I would like to spend a few blog entries rambling about the physiology of weight regulation.
This is really foundations, but it is an essential topic to be at least casually familiar with.
Many would be dieters are quite ignorant of this subject, and/or they are misinformed by various self styled gurus (ahem,
Big C). The misinformation is particularly acute pertaining to the relationship of fat regulation and post weight loss, body fat reduced states. Certain gurus have a vested interest in denying the fact that body fatness is tightly regulated and almost entirely outside of conscious control long term. This is because our society largely presupposes that obesity is a moral defect or a result of accidentally over eating calories. It goes against our moral beliefs that the obese state may be actually a relatively "normal/stable" condition, at least partially. Body fatness is not random, not accidental, not the result of over eating "rewarding" food, but actively regulated by the endocrine system and nervous system. It is not caused by "rewarding" food. Wanting to eat more "rewarding food" is merely one fragment of a symptom of weight regulation effects. As has been pointed out many times before, stating that "food reward" causes obesity is like saying "oxygen reward" causes respiratory/cardiovascular abnormalities. Respiratory rate is reactive to the concentration of oxygen/carbon dioxide in blood. Relatedly, eating behavior is the result of a myriad of energy deprivation cues. No one eats for any other reason. Fullness and satiety, by its definition, implies lack of further responsiveness to food cues.
Understanding this innate, unconscious, automatic regulation of body fatness logically means one cannot cannot arbitrarily reduce an aesthetically unsatisfactory body fatness long term via CICO dieting, much to the chagrin of the missionaries of puritanical masochistic self starvation, namely Big C & Stephen Guyenet.
This is obviously an enormous subject so I attempt to work at it in pieces ;)
Background:
I blogged a few weeks ago, toward end winter/early spring regarding how I was getting SEW FAT from sedentary activity and generous caloric eating that I was starting to have "ketotic nausea" again. For those unfamiliar with the concept,
"ketotic nausea" is a term I made-up describing the phenomenon of fat gain resistance to the point of uncontrollable negative energy balance when following a ketogenic diet. It is experienced when the physiological ability to assimilate consumed nutrition into fat tissue is
so poor that one experiences nearly maxed out nervous system and endocrine compensation in the form of nausea, very low appetite, and high energy/heat if they should consume a high energy intake.
Please bare in mind all obesity resistant people experience such compensation whenever they attempt to "over eat" food of any macronutrient breakdown; the adaptive response to hypernutrition is nausea, repulsion, food avoidance, anxiety, urge to exercise, and increased thermogenesis. On the other hand, people predisposed to obesity typically will not exhibit much innate compensation to hypernutrition;
there is little rebound compensation for hypercaloric eating in obesity. If anything obesity prone individuals like myself can tell you we are apt to experience increasing hunger and fatigue. As this study suggests, the difference between thin people and obese people is not "reward sensitivity" to food at meals, but rather adipose/body fat regulation defects in the post-meal state. This is demonstrated by food seeking behavior relatively shortly after eating in obese people, whereas obesity resistant people do not demonstrate this, and naturally consume less calories in response to eating a great lot of calories at any given time.
What this implies is that obesity does not occur at tasty "rewarding" meals, it is made
in between meals - body fat oxidation/regulation defects. Thin people will eat less after a large caloric intake, because the nervous system and endocrine system are antagonizing growth of the adipose tissue. Fat people will not eat less; fat tissue growth occurs, and caloric intake remains approximately the same later on. (It's interesting researchers hypothesize "cognitive training" might help reduce eating behavior; it seems they assume the fat people are eating more due to mindlessness as opposed to correctly assuming they experience more hunger. The moralizing/blaming is a default assumption, ha!)
I want to repeat this crucial point:
all healthy people normally and naturally experience food avoidance, aversion, nausea and repulsion when they attempt to over eat. They also experienced increased metabolic rate, anxiety, thermogenesis and a pressure to move and exercise in addition to the appetite changes. This is not some magical property of the ketogenic diet; all a ketogenic diet does is transform any individual into a relatively more obesity resistant one by raising the resistance to obesity threshhold.
The ketogenic diet is a therapy specifically for obesity (amongst other conditions). Whatever your baseline level of obesity resistance, the ketogenic diet typically increases it (sometimes quite substantially, as in my case and many others). Obese people find it anomalous and remarkable when we experience this change on a high fat low carb diet because the difference can be quite stark, for most of our lives we have responded to nutrition with lethargy and hunger. Thin people, however, have been experiencing this
their entire lives, and they experience it whether they over eat cake or over eat bacon. (
Sam Feltham's experiment certainly was entertaining, but my money is on this man not being able to gain much weight even if he did it on doritos. Well, maybe he'd be fatter on doritos and feel worse too, but I doubt he could ever gain much body fat even if he tried. )
I digress. What I attempt is to isolate this phenomenon - obesity resistance vs proneness - as being a total body phenomenon (as some isolated aspect of "brain" or "appetite").
What is the difference between extreme responsiveness to food cues, low satiety, high appetite, lethargy that characterizes obesity and associated intuitively with "a high carb" diet, vs "ketotic nausea" and implicit obesity resistance as I describe above?
Food reward doesn't help. Attributing obesity resistance to low responsiveness to food reward is like attributing my cardiovascular health and normal respiratory rate of 10-20 and HR of 70 to "low oxygen reward". You are taking the results of a system and assigning hierarchical importance to it. Food is "rewarding" when ones nervous system and endocrine system is primed to grow adipose. All normal people experience food reward when they are hungry, but then it terminates once the nervous and endocrine system responds appropriately to fed condition. What is occurring in obesity is increased food responsiveness as a RESULT of obesity proneness;
it is one of a myriad of effects that differentiates the obese from the lean, mind you.
The ketogenic diet increases obesity resistance, certainly, but it typically cannot adequately or entirely control obesity. Individuals such as myself are outliers and I am quite aware this is the case; my story is remarkable because of the degree of efficacy ketogenic diet exhibits in my own obesity. However, partial response is common, and a few respond virtually entirely as I have. I also hope to explain the "long term stall // pressure to regain" phenomenon that plagues so many dieters including myself. The stall is merely one facet of unconscious body fat regulation. Previously I described that ketogenic diets work by altering physiology to increase obesity resistance; weight loss exerts an opposite pressure, increasing body fat gain proneness. The stall occurs when the weight gain resisting properties of ketogenic diet are cancelled out by the weight gain encouraging effects of body fat atrophy.
As one gradually reduces body fat stores secondary to long term VLCarb diet the ability for ketogenic diets to further "work" to reduce body fat eventually slows and diminishes. The "ketotic nausea" which was a 24/7 proposition at 350 pounds, isn't so much at 150 pounds, basically.
As an aside, Carbsane with her shitty reasoning so typical of her would tell her naive readers ketogenic diets "poop out" and we "stall" simply because they don't work. This is a gross distortion to point of lie. Saying ketogenic/low carb diets don't work because all people typically "stall out" is like saying the diuretic furosemide doesn't work because people still have incomplete remission of the underlying illness while taking the diuretic.
"Well, if furosemide worked, my heart failure would be cured!" <Prior to furosemide your O2sa was 87% and your RR was 35 and your B/P was 95/65 and your pulse was 120 and you were coughing up blood and swollen like a balloon.
Introducing the therapy of furosemide helped normalize your cardiovascular system and vital signs is
pretty convincing evidence it does work, actually. No one ever attempted to say it would CURE you
completely. Heart failure patients do not get IV lasix and turn into someone totally disease free like myself; o2sat 98% on room air, pulse 70, B/P totally normal, zero edema. The lasix just prevents heart failure patients from dying and allows them to breathe and dramatically improves quality of life. It works very effectively but obviously doesn't
"cure" anything. A person with heart failure always has heart failure and all liabilities entailed within; furosemide therapy merely radically improves outcomes.
Ketogenic diets operate similarly in metabolic disorder and obesity.
It is grossly misleading for carbsane or anyone else to say low carb diets "don't work" because you only got down to 180lbs from a starting weight of 300lbs, but your goal is 120 lbs. It's nice that your random made up goal is 120 lbs like a 21 year old movie star, but the fact the diet allowed you to shed 160 lbs effortlessly / without self starvation ought to be evidence of its extreme efficacy in treating obesity, don't you think? Your average dieter / obnoxious self styled Carbsanian internet guru is highly medically untrained and ignorant, and generally unfamiliar with medical protocols. Medicine isn't borderline personality disorder reasoning; it's not a pivot between
total success and
total failure. Any medical therapy attempts to improve outcomes for ill patients and quality of life; it is always an analysis of risk:benefits. There is no such thing as TOTAL CURE or TOTAL FAILURE in medicine, with rare exceptions. Obesity is one of the only conditions I can think of where people expect *total remission* or else the therapy is deemed failure/ineffective.
TL;DR:
1) Body weight is tightly regulated and entirely outside of conscious control over a long term continuum of time.
2) Obese people exhibit poor compensation for hypercaloric feeding. Obesity resistant people unconsciously reduce caloric intake after hypercaloric feeding, secondary to decreased interest in food.
3) Attributing obesity to increased "food reward responsiveness" is confusing symptomatic effect with pathophysiological cause. Increased interest in feeding is one of many difference between the obese and lean; it is highly biased and false to focus on it to the exclusion of all other effects.
4) Ketogenic diets appear to increase "obesity resistance"; whatever baseline condition of adiposity, adopting a ketogenic diet tends to promote greater leanness for that person. The effect may be very pronounced for some individuals with pathological obesity (such as myself).
5) Weight reduction and body fat atrophy exerts an oppositional pressure, increasing weight gain proneness, eventually cancelling out the obesity resistance augmenting effects of ketogenic diets. Stalls then occur and no further weight loss is observed.
6) That ketogenic diet often exerts incomplete efficacy in the therapy of obesity does not mean it "DOESN'T WORK"; varying rate of response to therapies is par for course in medicine, and by all measures the ketogenic diet appears highly effective, safe, and generally well tolerated by most compared to alternative treatments.
Next I shall describe gross physiology of leptin and the SNS :)