Showing posts with label dopamine. Show all posts
Showing posts with label dopamine. Show all posts

Thursday, 8 October 2015

Brain Reward and Anabolic Steroids

Pine Cone and Peacocks from Vatican Museum
Testosterone displays effects on brain function in both males and females.

Emanuela Mhillaj and colleagues recently published a nice summary of what is currently known about the effects of anabolic-androgen steroids (AAS) on the brain.

Their review highlighted the potential for AAS to modulate brain reward function and potentially lead to a drug dependence type of abuse pattern.

Here are some of my notes on their discussion of AAS and the brain reward system:

  • Studies of brain reward and AAS use in humans is confounded by perceived user benefits in appearance, strength and athletic performance
  • Animal models of AAS and brain reward provide a model free of these confounding effects
  • Conditioned place preference (CPP) is a relevant model for reward study in rodents
  • Synthetic AAS compounds including nandrolone and drostanolone show rewarding CPP in both male mice and rats
  • This effect can be blocked by dopamine antagonists--dopamine pathways are key in reward modulation
  • Testosterone brain injections or implants produce reward response behaviors in rodents
  • Hamster models show reward behavior with intravenous AAS injection but not oral ingestion
  • PET imaging in rodents has shown upregulation of dopamine transporter protein
  • The endogenous opioid system may modulate reward and reinforcement mechanisms of AAS
  • Beta endorphin levels increase in brain regions of rats treated with AAS
  • In humans, AAS use is commonly associated with abuse of other substances including including alcohol, cocaine, opiates, cannabis and ecstasy

This multi-drug abuse pattern in humans with AAS complicates the assessment of AAS effects on dependence and behavior. It is possible that brain reward mechanisms and risk for abuse and dependence vary among humans. Risk for alcohol, drug or nicotine dependence may be a marker for higher AAS abuse risk in humans.

Additionally, in a study that I conducted, antisocial personality traits were increased in humans with illicit AAS use. Antisocial personality is a risk factor for alcohol and drug abuse as well as aggressive behavior.

Readers with more interest in the review article can access the free full-text manuscript by clicking on the PMID link in the citation below.

Photo of peacocks and pine cone is from the author's files.

Follow the author on Twitter WRY999

Mhillaj E, Morgese MG, Tucci P, Bove M, Schiavone S, & Trabace L (2015). Effects of anabolic-androgens on brain reward function. Frontiers in neuroscience, 9 PMID: 26379484

Yates WR, Perry PJ, & Andersen KH (1990). Illicit anabolic steroid use: a controlled personality study. Acta psychiatrica Scandinavica, 81 (6), 548-50 PMID: 2378247

Saturday, 13 August 2011

How Video Games Reward the Brain: TED Video




Tom Chatfield provides an overview of how games stimulate brain reward processing. Chatfield is game enthusiast who edits the arts and books section of the UK magazine, Prospect.  Here are my notes from the TED video.
 
Chatfield begins by stating he is in awe of the power of virtual games to transfix us.

Video gaming is the fastest growing of all forms of media ($50 billion per year).

People spend enormous time and money on virtual game rewards.  Farmville has over 70 million players around the world.

The good news is this gaming teaches us about brain rewards.

Video games produce huge data sets of reward processing.

We have evolved in special ways. Here are seven ways games teach us about brain rewards.

1. Measuring progress aids reward-games use constant score updating to reward players
2. Multiple long and short-term gains--by adding complexity, gamers are less likely to become bored
3. Reward for effort-every time you get something for effort, negative feedback is not very helpful
4. Feedback is frequent, rapid and clear
5. Element of uncertainty- uncertainty of reward is a neurological and psychological gold mine.  Dopamine is the brain's reward learning chemical and is released more with unexpected reward
6. Windows of enhanced engagement-in gaming, developers use moments of enhanced memory and increased confidence
7. Social interaction-playing with other people enhances reward and is more likely to keep gamers involved in the game

These principles have implications in business.  Real time energy meters could provide immediate feedback on progress in saving energy.

Implications are important for education.  We can use game technologies to enhance learning.

Finally, in government we may learn how to reward people to change complex behaviors and combat problems like obesity.

Games teach us the the key role of engagement--how to keep people involved in tasks to promote individual and social engagement.  If we can learn from how games promote engagement, we may have something very revolutionary.

Chatfield has written a book titled Fun, Inc where he outlines how virtual games can be a good place to learn new approaches in the real world.

I think Chatfield is on to an important issue here.  Why can't we take some of the principles of popular games and apply them to things like learning algebra or organic chemistry?  So far, educational software has not progressed at the speed or complexity of video gaming.  Perhaps by learning how gamers are rewarded and engaged in virtual reality games we can provide more effective online educational software.

Photo of Juno Beach, Florida sun rise with filter from the author's private collection. 

Monday, 11 July 2011

Cannabis Use Declines with Aerobic Exercise

Improvement in addiction treatment interventions in needed.  Many substance dependence individuals end up with with a chronic illness with frequent relapse following periods of abstinence.

Aerobic exercise appears to be a candidate for a treatment component in a variety of addictive disorders.  Aerobic exercise may produce a variety of changes in the brain that may influence craving and drug use.

Mechanisms induced by aerobic exercise that might influence drug craving and drug use include:

  • Alteration in the brain reward circuit
  • Increased release of brain dopamine and changes in dopamine receptor sensitivity
  • Decrease in anxiety and depressive symptoms 
Maciej Bukowski and colleagues at Vanderbilt University recently published a trial of cannabis craving and use in a series of subjects.  Regular cannabis user were enrolled in a ten session intervention that included ten 30 minute supervised treadmill periods.  Subjects exercised at 60% of their calculated maximum heart rate. 

All subjects met DSM-IV criteria for cannabis dependence.  Subjects were not involved in any formal substance abuse treatment program and did not express a desire to reduce or discontinue their cannabis use.  Subjects were using an average of 33.5 standard joint equivalents of cannabis at the beginning of the study.  The average daily cannabis use of the subjects is displayed in the plot below taken from the manuscript:



The plot demonstrates a significant reduction in daily cannabis use during the active aerobic exercise period. Daily joint use dropped from approximately six joints per day to an average of about two to three joints per day during the exercise period.  Following completion of the exercise phase, daily joint use climbed up again approaching the run-period levels.

This study was not done in a treatment-seeking sample.  It is unclear whether a similar effect would be seen in treatment seeking samples.  The study did not include a control sample.  Nevertheless, this study should stimulate research in treatment samples.  It suggests that regular aerobic exercise may be a valuable component of treatment for cannabis dependence.  Extended aerobic exercise may be valuable in the longer term reduction of cannabis use in those with cannabis dependence.

Chemical model of tetrahydrocannabinol (the psychoactive substance in cannabis) from the Creative Commons file at Wikipedia authored by Ben Mills.

Cannabis use Creative Commons Attribution License plot from Plos One manuscript authored by Maciej Bukowski and colleagues referenced below.

Buchowski MS, Meade NN, Charboneau E, Park S, Dietrich MS, Cowan RL, & Martin PR (2011). Aerobic exercise training reduces cannabis craving and use in non-treatment seeking cannabis-dependent adults. PloS one, 6 (3) PMID: 21408154

Wednesday, 2 March 2011

Decoding the Faces of Depression: Anhedonia and Dopamine



Diego Pizzagalli presented the March 2011 Warren Frontiers in Neuroscience Series lecture in Tulsa, Oklahoma on March 1, 2011.  Dr. Pizzagalli works at the Harvard Medical School affiliated Center for Depression, Anxiety and Stress Research & Neuroimaging Center at McLean Hospital in Boston.  He has been involved in research related to brain abnormalities in major depression as well as predictors of treatment response.  I will highlight some of the key points from his lecture and incorporate three recent research manuscripts related to this topic:
  • There are over 100 symptom combinations to diagnosis major depression (5 of 9 symptoms required)
  • Distinct depressive phenotypes (clinical presentations) are difficult to define--but the phenotype defined by anhedonia (pervasive lack of ability to experience pleasure) has significant research support
  • Depression with anhedonia also has a biological component--the brain reward pathways involving dopamine and the striatum.
  • Anhedonia has been linked to impaired dopamine function in these brain reward pathways
  • Anhedonia appears more heritable than depression and may be related to abnormalities in genes controlling dopamine neurotransmission
  • The dopamine reward pathway (substantia nigra-striatum-cingulate/prefrontal cortex) is vulnerable to stress (acute stress increases dopamine, chronic stress reduces it in the rat model)
  • He and colleagues developed a heuristic model of the functional neuroanatomy of anhedonia: both environmental and biological factors influence risk of depression: depression includes a decrease in the brains reward response, exaggerated stress responsivity and eventually a blunted mesolimbic dopamine system (and anhedonia)
  • Laboratory models and psychometric measures of anhedonia have been developed--studies suggest the ventral striatum (nucleus accumbens) is involved in hedonic coding while the dorsal striatum (caudate) is involved in positive re-inforcement
  • Decreased activation of cingulate and caudate with monetary incentive delay task is seen in untreated depression
  • Untreated depression (and anhedonia) also linked to decreased size of the caudate
  • Early life stress (abuse) may increase depression risk through dysregulation of mesolimbic pathways including left putamen and left pallidum
  • Stress even in healthy individuals impairs brains reward processing pathway
  • Some genes related to anhedonia may work through stress pathways, i.e. mineralcorticoids, corticotrophin hormone (CRH)
  • Future research will focus on further parsing of the heterogeneity associated with depression, developing animal models of reward tasks, using PET to better understand the role of dopamine in depression, using dopaminergic drugs (i.e. pramipexole) in stimulation models of depression and further study of the neurobiology of stress-induced anhedonia
I agree that evaluating the role of dopaminergic drugs in depression accompanied by anhedonia is worthy of basic and clinical research study.  Among typical antidepressants, only bupropion appears to have dopaminergic effects.  Other compounds such as psychostimulants also increase dopamine but carry the risk for abuse.  Several of the dopaminergic drugs used for Parkinson disease are beginning to see more use off-label for the treatment of depression.  I will look at this issue in a future Brain Post. 


Photo of Blake Griffin shooting free throw against Oklahoma City Thunder in 2011 NBA game courtesy of Tim Yates.

Pizzagalli DA, Holmes AJ, Dillon DG, Goetz EL, Birk JL, Bogdan R, Dougherty DD, Iosifescu DV, Rauch SL, & Fava M (2009). Reduced caudate and nucleus accumbens response to rewards in unmedicated individuals with major depressive disorder. The American journal of psychiatry, 166 (6), 702-10 PMID: 19411368

Wacker J, Dillon DG, & Pizzagalli DA (2009). The role of the nucleus accumbens and rostral anterior cingulate cortex in anhedonia: integration of resting EEG, fMRI, and volumetric techniques. NeuroImage, 46 (1), 327-37 PMID: 19457367


Pizzagalli DA (2011). Frontocingulate dysfunction in depression: toward biomarkers of treatment response. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 36 (1), 183-206 PMID: 20861828

Monday, 20 September 2010

Ending Emotional Eating



First of all, man am I glad to be back home. New York City was awesome this trip, and I’ll be writing about my food adventures there at http://180kitchen.wordpress.com/ very soon. But all in all it felt like a competition to see how much caffeine, alcohol, sugar, nitrates, and vegetable oil I could get into my system. I’m more than ready for a breather from that. I’ve never been so glad to see ground beef, coconut oil, sweet potatoes, and spinach. In fact, the burger I ate for breakfast this morning was so large I started singing “Everybody Wants Some.” I actually filmed it below. Any resemblance to a young John Cusack is purely coincidental.



Anyway, time to discuss what is a huge and extremely prevalent problem in the modern world – emotional eating.

As discussed in many prior posts, food triggers a response in the pleasure centers in the human brain, acting on pleasure neurotransmitters like serotonin and dopamine. It is no surprise that when many people feel a sense of chronic stress, anxiety, shame, guilt, and so on – food becomes not just a way to fuel oneself, but a form of psychoactive medication. And in general, what provides the highest pleasure response is…

1) Rapidly-absorbed foods like white flour and liquid sugars
2) Sweets, whether natural as in honey, refined as in sucrose, or non-caloric
3) Calorie dense foods – like French fries, pizza, brownies, ice cream, or cheesecake
4) Alcohol and caffeine-containing drinks and substances
5) Foods with flavor enhancers like MSG found in most fast food and highly-flavored stuff like Cheetos or Doritos
6) Foods with low water content – that are therefore very calorie dense (butter, oils, nuts, dried fruit, chips, crackers, cookies, bread)
7) High-calorie liquids such as soft drinks, fruit juices, whole milk, half n’ half
8) Large quantities of food in general, of any kind

This is a 2-way street, as eating some of these foods, particularly those with the highest capability of triggering a pleasure center response like a fast food meal with a large sugary drink and a dessert all mixed together in one hit, can in turn cause massive emotional fluctuations. First a high, followed by a crash, which is addiction pathology 101 and can be caused by anything that is unusually, and unnaturally, pleasurable.

It works the other way as well. Chronic stresses such as the loss of a loved one, self-esteem issues, relationship problems, being in an abusive situation, financial stresses, and other problems that are of a chronic nature have a tendency to activate the same hormonal changes that a famine is capable of inducing. That is, an increase in cortisol production as well as synthesis in fat cells themselves. Hypercortisolemia, induced by any form of chronic stress from famine (the reason we are designed to have this fat storage response to stress in the first place – marked by a drop in metabolism, reduction in fat burning, increased production of fat storage enzymes, increased appetite, increased cravings) to depression to sleep deprivation can all trigger an increased appetite for the things on the above list.

This is why calorie restriction combined with a huge exercise load has the following impacts on a typical person…

1) Increased alcohol, sugar, and caffeine cravings – along with foods with very high calorie density and huge quantities of overall food in general
2) Increased appetite
3) Reduced body temperature
4) Increased risk of infection
5) Decreased desire for physical activity (as well as sex and other calorie-burning activities)
6) And so on

Likewise, following the guidelines laid out in the THIS FREE EBOOK brings about the exact opposite set of changes.

Anyway, ending emotional eating is not difficult. In fact, most people have emotional eating issues to begin with because of chronic dieting, undernourishment, insufficient sleep, and excessive stress in the first place. It all starts with feeding yourself well as the FREE EBOOK explains.

Helpful tips include eating a diet that keeps you even keel emotionally. No one ever could have convinced me of the power of eating a well-balanced, calorically-sufficient, whole foods diet without excessive exercise and adequate sleep on emotions until I actually tried it religiously. Like Jon Gabriel mentions in this fantastic interview, “there are no more good days and bad days.” You are more or less anti-dieting at that point.

Another helpful hint is to eliminate substances you know you are addicted to WHILE EATING WELL and RESTING WELL. Eliminating addictive or problem foods that have been a target of emotional eating binges for years does not work if you are depriving yourself of anything. Otherwise you will increase your cravings for those “problem” foods as each day passes. With the right set of nourishment and minimal stress from intense exercise regimens – as well as plenty of time for rest and relaxation, there is simply no low serotonin and dopamine state occurring in your brain that causes the outrageous cravings to eat foods that spike those feel good neurotransmitters into the stratosphere.

By keeping yourself even keel with consistent sleep patterns, regular mealtimes, no skipped meals (or at the very least not skipping meals when you are hungry), and plenty of calories at each feeding to leave you feeling satisfied – there is simply no low state in need of medicating with food and drugs.

The real problem is that people are under all kinds of emotional stress, work stress, lack of sleep, and more while at the same time thinking it’s healthy to eat as little as possible, or at the very least go to war with fat, carbohydrates, or animal products while exercising as much as they can stand to.

This is what CAUSES emotional eating in the first place, exacerbated of course by the halo of guilt that a person experiences after eating junk food and the shame and loss of self-esteem that they feel over whatever excess fat they carry after each episode.

In short, emotional eating is caused by being at war with yourself and asking much more of your body and mind than you give in return. The big picture answer to emotional eating is to end that war.

Would you try to raise a healthy baby by depriving it of food, making it feel constantly scared, torturing it, yelling at it for being fat, weak-willed, and lazy, not letting it sleep, and forcing it to do a lot of exercise? No. Then why are you pursuing health by trying to do that to yourself?

Physical, emotional, and mental health is obtained by obeying your physical, emotional, and mental needs – not ignoring them and then beating yourself up over your cravings, fatigue, depression, and body fat.

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.

Monday, 19 July 2010

Anorexia Rehab

Over the weekend I was asked a question about anorexia, and since my thoughts and feelings about the disease are so vast, I saved my reply to this anonymous poster for its very own blog post (note, that is NOT a photo of the person who wrote the following)…

“I have had anorexia for 6-7 years now and I need and want out. I have gone from ‘conventional’ treatment where people shove ice cream and subs in your face to LC because it helped me mentally calm down and distress, then to VLC and then ZC then back up the ladder to VLC and LC now. I eat a shitload of protein and fat and slowly and upping my carbs. My blood sugar is shot. My adrenals are shit. My cortisol is well, shit as well. I have some incredible hypoglycemia problems. Like another person who commented on your blog, ANY form of exercise sends my blood sugar through the roof. My waking blood sugar is over 100 and stays there until I eat and usually post meal is anywhere from 60-90. I played around with Martin’s intermittent fasting because, yeah I am a dumbass. I am starting your book now, thank you.


I guess my question is this… you have read Ancel Keys ENTIRE starvation study and experiment. Well, I am like the prime candidate for overcoming what those people went through and getting my body out of starvation. Any steps, help, ideas are more than welcome.”

To begin with, anorexia is a lot more complex than most people give it credit for. It’s also a lot more dangerous and debilitating than many give it credit for as well. In the words of Furious Pete, former anorexic that nearly died from it – “it’s a bitch of an illness.”



Most assume that anorexia is purely psychological, stemming from body image issues and a desire to appear like supermodels or something like that. While this mentality can certainly instigate undereating and lead to the powerful physical and psychological addiction that best describes anorexia, once the disease has set in, to say that it is purely psychological is a huge error.

I liken anorexia to addiction. From what I suspect, most cases of anorexia begin with a desire to lose weight. When someone loses weight as we have been discussing at length over the past month, this is accompanied by a large rise in catecholamines – the adrenal hormones that break down both fat and muscle tissue to be used as fuel. This breaking down of body tissues is referred to as “catabolism.” Catabolism… catecholamines. Coincidence?

Along with the rise in catecholamines comes a rise in neurotransmitters dopamine and beta-endorphin. These are energizing. Pain goes away. A state of subtle euphoria sets in, and we get a little “high” from it. We are talking about opiate substances here, and they are very addictive – as addictive if not more addictive than actual opiate drugs. Dopamine… dope. Coincidence?

Anything that causes a big rise in catecholamines typically triggers a rise in beta endorphin and dopamine. That’s why you hear so much “buzz” from those who practice intermittent fasting for example, on how good they feel, how much energy they have, how clear and focused their thinking is, etc. They are getting a natural high, just like vigorous exercisers get. Very low carbohydrate eating often has the same impact, and while an anorexic can self-medicate by keeping carbs low enough to trigger dopamine and beta endorphin release, it is counterproductive to recovery for reasons explained below.

The problem is when a person with susceptible physiology meets activities and substances that spike these neurotransmitters to great highs. This is what makes the difference between a person that gets addicted and one that does not. What is susceptible physiology? Susceptible physiology is someone who naturally produces LOW amounts of these neurotransmitters for whatever reason – typically poor nutritional history on behalf of themselves and their parents I suspect, as nutrition needs to be excellent in order to have sound production of these neurochemicals (naturally weak adrenals may in part be responsible as well – and there’s no doubt that adrenal stressors heighten a person’s susceptibility to addiction).

When levels are naturally low, substances or activities that spike these neurotransmitters are particularly alluring. That’s because a person that naturally has low levels of these neurotransmitters correspondingly has a lot of receptor sites wide open to capture this small amount of dopamine and beta endorphin. Anything that causes a surge of these chemicals causes quite a thrill ride.

At the same time, spiking these neurotransmitters results in what is called “downregulation” in which some of those wide open receptor sites close down. This is precisely what makes anything that spikes feel good brain chemicals habit forming and addictive. With a low production of dopamine and lots of wide open receptor sites, life feels good, balanced, stable, and normal. But with a low dopamine production and closed receptor sites life feels slow, sluggish, depressing, painful, and so on – the opposite of a dopamine high.

Once dopamine has been spiked enough, and enough receptor sites shut down – even if dopamine production is still the exact same as it was to begin with, the person feels nothing but withdrawals and has the experience of insufficient dopamine, beta endorphin, or whatever. They need increasingly larger spikes of these neurotransmitters just to feel normal, much less good, just like any true long-term drug addict or alcoholic.

This is exactly the pathology of anorexia. A susceptible person starves him or herself. When that happens, beta endorphin and dopamine levels rise – making the person feel VERY good at first. If a person manages to fight their hunger signals hard enough, and long enough with a large motivating factor such as body image issues to override natural physical feedback…

Then receptor sites start to shut down. Undereating, at this point, then becomes self-perpetuating and the normal hunger feedback loop is broken. Resuming eating once again induces instant withdrawals for which abstaining from eating is the medicine. Undereating, from a functional standpoint, becomes a drug to get a dopamine and beta endorphin feel-good fix. Without it, a person feels miserable physically, and depressed, lethargic, and dark psychologically. At this point, anorexia is not something that can be cured with a Club sandwich any more than a heroin addiction can be cured with a Club sandwich.

Before I go indefinitely on this addiction/anorexia tangent, let me get into specifics in terms of the questions that were asked in the email I received above…

Recovering from anorexia is like recovering from serious drug addiction and should not be underestimated. Any person suffering from anorexia, if he or she has any hopes of recovery, must first be able to grasp what addiction is, how it operates, and what MUST be done to recover.

From this vantage point, the psychological pre-requisite for recovery can hopefully be mustered. That psychological pre-requisite is one of understanding how the body and mind work, and grasping fully why eating makes you feel shitty and depressed with an uncontrollable urge to stop eating.

I imagine a typical anorexic seeking recovery is at odds with themselves, frustrated as to why they can’t just eat when they know they need to, and confused at all the terrible physical and emotional trauma they experience when eating. To get to the other side, it really takes full recognition of the problem, how to fix it, and a whole lotta self compassion. Otherwise you’ll just beat yourself up for not eating instead of realizing exactly why you don’t want to, taking it easy on yourself because of it, and taking the proper steps knowing fully that it is going to be a major hellish battle that every cell in your body will try to resist.

To recover, I believe that there is no way around achieving “upregulation” in which the receptor sites for beta endorphin and dopamine open back up again – allowing you to feel normal with your naturally low production of those neurotransmitters instead of experiencing too little and having an unquenchable thirst for anything and everything that spikes it.

A very low carbohydrate diet, in the short-term, could very well make for a substitute for anorexia, as could very strenuous exercise, as could various psyche meds and stimulants. However, that is ultimately trading one form of addiction for another, and is not genuine recovery. However, it can make for a great stepping stone.

But ultimately upregulation must occur. For this to happen, it is essential to focus on doing everything possible to keep beta endorphin and dopamine levels as low as possible. This, ladies and gents, is brutal for someone with downregulated receptor sites for these chemicals. The withdrawals can be major.

For someone seeking to keep these levels as low as possible, major tactics include:

1) Eating frequent, starch-based, whole food meals at above-maintenance calorie levels. The food should actually be somewhat bland, in whole food format, with some, but not too much added fat or protein (protein raises adrenal hormones and associated neurotransmitters, and really good food, especially sweets mixed with fat, triggers a big release of opiates that you are looking to avoid). A non-vegetarian macrobiotic-ish diet would actually be decent for recovery. This will also help in fixing reactive hypoglycemia, which I would guess nearly all anorexics suffer from to some degree (although it too will exacerbate hypoglycemic symptoms in the short-term).
2) Sleep a lot, including regular naps.
3) Perform various relaxation techniques, from gentle yoga and breathing exercises to meditation.
4) Avoid stress as much as possible.
5) Avoid strenuous exercise.
6) Avoid stimulants.
7) Avoid drugs – recreational and psychoactive.
8) Avoid sweets.
9) Avoid anything overly pleasurable. The more miserable you are, the faster you are upregulating.

This is obviously a lot to ask for, and would require tremendous support from family members, loved ones, and potentially demand professional assistance like that required for a drug addict attempting rehabilitation. Unfortunately, I’d venture to guess that most professional eating disorder rehab joints, just like most drug rehab joints, provide many forms of self-medication from candy to cigarettes that lessen withdrawals and limit true fundamental healing of the core problem.

Once you have upregulated, be very cautious about meal-skipping, drugs, stimulants, stress, and other adrenal stressors that can cause a relapse, as your sensitivity to such things is greatly heightened in an upregulated state.

Bulimia shares a similar pathology. Know how miserable you feel right before puking and how euphoric and instantly healed you feel immediately after vomiting? That’s some endorphins for you. Addictive as hell if you do it enough to start shutting down your receptor sites.

For more specific lifestyle and dietary recommendations geared for overcoming addiction and more by lowering adrenal hormone activity via overfeeding, over-relaxing, and oversleeping, READ THIS FREE eBOOK.

More on reactive hypoglycemia in a blog post this Thursday – something many chronic dieters, hypometabolics, and adrenal gland punishers experience given sufficient time.