Monday 9 August 2010

Dopamine and Weight Loss

In the book 180 Degree Metabolism: The Smart Strategy for Fat Loss, I mentioned how the primary driver of leptin resistance and/or excess fat gain in general without the corresponding decrease in hunger and increase in metabolism is unknown. With some All-American speculation, I came up with what I believed to be the 5 most common causes of excess fat accumulation.

Dieting, stress, inflammation, and excessive fructose intake all got their own special chapters. In addition to that, I mentioned Seth Roberts and the Flavor-Calorie Association Theory of obesity that I got super nerded-out on last week in THIS POST.

Out of all causes of obesity; however, there is no doubt that Seth’s explanation – that foods that exert the most stimulus to the reward centers in our brains and thus causing a rise in weight set point (the “ponderstat”), is the most promising. Not only is it the most promising, but it helps to explain multiple phenomena. Let’s get into it a little deeper, and clear up some of the misconceptions that metastasized last week.

First off, I explained my current diet, which contains about 1/3 of the fat that I have been eating over the last several years (call it 60-70 grams per day averaged out throughout the week as opposed to 180-210 grams per day) as “bland.”

Oops, “bland” is a major misnomer. Actually, my food is FAR more flavorful than it has been over the past several years, as I have substituted things like spices and potent salsa LIKE THIS for butter, creamy cheeses, heavy use of coconut oil, and fatty cuts of meat. No one would argue that salsa has less flavor than any of the above-mentioned foods. My salsa is like a nuclear bomb hitting my tongue.

But what my food is, or at least was initially, was less pleasurable to eat. Eating boiled potatoes with salsa as opposed to eating fried potatoes covered in parmesan cheese and truffle oil has a different level of satisfaction – just like eating a strawberry on a lettuce leaf has a different level of satisfaction than eating a chocolate-covered strawberry topped with whipped cream on a shortcake.

Now, if you love potatoes covered with creamy Fromager D’Affinois, there’s no foreseeable reason to stop eating them that way. That wasn’t the point. The point, rather, is furthering the discussion about ways you can get your body to cooperate with losing weight if weight loss is something you are seeking. In other words, what can you eat that helps increase your metabolism in relation to your appetite?

First, let’s examine the extreme importance of that question. If it takes 3,000 calories to satisfy your appetite, and your metabolism burns 3,000 calories in a normal day, then eating to appetite will neither cause weight loss or weight gain. Sure, you could slowly replace fat with muscle while in calorie balance from doing something like Metabolic Enhancement Training, and I hope to post about that next week, but for the most part your weight is unlikely to change much while in calorie balance.

Actually, I shouldn’t downplay what is at least physically possible. Since 6 pounds of muscle and 1 pound of fat contain the same amount of calories, theoretically you could lose 10 pounds of fat, gain 60 pounds of muscle, and increase your weight by 50 pounds without a calorie surplus. You’re not likely to do anything like this to such an extreme, but mathematically, it is possible. Likewise, you could lose 50 pounds while in calorie balance on the other side of that coin. I’m sure Arnold, during his heyday, could have easily achieved a 50-pound weight loss while in calorie balance by doing a prolonged juice fast and taking a break from the weights and the roids.

But assuming no change in muscle to fat ratio - when your appetite is satisfied on fewer calories than you burn metabolically you will lose weight. Likewise, when you need more calories to satisfy your appetite than your body burns you will gain weight. This can happen at high calorie intakes which is most typical, or low calorie intakes (if you have to average 1,600 calories per day to satisfy your hunger but your body refuses to burn more than 1,500 on average, you will gain weight – more than 10 pounds per year with such a disparity in the appetite to metabolism ratio).

Okay, so that’s outta the way. Let’s get going further with the Flavor-Calorie Theory.

First of all, forget Seth Roberts and what he calls the Flavor-Calorie Theory. What he is really talking about is Pleasure Center Activation Theory (PCAT) of weight set point.

Yeah, it was time to bust out a new acronym. PCAT is a sweet one, and it can also be referred to as “Poodie Tat.” Too many people were getting caught up on “flavor” and not focusing on the real meat of the theory, which is that reward centers in the human brain that guide us towards foods that have the most bang for the buck exert a powerful influence over our weight set point.

The primary pleasure center substance is called dopamine – or “dope,” and it be some good shit.

It’s really very useful. The “land of milk and honey” was not called the “land of lettuce and lentil sprouts” because lettuce and lentil sprouts don’t activate the pleasure centers in the brain to the same extent of milk and honey – which are without question the most calorie-dense, rapidly-ingested, rapidly-absorbed calories that can be consumed on God’s green earth without some form of refinement (including cooking). Remember that liquids activate pleasure centers more than solids (to a certain extent – once the diet is 100% liquid that is no longer true… monotony rules and it has the opposite effect).

But modern foodstuffs and substances exploit the pleasure centers and spike dopamine to levels that real food, no matter how calorie-dense or flavorful, is simply not capable of doing to the same degree.

In terms of promoting a rise in weight set point, which increases the appetite to metabolism ratio (AM Ratio – kinda like AM Radio), the most powerful promoters seem to be substances that are the most sweet. Saccharine, Aspartame, and Sucralose (Splenda) cause much greater increase in the AM Ratio than plain ol’ sugar. Of course, throwing caffeine into the mix activates those pleasure centers even more. Diet drinks are the perfect obesigenic substances when paired with a calorie-dense meal. Say what you want about Stevia, but that is another dime-a-dozen sweetener for raising your weight set point – it just comes without so much of the neurotoxicity of aspartame, or the bowel destruction of sucralose.

Anyway, I will continue to try to poke holes in PCAT like I have over the past several years after coming across the work of Seth Roberts, but as of now I have little doubt that the PCAT explains most cases of obesity – and by eating foods that trigger a smaller dopamine response one can easily become satisfied on fewer calories and lose weight without a revolt from the metabolism (drop in body temperature).

More reasons why I find the Pleasure Center Activation Theory to be so compelling:

1) Ethnic groups with a history of eating foods that are not very calorie dense, or without a long history of alcohol use (which spikes the hell out of dopamine) are naturally FAR more susceptible to obesity, diabetes, and alcoholism than Whitey, who has consumed milk, honey, grain, and alcohol in abundance for thousands of years – and has consumed refined sugar and grain longer than most other Ethnic groups.

This suggests to me that many various ethnic groups have much more highly-attuned dopamine receptors (although dopamine is just one pleasure neurotransmitter, serotonin could certainly be involved as well) – to have a more acute sense for calorie-dense and rapidly-absorbed calories for the purposes of survival. When encountering alcohol as well as foods that are more calorie dense, highly-sweetened, and rapidly-absorbed, such as is the case with the Nauru of the Pacific (above) and the Pima of Arizona (the two fattest, most diabetic peoples on earth) who saw their sparse, lean, fibrous diets replaced by tons of animal and vegetable fat, soft drinks, refined grain, packaged junk foods, and alcohol, a huge rise in weight set point struck a large percentage of the population.

2) Alcoholism is considered to have a very strong hereditary component. Obesity researchers know very little about what causes obesity, but they do know that the strongest correlation by far is heredity. In fact, twins that are separated at birth and live separate lives with different families and different diets and influences almost invariably end up at the exact same weight – and even store excess fat in the exact same place on their bodies. Neurotransmitter profiles are certainly hereditary, and would explain the connections between both alcoholism and heredity and obesity and heredity.

3) It seems after hearing hundreds of testimonials for both weight loss and weight gain following my advice to eat to appetite of a “high-everything” whole foods (slower absorption) no sugar (unsweet), low to no alcohol diet, that the prime determinant of whether a person loses weight or not can be directly linked to the degree of pleasure center activation of the diet they ate preceding RRARF. In other words, if they were eating to appetite of fast food, doughnuts, Pepsi or diet drinks, white bread, and beer and switched to a whole foods diet with no sugar or alcohol, there was typically an instant drop in weight set point – causing rapid weight loss and presumably a big decrease in calorie intake.

Those who were eating a calorie-restricted diet, a carbohydrate-restricted diet, an already unsweetened diet with no alcohol, a vegan diet, a raw foods diet, or any other version of a diet that provided LESS pleasure center activation, often GAINED weight eating to appetite on RRARF and had a sudden increase in appetite and calorie intake.  These people were the equivalent, basically, of ethnic groups that are highly sensitive to weight gain when switching from a low-calorie density diet with very little alcohol and sweetness to standard "Western" fare. 

To read more about this, please check out the FREE EBOOK HERE

Final Thoughts…

The PCAT is a similar theory to the Thrifty Gene Hypothesis, except that the abundance of food is not the reason our “biology that once insured survival has now turned against us.” Rather, it is the nature of that food, not the quantity of it, that has taken the biological mechanisms of those predisposed to fat gain and switched on the fat storage programs. I believe these same mechanisms underlie many forms of addiction.

Unfortunately, even if this is the undeniable way that most people gain excess body fat and run into metabolic disease, trying to lose body fat and reverse disease remains a tricky thing to solve that reeks of tail-chasing (the PCAT chasing its tail, not a dog). It is tail-chasing because simply eating whole foods that have low-calorie density, like Joel Fuhrman’s nutritarian diet for example, which by definition is all about eating foods with the lowest calorie-density, upregulates the pleasure center receptors even more. So it in no way enables a person to be able to eat the calorie-dense foods that the rest of society eats, and that everyone enjoys, without becoming increasingly sensitive to their fattening effects. But I guess the good news is that the more you eat low-dopamine triggering foods the more tasty they become (trust me, when your pleasure neurotransmitters are upregulated enough, even the blandest food on earth will taste incredible).

This scores yet another big point in favor of the fat loss strategies of guys like Martin Berkhan and Joel Marion – who punctuate plain, whole foods-centric weight loss diets with major Cheesecake and pizza slayings. Berkhan has also been known to spank some Heineys.

Could it be that this acute, infrequent, monster dopamine rush is enough to keep the dopamine and/or serotonin receptors from opening up? Could this enable your average 100-pounds overweight Joe to take advantage of low-calorie density foods that induce weight loss while still being able to eat Brie-bombed potatoes and Jambalaya without falling off the deep end once ideal weight has been achieved? I dunno. We’ll see I guess.

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