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  #1   ^
Old Fri, Jun-01-18, 12:03
BillyHW's Avatar
BillyHW BillyHW is offline
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Default List Of All Obesity Cause Theories

Hey folks, I want to compile a list of all the various theories that have been proposed throughout history for the causes of and contributers to obesity. Please add any to the list.

Gluttony. You are fat because you eat to much and can't control yourself.

Sloth. You are fat because you are lazy and don't exercise.

Sedentary Lifestyle. You are fat because modern society, things like cars and computer jobs and video games, have led to a much more sedentary lifestyle, which makes you fat.

Thrifty Gene. We are genetically programmed by evolution to store up as much possible energy in the form of fat during times of plenty so that we can survive during times of famine.

Toxic Environment. You are fat because there is tasty fast food everywhere you look.

Marketing. The food manufacturers invented the Mattel And Mars Bar Quick Energy Chocobot Hour and we can't resist their mind manipulations.

Supersizing. Portion sizes have gotten out of control and are making you fat.

Hyper-Palatability. The food we make these days, especially processed food, is just so tasty we can't stop eating it.

Stress/Cortisol. Stress induces cortisol production making you fat.

Bad Sleep. Bad sleep or lack of sleep screws up your body and makes you fat, and people are getting less sleep these days than they used to because electricity and reasons.

Volumetrics. Concentrated calories make us fat because we don't feel full.

Genetics. You are genetically predisposed to being fat.

Fat Makes You Fat. Fat is higher in calories per gram than either protein and carbs, so eating fat makes you fat.

Empty Calories. Sugar/Pop is an empty calorie so it makes us fat.

Bad Habits. You picked up bad habits from your parents and family, which made you fat.

Snacking. Too frequent eating makes you fat, because you get a constantly raised blood sugar or insulin level.

Not Snacking. Larger, infrequent meals make you fat because the blood sugar and insulin peaks and valleys are larger.

Gut Biome. Something is wrong with the bacteria in your gut, which makes you fat.

Virus. There's a virus going around, that makes you fat.

Vegan Superiority. We were never meant to eat animals, therefore omnivores and carnivores are fat.

Agricultural Revolution. We were never designed to eat refined sugars, starches or dairy, which make us fat.

Casein is a drug. European-derived cattle casein protein acts like a drug in your brain, making you gorge on it and get fat.

Dopamine (Carb/Food Addiction). Carbs (or food in general), causes dopamine hits similar to drug and alcohol addictions. Fat people are literally addicted to food, but unlike drug and alcohol addicts, they can't go cold turkey, because we all need food to survive, and so it's particularly hard to beat a food addiction.

Artificial Sweeteners. Artificial sweeteners trick you into being fat.

Hyper-Glycemia. Excess and roller-coaster blood sugar levels caused by carbohydrate intake (especially refined carbohydrate lacking fibre) cause hunger and make you eat more and make you fat. Closely related to Hyper-Insulinism.

Hyper-Insulinism. High insulin levels make you fat, so therefore insulin-stimulating foods make you fat. Also foods that cause insulin-resistance (like possibly Sugar/Glucose/Fructose/Starch/Carbs). Closely related to Hyper-Glycemia.

Leptin-Insensitivity. Something is causing leptin-insensitivity, possibly hyper-insulinism which makes you hungrier and so you eat more and get fat.

Added to list after original post:

Affluence. - You are fat because you are rich enough to afford lots of food. In a number of societies being fat was seen as a sign of being well off, and was desirable.

Last edited by BillyHW : Fri, Jun-01-18 at 13:59.
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  #2   ^
Old Fri, Jun-01-18, 12:04
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BillyHW BillyHW is offline
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  #3   ^
Old Fri, Jun-01-18, 13:28
Verbena Verbena is online now
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Affluence - you are fat because you are rich enough to afford lots of food - You said "historical" reasons, right? In a number of societies being fat was seen as a sign of being well off, and was desirable. (That shouldn't be in the past tense; I believe there still are societies with that perception)
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Old Fri, Jun-01-18, 13:37
M Levac M Levac is offline
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There's only two hypothesis and they're mutually exclusive because causality is reversed, i.e. we grow fatter cuz we eat more, we eat more cuz we're growing fatter. CICO, where calories-in (CI) is greater than calories-out (CO). And carbohydrates-drive-insulin-drive-excess-fat-accumulation, where fat tissue is regulated by insulin, and insulin is disrupted/stimulated by dietary carbohydrates. All others are just variations of these two. Try to categorize your list like that, you'll see what I mean.

Also, check my blog (link in my signature) and the post titled "Paradigm - Progress". It could be considered a hypothesis on its own, though I prefer to think of it as a paradigm, a collection of hypotheses. This paradigm fits in the carbs-insulin-fat-tissue category. Just ignore the part about my personal health.
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Old Fri, Jun-01-18, 13:39
Verbena Verbena is online now
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#8 on your list - Hyper-palatability. Is this really true? I know it gets tossed around alot, but I personally cannot believe it. Yes, I know that processed and fast foods are "the bad guys" but everyone still eats them "because they taste so darn good". Or, low carbers don't eat them, but then are consumed by cravings, "because they taste so darn good". But really? Is it a factor of my age (66), or my upbringing, or my genes, or what? None of that junk appeals to me, never has. None of it elicits feelings of loss now that I "can't" eat it anymore. Why would I choose a substandard fast food hamburger over one I could make myself at home? Why would I think that cinema popcorn was superior to freshly popped corn that I used to make at home? Why would I prefer some over sweet cola to homemade lemonade (OK, I can sort of see that, through my friends' eyes, though I have never liked them myself)? Sorry, kind of a thread hijack, but I do sometimes wonder.
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  #6   ^
Old Fri, Jun-01-18, 13:55
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BillyHW BillyHW is offline
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Quote:
Originally Posted by Verbena
#8 on your list - Hyper-palatability. Is this really true? I know it gets tossed around alot, but I personally cannot believe it. Yes, I know that processed and fast foods are "the bad guys" but everyone still eats them "because they taste so darn good". Or, low carbers don't eat them, but then are consumed by cravings, "because they taste so darn good". But really? Is it a factor of my age (66), or my upbringing, or my genes, or what? None of that junk appeals to me, never has. None of it elicits feelings of loss now that I "can't" eat it anymore. Why would I choose a substandard fast food hamburger over one I could make myself at home? Why would I think that cinema popcorn was superior to freshly popped corn that I used to make at home? Why would I prefer some over sweet cola to homemade lemonade (OK, I can sort of see that, through my friends' eyes, though I have never liked them myself)? Sorry, kind of a thread hijack, but I do sometimes wonder.


I'm not endorsing any particular theory, I just want to create a list of all the ideas thrown out there, right and wrong. Debunkings are welcome in this thread for purposes of discussion. Please feel free to offer your debunkings of any particular theory people.

Last edited by BillyHW : Fri, Jun-01-18 at 14:00.
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  #7   ^
Old Fri, Jun-01-18, 13:55
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BillyHW BillyHW is offline
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Quote:
Originally Posted by M Levac
There's only two hypothesis and they're mutually exclusive because causality is reversed, i.e. we grow fatter cuz we eat more, we eat more cuz we're growing fatter. CICO, where calories-in (CI) is greater than calories-out (CO). And carbohydrates-drive-insulin-drive-excess-fat-accumulation, where fat tissue is regulated by insulin, and insulin is disrupted/stimulated by dietary carbohydrates. All others are just variations of these two. Try to categorize your list like that, you'll see what I mean.

Also, check my blog (link in my signature) and the post titled "Paradigm - Progress". It could be considered a hypothesis on its own, though I prefer to think of it as a paradigm, a collection of hypotheses. This paradigm fits in the carbs-insulin-fat-tissue category. Just ignore the part about my personal health.


I agree with your main point, but I just wanted to list all the variations. I realize there's a lot of overlap in these theories and they are not meant to be mutually exclusive.
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  #8   ^
Old Fri, Jun-01-18, 14:00
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BillyHW BillyHW is offline
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Quote:
Originally Posted by Verbena
Affluence - you are fat because you are rich enough to afford lots of food - You said "historical" reasons, right? In a number of societies being fat was seen as a sign of being well off, and was desirable. (That shouldn't be in the past tense; I believe there still are societies with that perception)


Thanks, I've added this to the list in the original post.
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  #9   ^
Old Sat, Jun-02-18, 01:42
M Levac M Levac is offline
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Ghrelin excess - makes us eat more, we grow fatter.

Insulin resistance - excess insulin makes us fatter, lean tissue is insulin resistant, and fat tissue remains insulin sensitive.

Fat tissue glucose sink - fat tissue is protective, it absorbs excess glucose, turns it into fat, fat tissue grows bigger.

Insulin-induced lipohypertrophy - caused by chronic hyperinsulinemia, cannot be reversed by diet alone, originally discovered in diabetes type 1 where we inject insulin in the same spot for years, specifically called insulin-induced lipodystrophy.

Leptin deficiency - leptin causes us to stop eating, absence of leptin allows us to continue to eat, we eat more, grow fatter.

Hypothyroidism - metabolism drops, we grow fatter.

Semi-starvation - metabolism drops, stays there (subborn metabolism), we grow fatter. The opposite is hyperactive metabolism.

Various vitamin and mineral deficiencies - all involved in some way in regulation of glucose and fat metabolism, we grow fatter.

Fatty liver - leads to liver insulin resistance, excess insulin, excess blood glucose, we grow fatter, diabetic type 2.

Inflammation - caused by fat tissue secretions (necro-something factor or whatever), caused by fat tissue excess growth, leads to further fat tissue excess growth.

Fructose - causes or leads to fatty liver, and so forth with insulin resistance and hyperinsulinemia and all that jazz, we grow fatter.

Ketones shunt hunger - carbs stimulate insulin, shuts down ketogenesis, absence of ketones, we eat more, we grow fatter. A well-accepted principle of low-carb, due to simultaneous higher blood ketones and lower hunger.

Metabolic advantage - low-carb diet causes greater energy expenditure than high-carb diet, balance determines fatter/leaner.

Thermic effect of food - foods cheap to digest and absorb make us fatter, foods expensive to digest and absorb make us leaner.

Yo-yo dieting - leads to low metabolism, we grow fatter.

Genetic predisposition - our parents were fat, that's why we're fat.

Generational epigenetics - similar to genetic predisposition, our parents were fat because of some environmental agent that altered their fat tissue and/or regulation thereof in some way, we inherited this alteration, that's why we're fat.

Pica - a form of eating disorder where we are compelled to eat something that isn't normally nutritious, a variation of pica where we are compelled to eat something that is caloric and/or stimulates insulin, we grow fatter.

Weak will, lack of willpower - we eat too much cuz we just can't help ourselves, we're morally defective.

We're already fat - we're heavier, less inclined to be active, become sedentary, we grow even fatter.

Age-related metabolism drop - the older we get, the lower our metabolism drops, we grow fatter.

Opiod peptides derived from food proteins (wheat gluten and alpha casein) - we get addicted, eat more, grow fatter.

Abdominal pressure on pancreas - high food volume increases abdominal pressure, pushes on pancreas, higher insulin secretion, we grow fatter.

Lipostat - something disrupts normal homeostasis of fat mass, we grow fatter.

Sedentary-induced insulin-resistance - activity leads to insulin sensitivity, lack of activity leads to insulin resistance, we grow fatter.

Stress/comfort foods - leads to eating comfort foods, leads to eating more, we grow fatter.

Self-image problem/comfort foods - any problem with self-image such as lack of confidence, failure or physical flaw, leads to comfort foods, leads to eating more, we grow fatter, leads to further self-image problem, etc.

Poverty - leads to eating empty calorie foods, we grow fatter.

Exertion - we work hard, get hungry, eat more, grow fatter.

Growth hormone deficiency - GH causes fat tissue to shrink and/or remain normal size, absence of GH allows fat tissue to grow bigger. GH also affects all other tissues including lean tissue and muscle, leading to change in metabolism and so forth.

Estrogen excess/estrogenic and/or estrogen-like foodstuff (soy anyone?) - women are naturally fatter than men by about 50% (for example, 15% bodyweight vs 10% bodyweight), excess estrogen in men causes gender modification (turns them into women, or gives them female traits), fat tissue redistribution more like a woman's, also modifies muscle distribution more like a woman's.


I had a link to a page that listed a bunch of drugs and medications that have the ability to make us fatter or leaner, can't find it at the moment, but this would be called something like drug-induced appetite/hyperphagia and/or drug-induced excess fat accumulation.
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Old Sat, Jun-02-18, 01:51
M Levac M Levac is offline
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Vagus nerve injury - vagus nerve links gut and brain, vagus nerve injury alters hunger/satiety communication, we grow fatter or leaner.
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Old Sat, Jun-02-18, 05:04
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teaser teaser is offline
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I think thrifty gene should probably be replaced by thrifty genetics. There was a study in mice looking at aggression, breeding aggressive mice to aggressive mice and then looking for "aggression" genes. They were hoping for a few major differences, what they got were hundreds of tiny variations.

The insulin resistance leading to obesity thing is sort of contested, alternately maybe once adipose is reaching a certain capacity, there's spillover into the liver and visceral fat depots, and this, increases insulin resistance. I think it's likely a mix, increased insulin is a vote for greater obesity, but the insulin is pushing against a lot of resistance.

In rodent models fructose is more of a model of insulin resistance, but there have been a few studies where feeding animals a high fructose diet for a while, which does make them insulin resistant, and then switching them to a "high fat" but importantly non-atkins diet makes them fat, in this case the previous insulin resistance might set them up to get fatter, though the researchers point to leptin (which doesn't exactly put insulin in the clear, anyways). But these animals didn't develop insulin resistance while getting fat, but before getting fat. Insulin drives fat storage, but trees don't grow to the sky, fat tissue past a certain size is resistant. Sometimes insulin being higher after somebody is fat instead of before is used as evidence that insulin is not fattening. Doesn't work that way, insulin is most fattening when our adipose is most sensitive to it.

So--if you manage to become insulin/leptin resistant without actually getting fat, maybe since your fat cells aren't overloaded, there's some other diet out there that you shouldn't be looking for that would allow you to add obesity to your other problems. If you get fat and insulin resistant at the same time, this is less likely, your fat tissue is nearer its maximal capacity.

https://www.ncbi.nlm.nih.gov/pubmed/18703413

Quote:
Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding.
Shapiro A1, Mu W, Roncal C, Cheng KY, Johnson RJ, Scarpace PJ.
Author information
Abstract
It has been suggested that increased fructose intake is associated with obesity. We hypothesized that chronic fructose consumption causes leptin resistance, which subsequently may promote the development of obesity in response to a high-fat diet. Sprague-Dawley rats were fed a fructose-free control or 60% fructose diet for 6 mo and then tested for leptin resistance. Half of the rats in each group were then switched to high-fat diet for 2 wk, while the other half continued on their respective diets. Chronic fructose consumption caused leptin resistance, while serum leptin levels, weight, and adiposity were the same as in control rats that were leptin responsive. Intraperitoneal leptin injections reduced 24-h food intake in the fructose-free group (73.7 +/- 6.3 vs. 58.1 +/- 8 kcal, P = 0.02) but had no effect in fructose-fed rats (71.2 +/- 6.6 vs. 72.4 +/- 6.4 kcal, P = 0.9). Absence of anorexic response to intraperitoneal leptin injection was associated with 25.7% decrease in hypothalamic signal transducer and activator of transcription 3 phosphorylation in the high-fructose-fed rats compared with controls (P = 0.015). Subsequent exposure of the fructose-mediated, leptin-resistant rats to a high-fat diet led to exacerbated weight gain (50.2 +/- 2 g) compared with correspondingly fed leptin-responsive animals that were pretreated with the fructose-free diet (30.4 +/- 5.8 g, P = 0.012). Our data indicate that chronic fructose consumption induces leptin resistance prior to body weight, adiposity, serum leptin, insulin, or glucose increases, and this fructose-induced leptin resistance accelerates high-fat induced obesity.

Comment in
Fructose-induced leptin resistance: discovery of an unsuspected form of the phenomenon and its significance. Focus on "Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding," by Shapiro et al. [Am J Physiol Regul Integr Comp Physiol. 2008]
PMID: 18703413 PMCID: PMC2584858 DOI: 10.1152/ajpregu.00195.2008


https://www.ncbi.nlm.nih.gov/pubmed/18703413


I think Seth Robert's Shangri-la diet deserves a mention as well. The basic idea is that exposure to food increases our body fat set point. Taking in flavourless calories, like sugar water or flavourless oils, or eating wearing noseplugs, or eating unfamiliar foods is supposed to lower the set point. This is not quite "palatability." It's more like the body have certain conditioned responses to food, more pleasant/stronger flavours send a stronger signal.

I'm not supporting this idea in its entirety, but the idea that my body acts as if it has an entirely different set point depending on my diet, Pizza and cheerios>Atkins>stricter ketogenic has panned out pretty well for me. But of course you notice these line up from most to least insulin.

Shangri-la dieters talk about appetite suppression, and of course if it really does work for them, a suppressed appetite equals a decrease in insulin. Sometimes Taubes and others argue that a low calorie diet is a low carbohydrate diet, so maybe that's why it works for those it does work for, but you don't really have to mention carbs there, even if you just dropped calories by dropping fat, that would drop insulin. The question is whether or not your body is going to throw a hissy fit when you do that.
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Old Sat, Jun-02-18, 07:38
M Levac M Levac is offline
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Two subsets of insulin-makes-us-fat:

1. During or immediately after a meal (post-prandial) - insulin is at its highest on a curve, more fat goes into fat tissue than otherwise.

2. In-between meals (fasting insulin) - insulin is higher than otherwise, less fat comes out of fat tissue over time.

Often the first subset is understood as the main idea behind insulin in discussions. And often I and others point out how the second subset is more likely. The reason is simple logistical efficiency. It's more efficient to store meal energy quickly into fat tissue (and other storage organs and tissues like the liver and muscles for glucose/glycogen), and it's more efficient to drain fat tissue in-between meals slowly. Perhaps as a result of natural selection, where eating a meal quickly lends more to survival than eating a meal slowly, and having a constant internal supply over a long period also lends itself more to survival.

The greater effect isn't with higher rate, but with longer period. This is due to the relative rate increase/decrease needed to obtain the same effect from either a meal or in-between. It's not that easy to stuff double the energy in a meal in the same short period (because the rate of storage is aleady so high), but quite easy to double or halve the rate of release in-between meals (because the rate of release is already so low).

The second subset can be rephrased as thrifty gene, but instead of "storing as much energy as possible", it's "releasing energy as slowly as possible". This then gives us yet another hypothesis:

Efficiency of energy usage - the more efficient we are at using energy, the slower the energy release from storage we can tolerate, the fatter we can grow. The converse is energy waste, where the more energy we waste, the less likely we are to grow fatter. For example, brown fat cells instead of white fat cells. A subset of this is the slower the rate of release from storage, the more efficient we become at using energy, and round we go.
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Old Sat, Jun-02-18, 08:07
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s93uv3h s93uv3h is online now
 
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Ancel Keys

low fat / high carb SAD diet

1977 Dietary Guidelines
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Old Sat, Jun-02-18, 08:42
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teaser teaser is offline
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From what I've seen obesity comes with an increase in fatty acid turnover in fat cells--so for the question of is release decreased, or storage increased, it's sort of both but with a net result of increased fat storage.

I'd say SAD diet instead of low fat/high carb SAD diet. I got fat on carbs, but they were fatty carbs. Also some of the evidence for things like volumetrics might depend on fatty foods. People eat fat free pizza etc. five days a week and then gorge on real pizza on the weekend. I know I did.

There are some rodent experiments with intermittent sugary or fatty diets. Fat free potato chips one day, fatty potato chips the next, was more fattening than giving animals the one or the other type of chip every day. Artificial sweetener with their chow one day, sugar the next was more fattening than sugar always or artificial sweetener always.
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Old Sun, Jun-03-18, 11:19
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BillyHW BillyHW is offline
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Plan: Keto + IF
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Unmindful Eating. You read a newspaper during breakfast, and without realizing it, you eat too much, therefore you are fat. Also eating while driving, eating while using your smartphone etc...
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