll keep eating until that is satisfied.
This would explain why the French tend not to be overweight and Americans are. Most standard American food is pretty tasteless except for salt, sugar and spices like chili.
Rich people, who can afford fresher, tastier food, tend not to be overweight. Poor people who eat a lot of starchy food tend to be fatter. I know correlation doesn't imply causation, but when a lot of correlations are consistent with a theory, they tend to support it.
Dr. Lustig is solidly on board with the food reward hypothesis. He does differ from most other researchers on the role of insulin in body fatness, although his position really is not the same as Taubes-- in denying the role of the brain, Taubes is in a weird world of his own.
I didn't make the claim that every scientist agrees with the FRH-- I'm sure there are some who don't, although I haven's seen any researchers publicly critique the idea lately. There will never be 100% agreement on any major scientific question. But it is still telling when experts converge on a hypothesis.
I don't understand why we should keep our focus on "normal, intact" people. You can easily gather several groups of people for a few months, control their diets, and then observe non-significant weight change in all of them. Now we need to come up with a new obesity hypothesis where food is not even a factor...?
People gain different amounts of weight in forcefeeding studies: "This fact alone is fatal to" food reward, or any hypothesis that revolves solely on calorie intake.
As for the insulin-induced hypoglycemia-induced calorie consumption point, try hanging around some competitive bodybuilders or search forums. See what happens when two bodybuilders are forcefeeding, one using insulin and another using winstrol. Spoiler: insulin users store more fat, depsite both forcefeeding.
The cry to study "normal" people when confronted with arguments of type 1s or hormonal injections just looks like a way to avoid having to provide any sort of mechanism of fat gain, due to complete reliance on calorie number per se: "Once you eat calories beyond a threshhold... fat gain just happens."
The fact that people gain different amounts of fat when force fed does not conflict with the food reward idea at all, it just suggests that fat mass is regulated, which I have explained many times on this blog. I have a post coming up on why some people gain more fat than others when force fed.
Those studies also do not challenge the idea that calories are important. In the absence of overfeeding, no one gains weight. When people are overfed, they gain weight, but some gain more than others. The difference is because some are able to ramp up energy expenditure. This is totally consistent with with idea that energy balance is the primary determinant of fat mass, it simply suggests that energy in and energy out are not independent variables.
Furthermore, if you look at underfeeding studies, calorie deficit is the sine qua non of fat loss. You can accurately predict fat loss via calorie deficit, and the heterogeneity between individuals is much smaller than what is seen in overfeeding studies. This is all totally consistent with my position.
Regarding focusing on normal people, two points. First of all, an important question is what causes fat accumulation to begin with. To answer that question, you have to start with normal, lean people who are not yet obese. I agree it's important to also study people who are not lean, but that has been done, and the evidence there is also not supportive of the insulin idea. Regarding diabetics, the argument that they gain weight when they inject insulin is being used by some as support for the idea that insulin causes fat gain in non-diabetics. I'm saying that analogy doesn't make physiological sense. There's a difference between injecting isolated insulin through a syringe, and the delicately regulated "symphony" of hormones, including insulin, that functions in a non-diabetic who is not injecting insulin. In this context, which is really what we're talking about when we're asking what causes obesity, insulin does not promote fat accumulation.
Okay, I will await your post on why some people are inefficient with overfeeding. But just the fact that that does happen somewhat discredits food reward as a complete hypothesis. As soon as one starts to explain the physiology of fat storage, we immediately know caloric intake is not the deciding factor--unless those mechanisms are unchangeable (but they obviously aren't).
The problem is with equating addiction-induced excess food to body fat. They are related, but they can be completely uncoupled--like smoking and lung cancer. I see this too from personal experience, as I have lived my life with an extreme propensity to binge (luckily with only healthy foods the last few years), yet I effortlessly stay very lean.
Even with only your own words, I don't see how one can logically conclude that insulin plays no role in fat storage. If it encourages glucose oxidation at the expense of fat oxidation, or suppresses FFA release, it is involved. Now that doesn't mean insulin=fat, but maybe all else equal it does. Besides, I have yet to see a good explanation for the FIRKO mouse by somebody trying to discredit the weak* insulin hypothesis.
*Like stated above: all else equal, more insulin leads to more fat (same statement with adipose insulin signaling), without any further implications.
As someone who currently lives in France and work/live with french people, I can say that croissants and other heavily fat and sugar-laden pastries, salty/fatty sandwiches, crepes, waffles, etc are more or less staples of the french diet, they're eaten by a large part of the population at breakfast and lunch. White bread with Nutella is pretty much standard breakfast for students, and from what I've heard, this is a habit most of them picked up from their parents. French student restaurants do serve some whole food dishes (though hardly unflavored), but also pizzas and pastas with various sauces, which tend to be the most popular choice by far, often with a sweet pastry for desert.
Granted you could argue this is a recent development and linked to the fact that France also has rising rates of obesity, but the vast majority of people of all ages I see having these dietary habits are not overweight, some of the leanest french people I know are also those who eat these foods most frequently, whereas you see the overweight choosing salads and sipping away on their diet cokes.
About studies that isolate food reward, I'm assuming you're referring to the rat studies that added artificial flavors to their diets. For one thing, as you pointed out yourself, adding artificial flavors did not cause fat gain in the context of a low-fat/low-sugar diet, though there is no reason it shouldn't according to the food-reward hypothesis.
For another I'm just skeptical that adding flavors to a diet is only an issue of food reward. Flavors are after all our primary guide to the nutrient content of a food, and fulfilling nutrient needs is of course part of the homeostatic system. Artificial flavoring may well be fattening simply because it tricks our body that a food contains a certain nutrient that we could use more of (hence the taste preference for it), yet because it doesn't, eating the food never satisfies our appetite for this particular flavor. I'd be willing to bet that in modern society, artificial flavoring is a heck of a lot more strongly correlated with obesity than food reward per se.
What I would consider direct proof that food reward is an independent factor in body weight regulation is either that blocking olfaction reduces susceptibility to gain weight on rewarding foods (interestingly I've read that obese people tend to have impaired sense of smell), or something like a diet trial where one group ingests their food in a palatable combination, whereas the other is instructed to ingest things like salt, sugar and added fat separately.
watch out-inneficiency with overfeeding likely has more to do with expenditure than intake. The calorie hypothesis (and food reward) will stay intact.
Also Stephan, how do you explain that pretty much all forms of dieting have terrible long-term success rates, even though they all involve substantially lowering food reward in one way or another? Frequent dieting is a strong predictor of future weight gain, and most people tend to regain more weight than they lost when they go back to eating freely. Neither of these phenomena seem to jive with the idea that lowering food reward improves long-term weight regulation.
The fact that many people can remain weight stable despite having food addictions shows the inadequacy of the reward hypothesis in explaining obesity. I'm not claiming that behavior reinforcement from food doesn't exist; I'm saying that it doesn't imply fat gain and doesn't explain it. Umm, assuming normal absorption, yea, overfeeding inefficiency has to do with expenditure. What else could it possibly be?
What is the "calorie hypothesis"?...Calorie intake is related to weight gain/loss?...Pure genius.
"You missed the point completely Nigel -- was that deliberate?"
You made a point?
P.S. You still haven't replied to THIS.
The problem with this debate is everyone is half right... Personally, I find that my "food reward" varies. I can tell you that after a Crossfit workout, the thought of sugary stuff is nauseating, what I crave is MEAT!
Meanwhile, in experimenting with "juicing" I discovered that my saiety increased sharply by drinking pure vegetable juices.
It's also clear that the brain is definitely significant. Look at the studies showing that diet sodas make you gain weight!
Ware the person with the anecdote, but I remember losing 10 pounds in 4 weeks on a visit to Germany; I found all the sausages super filling. Again, my personal experience tells me that soda is weight in a can; ice tea doesn't have nearly that effect.
I think the problem with low carb vs other hypotheses is that carb/fat/protein is too simplistic a view of food. One of the best weight loss tips I've ever had is to realize that you may be eating because you're thirsty; what you really want is water. Drink water.
What all that means is that both you and GCBC can be right; it may be that low carb diets, as implemented by Americans, lead to changes in eating and reward patterns that deemphasize certain foods. The body then responds to that by lowering insulin resistance, etc.
"The fact that many people can remain weight stable despite having food addictions shows the inadequacy of the reward hypothesis in explaining obesity."
The reward hypothesis explains over consumption, not necessarily obesity. What happens in between is highly individual. Some people may naturally increase expenditure, others may otherwise decrease intake. Some people do neither. This doesn't change the fact that consuming more than you expend results in gain (regardless of the macro)-some muscle (a lot more muscle if the body is stimulated with weight training) and some fat (a lot more fat without a muscle producing stimulus).
"What is the "calorie hypothesis"?...Calorie intake is related to weight gain/loss?...Pure genius."
I suppose I should have said calorie insulin hypothesis, not calorie hypothesis. By the way, your insulin vs. winstrol example speaks more of the effects of winstrol as a cutting steroid than it does of insulin as a fat promoting hormone.
Do other obesity researchers suggest tactics for losing weight based upon their conclusions about Food Reward? If so, how do these approaches map to your own strategy of five levels?
Hi Stephan. I have to admit I haven't been keeping up on the discussion on either "side" here. My impression is that there's a lot of fractionation ("factionation"?) where various camps have grabbed hold of some specific piece of the puzzle as the overall cause, rather than examining the interactions between the different subsystems involved in metabolic regulation.
For instance, suppose that (for whatever reason) some person's fat is not efficiently released to supply energy between meals. It seems pretty clear this individual's food reward response must be modified to make up the difference, otherwise they would eventually starve while getting fatter. Conversely, if there were some derangement of the hypothalamus which caused chronic overeating, the metabolic regulation of fat tissue would almost certainly have to respond, etc. So maybe I've missed something in the previous discussion, but I don't see how you can separate these things, or why you'd even want to.
It's disappointing that you would appeal to "scientific consensus". I'd like to see some quantitative assessment of the relative weights of various hypotheses given the evidence, something like a posterior odds ratio.
I have a bigger picture question when you have a moment. What is the current evolution of your thinking as to what causes the 'Diseases of Civilization'?
Why did Albert Schweitzer encounter no cases of cancer in Gabon? Why did Hutton find no cases in the Eskimo in Labrador? No cardiovascular disease?
This can't simply be a case of lack of overnutrition due to low food reward. The hippocampus is not causing heart disease and cancer, is it? Why to slim people in the US get heart disease and cancer?
Stephan, Your example of a meal at the home of your French relatives *does* sound hyperpalatable to me. I'll bet the ingredients were all fresh.
My parents lived in Paris for several years. They had a cook, and she shopped every day at a market. The food was fresh. The ingredients mattered. The train from Normandy was scheduled so that the morning milking would reach Paris by "lunch" time (main meal of day). Her meals were simple but delicious (except the time she tried to surprise us with corn on the cob and said she boiled it for 4 hours and the cobs never got tender).
I don't know about today, but then it was standard to shop daily. Americans would shop weekly and shove stuff in the freezer. Or eat prepared foods.
Fresh melon, fresh fish, good French bread, beans with olive oil, a bit of cheese, and fruit for dessert make my mouth water. A boxed meal or a chain restaurant meal does not.
"For instance, suppose that (for whatever reason) some person's fat is not efficiently released to supply energy between meals. It seems pretty clear this individual's food reward response must be modified to make up the difference, otherwise they would eventually starve while getting fatter."
WTF? C'mon people! Let's suppose we're humans living on planet earth.
A consensus is not possible but good to know the views and also ponder what should be the right approach after all,obesity can not be the order of the day.EMR
In the field of obesity, the divide between the basic scientists and the clinicians could not be any wider. Where are the clinical trials? When does food reward get made part of the nutritional guidelines?
I would love to hear your opinion on why the disconnect. Is there any plan to organize a clinical trial?
> insulin causes weight gain is because they've experienced it themselves
.... ( ! )
("factionation"?) where various camps have grabbed hold of some specific piece of the puzzle as the overall cause, rather than examining the interactions between the different subsystems involved in metabolic regulation
the word you seek is probably reductionism. Maybe "specialist fragmentation".
Whether correct or incorrect, reward theory seems to me the most integrative and least reductionist obesity theory I've yet seen, bringing together as it does a great many processes and signals.
> the reason people cling to the idea that insulin causes weight gain is because they've experienced it themselves
Maybe you typed "people" where you meant "diabetics that need to inject"?
"Regarding the carb-insulin hypothesis, I have yet to see a single shred of compelling evidence demonstrating that it's relevant in a normal human (rather than a diabetic getting lumps of fat from injecting mega-doses of insulin into the same place day after day-- that is not evidence)".
Please read "The Art and Science of Low Carbohydrate Living" by Jeff s. Volek, PhD, RD and Stephen D. Phinney, MD, PhD. Either read the book or go straight to the references to track down the studies.
Stephen, please understand (not read, understand) and critically evaluate
try not to make weak, invalid excuses like stalker and other name calling (IOW try not to pull your Taubes muscles)
Then read the following and evaluate it CRITICALLY, not as a gulled acolyte
"The Art and Science of Low Carbohydrate Living" by Jeff s. Volek, PhD, RD and Stephen D. Phinney, MD, PhD.
Great collection of papers - thank you.
I'm confused about something you wrote in your "glossary" on food reward:
"For example, if you eat a strong cheese for the first time, maybe it won't taste very good to you. As it's digested, your reward system gets wind that it's full of calories however, and the next few times you eat it, it tastes better and better until you like the flavor."
It's been my understanding that "food reward" was the simultaneous release of dopamine with the ingestion of highly palatable food so that "reward" was rather instant, as opposed to acquired - or maybe I'm just confusing myself (I'm good at that).
My interests in this science is to be able to "translate" it in as basic of layman's terms as possible (for a general audience), so any clarity would be much appreciated! Thank you ....
> so that "reward" was rather instant, as opposed to acquired
Even when people are not nomadic the taste of food changes regularly. New preparation methods, new foods (different types of meat, different nuts, fruits, vegetables - even differently-ripened foods) taste different.
Thus hard wiring preferences for specific tastes would not be adaptive.
Note that in addition to learning a preference for higher calorie foods, learned food reward makes food poisoning and toxicity less likely.
If the food reward system also rewards you for eating non-poisonous food, it only makes sense for you to eat food you've eaten many times before - that food has not poisoned you, so it's less likely to poison you now and in the future.
In this formulation reward in addition to rewarding for calories and various combinations of macro ratios is also a flip side of learned disgust and food aversion coin.
Hard wiring taste preferences also wastes brain space ... food that your ancestors ate but is no longer available should not be taking up space in our brains.
I was in France over the summer and was surprised how much they eat when eating out. But I was also surprised by how much they smoked while eating out. Some smoke between courses. It was the same thing when I was in Italy this winter. Both countries drink espresso after meals and throughout the day. Another thing was that their stress levels seem generally lower in those two countries. How might that affect obesity?
Does a high salt diet qualify as a hyper-palatable diet?
> so that "reward" was rather instant, as opposed to acquired
clarification on the above:
It's like Pavlov's dogs.
once you learn which flavours in your specific environment are accompanied by calorie dense foods the reward for the flavour becomes quick.
But that initial learning does take time. Take cheddar cheese as your example - that flavour could not have been learned by distance ancestors as being associated with high fat and protein - it was not available to them at all.
The very first time you eat it, so far as your body knows, it could be poisonous. your body/brain has to associate the flavour (and I bet the texture, chewiness, melting characteristics) to the calories.
After your brain/body knows the flavour is a shorthand (short-tongue?) for that combination of nutrients it can reward you immediately upon tasting it.
Apologies if this has been dealt with elsewhere, but I'd be interested in your comments on:-
Circulating glucose levels modulate neural control of desire for high-calorie foods in humans.
"...mild hypoglycemia preferentially activates limbic-striatal brain regions in response to food cues to produce a greater desire for high-calorie foods."
People with impaired glucose control get rebound mild hypoglycemia on high-GL diets. This is how insulin is involved in weight gain.
People with impaired glucose control also get postprandial hyperinsulinaemia, which causes severe lethargy. This drastically reduces calories burned.
I see where you're coming from, but postprandial hypoglycemia large enough to influence food intake is actually pretty rare. I read that paper, and they clamped people at 65 mg/dL glucose-- on the cusp of hypoglycemia. Almost no one goes that low following a meal; it's 20+ mg/dL below typical fasting glucose. If you ask an endocrinologist about it, which I have, they'll tell you that postprandial hypoglycemia is not a very relevant concept to common obesity. Non-diabetics who get symptoms like hunger that they call hypoglycemia are almost never hypoglycemic when you actually test their blood sugars.
Although, when your blood glucose control is quite impaired (severe pre-diabetes), it's possible that rapid large drops following meals could trigger a hunger response in some people. This is something that Jenny Ruhl brought up with me a while back. I don't know if it's been investigated but it makes sense as a possibility.
One other point-- hyperinsulinemia does not reduce calories burned. If anything, it increases calories burned via insulin-induced thermogenesis.
Obese people almost invariably have higher metabolic rates than lean people, and their fat cells release more fat than lean people-- there is nothing preventing the fat from exiting, it just isn't being burned fast enough so it goes back into the fat cell.
Thanks, Sanjeev, but you didn't answer the question (that I had posed to Stephan). While I appreciate your comment, it had absolutely nothing to do with my question & just added to the confusion. If Stephan can't answer it, I'll figure it out on my own. Thanks again.
Stalker? Taubes muscles? Acolyte? Name-calling is bad manners.
I was pointing out that credible research has been conducted by Volek and Phinney; others as well if you search. If you find their research has no value, fine. But don't call me names, it's in bad taste and only makes you look foolish.
As to the book, yes, I've read it, even critically. That's why I recommended it.
I had reactive hypoglycemia back in the 1970s when I did the early "wire desk" at a newspaper and had only coffee and a doughnut for breakfast, and I can assure you it's more than hunger.
I would perspire and get "the shakes," and this terrible feeling that if I didn't eat something, I'd die. The solution was a candy bar. When I didn't have to come in early and "reward" myself with a doughnut, I didn't eat breakfast and never had these symptoms.
I was Dx'd with type 2 diabetes 20 years later, and I've had real lows and I know the symptoms I had in the 1970s were low BG. At the time, my physician didn't believe me because he thought hypoglycemia was a fad.
I've also documented in a N = 1 experiment that rapidly falling BG levels cause intense hunger. I noted where the intense hunger occurred in a graph in my diabetes book, and it's definitely not low.
In one experiment, I went up to almost 200 and felt intense hunger when I had rapidly fallen to 160. This makes sense to me. The analogy I used in the book was that if you saw some broken glass at the bottom of a slide and your toddler was about to slide down and land on the shards, you'd rush to stop her BEFORE she reached the glass. I think the body is doing the same.
As I understand it, food reward is something that is learned.
When you ingest food that activates the reward centre in your brain, your brain "learns" this, and the next time you are faced with the prospect of eating said food, dopamine spikes causing increased desire and motivation to consume said food.
faced with the prospect of eating <- this is quite a flexible term, just thinking about said food will cause dopamine spikes, if your shown a picture of the food, or if you smell the food, all this causes dopamine spikes and will ultimately motivate you to obtain and eat said food.
Brain scanners done on obese people show that certain area's of the brain light up like fireworks when simply shown pictures of rewarding food. Thats the dopamine spiking and telling you "OI, LISTEN UP, THAT FOOD IS REALLY NICE, GO GET IT NOW!"
The reward feeling is instant, the feeling of euphoria and happiness you experience to eating rewarding food, is instant.
The release of dopamine comes before you consume food, its the signal telling you to get and eat the food. To put the food in your mouth.
I have a hard time believing that bacon, sausage, eggs, and cheese are NOT rewarding, because I eat it most days for breakfast and love it but am staying slim without restriction. However when I eat pancakes, cereal, and other sugary/floury carb-based foods I tend to overeat and gain a few pounds.
I'm open to alternate hypotheses, but to me it still seems obesity is more related to carb-food intake than to the taste of foods. I think Food Reward plays a role in food choices, but I don't buy the idea that it dictates the quantity. I still think that is driven by something else, and I still think insulin could be key here.
Thanks, Kindke. That is how I understood it as well, but I think I got tripped up on Stephan's wording.
You are a smart guy. The few pounds of weight gain after eating some carbs is definitely fat and is in no way related to any water weight gain.
When one follows a low carb diet and eats a few carbs, those carbs go straight to the fat tissue and stick like glue.
Thanks for the information. This Paleo diet concept is relatively new to me. Though the concepts seem sound and make sense. Everything in moderation!
Dude(ette?), you shouldn't joke like that! Misleading Dave with that BS is not nice.
I guess I misunderstood your question. for a biological process to be "instant", it has to be hard wired or reflexive; learned responses mostly can't be.
> that bacon, sausage, eggs, and cheese are NOT rewarding
For many people these don't excessively / abnormally activate the reward pathways.
They're fulfilling or "filling" or satisfying or satiating but that's a different issue from over-stimulation of those brain pathways; a different issue from some foods inculcating a drive to seek and consume more.
I can eat some cheeses (blue, aged cheddar) when I couldn't possible bear to look at another potato for fear of exploding. And soft boiled eggs with just the right goooey consistency, I could easily eat a dozen for breakfast every day, even more with salt & jalapenos or wasabi.
> However when I eat pancakes, cereal, and other
> sugary/floury carb-based foods I tend to overeat
> and gain a few pounds.
> I'm open to alternate hypotheses, but to me it
> still seems obesity is more related to carb-food
> intake than to the taste of foods.
sugary processed carbs are one of the classes of food most people identify as meeting the criteria for reward/(overfeeding trigger).
What you just wrote supports reward theory.
> supports reward theory
from 2 different angles no less
To really test out the reward theory in extremis do the potato only diet (no salt, butter, oil, sugar, condiments of any kind) for 3 or 4 weeks.
You misunderstand Food reward, just because a food taste good doesn't mean it's hyper-rewarding. The fact you eat those foods everyday to fullness and you maintain your weight means they're not highly rewarding. Re-read Stephan's post and older posts where he defines the terms more clearly.
Actually for me "in extremis" would mean cassava, which is the least rewarding starch I've tried so far.
I've found I actually like potato quite a bit. Not enough to overeat, but it's quite good. the yellow fleshed ones are the best.
Those are the starchy ones; nothing beats spinach smoothies (spinach only, no sugar or fruit or anything). When turned into smoothies I think there's enough starch liberated to provide enough calories to live but I would starve to death if I had to get my calories from that.
"Everything in moderation!"
The best weight loss advice ever given in the history of man kind. Mom and Grandma knew it all along, and it's not expensive or confusing.
I have experienced symptoms of low blood sugar since high school and I had a high sugar diet until I was about 30 years old. When I was 35 I had a 3 hr oral glucose tolerance test and my blood glucose was 60 at hour 3. I could hardly drive back to work. Of course, when the doctor called my test was "normal". From age 30 on I gradually cut way back on sugar, I eliminated soft drinks in my early 30s. I was already eating very low fat.
My weight was creeping up 1-2 lbs per year, by 45 I was 40 lbs overweight. So I kept cutting back calories and carbohydrates. So for 9 years I ate 1500 - 1800 calories a day with only 3 significant serving of carbs a day (oatmeal, 1 small slice of whole grain bread and 1/2 cup of brown rice a day) in addition to veggies and one serving a day of berries. My reward, I did not gain any weight for 8 years nor did I lose any. I still had symptoms of low blood sugar, but now when I tested myself, my glucose is in the 80s. I am not or have ever been diabetic, but most of my family is by age 50 and some of them are still thin.
About 1 1/2 years ago I cut added sugars to less than 10 grams per day. I lost 4 lbs in a couple of months and than stalled out. If I cut calories I would just have more frequent energy crashes. In October I cut out my 1 glass of wine or beer a day and I lost 4 more lbs over the next 2 months. I spent most of the time being hungry to extremely hungry and could not lose any additional weight.
In January, I read Gary Taubes new book and it convinced me that cutting carbs to less than 50 gms/day and increasing saturated fat would not kill me. So I replaced the 3 servings a day of carbs with fatty meats and even cheese. The first week I was miserable, I could feel the effects on insulin dumping into my blood before each meal and with no carbs to follow I would get tired and shaky. I am eating the same or above number of calories per day and I have lost 12 lbs in 10 weeks. My hunger level is much lower than before.
If this isn't the effects of reduced insulin on fat storage than what is it? I have eaten a whole foods, simple home cooked diet for 20 plus years and my exercise program has stayed exactly the same.
Stephan Guyenet said...
"Although, when your blood glucose control is quite impaired (severe pre-diabetes), it's possible that rapid large drops following meals could trigger a hunger response in some people. This is something that Jenny Ruhl brought up with me a while back. I don't know if it's been investigated but it makes sense as a possibility."
I can confirm that in the bad old days when I had impaired glucose control (by OGTT), I got the munchies when my blood glucose level fell from high to normal. I believe that people who do really well on low-GL diets also have impaired glucose control.
I'm glad to be able to report that I no longer have impaired glucose control and that I can now eat natural carbs to my heart's content.
@Swede, I know all about water weight. I'm really talking about food choices in the long term. Foods that are demonized like bacon, steak, hamburgers, and others high in fat seem to keep me thin unlike foods deemed healthy like cereals pasta, and other grains.
I guess it is convenient to have a hypothesis where you can pick and choose what foods are rewarding based on your own observations.
Stephan Guyenet said...
"One other point-- hyperinsulinemia does not reduce calories burned. If anything, it increases calories burned via insulin-induced thermogenesis."
I disagree. Thermic Effect of Activity (TEA) trumps insulin-induced thermogenesis. TEA is high on low-carb diets, but zero during postprandial hyperinsulinaemia "comas" (of which I've had many).
"If this isn't the effects of reduced insulin on fat storage than what is it? I have eaten a whole foods, simple home cooked diet for 20 plus years and my exercise program has stayed exactly the same."
Fewer energy crashes = increased calories burned due to Thermic Effect of Activity & Non-Exercise Activity Thermogenesis.
Mary, the diet has been known to work for a long time.
Long before insulin was discovered.
the diet works. Stephan writes it repeatedly; "low carb diets work for some". I write it. It works Spectacularly for some.
The diet is a different beast from the popular guess that purports to explain WHY the diet works.
Beyond your own "n=1" experiment, your individual testimonial, riddled with bias, just like everyone else, doesn't prove anything. I never take anyone's account of their diet seriously; most people seriously misreport and misinterpret this stuff.
"I could feel the effects on insulin dumping into my blood before each meal and with no carbs to follow I would get tired and shaky."
How do you know this was due to insulin "dumping" into your blood?
"If this isn't the effects of reduced insulin on fat storage than what is it?"
It isn't. 4-5lbs is likely water weight. The rest is due to reduced calorie intake or increased activity or both. But if you want to credit reduced insulin, with no proof, go ahead.
> Stalker? Taubes muscles? Acolyte? Name-calling is bad manners.
I didn't call YOU those names. Here's what I wrote:
> try not to make weak, invalid excuses like stalker ... try not to pull your Taubes muscles)
That's a suggestion/request not to try the same tactics the Atkins/Taubes supporters have been trying in vain.
It was also meant to tweak a few noses, hoping to get a few more of "the usual suspects" to comment here (I'm disappointed, I guessed a couple more would vent than actually commented)
If you really want Stephan's comment on the studies create a web page discussing the studies and post a link to that page here. You're requesting someone else do some work. Make it easy as you reasonably can for them to do it. before I would request such a thing I would at absolute minimum first search this blog to see if the individual studies have been discussed. I would also in fact check if James Krieger commented on the studies. Stephan's been known to share stuff with him. Krieger and Colpo I'd definitely check. Then at minimum post the links to the studies, full text if possible.
And how many times are you going to recommend the book anyway ... is the above comment, the 6th time? with no direct links to studies, no presentation of any good/bad/indifferent comment on study validity or quality, just the repetitive blanket vague assumption that anyone who reads it will agree.
click or copy & paste for work safety :
after all that, yes, your name calling accusation is completely valid - it's an invalid and lazy "argument" but ain't it interesting you didn't object to the actual name calling that did happen, being called a gulled acolyte.
Being an acolyte (in its most prominent definition) is not a bad thing 'tall in my mind. It's that qualifying word that makes it not good.
 not that they'll stop trying it, whether in vain or not. The Taubesians endlessly repeating "in-vain", intellectually invalid, unworkable, ineffectual, impotent behaviour? SAY IT AIN'T SO !!! 
 in case you didn't get it this is Einstein's quote somewhat reworked.
I apologize - my last comment was left in haste. I was just trying to bust your balls and mock your explicit (or implied) fear of carbs.
Bacon, steak and hamburger are indeed delicious foods. Eat them and enjoy my friend.
Stephan's either a saint or has luudes in an IV drip.
I would have blown a gasket months ago.
> I guess it is convenient to have a hypothesis where you can pick and choose what foods are rewarding based on your own observations.
The specific foods that qualify have been and are being quantified in several different ways that triangulate.
Subjective reports are only one triangulation direction.
Others include fMRI studies, neurotransmitter blockade studies, animal operant conditioning reinforcement, addiction research, opiate blockade studies, brain lesion studies (manually damaging animal brain regions, finding where a brain lesion is in humans with various disorders)
Dude, you should read "Good Calories, Bad Calories" by esteemed author Gary Taubes.
It will BLOW YOUR MIND!?!?!?!?!!?!?
> try not to pull your Taubes
it's a local joke/idiom hereabouts (a hockey-mad culture), a play on "pulled groin muscles".
May not mean the same elsewhere ...
I am a very disciplined person. I count calories and review what I have eaten during the day every evening and I weigh every morning. That is how I know I am eating the same or more calories per day - I do it deliberately and am enjoying not being so hungry often. The first 2 weeks I lost about 1 1/2 lbs (varied from day to day), so much for the water loss. Remember, I was already low carb before I switched to very low carb. Some weeks I lost no weight, those were also the weeks when I tried adding the oatmeal back at breakfast. I do eat a small quantity of roasted root vegetable at dinner a couple of times a week and salad and green vegetables every day, but I was already doing that. I simply removed the 3 small serving of carbs I was eating every day and replaced those calories with additional fatty meat, salmon or cheese. It is like a miracle to me that I am finally able to lose weight. I went from a very low fat, low carb, moderately low calorie diet to a very low carb, high fat diet and have lost 12 lbs in 10 weeks.
I bought a blood sugar meter years ago and monitor my blood sugar regularly. I started experiencing low blood sugar episodes - shaking, sweating, inability to communicate, confusion, etc. starting in high school. I was extremely thin until my late 20s despite a poor quality high sweets diet. I have always been active: socker, tennis, biking until I ruined my knees. I still walk 10 - 15 miles per week and do a strength workout twice a week, plus my knee exercises daily -no ACLs. Then I started gaining weight every year. I gradually improved my diet, cut out the sweets and finally carbs over my 30s and 40s to try to avoid the energy crashes - it interfered with work. As I said this kept me from gaining weight for 8 years in my late 40s, early 50s, a time when women tend to gain weight and become more insulin resistant. My fasting blood sugar continued to creep up, 95-110. Most of both sides of my family are diabetic by my age, so there is probably a genetic susceptibility to diabetes. 3 of my grandparents died before I was born from diabetic complications. Since,I have found most doctors to be unhelpful in regards to overweight and diabetes prevention, I have spent a lot of time researching the diet/obesity question. I have a lot at stake here and have been a lurker on this as well as many other blogs for a couple of years. With 2/3 of adults overweight or obese, we have to remember that there are real people here in desperate need of research to determine how to fix their broken metabolisms. I understand research on prevention is also necessary. Is it possible that the hypothalmus is driving a high insulin response to carbohydrate? I would get hungry before a meal, get hungrier just before eating and be even hungrier in the middle of the meal. I am a vey slow eater by the way. If I didn't eat soon enough after getting hungry I would experience a energy crash.
I would like to thank you for taking the time to keep up the blogging. I have found valuable information here, particularly a year or two ago when the blog was more focused on ancestral diets. I agree there may be something to the hyper-palatable hypothesis, but all of these industrial foods seems to be high in starches and sugar. I find a lot of these foods no longer taste good to me, switching to a whole simple food diet 20 years ago has changed my taste buds.
> Dude, you should read
that's dWeWd 2U d00d
Where would one find such a magical tome, obviously penned by one so wise in the ways of science
Under short stories? swords & sorcery? nah ... must be romance
> Mom and Grandma knew it all along
clearly They never read gc,bc
"The Art and Science of Low Carbohydrate Living" by Jeff s. Volek, PhD, RD and Stephen D. Phinney, MD, PhD.
Mom & Grandma should Either read the book or go straight to the references to track down the studies.
"You misunderstand Food reward, just because a food taste good doesn't mean it's hyper-rewarding. The fact you eat those foods everyday to fullness and you maintain your weight means they're not highly rewarding. Re-read Stephan's post and older posts where he defines the terms more clearly."
I eat cocoa puffs, pizza, Pain au chocolat and drink Coca Cola every day without gaining weight (neither do I go hungry or count calories), while eating other things like Nutella pancakes, ice-cream and candy on a weekly basis, does this mean these foods are not hyperrewarding?
Thank you for validating my point about name calling. Try not to be so angry.
@Collden The FR hypothesis doesn't imply that every person will fall victim to obesity because of an abundance of rewarding food. There are millions of people who can eat any food they want and at any quantity they want, and their body does a tremendous job in regulating their intake such that they never gain weight. This was me for the first 20 years of my life. At age 30 I spend more time exercising than ever before, yet I've become completely intolerant to highly refined carb foods such that I will easily gain 20 or more pounds if left unchecked.
I'm curious if anyone here has read "The Art and Science of Low Carbohydrate Living", and if so is it bad science? I know you might tell me to critically review it for myself, but I don't have the expertise to distinguish between fact from fiction. That is why I visit this blog among others, to get an interpretation of the works.
Give up now my friend. Go on your merry way and continue to enjoy life. Come back here if and when you get fat or chronically sick.
I wonder if your reactive hypoglycemia is the result of a chromium deficiency as mine was:
Something to think about at least.
I admire your patience as much as your work.
Thadeus/Sanjeev, my parents were semi-obese when I was born, I personally had a BMI of 30 already in my late teens. At 18 I decided to get lean, only to spend the next 5 years manically counting calories, following various diets like Low-carb, and eating absolutely zero junk food (except when my willpower broke down of course, which was often). Right after my year of low-carbing when I embarked on an overfeeding experiment,using nothing but whole foods with lots of saturated fat, starchy tubers and zero sugar, I gained 70 pounds in 5 months. I did certainly not use to be a "naturally" lean person, yet over the past 2 years I have improved my metabolism to the point where I can eat just about anything I want while maintaining the leanness I had in my calorie-counting days.
And the greatest improvement has really come in the past year, a period in which I've successively increased my consumption of sugar, salt, refined cereals, and highly rewarding foods in general. This is partially why I have serious issues with the food-reward theory of obesity. Stay on a low-reward diet and you will most likely
2) Become increasingly susceptible to gain weight by eating rewarding foods
1) Increasingly crave the rewarding foods that you deprive yourself of despite them being all around you
As such I strongly doubt that a low-reward diet is a good long-term solution if you want to avoid gaining weight .
Thanks for relating your experience. I'm glad you found a strategy that's working for you. There is a subset of people who respond very well to carb restriction (i.e. seemingly better than other approaches). I know some of these people personally, and for them it's been very helpful. I also know others who have gained fat on the diet.
I suspect your prior diet was effective in the sense that you gained less fat than you would have otherwise.
I'll be honest, I'm wary of very low-carb diets in the long term, because they often have negative effects on mood, sleep, lean mass, blood lipids and other things. But as with anything else, the response will vary between individuals.
Thanks, I have to admit it's been especially taxing lately.
Dave, my guess would be that overexercising and avoiding carbohydrate-dense foods has left you severely chronically stressed which is why you are so highly susceptible to gain weight when you give in to carb cravings. It might very well be you would become far less susceptible to weight gain in the long-term if you allowed your body to rest and gave in more freely to your food cravings.
@Collden, I've been battling to keep my weight to where it is right now with just calorie restriction and exercise for years. It was always a challenge as I would get excessively hungry and regain the pounds I lose within a few weeks. Only just a few months ago I discovered low-carb eating. So low-carb has actually been the path of least resistance for me, but still I want to better understand why. I'm a skeptic though, so I have a hard time deciding between FR and insulin at this point.
(I'm not terribly familiar with the food reward hypothesis so I apologize if this has already been covered and I missed it.)
How does the food reward theory explain the recent trend of obesity in infants?
"(I'm not terribly familiar with the food reward hypothesis so I apologize if this has already been covered and I missed it.)
How does the food reward theory explain the recent trend of obesity in infants?"
It doesn't. Infants are fed (by their parents) on utter crap like THIS, instead of breast milk.
The infants then acquire a lifelong taste for sugar. Job done!
> How does the food reward theory explain the recent trend of obesity in infants?
yes I don't think it has much to say about infant obesity.
prenatal environment (the mother's been dieting for 20 years so the infant may get "famine signals")
homogeneity/uniformity (which may tie into reward) - mother's milk's contents and taste vary with the mother's diet, infant formula is UNIFORm. Even if the formula itself were nutritionally perfect, the homogeneity/(industrial uniformity)/(standardized chemical composition) might still be a problem
for more reading (if you're interested) on what gestational environment can do, Look up the "Dutch Hunger Winter" and some of the critiques of Taubes' work re: the Pima.
I would post links to the Dutch historical episode but the Robert Sapolsky lectures I heard are copyrighted material & not available on the web. There were wiki entries on it though.
this may get you started
or copy & paste into your url text box to ensure work safety:
Sorry if I'm misunderstanding, but infant formula isn't anything new, (even the terrible ones). And I have no doubt that it has consequences later in life, but how does an infant become obese based on food reward at six months? Babies can't exactly control their intake.
Sorry if I'm misunderstanding, but infant formula isn't anything new, (even the terrible ones). And I have no doubt that it has consequences later in life, but how does an infant become obese based on food reward at six months? Babies can't exactly control their intake."
Which part of "It doesn't" didn't you understand? That said, it's not impossible that infants may cry more when deprived of their sickly sweet high-calorie milkshake, resulting in their parents feeding them more often and in larger amounts.
The advertising of utter crap has increased drastically over the years, resulting in an increase in the percentage of parents feeding their infants on the stuff. Hence, the recent trend of obesity in infants.
P.S. Sorry if I come across as a little snippy, but it's nearly 5am here and I really should be in bed!
> can't exactly control their intake
They don't have complete control but they don't have zero control either
And "control" is not the same as "conscious control" or "conscious choice".
even "neural control" is not the same as "conscious control" or "conscious choice".
I did try chromium picolinate, I think it was the early 90s, and it made my reactive hypoglycemic worse. At the time some research came out that this chelate of chromium was supposed to increase insulin sensitivity, and I discontinued taking it. I do take a multi supplement every 2 to 3 days as insurance, that contains the GTF form of chromium.
I had previously read your concerns about low carb diets and that they could cause insulin insensitivity, so I am making a effort to eat some carbs. Tonight I had about a quarter cup of mixed roasted rutabaga, turnip, gold potato and beets along with whole chicken pieces and brocolini. I have also continued to eat a quarter cup of berries daily and 2 to 3 tablespoons of whole fat yogurt - used to be no fat yogurt:) So far my mood has been calmer on this diet and I am having a lot fewer episodes of shakiness and when I do have them they are very mild.
One test I would do all of the time would be to hold one or both of my hands up in front of me with the fingers spread apart and monitor the trembling of my fingers. It is nice to have my fingers remain steady most of the time now. My brain also functions much better now. Whenever I would get the symptoms of low blood sugar, I could get so incapacitated I could hardly think or talk and be extremely tired. On more than one occasion, I had to pull over while driving and simply lie down in the back seat until I could recover. I always carry a supply of nuts with me. One time on the way driving home after swimming at the Y with my son, I had an especially bad low blood sugar attack. I pulled off the road and could hardly figure out how to use the cell phone to call my husband to come get us. By my mid 40s when I was able to check my blood sugar while having these symptoms, my blood sugar would be in the 80s and few years later the 90s instead of 50s or 60s when I was younger - exact same symptoms though. Even a few months ago before further reducing my carbs, my 1 hr blood glucose never goes over 130 and was usually below 100 by 2 hours. My fasting blood glucose was 96 to 110.
The results from my 3 hour blood glucose test in 1994 were:
1 hr 122
2 hr 87
3 hr 60
I had to really push my doctor to do the test, since "non diabetics cannot be hypoglycemic". My doctor office called and said the results were normal, I only found out otherwise after requesting copies of the lab myself. This was not the first time I was told a test was "normal" and I later found out that it wasn't, after getting my own copy. I highly recommend that everyone should get copies of their lab work, to keep in a file and check it themselves.
My husband and son are also loosing weight even though they still eat bread, rice and oatmeal daily. I have forced them to cut back on the little sugar they were eating and the whole family is eating more fat. Of course neither one of them needed to loose weight.
As far as my blood lipids go I have a history starting with my first test at age 20, of above normal triglycerides and low HDL. At course at age 20 I had no idea what that meant.
It does seem like your post here has really turned into mud slinging, don't blame you for moving on. I think food reward could be the slippery slope down into metabolic dysfunction.
I sure ate a lot of sweets growing up, mostly home baked of course. In high school, I used to make a double batch of cookies, 2 pies and a cake every Saturday and this was for a family of 4. I thought the whole purpose of eating dinner was to have dessert. It took me years to break that habit.
Sorry for the long post, I just seem to be on a roll.
coffee with no or little food is a potent stressor (as in release of corticoids) most likely sending your BG down
No worries, 5am is pretty rough. Just to clarify then, you are NOT in support of the food reward theory? (I guess I assumed whoever responded would be in support.) And I totally agree that infant formula is atrocious, but I find it hard to believe that it could be as simple as formula = fat baby. It seems like people would catch on and stop feeding it the formula, thus reversing the problem. I feel that there must be something metabolic underlying this, which brings me to:
Interesting stuff with the Dutch famine, although I am dubious as to how applicable it is to the current problem. While I can completely understand an epigenetic problem emerging from direct malnutrition in the womb, I can't imagine this is paralleled by a "famine signal" existing along with the presence of ample nutrients for the fetus. And this would only apply to obese mothers who have also been lifelong dieters, which I don't believe is the case. Or are you suggesting a distinct epigenetic manifestation from the abundance of nutrients likely available in an obese mother?
My understanding (or at least my opinion) was that relative insulin resistance of the fetus was determined by the state of the mother, explaining the prevalence of pre-diabetic babies among diabetic mothers. This suggests (to me) that insulin resistance is the heart of the problem, but I'd like to hear a food reward argument against. Are these separate phenomenon? or am I missing something?
And I'm not sure I see the point your making about "control."
No worries, 5am is pretty rough. Just to clarify then, you are NOT in support of the food reward theory? (I guess I assumed whoever responded would be in support.)"
I am totally in support of FR (and insulin) as factors contributing to obesity. You really need to read my blog!
FR does not directly apply to infants, as infants cannot directly control their food intake. They try to increase their food intake by crying.
Would you care to expound more on your methods?
I'm just trying to flesh out your argument. Babies try to increase food intake by crying: Do they succeed? Are you suggesting that babies are being overfed? Or are you suggesting that infant obesity results from a separate mechanism, and food reward kicks in later?
I'm just trying to flesh out your argument. Babies try to increase food intake by crying: Do they succeed?"
Sometimes, yes. Sometimes, no.
"Are you suggesting that babies are being overfed?"
"Or are you suggesting that infant obesity results from a separate mechanism, and food reward kicks in later?"
No. Food reward only becomes relevant when the infant can get his/her own food.
> FR does not directly apply to infants, as infants cannot directly control their food intake
When sated they can refuse to eat more, leaving some in the bottle.
And when a parent sees the baby trying to get more out of an empty bottle I have assumed the baby needs more, I assume any parent would think the baby needs more.
We need mothers who have breast fed to tell us who controls the amount ...
> I have assumed the baby needs more
when taking care of a baby; not been a parent myself yet
Thank you for validating my point about name calling. Try not to be so angry.
Anger is for a few seconds to a minute.
Gullibility ... not so much.
Apologies for taking you off your preferred topic, pushing that book - here, let me help get you back on track with your personal mania
"The Art and Science of Low Carbohydrate Living" by Jeff s. Volek, PhD, RD and Stephen D. Phinney, MD, PhD.
Either read the book or go straight to the references to track down the studies.
Wasn't proposing Dutch Winter Hunger mechanisms as the solution.
It's one avenue of research I stumbled on after some online discussions regarding Lustig's "fructose is a poison" talk. I found the infant obesity idea interesting and have done some reading when I had the time. This is one avenue I keep tabs on intermittently out of curiosity.
If I may poke a quandry I'm having in here.
On a 700-800 daily Calorie, Level 5 reward diet consisting of potatoes, chicken breast and spinach. What should be done for vitamin/mineral deficiencies on a low-reward low-calorie diet? Is multivitamin supplementation necessary?
Does low-calorie typically run the risk of getting sufficient nutrients over a long enough period of time?
So infant obesity is strictly because of parental overfeeding? I find this almost impossible to believe. People are smart enough to give the baby less food if its becoming obese. Not to mention that I've known several parents of newborns, and the bottle is a way to shut the baby up when its crying, no matter what the reason. Attempting to overfeed the baby is nothing new.
The level 5 "simple" diet is not something I envision going on indefinitely, but rather a tool to produce fat loss in the short to medium term. The idea is eventually to return to a higher level, whatever is sustainable for you and meets your goals. The point is that the diet should not be extremely restricted in food variety forever.
I think the foods you selected should provide enough micronutrients to meet your nutritional needs as long as it isn't continued indefinitely. The only concern I have is that it may be too low in fat for some people (especially if the chicken breast is skinless). Two options to increase variety would be 1) change which three foods you eat each week, and 2) have a couple of planned 'cheat' meals per week where you eat food that's more diverse.
I'm not a physician, I can't give medical advice, and I don't know the medical details of your situation, so these are just ideas for a rational adult to consider and discuss with a physician before taking action.
Thomas, I've been most influenced by 180 Degree Health, would recommend you to explore that site.
"So infant obesity is strictly because of parental overfeeding? I find this almost impossible to believe. People are smart enough to give the baby less food if its becoming obese."
You overestimate people.
as a mother who breastfed my child (who is 19 now), I can tell that amount of food child consume is self-regulated. When breast is very full at the beginning of feeding, milk gets released very easily and freely but less easily than from a bottle. Eating is a hard job for a little child, when it gets tired and full, it fells asleep, if it is not getting enough food, it awakes sooner in order to eat, the more milk is sucked, the more gets produced. If the child leaves some milk in the breast, less milk gets produced in a future. No sane mother tries to limit the amount of milk for her baby. Also, a hungry child has a defense mechanism - it can easily drive family, especially mother, insane by crying, it is more than just some crying.
Before I had my son at 32 yo, I went on diet several times, it didn't cause any tendency to a fatness in my offspring so far. I am from a society where people eat self-cooked food. Such system doesn't prevent diseases of civilization and obesity in society, but keeps children and most young adults in normal weight.
Thanks for the input Galina.
That's what I have seen before with women friends and relatives who breast fed.
And for those that bottle fed it's been pretty consistent that the baby decides when they've had enough and they can communicate in several ways they want more.
Any caregiver that can see the (IMHO usually clear) signs will respond to the cues the baby gives saying the baby is still hungry. And if the baby's reward system gets triggered in a similar way to kids and teens and adults respond to a cafeteria diet, voila ... the baby's hunger lasts longer and happens more frequently.
Excellent. Although FrankG has a good point too.
I think it is more complicated.
I am not a defender of a bottle-feeding, but I don't personally think it ultimately determines the weight of a grown-up person. I don't remember any overweight child in my class, while some were not breast-feed as infants for sure - breast-milk substitutes were available in Soviet Union and people used it because some mothers couldn't breast-feed or for some other reasons. Sorry, but I have to repeat it again, in the society with the luck of manufactured and fast food people gained weight later in life, smaller amounts, but not young individuals and children. Another personal opinion - in order for a very young child to gain an inappropriate amount of weight, he/she should be fed frequently,and given a lot of sugar, especially in a liquid form. People in McDonald give children a toy with meals for a reason - just a food even manufactured to be addictive is not an attraction enough.
I think it is very important to get used to some normal food during one's childhood. When my son went to a university in different town and was required to eat in a cafeteria for his first year, he couldn't take it any longer after a year and started to cook his own food afterwards. He is not particularly skillful in cooking, somewhat lazy, so his dishes are quite simple, but for him it is more attractive food than over-flavored manufactured one. The attractiveness of cafeteria food is overrated. It is a very convenient way to eat for thous who got used to it and can stand it. I immigrated initially to Canada (Vancouver,BC), then to USA. I know a lot of immigrants, most of them avoid commercial foods and cook their own because it is what they prefer. Traditional food doesn't keep them thin and healthy. It is just a better way to eat than SAD.
Well we've covered about half of the battle. But how does food reward explain why this has only started occurring recently. Bottle feeding has been around for a long time, and even the modern incarnation of formula has remained relatively the same since the 1970s. Shouldn't we have been seeing obese infants (albeit perhaps in smaller numbers, I don't know the exact stats on bottle-feeding vs. breastfeeding over time)since the introduction of the hyper-rewarding formula?
IcedCoffee, perhaps your memory is poor due to the excessive consumption of iced coffee.
Somewhere up there ^^^^, I wrote:-
"The advertising of utter crap has increased drastically over the years, resulting in an increase in the percentage of parents feeding their infants on the stuff. Hence, the recent trend of obesity in infants."
Do you have any evidence to refute what I wrote?
Sorry if I was unclear.
Although formula might be used more now than when it was introduced, (I have no idea what the figures are on this,) this would still suggest that infant obesity should have always been around, and the only difference over time is the number.
But that's not what we are seeing here. Infant obesity is a distinctly recent phenomenon, which is why I am skeptical that it is simply infant formula that is the issue (although it is clearly an issue)
And its totally possible my logic is off from over-consumption of icedcoffee, speaking of which . . .
Probably, it is to late to comment, but the weight and size of new-born babies is on the rise. They manage to start their weight-gain while inside the womb.
There was once a scientific consensus that the earth was the center of the universe. This post sounds a lot like you're thoroughly convinced of your own theory, which I think is rather dangerous.
While a lot of people might think reward is involved, that does not a consensus make.
> scientific consensus that the earth was the center of the universe
confusing science with religion
confusing people with incentive to disagree and establish a career by proving everyone else is wrong with people incentivized to always agree
> that does not a consensus make
heh ... maybe that's why Stephan's post was about "approaching a consensus", not about "a consensus as been made"
your comment indicates incoherence on science, process, religion and confusion on when, historically, people started being skeptical and scientific, and a failure of basic reading comprehension. I hope you are not this way in real life.
I appear to have angered Sanjeev. I hope he can get over it.
My point was that suggesting science is even approaching a consensus on food reward just sounds too self-affirming and might encourage self-affirming research, which has led us down the wrong path before.
This is great, thank you! And it leads me to ponder:
How fitting that the only instance where Twinkie-level palatability would have ever occurred throughout evolution would be, appropriately, in times of starvation/metabolic slowdown/emergency storage mode, in which that old dry leg of meat was suddenly elevated to Twinkie-level reward status. It never occurred to me that yumminess and starvation mode had such a long steamy love affair.
Anyhow, thanks again for the enlightening overview!
Absolutely fascinating blog post - thanks for putting it together. Very informative.
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