Dopamine is a neurotransmitter (chemical that signals between neurons) that is a central mediator of reward and motivation in the brain. It has been known for decades that dopamine injections into the brain suppress food intake, and that this is due primarily to its action in the hypothalamus, which is the main region that regulates body fatness (1). Dopamine-producing neurons from reward centers contact neurons in the hypothalamus that regulate body fatness (2). I recently came across a paper by a researcher named Dr. Hanno Pijl, from Leiden University in the Netherlands (3). The paper is a nice overview of the evidence linking dopamine signaling with body fatness via its effects on the hypothalamus, and I recommend it to any scientists out there who want to read more about the concept.
Increased dopamine signaling, particularly through the dopamine D2 receptor, can attenuate and in some cases reverse obesity in diet-induced obese animals, seasonally obese animals (squirrels, Syrian hamsters, etc.), and overweight/obese humans (4). Not only that, it can increase resting metabolic rate and attenuate the metabolic abnormalities associated with obesity even before the fat is lost, which emphasizes that these circuits control metabolism directly, as well as indirectly by influencing fat mass (5)*. Conversely, people who have genetic or drug-induced reductions in D2 receptor signaling gain fat at an accelerated rate (6, 7).
Together, this supports a hypothesis that I've scarcely seen in the scientific literature: that reward centers, and probably food reward itself, can directly influence body fatness and metabolism. Other people have made parts of this argument, however, I've never seen anyone put together the evidence from psychology, pharmacology and neurobiology into a single coherent hypothesis.
Addiction and Obesity
Speaking of dopamine D2 receptors, people who produce fewer of them due to their genetic makeup not only tend to gain more weight, they're also more susceptible to addictive behaviors such as drug abuse and excessive gambling (8, 9, 10). In other words, they respond differently to rewarding stimuli than others and are more susceptible to developing pathological relationships with high-reward things.
When you look at D2 receptors in the human brain, the more fat a person carries, the fewer D2 receptors are available for binding dopmaine** (11). This is the same thing one sees in the brains of people who are addicted to drugs (12). In the case of drugs, reduced dopamine signaling may lead to increased drug-seeking behavior to compensate for a "reward deficit". This is based on the hypothesis that highly rewarding drugs or foods eventually cause the brain to become desensitized to food reward, creating a vicious cycle in which people seek out more and more food reward to reach the same level of reward signaling in the brain. In his nice review article "Food reward, hyperphagia and obesity", Dr. Hans-Rudolph Berthoud and colleagues refer to the chronic intake of highly rewarding food as an "escalating, addictive process leading to obesity" (13). Rodents that are accustomed to eating human junk food will endure foot shocks and extreme temperatures to obtain it, even when regular chow is freely available in unlimited quantity (14).
Commenter "mem" recently pointed me to the research of Dr. Robert Pretlow. He has a nice slideshow online that describes his research (15). He set up a support website for overweight youths, and uses it to conduct his research. He has some interesting observations:
- Many youths describe themselves as addicted to junk food. They know it's unhealthy but they have little control over their cravings.
- Many say they use junk food as a way to cope with stress-- unstable home life, school pressures, lack of sleep, etc.
- Some find that their cravings subside and weight decreases if they can avoid junk food for enough time.
- Ice cream
- Potato chips
- Fast food
Putting it All Together
I believe the evidence as a whole shows that chronic consumption of foods with an excessive reward value causes abnormalities in parts of the brain that regulate body fatness, metabolism and reward/motivation. This can lead to weight gain and metabolic problems, and favor addictive and compulsive relationships to food and other things. The combination of readily accessible, cheap, high-reward food, and stressful lifestyles that drive us to eat it, is probably a major contributor to overweight, obesity, diabetes and perhaps other health problems in affluent nations.
* Thanks to commenter "Gunther Gatherer" for pointing this paper out.
** Specifically in the striatum.
*** Thanks to reader JBG for sending me this.
Another Great Post! just curious about something. I struggle with an addiction to coffee... After reading your articles, and Seth Roberts book, I decided to stop using cream and sugar in my coffee. This has helped curb my appetite for coffee, but I still crave a black coffee in the morning (even though the taste is blah). Would the black coffee fall into food reward or drug addiction? What about alcohol? The 2 glasses of red wine that accompany most of my nights, are they food reward or drug addiction? In other words, will these lead to weight gain like other types of food reward? Or am I just a mild addict of legal stimulants/depressants?
Brilliant series of posts Stephan. Thanks for posting these in the public domain.
BTW, this post is appearing completely in the google reader itself. Just FYI.
This is starting to make a lot of sense.
Also, if you consider Chris Masterjohn's recent post about how traditional diets that successfully minimized diseases and dental caries weren't just accidents but careful accumulations of dietary wisdom, does it make sense to think of relatively bland traditional diets as not that way by geographic necessity but by design, to prevent overeating? Obesity would be even riskier in a pre-medical milieu, especially given a need for mobility, agility and speed - and individuals who overconsume food may risk depleting food supplies prematurely or unevenly. Possible?
What I understand you to be saying is that dopamine signaling doesn't just influence metabolism through altering our behavior (particularly our food choices): it has a direct and significant effect on metabolism by itself. Correct?
Stephan, as the various research articles you point to indicate, the dopamine-obesity connection has been put out there before. I think maybe the reason there isn't an established dopamine school of weight gain theory is that the connection doesn't go anywhere. Since everyone is under stress, but not everyone deals with stress via junk food, you are left either (a) looking for a non-dopamine physiological mediator or (b) falling back on looking at an extra-corporeal mediator, which leads back to the realm of questions about "will power" and "social conditioning" and the like.
Also there are problems with some of this research. For example, as Gina Kolata has pointed out, people's self-reported anxiety-eating does not seem to be connected to weight gain as there are equal numbers of thin people who indulge in this practice. And in the current state of culture and education, I would not trust any self-reporting by children on the reasons that they over-eat.
My personal experience with anxiety, eating, and weight gain is that I used to feel that I ate junk food (especially, cold cereal) out of stress, but looking back I think it is equally likely that I experienced anxiety when I skipped junk food. Today, I can go for 2-3 weeks or more eating well and then experience intense cravings for junk food, and I cannot identify that these cravings are connected to increased stress. Are these periods of physiological low-dopamine? Is there research showing that dopamine levels cycle at all?
Re feedback loops in general, an interesting anecdote: When I went on the Atkins diet back in the '90s, I noticed that I was over-eating a lot foods that I did not like. For example, at a church social event, store-bought cookies would be put out, and I would eat these until they were gone regardless of how I felt. On Atkins, I realized I was eating like this because I didn't like the cookies: they were gastronomically titillating but not satisfying at all. I suspect poor quality leading to dissatisfaction and subsequent increased consumption is an unidentified factor in many people's eating patterns.
Hmm... These dopamine things remind me of what Julia Ross wrote in her book "The Mood Cure" about some amino acids:
"Raymond Brown, Ph.D., a San Francisco psychologist and addiction specialist, conducted a study in 1989 comparing groups of cocaine addicts who had been given an amino acid formula high in tyrosine and L-phenylalanine with those who got no amino acid supplementation. The results were dramatic: The success rate after ten weeks for those on the amino acid formula was 80 percent; for those not on aminos, it was 13 percent! Says Brown: "I would never again try to work with addicts without amino acids.""
And here's the study abstract link: http://www.ncbi.nlm.nih.gov/pubmed/2374070
Problem is... Where's the full text? :|
Pam Killeen's book is also full of interviews in which various professionals praise those amino acid cures in the addict rehab programs. It's very interesting but I wish there was some clearer proof for that.
I remember reading about this on sciencedaily some years ago (http://www.sciencedaily.com/releases/2001/02/010205075129.htm; http://www.sciencedaily.com/releases/2009/07/090727102030.htm). The findings were particularly interesting because it sounds like the reverse of what you'd expect: that obese people just love/are highly rewarded by food and eat lots in consequence. My immediate suspicion, upon hearing that the obese had fewer dopamine receptors was that the obese were getting *less* reward out of the same food that would aptly reward lean people and were eating more/more rewarding food in general in order to meet their 'reward requirements.' Of course an alternate interpretation would be that this is a sign of the body reducing the reward it gets from food (as its supposed to) when it has excess fat.
I do wonder if some part of this is that when people lose the physical inclination to eat (due to being overweight) they respond by seeking out especially highly rewarding foods that they actually will feel rewarded for eating. I think I've experienced this when ill: I don't feel like eating most food, but because I want some source of pleasure/distraction/I believe I ought to be eating, I'll seek out something highly rewarding instead (I've observed this in other people as well).
Hi Stephan and many thanks for putting this all together so beautifully. I have two additional questions regarding dopamine, reward and obesity:
1) You hinted at bitterness being something that humans are averse to. It stands to reason that adding bitterness to foods would substantially lower their reward value. Do you recommend adding things like horseradish (not nice-tasting mild horseradish sauce, but the real thing), bitter almond, and other things to foods for those with weight loss problems?
2) The fact that faulty dopamine communication is not only related to obesity but also to other addictions implies that abstaining from OTHER addictions could also help those with sluggish weight loss. Gambling, caffeine, chocolate, pornography, work ("workaholics"), video games, and other addictions known to be related to overwhelmed dopamine receptors may all be part of a general overstimulating Neolithic lifestyle in which ANY ONE of these things causes ALL D2 receptors to be affected. Do you think reducing ALL Superstimuli from one's lifestyle would also help one develop more general D2 sensitivity, and so enhance your receptors for eating? Would attending to a gambling or caffeine addiction cause a knock-on effect when eating?
The love-bonding-thing might be involved in this as well:
we identified two direct regulators of ghrelin, oxytocin and dopamine
Oxytocin is expressed in the myenteric and submucous ganglia and nerve fibres along the entire human GI tract. The role for oxytocin in the physiology and pathophysiology of the bowel remains to be settled.
And here, these complement the studies you gave quite nicely:
All about how dopamine agonists LOWER BASAL INSULIN, while disruption of dopamine signalling causes glucose intolerance. Superstimuli directly causing the metabolic syndrome? Fascinating.
Sorry, one more:
Spughy wrote: "does it make sense to think of relatively bland traditional diets as not that way by geographic necessity but by design, to prevent overeating?"
There was feast and famine in traditional societies but no opportunity for people other than village leaders to chronically overeat. Plus, the key food reward ingredient of sugar was not readily available year-round, and oils suitable for cooking and frying were too valuable to be consumed in abundance.
Chris wrote, "Since everyone is under stress, but not everyone deals with stress via junk food, you are left either (a) looking for a non-dopamine physiological mediator or (b) falling back on looking at an extra-corporeal mediator, which leads back to the realm of questions about "will power" and "social conditioning" and the like."
Everyone is under stress, but some people experience chronic stress more than others, and there are the related feelings of depression and unhappiness. A study by Princeton's Woodrow Wilson found that rises in income corresponded with rises in happiness up to $75,000. Financial instability is a great source of worry that would drive people to seek comfort food. Last year, the Atlantic Monthly article "Cultivating Failure: How School Gardens Are Cheating Our Most Vulnerable Students," the author challenged the notion of food deserts as a cause of poor people eating unhealthy food and suggested that poor people bought junk food because they wanted food that would make them feel better, at least temporarily. Junk food is a narcotic of the poor.
Another factor is taste acquisition. I used to live in Asia for many years. Middle-aged and elderly people there do not like junk food. The strong salty, sweet, and greasy flavors overwhelm them. By gradually adopting a local diet, I unacquired my preference for processed foods. Now that I'm back in the US, when I go to an American casual dining or fast food restaurant with friends, I stare at the for a long time, looking earnestly for something I'd actually want to eat.
Regarding bitterness, I've found that unsweetened chocolate suppresses my appetite.
What about the reverse--how would something like octreotide affect dopamine signaling?
It is interesting as well that the anti-psychotic olanzapine (zyprexa) - a drug which binds to dopamine receptors to reduce its activity in the brain - almost as a rule causes massive weight gain and a diabetic state.
If unnaturally palatable foods cause people to overeat constantly to activate desensitized reward centres, how do you reconcile that with the fact that most obese people eventually become weight stable?
At that point they wouldn't be overeating to activate these centres - they would be in complete energy balance. They strike a balance between the gratification of eating and calories ingested - just at an unhealthy weight.
It makes more sense that overly palatable foods somehow increase the body's set-point in some way.
John, the chocolate thing is interesting. The cocoa bean itself is very bitter, almost inedible without sugar, so would presumably lower food reward if eaten at 100% cacao. But the caffeine and theobromide in it raise dopamine temporarily, resulting in an increased food reward. But then again, how much can you really eat if it's 100% cacao? It's just not satisfying at all.
Add high sugar to the mixture and that's where people find it addictive. Is it the sugar that's really supplying the hit, or the cacao itself? Whenever I drink coffee, even black, I still get addicted, so I'm inclined to stay away from it. Dunno if chocolate would give me the same symptoms.
But with your experience in mind, I do think trying plain horseradish, bitter almonds, mustard seeds or other things might supply the appetite lowering effects without any conflicting caffeine or theobromide to worry about.
Gunter Gatherer: I find that the higher the cacao content, the less I eat. I haven't found anything much over 70%, but when I get down to regular old Hershey bars, I eat much more. So I stay away from the sweet stuff!
Stephan, how do you square the fact that increased dopamine signaling is anti-obesogenic, but highly rewarding food is supposedly obesogenic? Doesn't rewarding food stimulate more dopamine release than non-rewarding food? Is there any evidence that eating rewarding food leads to decreased dopaminergic tone?
Have you read the 2002 review by Barsch and Schwartz on energy balance ?
I certainly liked figure 4b (model of dopaminergic regulation of food intake) and the paragraph titled "Why we eat: new roles for old neurotransmitters".
Back when I first learnt about leptin and body fat regulation, I immediately imagined a feedback loop where the hypothalamus converts hormonal signals into an electrical "energy balance" signal. And this electrical signal then proceeds downstream in the brain to do its job. An admittedly simplistic mental model, but it allowed me to make sense of a lot things.
For example, when I learnt about Robert Lustig's idea that elevated fasting insulin interferes with leptin signaling , I immediately understood why that might increase fat mass: the "perceived" amount of leptin by the hypothalamus would be lower → higher fat mass.
Similarly, when I read your first post on food reward, it wasn't a big stretch for me to think that the electrical "energy balance" signal in the brain could be modified by that same brain. And when the brain changes the signal, this will impact the feedback loop in a similar way as changing hormone levels (e.g., leptin, insulin, ghrelin, PYY, CCK).
The review by Barsch and Schwartz nicely provided a possible mechanism for how the brain might modify the electrical "energy balance" signal.
Your post provides even more pointers.
Keep up the great work.
 Barsh G.S., Schwartz M.W. Genetic approaches to studying energy balance: perception and integration. Nat Rev Genet. 2002 Aug;3(8):589-600. http://pmid.us/12154382
 Lustig R.H. Childhood obesity: behavioral aberration or biochemical drive? Reinterpreting the First Law of Thermodynamics. Nat Clin Pract Endocrinol Metab. 2006 Aug;2(8):447-58. http://pmid.us/16932334
So would you expect something like the tea chemical theanine, which reportedly increases brain dopamine levels and apparently does not cause habituation, to be an aid to insulin sensitivity and weight loss? Could this, perhaps along with caffeine, explain the purported weight restrictive properties of tea?
Mighto'chondri-al (sorry if I'm butchering the spelling) mentioned in a previous post that increasing nitrous oxide in the bloodstream might increase the sensitivity of the dopamine receptor.
I then thought of something else that increase NO in the bloodstream, the amino acid arginine.
I had a quick check to see if this would be a plausible way of reducing weight. I found this rat study showing that rats supplemented with arginine seem to have much less weight gain:
Recently I came across mention of a diet product that appears to be based on a theory like Stephan's. The originator presents credentials:
and wrote a book about the subject more than a decade ago:
which was apparently accompanied with a commercial product, now discontinued.
There is now a new product:
but my guess is that it does not work particularly well, even though it comes with an updated version of the book:
There are ten reviews, five 5-star ones and five 1-star ones...but four of the five 5-star ones came in the first month after the Amazon launch, strongly suggesting shill sources.
I haven't looked at the books or any of the materials available via the websites, but he *seems* to be talking Stephan's talk, even if his efforts to produce a commercial dieting shortcut may not be doing well.
gunther gatherer wrote: "Whenever I drink coffee, even black, I still get addicted, so I'm inclined to stay away from it. Dunno if chocolate would give me the same symptoms."
Caffeine is highly addictive, at least for some people. I have to be careful about consumption because I experience horrific withdrawal headaches if I consume 2-3 cups of caffeinated coffee for a few days and then go without.
Caution (and a bad sign) -- As I was closing tabs after completing the previous comment, I seemed to be trapped on one of the trysensa pages, with it repeatedly asking me to check a box to start a conversation with "a live rep". Clicking the close box on that dialog box three successive times finally got me out.
A narrated slideshow of army rations from around the world by photographer Ashley Gilbertson. Sorry if it's slightly off topic, but very interesting, and quite telling:
@ Gunther Gatherer -
Bitters also aid in digestion and assist the body in absorbing nutrients. I've taken to starting pretty much every meal with a bitter. This might take the form of a bit of unsweetened tea with lemon (tea and lemon are both bitters) or some raw undressed spinach or endive or escarole that I eat before eating anything else on my plate. It's a new experiment for me, but it seems to be helping with digestion issues if nothing else.
thanks for a nice article.
"rewarding" factor sounds different from satiating.
you also forgot donuts (such insidious food, but seems to be a default "free breakfast" during conferences/meetings in a corporate Americ! or perhaps it's probably implied)
although i'm not sure chronic stress is such a big factor?
my great grand parents & grandparents experience multiple wars, shortage in food & everything.
so how can the stress of modern people be greater than theirs? when they didn't even know if they could live to see the next day?
but the previous generations, for those that were lucky enough to survive seem to have less "civilized diseases."
I had the same question as Collden. If eating highly rewarding food makes you fat, shouldn't that imply that people with low dopamine sensitivity should tend to be thin, because for them all food has low reward value?
Conversely, if people with low dopamine sensitivity overeat because they're trying to get the same dopamine hit that people with normal dopamine sensitivity get from normal amounts of food, shouldn't that imply that eating high-reward food should lead to weight loss because it allows us to get the same dopamine hit with less food than it would normally take?
I read the first two paragraphs and got SO EXCITED that you finally saw the light... you seemed to be echoing what I spoke before , presumably you read the research and saw what i already saw.
Then I read the third paragraph and got all :(.
How on earth do you conclude from the data (that high dopamine signalling PREVENTS obesity/metabolic disorder, and low dopamine signalling CAUSES obesity/metabolic disorder) that obesity is an addiction process???
YOu do realize that in addiction, dopamine receptors are being chronically stimulated?
You do realize that all addictive people become emaciated and stop eating food, right, because of this aforementioned hyperactivity of dopamine?
You do realize that over eating and weight gain only occurs in the recovery period, when a person is no longer receiving the drug-induced dopamine stimulation?
You seem to have missed all of the evidence which shows that in people genetically predisposed to seasonal adaptation aka "obesity", it's the food itself that leads to low dopamine binding. The food, the GLUCOSE, is the trigger for the dopamine receptor downregulation. THis means no dopamine sensitivity, this means obesity.
It is rapidly corrected upon food restriction.
No, obesity is not a case of food addiction - the dopamine situation is all fixed as soon as you get them off glucose. The same cannot be said for a heroin or meth addict.
THe dopamine receptor downregulation in obesity is functional and likely evolutionarily conserved, just as it is for hibernating animals. Certain humans among us are programmed to have zero dopamine sensitivity when eating lots of carbs and calories. It's not addiction, it's quasi hibernation preparation.
People confabulate all sorts of reasons for why they do what they do. Asking an 11 year old why he eats junkfood will tell you nothing except the cognative rationale for why the 11 year old is eating too m any calories over a long term continuum of time.
People ask me how I can possible have such meticulous attention to detail required to draw lifelike portraits. How do I possibly pay attention that well? How do I know where to place the lines and how much pressure to apply to the paper?
Answer: my brain makes me do it.
I can tell you it's a choice I'm making or that I practiced really hard or that I studied art but the truth is the neuroanatomy I have is wired in such a way that i am capable of producing meticulously detailed drawings. I don't know about the brain regions responsible, or the configuration of structures, but it's there and it's nothing I have to try at. It's how my brain was made. I am an EXTREMELY detailed elaborate personality.
When an 11 year old says he is "addicted to junk food", the 11 year old has never heard of dopamine, or dopamine receptor do9wnregulation in humans predisposed to obesity, and all he knows of hibernation is that bears do it. He does not know that in animals which hibernate a critical hypersensitivity and resultant downregulation of dopamine receptors is what causes squirrels and bears to move less, eat more, and gain body fat. He does not know this is an evolutionarily logical behavior and it is not "addiction to food" but rather an adaptive response to predicting seasonal food availability.
The 11 year old does not know his metabolism / nervous system's genetics were selected in nomadic american tribes, or african tribes. He looks white. He wouldn't think of himself as a hunter gatherer. As a result of these genes, just like a squirrel or a bear he too has a mild hibernation capacity which is triggered by a year round high carbohydrate diet. Such a diet causes a similar dopamine receptor downregulation, and it is so for the exact same purpose as a bear or a squirrel - to capitalize on seasonal food excess because such food trends (high carb) tended to predict food deprivation when the genes were selected. Carbs surge right before famine. Some humans among us = those with hunter gatherer genes - respond to high carbs with low dopamine just like a bear responds to fall with dopamine receptor downregulation.re
I have a feeling that you considered my pervious posts, felt I was correct, but was ultimately unwilling to modify your original position (that food reward causes obesity), so instead you took my points on dopamine and obesity and just IRRATIONALLY conformed them to your food addiction hypothesis.
Let me use your logic and test your reasoning.
You constantly tell me that leptin should prevent all forms of obesity, because leptin suppresses appetite and increases metabolism, therefore should prevent over eating or appetite or low metabolism related to other conditions.
If this is true, why then do you think that food mediated dopamine (we are arguing fatties get a dopamine high, right) would lead to MORE eating and weight gain and inactivity?
If the dopamine system of fat people works normally in response to food (i.e. fat people are just as likely to have low dopamine from food as thin people, the only difference is that their "Food addiction" leads them to eat soooo much that their dopamine receptors downregulate, just as is the case for a heroin addict)....
...If this is true, why then does the high dopamine stimulation never prompt anorexia, activity, and metabolic profiling consistent with thinness?
It certainly does for all other cases of addiction. A person riding that high horse stops eating food and becomes euphoric because opiates lead to dopamine disinhibition.
A person smoking meth and crack does the same.
All junkies are emaciated because they are brutalizing their dopamine receptors with drugs.
IF WE ARE TO FOLLOW the logic that fat people are eating so much food that they are OVERSTIMULATING dopamine to the point of downregulation, do you not see this should be self terminating and the food addict must then become euphoric, anorexic, hyperactive and very thin just as other drug addicts and alcoholics do?
REmember, the reason there is no dopamine receptor binding in addiction is because the chronic overstimulation reduced receptor number. This is also why they are thin and anorexic.
THe obese person never experienced anorexia, thinness, or acitivty - quite the opposite, the moment they began eating they started eating MORE and moving LESS and it got progressively worse and worse.
Doesn't this suggest to you that in obesity there never is a period of dopamine receptor hyperactivity?
Doesn't this suggest to you that obesity is therefore not an addiction process and dopamine overstimulation is not figuring in, but quite the opposite is true... high glucose is triggering dopamine receptor DOWNREGULATION and this occurs without any dopamine hyperactivity period.
The obese have much more in common with people taking antipsychotics than they do people taking stimulant or other addictive drugs.
They go stright to "no dopamine", there is no "high dopamine" phase, thus it is not addiction. IT is straightforward dopamine insensitivity. It is NOT secondary to addiction/pleasure/drug like overstimulation of dopamine receptors.
PS when I was a fat hypoglycemic kid, food was the best thing ever too.
Even know when I go through periods of low catecholamines (as was the case the past few weeks) I get veeery tired very hungry very dim and unmotivated gain fat easily etc.
Then I took some magnesium and poof my brain started making neurotransmitters. My mood brightened my energy increased and my appetite plummeted and I had toins of motivation just like before.
Did i develop - and cure - a food addiction in 2 wks? Or did fluxing levels of dopamine due to drug withdrawal cause this shift?
I feel as if you (and other researchers) view dopamine receptor insensitivity in obesity as being evidence of food addiction, just because addicts share this commonality, are being tragically narrow sighted.
Diabetics who are type II and type I both have high blood sugar, both have high A1cs, both have neuropathy, both have kidney damage.
The difference is that one is thin and one is fat, one makes insulin and one does not, one responds to insulin normally and one does not.
Making any kind of prediction about the pathogenesis of either form of diabetes based on the fact type I and type II diabetics have similar complications is bound to be wrong. The end result may be the same (high blood sugar), but the way one person go there is ZERO PERCENT, NOT EVEN SLIGHTLY pathologically related to how the other person go there. The type I diabetic simply has no insulin making cells. The type I diabetic has an abnormal immune system. The type II diabetic is normal and makes insulin but he has a widespread complex metabolic disorder. There is NO SIMILARITY IN PATHOLOGY even if the result of the disease process looks the same.
When you look at an obese person with no dopamine receptor binding, and you look at an emaciated wired cracked out junkie with no dopamine receptor binding, it is a MASSIVE MISTAKE ot then predict that obesity is anything like addiction just because junkies also have low dopamine eceptors.
If anything, the fact that the obese person is the polar opposite phenotype of the addict ought to suggest that the disease process is very different. Knowing what we know about dopamine, intuitive logic should suggest that dopamine hyperactivity is not figuring into obesity.
Any every and all cases of dopamine hyperactivity will cause a relative decrease in eating, decrease in sleeping, and increase in activity and energy. Look at a manic person, look at a meth addict. They are high on dopamine.
To see another disease phentoypically similar to a garden variety fat person, go find that manic depressive in november when his brain craps out and he is in depression. You GENERALLY find immobility, torpor, hypersomnia, hyperphagia (fancy word for eating heaps) and weight gain. Manic depressive typically get atypical depressive symptoms, the polar opposite of mania.
Manic depressive illness is a good example of the throes of a hibernation-like process. Probably because it too like obesity is an evolutionarily conserved form of seasonal adaptation.
Love this series! The cult of low carb is thankfully dying an ignominious death. Woot!
Dr. Curmugeon Gee wrote: "although i'm not sure chronic stress is such a big factor?
my great grand parents & grandparents experience multiple wars, shortage in food & everything.
so how can the stress of modern people be greater than theirs? when they didn't even know if they could live to see the next day?"
You're right, but the other element besides stress is easy access to food rewards, which most of our ancestors did not have. 25% of WWII recruits were rejected because of malnutrition whereas today a similar percentage are turned away for being obese. As I mentioned before, I don't think it's stress but more accurately depression and unhappiness that drives people to seek food rewards. 100 years ago people had much less but they were interconnected through extended family, church, and neighborhood ties. Even if they were unhappy, they couldn't just jump in the car and drive to the nearest Wal-mart to fill up a shopping cart with pizza, chips, and pop, all paid for a SNAP EBT card.
Hmm... As you mentioned junkies who live their lives on dopamine highs, suppressing their hunger and becoming emaciated, I think I share some properties with them. For example, I get easily stimulated by computer usage and I feel computer addicted and it seems to suppress my hunger and impair my digestion etc... I also ate low carb diet and felt almost euphoric until I almost burned out. Now I'm eating diet similar to Perfect Health Diet(.org)
Do you have any ideas for such people who want to fix their system. It's just difficult to avoid all stimulants.
(I'm sorry for going a bit off-topic)
You make some good points, but your characterization of how people use their SNAP (Food Stamp) benefits is inaccurate. I did research on this when I worked for an anti-hunger organization. People who used Food Stamps (as they were then called) made more nutritious choices, dollar-for-dollar, than matched samples of people who did not (matched socio-economically). One reason may be that healthy food often costs more, and they felt that they cold afford better choices.
Hating on SNAP benefits is hating on a social program that is actually efficient in doing what it purports to do - increase food security.
The primary symptom of food insecurity isn't hunger, by the way, though that's in the mix (it tends to be intermittent, but it's definitely real). The primary symptom is poor health caused by an impoverished array of food options - limited by price, location, perishability (fresh vegetables rot fast), and limited cooking facilities (some people live in motels or have had their utilities shut off).
Ironically, having been in the hunger relief biz, now that I have two young children and we're living just on my spouse's wage, we are now benefiting from SNAP.
The benefits help many people and families from falling into a downward economic and health spiral. They also aren't designed to cover all of a household's food costs, so there's not surplus for soda and chips. People may still buy those things, but don't blame SNAP for that.
The point of DogwoodTree05's I agree with is, not only are our potential responses to stress different than in the past, but stress is a bit different. There's more social isolation, which, for social animals like us, is a different kind of stress than we evolved to deal with - such as famine, tigers, war, floods. It's easier to face those things when someone has our back. Immigrants to the U.S. who lose their traditional family structure soon start having higher rates of depression, alcoholism, and so on - matching U.S. rates rather than their home countries (comparative rates depend on the immigrant group - I've read of this phenomenon with Mexican and Japanese immigrants), even though their standard of living may rise.
Stephan also wrote about the stress of lack of control over one's life - of being on the lower end of a pecking order. As society's gotten larger and more complex, most of us are someone's employee in a non-democratic decision-making environment. I'd add to that uncertainty and insecurity about one's worth and role. I'm not an expert in hunter-gatherer social structures, but in a smaller community you might have more of a sense of shared decision-making, if not autonomy.
Wouldn't any amino acid increase NO in the bloodstream, not just arginine?
I would suspect one of the best things for D2R then would be a plain steak. This could be why high protein diets show initial weight loss, simply from waking up D2R sensitivity that had been long dormant on Pritikin and Ornish, etc.
New study on food reward:
Food reinforcement, energy intake, and macronutrient choice
Results: The results showed that the relative proportion of responding for food compared with reading (RRVprop) was positively related to body mass index, laboratory-measured energy intake, and usual energy intake. In addition, RRVprop was a predictor of sugar intake but not of total carbohydrate, fat, or protein intake.
Conclusion: These results are consistent with basic animal research showing that sugar is related to food reward and with the hypothesis that food reward processes are more strongly related to eating than are food hedonics.
I'm trying to let this play out but the suspense is killing me! So what are we back to? The tendency towards obesity is back to genetics? Or what drives this dopamine response to food? I am still hazy on how the food reward concept fits with everyday examples of things we all see and get frustrated by. I was in a coffee shop this morning eating some bland eggs struggling to keep my weight from going higher while watching two lean & muscular guys my age (mid 30's) eating donuts. Maybe their reward wasn't high because of the dopamine connection but then how do I get their dopamine response working for me?
surely the "chronic stress" my forefathers experienced (_decades_ of war & shortage) had to be much greater w/ ours.
I just wonder if the support (family, friends community), a sense of hope can offset their hardship.
If it's non-caloric, then I would put it in the drug category. I think alcohol is both, and I also think drinking a lot of alcohol (esp beer) is a good way to put on weight.
I think most cultures ate bland food because they had no choice.
Hi J. Stanton,
Yes. Bromocriptine, a dopamine D2 receptor agonist, is an FDA approved drug for the treatment of type 2 diabetes.
I'm not suggesting stress causes everyone to overeat highly rewarding food, but it does in some people. Everyone differs in their susceptibility to diet-induced obesity.
Hi David Moss,
Yes, research suggests that obesity is associated with a "reward deficit". Some interpret this as a driver of additional food consumption, although a viable alternative is the idea you mentioned that reward circuits are deliberately dampened in cases of excess fat mass. In fact, there's good evidence that occurs. Leptin and insulin both suppress reward signaling... but that may go awry in obesity.
Adding mild bitter flavors is one potential strategy. I don't know whether it would work or not, but it might.
We've been thinking along the same lines about whether other high-reward stimuli (TV, video games, drugs, etc) could contribute to the problem. I don't know, but it's possible. I think it could certainly be worthwhile to try cutting out a variety of high-reward stimuli for a while to see if it helps. I also think meditation is likely to help, because it's the ultimate low-reward state and I truly believe based on personal experience that it resets reward sensitivity, at least if you do enough of it.
Yes, I think excessive reward increases the setpoint. All available evidence I'm aware of suggests that most if not all overweight and obese people "defend" their elevated fat mass.
Hi Collden and Brandon Berg,
It's about short term vs. long term. In the short term, highly rewarding food does increase dopamine signaling. In the long term, neurons seem to become desensitized (perhaps due to downregulated receptor density) and it takes more rewarding stimuli to achieve the same level of reward signaling.
Just read it. Yes, it's a nice review. I think they left a lot out though!
Hi David Pier,
I would not assume it's that simple. What part of the brain is seeing the increased dopamine, and how does it react to increased dopamine in the long term? The only way to see if it causes weight loss by that mechanism is to test it empirically. The system is too complex to predict the outcome IMO.
I doubt Blogger was responsible for that, you may have malware on your computer.
Hi Dr. Curmudgeon,
You can't stress binge on high-reward foods if there are few or none available. I don't know how your ancestors lived, but industrial convenience food is much more prevalent today than it was even 40 years ago in the US. In other countries, the difference would have been even more exaggerated.
I'll be setting out some practical ideas soon enough. Everyone is different and some people can eat donuts and not gain fat, at least for a while.
Hi Stephan. What is your experience with meditation then? I've never tried it, but I can imagine it beats going to the gym for fat loss.
FYI, the June 2011 issue of Discover magazine has an article by Dan Hurley entitled "The Hungry Brain". I'm sure readers of this blog would find it filled with familiar material. I couldn't find it online however.
I'm curious how this may relate to reward as a whole. If you bring food reward down and bring it up in other areas [sleep quality/quantity, sex, relaxation activities, etc] would you expect that to have a positive/negative effect on D2 receptor sensitivity or no effect at all?
I just read this blog post -
- and now I'm a little bit confused by the exact role of dopamine in all this. Dopamine activity creates wanting, not pleasure. In a drug addiction cycle, the action of the drug changes the state of the brain such that future desire or wanting of the drug is increased. There a positive feedback mechanisms and there are negative feedback mechanisms. If large hits of dopamine desensitize a person to dopamine that means that they will need more dopamine to achieve the same effect as prior to the adaptation. If dopamine mediates wanting this means that becoming desensitized to dopamine should create a situation where desire for the object in question is decreased. If large hits of dopamine rather than desensitizing are sensitizing, then they will cause an adaptation such that less dopamine is required to create the same level of desire and wanting in the future is increased. It seems like the dopamine system may work on a positive feedback mechanism of senstization rather than desensitization. With dopamine mediating wanting rather than reward this puzzle becomes more complex. What then mediates reward? Endorphins? Perhaps dopamine works on a positive feedback schedule and endorphins work on a negative feedback schedule.
As far as I know, arginine is substrate for NO, other amino acids are not.
gunther gatherer said... 1) You hinted at bitterness being something that humans are averse to.
My understanding is that bitterness signals things that may be teratogenic. This is why women are more likely to be supertasters (have more taste buds for bitter) than men. It is adaptive not to birth monsters.
Thanks Al. I also read that emotional/mental functions aren't delegated to different neurotransmitters. Rather different functions are carried out by different circuits which often use the same neurotransmitters. So the idea that wanting is a function of dopamine but pleasure isn't is a bit oversimplified on that basis alone. Probably the wanting and pleasure circuits both use several different neurotransmitters including dopamine. This probably explains why psycho-pharmacological treatments always have side-effects.
On whether non-food reward centers actually affect bodyfat percentages:
From a study done in India. Those who count their own cash for a living have significantly higher % of obesity than those who count others' cash. Though both cash counters were comparatively fat anyway. Best bet is not to count cash:
Here's the whole PDF on that study mentioned above.
The theory is that money is now perceived the same way as highly rewarding food was during our evolution. Hence we feed our reward centers just by acquiring it and trying to make more. No one can deny that money can be an addiction too.
Though there is the confounding factor that when you count your own money, there is more stress involved than when you count someone else's.
"Hibernation is not something humans do;"
This is where you stephen are fundamentally wrong. No we do not hibernate but yes our physiology shifts in preparation for winter, just like a bear. No it is not as extreme as hibernation but yes we do experience major shifts in how our bodies work.
Re: Cold climate dwellers and COMT variations - I can't say i've read the research myself, but in terms of body temperature regulation, you are absolutely incorrect when you say dopamine stimulates warmth. The primary purpose of dopamine in regard to body temperature regulation is to reduce core body temp. This is why dopamine is associated with warm weather environments - more dopamine signaling in thermoregulatory brain regions reduce core body temp.
There is a severe side effect of antipsychotic medication called "NMS", neuroleptic malignant syndrome. A significant chunk of this deadly syndrome is a direct result of body temperature becoming extremely elevated due to dopamine blockade in the hypothalamus, leading to an elevated temp, rigid muscles, rhabdomylosis, which then leads to attendant problems.
People on antipsychotic medication (dopamine blocking) are advised to avoid warm climates - they NEED to remain in cold, winter-like environments to avoid triggering the syndrome.
So when you argue that cold dwelling humans are more dopaminergic, that makes zero sense and is not consistent with human physiology. Dopamine primarily evolved to be dominant in warm climates, so much to the point that it has a primary function of inhibiting increased body temperature so as to maintain an internal environment conducive for surviving warm climates.
The fact that their behaviors are so lax (dopamine makes you move around , stimulates 'psychomotor activity) aruges against the inuit of being more dopaminergic.
Here's more on modern-day money acquisition being a darwinian "exaptation" of our brain's prehistoric food environment.
Another study which changed the environment and found subjects gave less charity when they were hungry, and when given an olfactory food cue, they gave out less money compared to those in a room with no odor.
Great article, Stephan.
On a side note, I was wondering what you thought:
Dr. Jeffrey Friedman has said in his lectures that there is no evidence at all that he is aware of that the composition of the diet matters as far as body weight and body fat. (for example eating at McDonald's very often, Atkins vs Pritikin etc.)
This directly flies in the face of many "Paleo gurus", but Dr. Friedman is a world renowned source of information.
I agree with Dr. Friedman conditionally. I think that for a person in energy balance, the macronutrient composition (mostly fat:carb ratio) of the diet may not be very relevant to body fatness, within reason. However, people do seem to gain less fat when they're overfed with carbohydrate rather than fat.
Also, the palatability of the diet makes a big difference, and can influence ad libitum food intake. That can be independent of the diet's nutrient composition, or they can change together. Carb-restricted, fat-restricted, and other reduced-palatability diets decrease spontaneous energy intake and fat mass in overweight people.
Stephan, I notice you have not made any kind of reply to itsthewooo's comments. I find her knowledge of this subject extremely pertinent and I wonder at your avoidance of replying to her. I would like to read some kind of response from you, because as it stands I think she seems to have a better grasp of this subject than you do.
Funny you should her praise her knowledge when she hasn't provided a single reference for any of her statements in this thread.
I can't speak for Stephan, but I'm ignoring her because her comments are flippant, rambling and unsubstantiated.
Not to mention arrogant. Kitty is probably ItsTheWooo2 herself.
I think this about sums it up:
"I can't say i've read the research myself, but in terms of body temperature regulation, you are absolutely incorrect when you say dopamine stimulates warmth."
@Mirrorball - Thanks for the giant LOL.
This paper is a correlate to George F Koob work in addiction neurochemistry but still misses the bigger point of what drives obesity. The reward tracts are outflow tracts from the hypothalamus. Their is no data that shows that they can effect the lateral or posterior hypothalamic functions. Moreover, when I section these reward tracts in humans of they pulp their frontal lobes in trauma we don't see obesity. However, when we see a CVA or trauma or iatrogenic injury to the lateral hypothalmus we see unreal obesity. I think the series because you really have thought it out well. But this is the distal reflex in the leptin story. The central effect can be caused multiple ways but the real target is a small group of neurons gone unmentioned. Dr K
Hi Dr. K,
The reward centers are not primarily in the hypothalamus. They're mostly in corticolimbic and midbrain areas-- such as the nucleus accumbens and the VTA, although the lateral hypothalamus is an exception.
The lateral hypothalamus integrates homeostatic information from other hypothalamic areas (such as the arcuate nucleus) and reward information from the midbrain and corticolimbic structures. I think it's a good place to look for an interaction between the two. Orexin neurons could be involved, but orexin itself probably isn't. However, lesions to the LH cause weight loss, not weight gain (e.g, http://psycnet.apa.org/journals/com/70/1p1/25/). Lesioning other hypothalamic areas such as the arcuate or the VMH can cause hypothalamic obesity.
There is quite a bit missing here - There are several different ways of increasing dopamine releasers (amphetamines), MAOIs, agonists. Some of these lead to weight loss - some to gain.
High average level of dopamine or agonists causes down regulation of post-synaptic receptors.
There is a clear connection with carbohydrates and seritonin levels as you can read about in Dr. Wurtmans papers. Chronic consumption of carbohydrates cause a down regulation of postsynaptic receptors - re-regulation can take 6-8 weeks.
Amphetamines can stimulate appetite when the drug wears off to a point that there is a net increase in appetite.
Many foods directly effect dopamine secretion via stimulation of the oral cavity - spicy hot foods - crunchy chips, carbonated beverages.
PS: Some people lose weight on therapeutic dosages of amphetamines - some gain weight!
If this dopamine reward was all that drove appetite, life would be simple - it is much more complex.
Many people have had weight loss with SSRI that increase seritonin - ending the cycle of eating to feel secure and less anxious.
The question isn't so much if a food reward effect exists - but that of magnitude! Is it what drives the obesity epidemic? You haven't sold me on dopamine being the key cause of the change in the last 50 years.
I think you greatly underestimate the number of people that eat carbs as "comfort foods" -- the seritonin addiction has been rather well studies - less has been researched about the down regulation that causes longterm effects.
I'm not kitty, stephan can verify we have different IPs.
Yea, meanwhile I'm ~116 pounds and cured myself of morbid obesity without surgery or drugs.
The rest of you were either naturally thin like stephan, or you are fat and will remain fat because you keep looking to "gurus" and don't think critically or read.
"Yea, meanwhile I'm ~116 pounds and cured myself of morbid obesity without surgery or drugs."
That's not even true, you are taking leptin injections. And if you had lost weight without drugs, you would hardly be the only one. I myself weigh 125 lb now, previously type 2 obese, and I lost weight without surgery or drugs for real. But why am I replying to you? I should have followed Stephan's example and just ignored you until you learn that you don't know shit, just like everybody else. You just think you do. You would do much better to try to learn something and explore new possibilities with an open mind. That's how we get a little less ignorant, by not being arrogant and listening to what other people have to say. I'm done with you now.
This lecture remind me of this series:
Parents who offer food as a work incentive and use food to control a child's behavior are contributing to childhood obesity. Food rewards lead to poor nutrition habits.
I'm not even on the same continent as Wooo
I have been following Wooo's posts and blog for about 4 years, that is why I understand that she knows whereof she speaks. She has walked the walk; that will always count more for me than talking the talk.
Woo2, on your blog, you comment that you may be "congenitally partially leptin deficient." Of course, if so, I hardly think that your weight loss experience extrapolates to the entire obese population.
I come from the perspective of the compulsive overeater, and Stephan's theories resonate with me considerably (and pretty much in practice) -- tho I have a semantic quibble with whether it's a question of food reward raising or lowering fat setpoint vs overriding appetite mechanisms.
BTW, earlier this week you wrote: "I have definitely absolutely gained body fat. ... I am even hopeful that perhaps tomorrow I will wake up energetic with no appetite. One can dream, eh?"
If that's your definition of cured, I think I'll stick with Stephan. kthxbai!
Lucas, the Kenyon lecture is fascinating, especially the stuff about olfactory function and lifespan.
Since olfactory sensation is about 90% of taste anyway, maybe this intersects with our reward center discussion.
Does anyone know how olfactory sensation affects the limbic system?? Particularly dopamine?
You surely have a lot of knowledge. we all give you that. Most bloggers, including Stephan, always welcome comments from readers, even if they disagree with the content. In fact, many times those are the comments that drive the best conversations and sometimes even reveal new pieces to the puzzle. I'm sure, in some ways, you've done that as well.
But here's the deal. Your approach and your comments are often too abrasive. You have to remember (and respect) that this is Stephan's site. Posting multiple comments in a row that nearly max out the character limits with rants is not respectful. If you have that much to say, just stick to your own site and put it out there for everyone to read.
I've seen Stephan take the time to directly address your concerns in the comments of the other posts. But there just comes a point when enough is enough. I don't really gather that anybody is doubting your personal experience, but also nobody can write articles and do quality research to reach the masses based on one person's weight loss experience. Most people cannot (or rather will not) achieve your results. You are to be commended for your success.
I can't speak for Stephan directly, but I would lightly suggest easing up a bit. Be happy that you have conquered your own personal bod. But try to balance your desire to share your knowledge with remembering that folks like Stephan are doing a great work. I find it odd that your seem hellbent on fighting him on this series. He is not the big bad wolf.
Come to think of it, I think I read on Seth Roberts' blog that people were losing lots of weight by wearing nose clips when they ate.
Kenyon's olfactory knockout worms basically had nose clips on all the time, so they couldn't ever sense food.
Has there ever been a study on lifespan/metabolic factors/body weight of those who lost their sense of smell?
there are many who've cured their morbid obesity, including myself, without drugs and have kept it off. i know some of these people and i also help the morbidly obese on their weight loss journeys. here's the kicker- many of us have done it using different methods or a combination of methods. the reason i am reading this series by stephan with such interest is because i am seeing how his explanations of the mechanisms line up with what i've experienced and what i've observed personally and from those i help. more often than not, they are lining up pretty well. according to what i've read, there are a group of people out there who are indeed leptin deficient and injections help with weight loss, however, that is not the case with vast majority of people who are suffering with obesity. i think that hypothalamic inflammation and leptin resistance are the underlying causes and are the results of the hyperstimulative modern western diet and the use of industrial seed oils. i would post studies on this, but since you didn't, no need to show off.
i thinks stephan's ignoring of woo is justified because this is the second time during this series that she's stormed onto his comment section in a rude manner- this time almost accusing him of plagiarizing her work. pretty damn laughable for the woman who doesn't cite the studies she's referencing. there are many smart and opinionated people who come to this cite to read stephan and start a dialogue with him and most of the interaction is polite and civil even if there are disagreements. i'm not a scientist but have a great interest in these discussions because it helps me to help others who are trying to make the same journey out of obesity that i have. i think the vibe she brings to his message board is not a good one and she comes off as over the top and knowing all of a very complex subject that many very smart people around the world are just starting to get a grasp of.
The rest of you were either naturally thin like stephan, or you are fat and will remain fat because you keep looking to "gurus" and don't think critically or read."
I fluctuated from obese to skinny my entire life and now over a year later I've kept off 40 pounds at ~15% BF.. no drugs or surgery. How? Just plain old being mindful of calories and having a diet consisting of foods I like that's also high protein. Plus a moderate amount of weight lifting to preserve muscle mass.
I knew a man (former boss) who was overweight to obese who had lost (perhaps never had) his sense of smell. Apparently, that doesn't work for everyone.
In addition (I'll look up study later, but you can Google it), kids who've had recurrent ear infections and kids who've had their tonsils out both are at increased risk for obesity because they are more drawn to foods that are especially fatty or sweet, as they've lost some ability to taste.
I'm trying to figure out how this all fits together, since elderly people often lose weight because of a lack of interest in food caused by decreased ability to taste.
"However, people do seem to gain less fat when they're overfed with carbohydrate rather than fat."
What makes you think this? I tend to be the exact opposite. Although, maybe it is harder for me to overeat if I have more fat in my diet, thus never reaching the overfed state.
What about this
Potato Chips Cited as Culprit in U.S. Weight Gain, Harvard Says?
So potato chips and french fries are out, and it would seem to make the overall prognosis for the potato very grim. We know that potato chips are definitely high reward food but, on the other hand, potatoes themselves have low palatability.
Authorities try to pick one food that is the source of all problems -- are they misfiring?
Thanks Mighty Al, that explains some of Seth Roberts' blog testimonies.
Helen, I googled it and you're right about the ear infections and tonsils. Come to think of it, I had a botched wisdom tooth extraction in 1996 that left the right side of my tongue numb for years, which happens to coincide with when I started to gain weight, lose hair and come down with most of the metabolic syndrome I've just spent the last 6 years recovering from.
But I did recover eventually, once I got the formula right. The plasticity of the brain will allow the limbic system to grow back to normal, as far as I understand.
David, I think this study says a lot more about industrial foods and omega-6-laden veggie oils than it does about the potato.
Luckybastard and Jack
I think it is pointless taking the messenger to task for the manner of their conveying the message. Surely the 'meat' of the message is the thing any intelligent person who is interested in the truth should be focussing on?
Wooo has cited and commented on many relevant studies on her blog. Perhaps you should go there for more background.
Hey mirrorball - I lost weight at 20 years old (I am now 28). I didn't take leptin injections until 25. I no longer take leptin injections, I stopped them a few weeks ago. I have sinced gained some weight but I was, can, and will maintain my weight loss with or without leptin. Leptin just makes it natural and effortless like all you naturally biologically non-obese people (or people who barely lost any weight... theres a big difference between losing 160-170 pounds vs losing 40 pounds, lemmietellu).
SOrry but i DO know shit. You don't accidentally lose 160 pounds and maintain a BMI of 18-19 without having a meth habit or being anorexic or having gastric mutilation surgery. Yes, I used leptin for 2-3 years (between 25 until a few weeks ago) but I had lost weight 5 years prior to that. JUST SAYING.
I absolutely do listen to new information, but that doesn't mean I agree with everything I read just because the person saying it says it in a convincing way. The food addiction/reward hypothesis has 0% not even sightly not even a little bit relevence in my weight problem or weight control.
This may be relevant for mild weight problem but you don't store hundreds of pounds of fat because your brain finds food rewarding - that can only occur when the hormones and enzymes regulating fat storage vs fat use are severely FUBAR and it takes more than loving TWIX bars to do it.
And, not to mention, food addiction - if it was REAL - would and will eventually trigger euphoria and low appetite and low sleeping and all other signs of high dopamine/addiction. This seems to occur in obesity resistant people (when they over eat their favorite foods) but it does NOT occur in obesity... and obesity is the very group of people stephan is trying to apply a dopaminergic/food ramping up dopamine link to. Ironically this seems to be the only group of people who do not get high dopamine signs after eating. Thin kids run around after eating sugar and get hyper and have trouble sleeping because their body works normally - if they eat a lot of high sensation food like sugar their dopamine signaling ping pongs and they don't get fat. This does NOT happen for fat kids or fat people; the more they eat the more torporous they become.
There is NEVER a period of hyperactivity/anorexia/sleeplessness en route to obesity, this argues strongly against a hyperdopaminergic role , thus argues against an addictive process.
I had a physics professor without a sense of smell. He was overweight (Cynthia does great work though). I think blogblog commented on Hyperlipid (maybe it was here) about people losing their sense of taste and still eating the same amount. But, as Stephan has pointed out in the study he originally cited, lean people didn't significantly reduce their calorie intake even with the low reward liquid.
OK beth, when you get ANYWHERE NEAR MY WEIGHT , and keep it off for 8 years, then talk to me about how well you are maintaining. Until then, stick with your gurus and stay fat. KTHXBAI!
BTW my blog is a place where I vent, I have for the most part stopped writing informational pieces and deleted them all. I go through phases, moods, thoughts feelings intense and all, I vent. WHen I stopped the leptin for a while - a couple weeks - it was very difficult but I have since adapted.
I will be glad to let you know my appetite and energy has vastly improved since writing that. I have lost some weight. Oh and by the way I am a size zero, I have a 24 inch waist and 35 inch hips. Everyone tells me I'm extremely tiny. Even if I gained 10 pounds I would STILL be thin. Even if I gained 40 pounds I would NOT be overweight by a BMI chart.
I am maintaining fabulously, actually, if I don't say so myself.
Just a piece of advice I"m sure you don't care to hear, but in my experience people who label themselves "food addicts" usually have other reasons why they are eating that are physiological. I've never met a self described food addict who lost weight permanently. Oprah is an archetypal example. Oprah is a woman who needs to stop eating junk food (diet or otherwise) and carbs and anything like it and start eating a low carb high fat diet. She will never be thin because she won't do this. She does EVERYTHING IN HER POWER to avoid this conclusion, and part of that is telling herself shes a food addict. If you're a food addict, no need to go on a metabolic correcting high fat low carb diet, right?
In my experience, people who label themselves food addicts are trying to avoid a physiological basis for obesity, so to justify continuing to eat food they enjoy eating. It's not out of addiction but sheer lack of motivation to make unpleasant changes...
If there is no physiological intolerance to sugar/starch, no need to dramatically reduce those foods...right? If it is just a mental problem, all you need to do is set limits and think and meditate or other nonsense, and you can "moderate" those foods like everyone else.
It's sort of like that "I'm just going to have one more cigarette then I"ll quit tomorrow" mentality. You're justifying inaction with a physical disorder by telling yourself you are acting (when in reality you are not).
Food addiction is just a self delusion which keeps people eating the foods they METABOLICALLY, ENDOCRINOLOGICALLY, NERVOUS SYSTEM-WISE can not tolerate. The pathological eating is a result of the metabolic abnormality, it is NOT a mental or emotional problem. Strong emotions about food do exist in obesity, but they are the result of metabolic / endocrine/ nervous system problems, they are NOT the cause. This is sort of how strong feelings about cigs are the result of nicotine addiction.
I've been there. You cry and scream for food and think about it all the time.
But the way to end this - you need to frame it as a body issue, and any mental/emotional stuff is just another symptom of that. Normal people with working bodies eat normally, and even when they eat a lot they still eat normally over a long term period of time because their bodies work.
I think the reason people have such a hard time sticking to low carb is not because carbs are so awesome... it's because they are murky and do not believe or adequately understand the science. When you absolutely get it and understand, it's very easy not to eat carbs anymore. Eating carbs feels like eating glass or poison, i mean duh it just so obviously makes you feel like crap and causes sickness. Why would you do that to yourself, it's going to cause disease? Carb free alternatives exist for almost everything, and low carb food usually tastes better anyway. It takes a little effort sure but how much do you enjoy feeling good? I certainly enjoy feeling alive much more than I do a nasty take out meal and other conveniences. When you absolutely must be lazy, hay, a satchel of peanuts and a sugar free coffee full of cream is about 0.1 seconds of effort and does the job in keeping you thin and fed.
I know the thing that keeps me sticking to low carb is being very clear in my mind about why obesity happens and how to control it. If I didn't understand this as well I probably would cheat more often and would not be thin as a result.
I have an easy time ignoring everyone, ignoring doctors, ignoring "experts" and thinking / solving for myself. This has helped me all throughout my life and if not for this ability I would still be fat. Amongst many other issues I've had and re/solved.
My success isn't because I"m fundamentally different than other fat people physically...it's because my personality is. I can research, I can think independently, I can say that experts are idiots and have things all wrong, I can do what I know is right without caring that the rest of the world thinks I"m a freak. My fat coworkers all eat low fat tiny meals, they think I"m absolutely insane for eating the way I eat. They think it's just the whims of a crazy person doing crazy things like eating weird food in weird ways... like a schizophrenic making hand gestures at no one. Who's insane, me at 116 pounds and tons of energy or you whos STARVING and staying fat only to quit the diet when you cant take it anymore? OKthx.
If I were bound to experts and opinion I would probably either be fat and ignoring it or fat and starving myself on tiny meals stripped of fat with a small portion of rice. I sure as hell wouldnt be thin.
So all of you who call me obnoxious arrogant a know it all etc... THANK YOU ITS MY FAVORITE PERSONALITY TRAIT.
I'm confused. I hear what you're saying but I thought Stephans point was that the dopamine reception was not doing it's job...which seems to be what you are saying as well. Am I misunderstanding?
yah well if i were stephan, i would block your account from posting. what good does it do to try to help people if you those people feel that you are super annoying, you know it, yet you continue anyway, even piling it on heavier. good grief.
I've patiently tolerated your comments, despite the fact that they're often insulting to myself and others, because I want to allow alternative perspectives. But you're pushing your luck. Taunting other commenters for being overweight is crossing the line.
If you can't participate in an adult manner, you can't participate at all. This is your warning.
Woo, I can't decide whether it's leptin, dopamine, or pink elephants that stimulate you to write such inflammatory, insulting posts to this low-key group of blogreaders. You've generously provided us (and I'm perfectly comfortable saying "us" at this point) all with the evidence necessary to conclude that you are aggressive, irrational, self-aggrandizing, and myopic. Operating in your solipsistic way, you've failed to entertain the possibility that any one of your fellow readers shares your physical or social plight. Why do you think we're here? To be entertained by the fireworks you're shooting off? Perhaps because we're all thin, muscular, and healthy and simply decided one day that the twinkie/coke diet keeping us that way was suddenly undesirable, without some compelling evidence to the contrary? Very few of us are scientists, some read studies, some don't, but all of us have a vested interest in health and listen to Stephan et al because they are willing to share their educated insights. Stephan doesn't get a free pass and his arguments have been cogently and fairly criticized here (not by you, I'm afraid). While his approach is measured, careful, and relies on the scientific research with which he is deeply involved, yours is based on self-righteousness and ad hominem irrationality. I don't doubt you are passionate and, perhaps, well-informed, but your tactics are anti-social and anti-scientific and provide little in the way of meaningful shared discourse. Moreover, they are increasingly intolerable and will probably get you booted soon enough.
Apologies Stephan, I didn't see you'd written something as I was making my post.
Wooo said, I think the reason people have such a hard time sticking to low carb is not because carbs are so awesome... it's because they are murky and do not believe or adequately understand the science. When you absolutely get it and understand, it's very easy not to eat carbs anymore. Eating carbs feels like eating glass or poison..
That's my experience as well. I came to low-carb with a degree in medical biochemistry. I knew it was based on science, and once I realized that it worked on a practical level, it was not hard to leave behind all but a few incidental carbs per day.
Stephan said, However, people do seem to gain less fat when they're overfed with carbohydrate rather than fat.
That is definitely not my experience. In a low-carb context, fat slows gastric emptying and promotes satiety far longer than an equal number of carb calories would do. And fat does not produce a drop in blood glucose that signals the need to look for more food an hour or two after eating. On the other hand, it's possible that Stephan's statement applies to individuals who (unlike me) have normal insulin signaling.
i've been a fat boy my whole life (maxed out at 340lbs) until i went to a paleo carb diet to finally get the weight off (now 225@15%bf). i started off vlc for a few months but then i started adding back in starch post workout. i really think that little trick did wonders for leptin sensitivity as well as re-teaching my muscles how to properly accept glucose after they've been emptied out and upping insulin sensitivity. i think using this strategy also keeps the liver from having to deal with too much excess glucose. i stress again that i gave myself a few months of being vlc before i employed this strategy.
i hear many people who have been vlc and lc a long time say that their insulin signaling is off and they can never do a moderate carb diet- i used to say this also. with my experience and seeing other people go back to eating starches moderately, i'm wondering if the insulin resistance you are experiencing is of the physiological variety and not of the liver. i don't have any answers concerning this- just my experiences and observations, but i'd love to hear what you think on this matter...
Part 1 of a two part comment-
Well, I certainly feel that Stephan is onto something important. Stephan's theory speaks to the evolution of a pandemic in obesity over the the last 30 years.Is Stephan saying that this accounts for ALL individual cases of obesity? No, he is not. But this is what I see as huge feeder-theory when looking at a pandemic situation.
I very much like the way that all the factors that I see as drivers have been tied together. As someone who has practiced in healthcare for 30+ years, one of my greatest frustrations has been the lack of effective synthesis from multiple disciplines of highly pertinent information/clinical observations, from multiple sources to produce WHOLE "answers."
I think that the stress piece in modern life is paramount and cannot be understood rightly without some thought. Different kinds of stress are experienced in very different ways.For instance, rationing of say gasoline which comes about due to war efforts(as in WWII) would be experienced
in a very different way from the rationing that that occurred in the 70's which invovled no common purpose or "noble" cultural/nationalistic cause, but rather was experienced very angrily by many people as simply deprivation.
To give a single, simple example, what I call the background noise stress of my work changed radically with computers and cellphones. 10 or so years ago, it was not a given that I would have a cellphone to begin with. Now it is an absoute given that I have one and furthermore that I additionally carry a "company" cellphone AND notify everyone in the hierarchy of my home, personal cell and work cell numbers AND that I will basically always be reachable by one of these, 24hrs/day. In my office, the sheer number of emails from all the divisions that I had responsiblity for, in a morning's time, was staggering.Calvin Coolidge once said that if 10 problems were coming at you like cars down a road, if you just stayed where you were, about 7 of them would fall into the ditches on the side of the road before they ever got to you.
This is a good example of how things have really, really changed.
There is no longer that time lag in the road. All the cars/problems reach you in as long as it takes to punch a few numbers or letters or zing off an angry email. These are small examples, but I am sure that everyone reading this blog can heap on like examples.
These are the result of cultural changes and they are chronic - no end in sight, which is how they are experieced by people. This is very different from acute, time limited stressors, especially when the stressors are experienced as necessary for the attainment of a specific,desired goal.
Some comments arose that basically had to do with availability. We can look at specific areas and see where availability plays hugely into abuse/dependence/addictive issues. Pharmacists have what I am remembering as, I think, the highest rate of addictions issues of any profession. Is this because pharmacists are somehow far more addiction prone than say landscapers? No, but they have the ready availability in their everyday work of controlled substances and, they have very high stress work. Huge high stress and feelings of lack of control +access.
Stephan - I don't like "taunting" people but when certain posters (who they themselves are not successful at weight loss) are mocking personal journal entries regarding problems maintaining weight 2 weeks ago, then they should expect similar vitriol. They don't know me at all or how difficult or easy it is for me to lose or maintain weight, all they did was search my name and pull up ONE entry and then say "ha, you fail at weight loss" because of a bad few days... I mean, come on, they have to expect me to at LEAST say "and you as well".
Part 2 of a 2 part comment - too long for one post -
Cross addiction and poly addiction are so common as to be the norm rather than an exception. Recovering substance dependent people often put on lots of weight and it is not uncommon for them to become obese or morbidly obese.I have personally and professionally known of several cases where women who had bariatric surgery and were either non-alcohol drinkers or truly occasional-social drinkers, developed alcohol abuse/dependency. I have also seen many cases of opioid or benzodiazepine abuse/depndence development when there was no prior issue, as well as mega shopoholism.
I like this blogpost by Dr. Sharma. My view is slightly different in that I think what he refers to as "process" versus actual "food" addiction is often a combination. The behaviors leading up to the reward become an essential and highly pleasureable part of the entire process in some cases. AND, perhaps there is not an addiction to a specific food, BUT, I would bet that the foods sought are right off of Stephan's list - highly industrialized-food-like-substances, which I believe become compelling beyond conscious comprehension.
Some made comments about kids and their credibility in reporting. As someone who has worked very extensively with children and adolescents, this saddens and concerns me.Kids need to be heard. I have worked with far too many severely depressed kids who had been having auditory hallucinations (present in approximately 25% of severely depressed kids) who had been hearing these denigrating statements or bizarre music or God telling them how horrible they were for months if not more than a year, without telling ANYONE, least of all their parents. Suffering, stressed kids frequently suffer in silence or act out in angry (kick the trashcan) actions or act-in (seeking hyperpalatable foods as per Dr. Pretlow.)If we don't listen to kids, as we are not doing a very good job of doing culturally, it is at our own continued peril.
I also think this link figures highly into it all...
This has gotten too long, so I'll sign off with my favorite quote by Bruce D. Perry, MD, PhD regarding the USE DEPENDENT development of the brain, particularly in kids.Perry is one of the leading researchers , clinicians and systems changers in child trauma in the U.S.
Use-dependent: This refers to the specific changes in neurons and neural systems following activation. Repetitive, patterned stimulation alters the organization and functioning of neurons and neural systems and, thereby, the brain
OK Woooo, I'm game, I can't follow you because your tone turns me off. Gimme your secret. We got a guy (Stephan) who is genuinely interested in helping others in losing weight. Peace of mind to you. Thanks.
Rob - you basically do what I do. I eat food I ENJOY (so much for the reward hypothesis), avoid food I don't like, and eat low carb, glucose control. Of course I';m mindful of calories but when I'm hungry I always eat, I always make sure I eat enough I don't starve for long periods. That never helps IMO. I focus very much on nutrition particularly pertaining to glucose regulation. I take chromium / GTF, inositol, acetyl-l-carnitine, I recently began supplementing with magnesium and l-tyrosine again which has helped very very much in post-leptin lower dopamine state. I take st johns wort for depressive tendency, which helps my weight and glucose tolerance as well (one, it augments catecholamines dopamine which we previously established is fundamental to normal weight, two, it directly a affects GLUT signaling reducing glucose intolerance).
I have also seen a lot of benefit from piling on flax seeds and EPA/DHA pills. Recently started coconut oil again too and find that is helping.
Since adding in coconut oil, magnesium, tyrosine, and altering my st johns wort routine I've regained tremendous energy and decreased my appetite. Not to the point it was on leptin, but much better than it was before.
Ironically the one supplement that was supposed to be magical (vitamin d3) never seemed to do anything for me. It did result in me getting sick more often though.
My capacity to tolerate glucose food is infinitely better than it was before doing these things.
We pretty much do the same thing I suspect that intuitively you make sure your glucose stays stable, because when it is not stable it is far more difficult if not impossible to prevent fat gain.
Interesting that both of us are maintaining weight and part of the secret is eating food we enjoy, making sure our meals are high reward?
A few years ago they were saying that was the key to weight control - eating very flavorful rewarding foods so you become satisfied easily. I tend to find this does help, but only in the context of a glucose controlling diet that does not destroy your nervous system like a hyperglycemic diet/lifestyle will in an obese prone individual.
If I ate bland food, I am pretty sure it would be more difficult to control my weight.
I think the issue is whether or not the person is really watching their intake and glucose and insulin, consciously or intuitively. If you are doing so, eating a bland diet will only make it more difficult to maintain. If you are not, it may help you ironically by causing you to eat less "bad for you" food.
Would you say that the food reward theory you currently espouse creates a line of distinction between foods that have a pleasant flavor and foods that are designed to have properties or combinations that superstimulate?
I can't imagine that humans are designed to thrive on food that tastes bad...but an average value meal from any drive through will deliver a meal you could never ever replicate outside of an industry designed for that purpose.
The bland tube feed diet did strongly imply that obese were seeking something from food other than fuel...when the food did not provide it they were no longer interested in consuming it beyond basic calorie needs. In an artificial environment obviously, so how about outside of that?
All foods naturally have some flavor. Is it a question of degree regarding stimulation? If so would a low carb favorite of heavy cream + flavored coffee + artificial sweetener could be considered a superstimulant?
Don’t go away. I like your opinions. You can make the same points without being quite so inflammatory.
It's just a blog - lighten up! You can learn more from an outlier than you can from a choir boy.
I don't if I'm intuitively controlling my glucose, insulin, etc. or not but it doesn't matter to me. The reason I haven't regained because I've consciously stayed in energy balance this whole time, that doesn't mean I don't overeat some days. I do and when that happens I adjust my intake the next day or days.
And just to be clear I don't eat low carb, I almost never go below 100g a day and on lifting days it's a lot higher. I'd say my diet is a 50/50 whole foods and processed foods, for example at almost every meal at home I have a piece of corn bread or a mini chocolate muffin.
No guilt, no worries about insulin, glucose or anything. I know how much food I'm putting into my body, usually it's exact (like at home) and other times it's a rough estimate (e.g. at a restaurant). I also know what my maintenance calories on my lazy days and active days.
But again this business about glucose control to prevent fat gain, there are days where I'm ravenous (usually because I've eaten more processed foods than usually) but I don't allow myself to over eat. And like I said if I do, I lower my intake the next day.
@luckybastard, thanks for reading my rant. My insulin resistance is probably mostly of the physiologic type because I've been very-low-carb for about eight years. I simply don't enjoy eating carbs any more (the smell is great, but for me the mouth feel is ghastly).
The reason I suspect that my insulin signaling is somewhat "broken" is that I did zero carb for a while and discovered that my fasting blood sugars were consistently above 100mg/dl. This basically doesn't happen in healthy zero-carbers below age 50, and it made me conclude that I was a not-so-healthy zero-carber above 50. I did have to add some carbs back to get the fasting blood sugars into the 80's. However, because I don't lift or do strenuous exercise, adding starches isn't something I'm motivated to do. But you've given me something to think about.
thx for sharing. i've found that cycling and slowly ramping up carbs is a good way to get leptin sensitivity back as well as work out of that physiological insulin resistance- at least for me. i hope you can find some success with cycling...
i do strength train twice a week so that may have also helped.
Might-o'chondri-AL, I believe the mechanism you describe can explain a lot of what Stephan Phinney found in his elite cyclist study in the 1980's where he feed them a high fat diet. After adapting to it, their performance was better or the same as under high carb feedings. It seems that this state preserves glycogen by shunting to fat burning (and possible generates more mitochondria).
BTW, I really appreciate itsthewoo's input and find it very enlightening and valid.
Dr Guyenet......come read my blog listed today. I wrote it just for you. http://jackkruse.com/why-sleep-and-leptin-are-yoked/
Normally would never do this......but I want to stimulate you.
I think part of the problem is you are taking stephen's hypothesis as fact. So far, only stephen has put forward that appetite and enjoyment/desire/craving for food is motivating obesity - I don't agree. I fundamentally REJECT this idea. Certainly motivation to eat is part of obesity, but it is absolutely wrong that obesity is an addiction process, it is WRONG to assume that just because insulin in the brain tends to be anorexiant, that necessarily means the higher one's insulin the less hungry they are. This is an irrational conclusion.
Multiple factors can operate at once in affecting whether or not one is motivated to eat. This seems to be a fundamental difficulty we are having in this discussion (much like the "leptin resistance" idea - just because normal leptin signaling prevents further weight gain, this does not necessarily mean whenever someone gets fat it must be because their leptin is "resistant")
Insulin is one factor and does suppress appetite, but do you know what REALLY augments appetite? A drop in blood sugar. You can have high insulin, but if your sugar goes from 140 to 75 in an hour precisely because of that high insulin, you better believe you are going to be crying and screaming for food. You know what else augments appetite? Low dopamine receptors, low stimulation of the d2 receptor. Low FFAs.
Ive lived this. Trust me, you can be full for an hour after eating then you feel that trembling, that edginess, and you know your sugar is bottoming out and you can't help but eat.
This is why I don't believe in "food addiction" or emotional eating. Yes, when your blood sugar is swinging left and right, you're going to be extremely emotional. That's a DUH. It's not an addiction any more than someone with COPD who can't breathe is "addicted to oxygen".
I know precisely Why I can "burn off" fat on a low carb diet. I vividly remember 8 years ago when I inducted into the atkins diet. I was just 20 years old, I just stopped being a teenager, my life was a complete wreck, my brain was trashed from depression, I didn't know if it was day or night, I was sleeping 12 hrs a day, and I was growing fatter year by year. I never felt full.
I honestly had no will to live, my brain had no motivation, n o capacity to care about anything. It was a physically real disability - an inability to see or care about a thing.
Well, it was march, and I think that light creeping into my window gave me a bit of motivation (I am extremely sensitive to light, mood wise) and I decided to try to make some changes, and by CHANCE I went on the atkins diet.
Within 2 days my entire body changed. It was a miracle. I started hemorrhaging fat from my fat cells, this is exactly how it felt to me. When I did not eat carbohydrate food and did eat fats, my fat cells just POURED OUT fatty acids, much like a diabetic who is in ketoacidosis, except in my case it was a normalizing of abnormally high insulin levels and thus a normalizing of adipocyte fat content.
I had no need for food, and if I tried to eat, the extra fatty acids rapidly produced nausea preventing me from eating. It was as if my body was saying "hey, why are you eating more fat, we are using well enough from our abnormally full fat tissue".
The only time I could eat is if I ate something insulinogenic like a few grapes. This would raise insulin enough that presumably my FFAs dropped and I could tolerate eating more (although, naturally, this would prevent weight loss, and i had no reason at all to do that).
Also miraculously my depression become about 80% better in a few days. I believe this is due to a combination of stable blood glucose, combined with the theraputic effect of ketones, combined with upregulating my deficient dopamine receptors (as it has been shown in studies, glucose excess in the brain causes downregulation of dopamine receptors in humans prone to obesity and is fundamental to the process).
I gained the will to FEEL, TO CARE, TO HAVE MOTIVATION. This is another thing I vividly remember - feeling as if things had meaning for the first time in many months if not years.
Observing this change, like a lightswitch, motivated me to learn ravenously and here we are today.
The skeletal muscle insulin resistance of an extreme ketogenic diet is absolutely temporary and is reversed upon eating a high carb diet for a few days. It is basically like "inducting" into a ketogenic diet, except in reverse.
My problems with glucose far precede my low carb diet.
Trust me on this, you're wrong. I cannot tolerate glucose and carbs, nothing I do can change that, it is a genetic trait which is evolutionarily conserved that I happened to inherit from my grandmother who herself was just one generation away from being a tribal nomad in the north african desert. I am like many others of african, hispanic, or mixed caucasian descent - we get fat when we see too many carbs, it's functional and it's evolutionarily logical in the environments we herald from.
I should also mention about the same time I started feeling the will to care and as if things had any meaning at all, I also stopped sleeping 12 hrs a day and started sleeping only 6 or 7. It was strange needing so much less sleep, just as strange and foreign as feeling as if life had meaning.
I relate it all to dopamine, my brain grew dopamine receptors, and lower insulin / blood glucose stopped moping it up as it tends to do. Google hypocretin - this hormone works like a lightswitch in the brain, do you know what suppresses it? High glucose in the brain. Narcoleptics are deficient of hypocretin, but people chronically hyperglycemic have low hypocretin in the brain as well. Hypocretin signals to every part of the brain "hay HAY HAY BE ALERT AND MAKE DOPAMINE AND NOREPINEPHRINE ".
Hypocretin also controls metabolism, augmenting it.
The irony is hypocretin, when initially discovered, was believed to promote obesity as it stimulated appetite - it was thus called orexin. The major irony is this is the polar opposite of what it does; hypocretin is essential for normal wakefulness, normal stimulation, normal metabolism, and increased appetite is merely a symptom of increased metabolism and movement, just as increasing fT3 uptake will result in an increase in appetite (meanwhile, hypothyroid people with inadequate T3 will have very low appetite in spite of gaining weight and body fatness). Using energy promotes appetite.
I believe high blood glucose suppresses hypocretin and this is fundamental to the epidemic in depession and ADHD in western society. You can't pay attention or care if your shooting excess glucose in your brain all the time.
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