Blog

18

2

In his latest salvo in the carb/insulin vs food reward battle, Gary Taubes writes (emphasis mine):

Well, for starters, the food reward/palatability hypothesis can’t explain the kinds of observations about obesity and weight regulation that I’ve been arguing in my books must be explained by any viable hypothesis of why we get fat. This is the primary issue, obviously, as a hypothesis that can’t explain the necessary observations is a failed hypothesis

Interestingly enough, Evelyn/CarbSane agrees that there must be a single hypothesis:

Taubes is right about one thing: a hypothesis must explain the epidemic

Hmmmm. Well, allow me to channel Wanda Sykes ... I think that must be one big a** hypothesis!

Seriously, it seems to me there are a number of things that may be contributing to the obesity epidemic, including industrial food, environmental toxins/chemicals, epigenetics (pre-natal/post-natal diet), other cultural factors (external stresses, types/amounts of physical activity), and probably many others I'm not listing here.

I like what Harry Rutter, director of the National Obesity Observatory in the UK said in his editorial Where next for obesity? -- obesity is a complex problem, not a complicated one:

The distinction is important. A complicated system might contain many different elements, with various interactions, but it is knowable and ultimately predictable: a Saturn rocket is not simple, but plans for it exist, and to calculate its trajectory and send astronauts to the moon and back is possible. A complex system does us no such favours. It is non-linear, subject to unexpected and unintended consequences, contains feedback loops, and displays emergent properties—it is more than the sum of its parts. This kind of wicked problem needs a different set of approaches to understand it and deal with it from those needed for issues that are merely complicated.

What do you think? Is there a single hypothesis that is likely to explain the obesity epidemic?

flag
1 
A single hypothesis can be multifactorial... – conciliator Nov 13 2011 at 0:05
Sure, that's my point re the one big *ss hypothesis. But it seems like many folks are focusing on one thing ... a la the 6 blind men and the elephant. – Beth-WeightMaven Nov 13 2011 at 0:17
"we eat too much...but why?" is the question. – ROB Nov 13 2011 at 19:12

12 Answers

12

Faith - yes there will someday be a single hypothesis that will explain the obesity epidemic...someday, maybe not in our lifetime, but....IT WILL BE MULTIFACTORIAL!

Possible factors

  • Hormonal (ala Taubes, et al)
  • Reward (ala Guyenet, et al)
  • Epigenetics (ala Cate Shanahan, et al)
  • Neolithic Toxin consumption (ala KGH, Cordain, et al)
  • Micronutrient deficiency (ala Paul Jaminet, et al)
  • Energy balance (ala conventional wisdom)
  • Mitochrondial dysfunction (ala J. Stanton, Peter at Hyperlipid)
  • Psychological factors (ala Emily Deans)
  • TBDs....if only we knew what those are

EDIT: Preemptive strike - the names I listed are just a few of players. Yes, there are others. The point of inclusion is that there are many people on the hunt. Maybe if we collaborate rather than compete, we can move this ball forward quicker.

Also, I do not currently agree with the carb--> insulin --> obesity paradigm. However, that low carb is effective as a therapeutic measure is not in question to me based on so many success stories. Do hormones matter...of course they do. So the point being that causation vs remediation are two related but different matters.

link|flag
2 
You spelled Cordain wrong! Now it looks like an instrument that people play in the French subway. (a Cordian). – Kamal Nov 12 2011 at 20:31
5 
Thanks Kumar, fixed it. Such the spelling snob you are. Kepp relax, enjoy you sucess, and the lovelee time – Aravind Nov 12 2011 at 20:33
4 
Simon - are you fucking kidding me? Yes, that what explains in the affluent area I live that there are so many obese people. – Aravind Nov 12 2011 at 20:48
2 
Poverty is definitely associated with (and probably a contributer to) obesity, but I see no reason (and I live in the UK) to think that (supposedly) increased social security causes it. I suspect (given that a stronger welfare state would reduce poverty) that increased social security would decrease obesity. – David Moss Nov 12 2011 at 21:31
6 
One "hypothesis" explains all obesity: Energy Balance. It's how it gets unbalanced. Sometimes there's an underlying genetic/hormonal issue (e.g. leptin deficiency) that drives overeating, then there's Lustig's hypothalamic obese kids (hyperinsulinemic with all else normal, overeat/underactive). There's the starving children/fat adults (starvation during development leads to greater fat/lean mass ratio and lower BMR), etc.etc. Gut flora? Rodents are hindgut fermenters. The list can go on. – Evelyn aka CarbSane Nov 12 2011 at 21:54
show 9 more comments
12

I like your post very much.

Maybe my little brain has a hard time grasping all of this, but...WHY DO SOME GURUS FEEL THE NEED TO PIMP THEIR HYPOTHESES AS "THE ONE TO RULE THEM ALL"?

You don't have to take very advanced biostats or mathematics to understand this simple concept: the reason multivariate regressions are done is because there are multiple variables. When it comes to human physiology, there are a bajillion variables, and when you add in environmental/emotional/etc factors and mix-and-match them, each person is going to be quite unique in the etiology of their weight gain.

I've gained weight eating fat, and lost weight eating fat. I've gained weight eating carbs, and lost weight eating carbs. I've tried lower food/tech reward and found it to be a nice way for me, personally, to reset some things that had spiraled out of control. Ketogenic diets also work great for me for certain purposes. But why try to push your individual experience or individual research on others?

If I remember correct, science increases in complexity as you go from the foundation on up: math to physics to chemistry to biology to physiology. Weight gain involves a bunch of those plus social factors. Why pretend to know all the answers? Everything is probably a little bit right. Except for healthywholegrains and arterycloggingsaturatedfat, that is.

link|flag
2 
Pimps and hos, bro. BTW - Now that you are saying it is multivariate like I did, I will have to change my opinion. – Aravind Nov 12 2011 at 20:24
3 
I wouldn't mind the pimping so much if it didn't seem like it was getting in the way of discovering what's really going on. – Beth-WeightMaven Nov 12 2011 at 20:27
1 
That's a slippery slope right there-- if you change your opinion, I'll have to change mine, and on and on. – Kamal Nov 12 2011 at 20:27
1 
Back in Black? Black Like Me? Jack Black? Okay, nap time. – Kamal Nov 12 2011 at 20:32
5 
People get fat because we eat more than we need to maintain bodyweight. Why do we eat more than we need? Food is extremely available, and we have made it more palatable than it was ever meant to be. Socially, we are pressured to eat. Physiologically, our bodyweight regulatory mechanisms are biased towards fat gain because our bodies love us so much they don't want us to starve to death. And finally, we are more sedentary than we have ever been throughout our evolution. I think that covers the main bases. Insulin is honestly not that important. You can get and stay fat on a ketogenic diet. – conciliator Nov 12 2011 at 23:48
show 6 more comments
11

No, there isn't a single hypothesis that covers ALL obesity.

But much of obesity has to do with the HPA axis dysregulation.

And there are lots of super-dysregulating paths that have not been a part of our thinking and discussion here..

There are many ways for the HPA axis to get dysregulated/inflammed, as well as for brain development to get very, very skewed (brain development is use dependent.) At certain times of your life prominently, for just one, in the early teens, your brain is busy pruning what I think of as neuronal "arbors" that are not used, and developing neuronal "arbors" like wildfire that ARE used. Depending upon what your brain is exposed to, this can be a big, big deal and spawn big, big problems. Just take one simple thought...we needn't get all fancy about this. What if your brain as a 14 year old is constantly experiencing insults due to the environment that make you spew cortisol(and other juicy chemicals!) like crazy. Do you think this might affect your brain? Do you think it is possible that these brain effects could be very wipespread, ie., affect more than one "function?"

So, let's look at some that we haven't looked at -

http://www.weightlosssurgerychannel.com/breaking-wls-news/childhood-obesity-often-linked-to-trauma.html/

Let me say that with this link, I do not agree with the conclusion, but I understand that the conclusion had to be "sold" to the general public on a TV station, so it had to be greatly simplified. Perhaps you can apply your super hacker brains to what might be the effects in the brains of these people whose brains were bathed in at least cortisol, people who could be described as never feeling safe. Might they have developed some cortisol related conditions? Might an outcome of their brains being bathed in cortisol ad infinitum have led to the inflammation of the HPA that we know occurs through a variety of mechanisims, leading to probable depression, anxiety and other states originating at young ages, AND a high probability, in my opinion, of lots of endocrine system disruption/dyregulation that can greatly affect energy use and appetite/feelings of hunger?

http://www.nospank.net/stevens.htm

In this link, I think that their projection that trauma (think: brain changes) becomes a path to obesity for about 8% of the obese is probably conservative. But still, combine that with Lustig's identification/defining of a syndrome of vagally mediated beta cell hyperactivity that leads to insulin hypersecretion and obesity and which is treated by insulin suppression, a phenomenon which may occur in about 20% of the obese population, and we are now batting about 28% of the obese population.That's a big chunk of the total.

http://www.chc.ucsf.edu/coast/faculty_lustig.htm

Now, take a think on the following...The purpose of this "answer" (the entire post, including all of the above) is not to be an "answer." It is to broaden the thought pool for thinking about the question.

"This study not only confirms that ADHD is a highly prevalent condition in severely obese patients, but that the treatment of ADHD is associated with significant long-term weight loss in individuals with a lengthy history of weight loss failure.

Levy suggests, as I did in earlier postings on this topic, that ADHD should be considered as a primary cause of weight loss failure in obese patients."

http://www.drsharma.ca/still-more-on-adhd-and-obesity.html

"Attention deficit disorder with or without hyperactivity (ADD or ADHD) and impulsiveness has been associated with increased risk for weight gain in both children and adults. In one study, ADHD was present in over 25% of all obese patients and 40% of patients with class III obesity. Reasons for this prevalent co-morbidity are unknown, but brain dopamine or insulin receptor activity may be involved.

Patients with ADD or ADHD usually manifest a long history (since childhood) of impulsivity, lack of concentration, decreased attention, inability to complete tasks, impairment in school or work performance and social dysfunction. Being “hyperactive” in the sense of the DSM-IV diagnosis of ADHD does not prevent the development or persistence of overweight and obesity in children."

http://www.drsharma.ca/obesity-attention-deficit-disorder.html

"Regular readers will recall that almost 30% of adults with severe obesity may have signs of attention deficit hyperactivity disorder (ADHD) and, when present, this can be a major barrier to weight management."

http://www.drsharma.ca/obesity-cognitive-behavioural-therapy-for-attention-deficit-disorder.html

"Childhood maltreatment or adverse experiences in five domains (emotional abuse, physical abuse, sexual abuse, emotional neglect and physical neglect) have been reported as highly prevalent in patients with binge-eating syndrome. In one study, 83% of patients with binge eating reported some form of childhood maltreatment: 59% reported emotional abuse, 36% reported physical abuse, 30% reported sexual abuse, 69% reported emotional neglect, and 49% reported physical neglect."

http://www.drsharma.ca/obesity-abuse-neglect-and-post-traumatic-stress.html

Now, some more nice science background from one of the best of the best:

"Childhood is a dangerous time." "The home is the most violent place in America."

http://www.lfcc.on.ca/Perry_Core_Concepts_Violence_and_Childhood.pdf

"We are not designed for this modern world. The human brain is designed for the natural world. Small, multi-generational family groups living together."

http://www.mentalhealthconnection.org/pdfs/perry-2009-presentation.pdf

http://www.healing-arts.org/tir/perry_childhood_trauma_the_neurobilogy_of_adaptation_states.pdf

And a piece of PubMed research, because PubMed excites us so:

http://www.ncbi.nlm.nih.gov/pubmed/18193182

http://www.ncbi.nlm.nih.gov/pubmed/15761171

http://www.uppitysciencechick.com/rohde_abuse_dep_obesity.pdf

For those who are prone to deeming the "psychological" to being "all in the head," be very, very clear that I disagree with you. And so does science.

With imaging, changes in the brain can be seen. Changes in the brain resulting from psychotherapy, which for too long was seen as another "all in the head" therapy, can also be seen/measured.

http://www.psychiatrictimes.com/display/article/10168/1926705

And to be really, really clear, nowhere in this post am I saying that if you are or have been a significantly overweight or obese person, that YOU suffered childhood trauma, have ADHD, or have suffered other linked adverse experiences.

This is a response to the question. And as I made clear from the outset, I do not buy into any single hypothesis for obesity, though I see some as far more compelling than others.

The purpose of this answer is to broaden the thinking field.

It is not to "prove" the information that I have presented, which is simply to get the "wheels turning."

I will leave you with a favorite quote:

"If 20 million people were infected by a virus that caused anxiety, impulsivity, aggression, sleep problems, depression, respiratory and heart problems, vulnerability to substance abuse, antisocial and criminal behavior, retardation and school failure, we would consider it an urgent public health crisis.(This was written in the mid 90's. Were Perry writing it now, he'd add obesity, I am sure.)

Yet, in the United States alone, there are more than 20 million abused, neglected and traumatized children vulnerable to these problems. Our society has yet to recognize this epidemic, let alone develop an immunization strategy." - Bruce D. Perry MD., PhD, The Child Trauma Academy

.

link|flag
1 
Nice answer mem! – Aravind Nov 13 2011 at 3:06
1 
good stuff here... – JayJay Nov 13 2011 at 14:53
2 
it is interesting... i could throw up the same studies to prove almost any point though, you can link ANYThing back to the brain – Mallory Nov 13 2011 at 17:11
2 
Mem, thank you for taking the time to post such a thought-inspiring answer. – PaleoGran Nov 13 2011 at 18:45
1 
My mind just exploded. That's a hell of a post, mem - give me a week to digest it all. – Jac Nov 14 2011 at 19:33
show 3 more comments
9

Our bodies and minds have evolved to respond to the properties of certain foods (and activities) that trigger hormonal, physiological and neurological responses within.

We are now eating foods that have been engineered to stimulate a subset of particular responses, but do not carry the nutritional payload expected by the body for that particular 'food signature'.

EDIT: Food engineers target those responses that translate to economic gain for the food-manufacturer.

You can imagine how in our evolutionary past Hebbian learning would tightly bind the nutritional quality of food and palate/taste...and perhaps even activity (predators hunt when hungry, whereas we jog having carbed-up).

Activity and lifestyle are also important factors - not to burn off energy, rather as a mechanism with which our body can understand the world - through energy expenditure and so forth.

How can I best summarise this....if someone opened up a computer and chucked a load of seawater in to it how would you work out which bit got destroyed first? The motherboard? CPU? RAM? Some other bit? By this I mean that there are several important functions within the body - not simply organs, but also messaging systems in the form of hormonal cascades and so forth. You can screw up any one of them, or several at the same time - and cause deleterous effects 'downstream'....be wise with your choice of 'inputs'.

link|flag
Dude this is a great comment and you and I see this issue. Plus one. – The Quilt Nov 13 2011 at 16:09
And this is why I have some days of very high protein, some days low protein, some days high calories and some days of low calories (IF), some days high carn and some days VLC! And this is also why there is seasonal bias in my diet (and in my sleeping patterns and in terms of exposing myself to cold). I have freed my 'inner actuary' to manage the BF for me and let him choose the appropriate metabolic pathway! – Asclepius Nov 14 2011 at 13:11
I should probably take this opportunity to publicise J Stanton's Why Are We Hungry series which gives a scientific backbone to this idea: gnolls.org/2304/… – Asclepius Nov 14 2011 at 15:18
ASCLEPIUS. u rock!!!!! – grace Nov 15 2011 at 6:09
4

When I look at factory company photos from the 1920s through the 60s with all the employees lined up on risers, there is never a fat, obese, slightly overweight employee...ever.

They ate real food like lard, butter, beef, chicken, unadulterated veggies and no fruit from places other than the local environs. No hybridized dwarf wheat, no hydrogenated anything, no margarine, none of the unpronounceable ingredients on packaged "foods", no soybean,canola,veg,saffower or other frankenstein oils.

The one hypothesis that makes sense to me is the introduction of "foods" that our bodies only know how to store. And that has only happened since the mid sixties.

We are living the legacy of Ancel Keys and the lipid hypothesis that eating fat will kill you.

That is the only hypothesis that works for the advent of obesity. Take away neolithic foods and the obesity epidemic would abate.

link|flag
1 
From 1920-1960 fruit usually came from a can. Strawberries were in season for about 3 weeks. The only lettuce was iceberg. – thhq Nov 13 2011 at 3:58
3 
Fruit in a can did not contain HFCS back then. And my parents were both office workers during the early 50s and both were slim and athletic. Then started the decline into fatdom in the 60s as newly minted neolithic convenience foods were introduced. Both died of complications of fatdom far too early. Butter was good sat fat. And bacon grease was the favorite fat of my gmother and mother used Crisco for making pies. The flour was not highly hybridized in the 40s-50s by Monsanto. – Dextery Nov 13 2011 at 4:46
1 
@thhg Tell me why the lipid hypothesis did not result in the advent of obesity. People avoided real food and were sold margarine and Crisco as a superior replacement for lard. Boxed wheat products were not GMO. Frankenoils replaced butter and lard. Very few people prior to Ancel were fat. – Dextery Nov 13 2011 at 17:04
3 
Dude, the title of the posting is "Because everything you think you know about obesity is wrong" Obviously you did not even bother to open up the link before you got your feathers ruffled. – Dextery Nov 13 2011 at 21:42
3 
Ahh Zoe... A woman who lost some weight and maintained it on a high fiber high veggie, no animal flesh ovo lacto vegetarian diet but tells others to eat otherwise as the key. – Evelyn aka CarbSane Nov 14 2011 at 2:54
show 8 more comments
3

I wonder if part of finding the one-hypothesis-fits-all will be a series of trials with human volunteers of at least 2 types: healthy folks with great metabolism and obese folks with clearly deranged metabolism. I'm thinking the easier challenge would be showing that the deranged metabolism can be shifted back to healthy using the hypothesis, but the tougher challenge would be shifting healthy subjects to a "sick" metabolism (and back) due to ethical issues.

Anyhow, if you can't affect metabolism in predictable ways how can you prove a hypothesis?

link|flag
3

I had thought about posting this as a question, but any port in a storm. Here's my hypothesis.

Obesity is caused by fast food.

Feel free to gut it, but here's why I believe it, in short form. Easy food accessibility, fast eating, and good flavor result in overconsumption before satiation can happen physiologically. Super Size Me illustrates the hypothesis.

The techno body-as-chemistry-lab hypotheses are just not broad enough to describe obesity as a social phenomena. We're not gathered on the game trails anymore because it's so easy to use the drive throughs.

link|flag
4 
This is actually simplistic but if one had to put it in 6 words, there could be none more accurate. Fast food = cheap. Fast food = engineered and tested by food scientists to maximize "eat more". Fast food = high calorie/low nutrient/low protein v. carb&fat. Fast food = no effort to attain, heck drive thru! Fast food = ready in 0 min (or under 10 for frozen/packaged crap). Fast food = higher in sugar/salt/fat than palatable w/o emulsifiers/stabilizers/magic. Fast food = not knowing what's in there (or wanting to). Fast Food = Fattening Food. FF = FF. Can we put that eq on the Quilt?? – Evelyn aka CarbSane Nov 12 2011 at 22:05
7 
Does fast food contribute to obesity in many cases? Yes. Is it THE cause of obesity? No. I'm sure there are millions of obese people who don't eat fast food. Also, much of "Super Size Me" has been debunked by Tom Naughton in "Fat Head" ( fathead-movie.com ) – Ed Nov 12 2011 at 22:07
2 
What struck me this morning was how I've been conditioned to bolt down my food. If I do that leptin and satiation don't have a chance. I used to eat rapidly until I was volumetrically full which is way beyond being satisfied. Now I savor my food and take my time eating. – thhq Nov 13 2011 at 0:15
1 
My n=1 has nothing to do with fast food. I think I had my first Macca burger when I was in my 20s, and I was obese by then. – Jac Nov 14 2011 at 19:37
I was fat eating 60's home cooking. No sense of portion control, just eat until full. It was mostly fat/sugar/starch because meat was expensive. We drove 40 miles to get a mcdo burger back in the day, an exotic treat for fifteen cents. – thhq Nov 14 2011 at 20:38
3

Hi Beth ... Just to clarify my position, I do NOT believe there is a single hypothesis that can explain obesity. Indeed to say there is one single hypothesis is downright ridiculous in my opinion. Perhaps I need to be more careful in my wording there, because when we're talking about obesity hypotheses these days, the focus is basically on the epidemic. Specifically: Why did obesity rates snowball from sometime in the late 70's to mid 80's?

This is where Taubes' hypothesis fails before it even comes out of the gate. I grew up during that time so I know what we ate as kids that did not make us all rolly polly pudge balls. Back when "kid's cereals" went by names like Sugar Frosted Flakes ... and kids put more sugar on top of that.

So let me rephrase a bit and say that any theory of modern obesity must be consistent with the observation of the obesity epidemic we are seeing. It does not need to explain all of it, but it must be consistent with it at the very least.

In this regard, Stephan Guyenet's rendering of food reward comes closest but doesn't account for what I believe to be other factors. Perhaps this is why he called it A dominant factor. Activity does play a role, and I'm not talking exercise, I'm talking little stuff that adds up. Taubes doubled down in WWGF. It's the carbs, insulin, only the carbs, and calories have nothing to do with it. Dietary fat has no influence on body weight.

link|flag
1 
And parents made brownies, cookies and cakes on weekends and pancakes with maple syrup ... and fruit was locally grown and very ripe vs the cardboard sold as fruit today (much less sweet.) Also, kids drank whole milk and ate lot of bacon and sausage and sandwiches with mayo for lunch--and were skinny. – Nance Nov 12 2011 at 21:08
1 
i was born in the 60s and Mom knew nothing about nutrition having been raised in a broken family; no one passed on any food wisdom to her. i was fat before i hit my first birthday and both my sisters became over weight in their early 20s. i still struggle with weight inspite of decades of effort. conversely my children have no issues with weight. – sage_ Nov 12 2011 at 21:34
2 
Wrt 'food reward' - I have known obese friends whose weight was stable at 30%BF. They'd diet down to 15%BF, then (eventually), give in to their old ways and rebound back up to 30%BF where once again (and despite their bad diet), their weight would eventually stabilise. I'm sure we all know folk like this. So how can food be hyperpalatable for them until they are back upto to a particular level of obesity, from where suddenly, according to the idea of hyperpalatability, they suddenly find previously hyperpalatable foods no longer hyperpalatable? – Asclepius Nov 12 2011 at 21:43
1 
@Asclepius: I think Stephan would answer this with a reset of the setpoint which I tend to disagree with. I think it speaks to "passive overeating" of calorie dense foods. In this way, folks need not be gluttons in the classic sense -- after all, I know obese people who eat two sometimes just one meal per day. But have you checked the calorie counts for a "normal" meal at any of those family style restaurants? Easily enough calories for Mark Sisson for a day. So you hit on it -- they return to old habits, then gain back until they are in caloric balance. – Evelyn aka CarbSane Nov 12 2011 at 21:48
Evelyn, thanks for the comment. I find your comments/blog posts re the affects of perpetual overnutrition compelling as well. – Beth-WeightMaven Nov 13 2011 at 0:31
show 6 more comments
3

It is really basic. We have, in our society a combination of unlimited food availability, in most cases, and no requirement to expend energy in order to get the food. We don't pick it, catch it, chase it..........we just buy it. Your body uses energy. When you move more, it uses more energy. If you can walk into a store, reach into your pocket and pay someone for it, you haven't expended much energy in relation to the caloric intake. It's really that simple. Lots of information about this subject at www.PrimitiveHealth.blogspot.com

link|flag
1 
And when we walk into the store, we don't buy that standby appetite suppressant tobacco as much as we used to. So defy conventional wisdom and your surgeon general! Smoke em if you've got em! – thhq Nov 13 2011 at 14:55
I don't disagree with this, but the interesting question (to me anyways) is what protects the 30% or so who don't become overweight or obese in this environment. Is it all genetics? – Beth-WeightMaven Nov 13 2011 at 15:45
Here's an idea beth. 100 years ago we were all more tribal. We ate our national diets, whatever they were, and conformed to certain cultural norms. All of this is fading, for better or worse. I can eat any diet, anywhere, anytime, but I'm missing the cultural norming to know how much sauerbraten, or pho, or chili verde is enough. Perhaps the 30% is a relict population which maintains its cultural memory. – thhq Nov 13 2011 at 16:40
I think the cultural aspect is critically important too. – Beth-WeightMaven Nov 14 2011 at 12:10
3

Beth this is a great question and plus one for asking it. My answer is short. No I don't see it that way at all. It is many domino's hitting our biochemistry often and sequentially that erodes efficiency.

link|flag
2

I think Taubes does a better job of explaining how people don't get lean or get flabby vs. actually get obese. Presently, I'm convinced that it's the result of the massive recent increase in dietary excitotoxic amino acids (typically in the form of MSG and aspartame) that damage the leptin receptors of the hypothalamus' arcuate nucleus (which is unshielded by the blood-brain barrier).

link|flag
Interesting! Me, I find both brain and body arguments compelling (before Peter@Hyperlipid went all in with Taubes, he had a great post re NADS-related hepatic failure). I just wonder whether these are chicken or egg issues. – Beth-WeightMaven Nov 12 2011 at 20:16
1 
You don't need to blame excitotoxins. You could simply say that humans bodyweight regulatory mechanisms are biased towards weight gain as a result of our evolution. If a rat gets fat, he cannot escape predators. If a human gets fat, he can survive a famine. It could be as simple as saying humans are predisposed to fat gain. No need to invoke leptin, which works marvelously at its main function: to stop people from starving. – conciliator Nov 12 2011 at 23:45
1 
And besides, acute overfeeding of fat doesn't trigger increased satiety through leptin increases, it does it by suppressing ghrelin. In the long term yes adipose tissue creates leptin. And NEAT, which is also hugely important, is not under the direct power of leptin. Orexins are important here too. So are catecholamines. We have many mechanisms of maintaining bodyweight, and yet they all suck, in general. Except in cases of losing weight, they all seem to work. To me, that implies the methods aren't broken, they are just meant to work better for keeping us plump than keeping us lean. – conciliator Nov 13 2011 at 1:03
2 
I will be sure to not INJECT my pet RATS with LARGE quantities of MSG. On a more serious note, it is a very interesting paper, but we have to keep in mind there is human research that should take precedence. The amount of things that work on rats and do not work on humans is truly mind boggling, and also sad, because I think we could solve the rat obesity crisis. Human research finds drops in leptin levels correlate to increased hunger when on a diet, which seems to imply leptin is working well and not saturating receptors. – conciliator Nov 13 2011 at 1:51
1 
One could not argue that they are being injected unless they are actually being INJECTED. There is a nontrivial difference between injection and ingestion. And if you want to use epidemiological studies I can go find a whole host of evidence for whole grains being healthy. I can also point to obese people who don't consume MSG or aspartame. Not to mention that obese people who lose weight don't display signs you would expect of those with some leptin deficiency such as hyperphagia. Obese people who diet down gain the weight back due to psychological reverting to old habits. – conciliator Nov 13 2011 at 6:07
show 13 more comments
-1

Three words: Taubes Taubes Taubes.

EDITED TO ADD:

The question is, what caused the epidemic, which means we can ignore the baseline rate of obesity that existed in statistical studies before the advent of the epidemic. Thyroid problems? Ignore 'em! Pituitary problem? Fuggetaboutit!

That stuff does NOT count!

What counts is, the low-fat high-carb heart-healthy propaganda that sent the whole nation into a death march. That's what counts!

link|flag
4 
Meh. Taubes is crayon science. And it is more of the weight-loss kool-aid - "just do this one thing to lose weight" – cut calories, cut fat, cut carbs, eat grapefruit, eat paleo lemon squares, etc… – Paleo2.0 Nov 12 2011 at 23:14
4 
Let's hear more about these lemon squares plz. – Travis Culp Nov 12 2011 at 23:25
3 
If you love him so much, why don't you marry him. – Bread-Eating Beelzebub Nov 12 2011 at 23:25
I'm still not getting it huey. Your response can be taken a couple of ways. First one is that Taubes is the cause of the obesity crisis. I don't think so. Second one is that it's football Saturday and you're shouting out a cheer for Taube's hypothesis – thhq Nov 13 2011 at 0:07
1 
huey, also please refrain from posting sexual stuff about me (or others). – Bread-Eating Beelzebub Nov 13 2011 at 0:10
show 3 more comments

Your Answer

Not the answer you're looking for? Browse other questions tagged or ask your own question.