Yet Wim is not a genetic freak or Tibetan monk. He is a 52 year old Dutch man without much body fat. He believes that anyone can adapt to the cold and learn to control body temperature.

In this article, I will try to answer two questions:

• How does he do it, and can anyone really do the same?
• Is this basically an impressive stunt, or is there any benefit to learning Wim’s methods?

No stunts.  First, just to be clear about what Wim has been able to accomplish,  take a look at these two short videos:

1. Wim running a half marathon in the north of Finland:

2. Wim swimming 50 meters under arctic ice:

An enjoyable account of Wim’s remarkable adventures and methods is detailed in the book Becoming the Iceman, co-authored by Wim Hof and Justin Rosales.  Rosales is a college student who became so intrigued with Wim’s abilities that he managed to earn enough money washing dishes–while still attending classes–to travel to Europe and learn Wim’s methods.  The chapters alternate between those written by Wim and those by Justin. While their account suffers from a lack of editing and is sprinkled with grammatical errors, the excitement of Wim’s remarkable sense of fearless adventure and Justin’s learning process make this book a real page-turner.

Changing how body temperature is regulated.  How does Wim Hof manage to keep his core body temperature elevated, maintain peripheral circulation, and avoid frostbite and hypothermia?  Nobody knows for sure, but there is no doubt that he does it.  Dr. Kenneth Kamler, an expert on hypothermia, frostbite and high-altitude medicine, who has himself climbed up Everest, has observed that Wim’s trained body responds differently than yours or mine.

The normal response to extreme cold exposure starts in the peripheral blood vessels in the extremities  – the ears, nose, fingers and toes.  Blood flow in the extremities at first increases, in order to stimulate warming.  If the cold exposure is prolonged more than a few minutes, goosebumps and shivering kick in to induce warming of muscles and skin.  But if the exposure continues beyond that, a process of biological “triage” takes place.  To preserve the high priority  organs – brain, heart, digestive tract — the body shuts down blood flow to the extremities to prevent further heat loss. The peripheral veins snap shut to segregate warm interior blood from cold peripheral blood. After all, these extremities have a lot exposed surface area, so cutting them off greatly conserves heat.  But the cost of doing this is frostbite and the irreversible tissue damage that often results if the cold exposure is sustained for more than a brief time.  Finally, when the core temperature falls below 95 F, the various stages of hypothermia set in, ultimately leading to death if sufficiently prolonged.

But Wim, and Tibetan practioners of the ancient art of Tummo, are able to significantly alter this normal process.  As Kamler explains, the key adaptation occurs within the brain during meditation–specifically the yoga and controlled breathing exercises that Wim and the tumo practitioners follow.  Of these exercises, breath retention exercises are key.  As a result, there is a significant activation of blood flow and electrical activity in his frontal cortex and hypothalamus — areas that regulate peripheral nerves and veins involved in the regulation of body temperature.   Normally, the circuit between the hypothalamus and these temperature control circuits is involuntary, governed by the autonomic nervous system. Kamler reasonably speculates that,  through meditation, Wim is able to override the normal function of the hypothalamus, allowing the peripheral veins to remain open and heat the extremities, preventing injury.  He points out that Wim must be generating heat and distributing it more efficiently, but he admits having no idea mechanistically how Wim’s meditative techniques accomplish this.

The monks who practice Tummo are able to tolerate cold, but they do so in a meditative pose, while sitting. They speak of being able to generate an “inner fire”.  Wim Hof’s method has diverged from that of classical Tummo. He has innovated significantly, since he is able to control his body temperature while moving about, in fact while exerting himself under conditions of running, swimming, or high altitude climbing which would be challenging for most people even at ambient temperatures! Yet, while Wim is certainly a one-of-a-kind personality, he is insistent that anyone can apply his techniques. His success in teaching Justin Rosales and others seems to bear that out. More recently, Wim  has devoted himself to training others through seminars and training expeditions.

Other abilities.  Wim’s ability to voluntarily control what what we consider to be automatic, involuntary responses does not stop at tolerance of extreme cold.  He has also learned to tolerate extreme heat, consciously overcome pain and cramping, and even moderate his immune response to endotoxin.  A fuller discussion of these abilities is given in Becoming the Iceman.

Possible benefits.  I’m particularly interested in Wim Hof, because of my own positive experience taking daily cold showers.  As I discussed in my post, Cold Showers, making a daily habit of cold showering results in a remarkable degree of adaptation.  The initial intense discomfort of cold shock rapidly shrinks in both intensity and duration, and the self-heating process of thermogenesis becomes more prominent after only a few weeks of the daily habit.  I’ve found benefits in weight control, mood enhancement, and generalized stress resistance.  I’ve not had any colds since starting cold showers. When my family was suffering with a stomach flu that lasted several days, the net effect on me was a 12 hours of achiness which I slept off on a single night, with none of the nausea that they had.

Could more aggressive exposure to the cold provide benefits that go beyond that of daily cold showers?  Hof and Kamler have suggested that the ability to open up peripheral veins and capillaries may help to enhance more than just temperature regulation.  It likely improves blood circulation overall, particularly in the smaller peripheral vessels. Because there are so few individuals that do what Wim Hof does, there is not yet any body of clinical science regarding the benefits to circulation.  But it is not hard to speculate that cold exposure could be a great way to fend of a wide range of cardiovascular and circulatory maladies.  So it intrigues me.

Total cold water submersion.   Cold showers are great, but what Wim Hof does is far more extreme.  Not only is the temperature of the water significantly colder — 32 F vs. the 55-60 F of my showers — but the total body immersion involves much more extensive skin surface area contact, meaning more rapid heat loss. A few times a year, I go for a brisk 10 minute swim in the ocean.  Here where I live in northern California, the ocean temperatures range between 53 and 60 F, similar to my shower water, and ocean swims are definitely more bracing than the cold showers.

My first experiments.  I want to see if I can up the game beyond cold showers. I first read Tim Ferriss’s account of cold water exposure in his book, The 4-Hour Body.  In his chapter “Ice Age”, he recounts the method of Ray Cronis, a NASA scientist who was able to lose almost 30 pounds of fat — fat, not weight — in 6 weeks, by taking cold walks, cold swims, and by drinking cold water.  Ferris himself tried immersing himself in cold baths — with added ice — for 20 minutes.  But he first heated himself to the point of sweating by consuming a thermogenic cocktail of ephedrine, caffeine and aspirin.  So what Conise and Ferris did doesn’t really approach the level of unmediated cold exposure undertaken by Wim Hof.

I want to see how much I can directly adapt to the cold.  My first effort will be to attempt this without any special meditative technique or breathing method, and certainly without taking any thermogenic medications or supplements, as Ferriss did.  So I did my first experiment today, and here is what I did and what I experienced:

I filled a bath with cold water, which I measured at 58 F (14 C).  I first submerged my legs.  It was painful, so I decided to allow myself to adjust before filling the tub with more water. Fortunately, after about 2.5 minutes, my legs no longer hurt and by 4 minutes they felt a kind of paradoxical warmth and I could wiggle my toes again. So I filled the cold water up to my chest when laying back. I was completely submerged at 9 minutes.  At first, this was very uncomfortable, and I started shivering. I felt some numbness, but that went away and I was comfortable again at  14 minutes. I could easily flex my toes and fingers. I continued laying in the tub, submerged up to my neck. The sensation alternated between shivering and coolness. I stayed in until 20 minutes had passed from the initial plunge.

After I got out of the bath, I felt warmer and tingly at first. But 5 minutes after getting out and drying off, I started feeling very cold and shivering uncontrollably. I was not really expecting that; I thought I would instantly feel warmer, just as I always do after stepping out of a cold shower. But in the book Becoming the Iceman, Justin Rosales and Wim Hof describe a phenomenon they refer to as “the afterdrop”, an experience of getting colder after you emerge from cold water. This is exactly what was happening to me. I needed to  put on warm clothes and move around to fight off the shakes. I was still cold and shivering 30 minutes after emerging from the cold bath, and my fingers were stiff, making it hard to type up my notes.

However, a full hour after finishing the bath I started to feel great. I became warmer throughout the evening, even though it has been a chilly evening. Psychologically, I have been quite alert all evening long. So there is some evidence of adaptation, even though the experience has been quite different than what I would have predicted from my familiar habit of cold showers.

I plan to continue experimenting with cold baths over the coming weeks, varying both the duration and the water temperature.  I’m interested to see how readily I adapt, and what other benefits or problems occur along with the adaptation.

Our drives are largely governed by two small primitive brain structures, the hypothalamus and the amygdala – shown in red in the drawing at right.  Remarkably, these two tiny structures are respectively the size of a pea and an almond — representing less than 1% of the brain’s three pounds of neural matter. Together, they constitute the control center of the paleomammalian brain–the “limbic” brain that governs our basic urges and desires as well as our homeostatic “set points” for temperature, sleep, body fat and behavioral urges like sex drive and aggression.

You can attempt to change your behavior by conscious determination and cognitive therapies.  But most attempts at intentional change are temporary and are doomed to fail in the long term because they are strongly resisted by powerful homeostatic processes encoded in our limbic brain.  Modern medicine recognizes the importance of homeostatic drives, and has developed pharmaceuticals to override them with diet pills, sleeping pills and antidepressants.  In fact, these medications do shift the balance of neurotransmitters and neural activity — at least in the short term.  But such chemical interventions are short-sighted “crutches” that promote dependency and come with side effects.  Often they exhibit  a “tolerance” effect: the brain’s control system fights back and weakens the impact of the medication.  To maintain the benefit, doses are increased, but this strategy may not always work.

This article will explain how the hypothalamus and amygdala contribute to the regulation of basic drives like eating, sleeping and sexuality, and how the amygdala can actually override the hypothalamus by enhancing the reward value of foods and other stimuli. (As I will explain, however, my take on “food reward” is different from that of Stephan Guyenet and other advocates of the Food Reward Hypothesis). This dual-control model can help explain anomalies such as obesity, addiction, and disordered sleep.

Finally,  I will provide suggestions on effective and natural ways to re-program the hypothalamus and amygdala and change your homeostatic set points, using the principle of hormesis.

Hormesis. Readers of this blog are familiar with hormesis:  a biological process whereby a beneficial effect (improved health, stress tolerance, growth or longevity) results from exposure to judicious doses of an agent that is otherwise detrimental at higher doses.  The many examples of homesis we’ve discussed on this blog involve adaptations that roughly fall into three categories.  The first two categories are quite well-known:

Structural adaptations to organs and tissues:

• Muscular growth, from weight lifting
• Adaptations of the foot and leg, from barefoot running
• Reversal of myopia, from use of anti-corrective lenses
• Other examples: calluses, suntanning

Defensive adaptations against foreign subtances:

• Immunotherapy to overcome allergies
• Endogenous defenses against oxidants and “xenobiotic” toxins

The third category is perhaps a less well recognized form of hormesis:

 ”Psycho-metabolic” adaptations:

• Hormonal and enzymatic adaptations to caloric restriction and fasting
• Psychological and weight loss benefits of cold showers
• Cue exposure therapy to overcome addictions
• Sleep restriction therapy to counteract insomnia

Psycho-metabolic adaptations. Let’s now expand upon this third category of adaptations, focusing on how certain types of stimulus or “stress” can bring about long term changes within the brain’s control system — the hypothalamus and amygdala.  These adaptations can induce broad sets of changes to your metabolism and psychological functioning.   These changes are long term adaptations — to be distinguished from short term or “artificial” changes that can temporarily induce weight loss, boost metabolism, energy level, wakefulness, or sex drive.   A true change in “set point” requires a sustainable physiological change that is reflected in real alterations in neuron density or receptor sensitivity within the brain.  In turn, these changes to the brain result in systemic changes elsewhere in the body.

In previous posts, I’ve touched upon a few topics that relate to the general thesis of psycho-metabolic adaptations that involve changes to the brain:

1. In “Change your receptors, change your set point“, I presented evidence that individuals suffering from obesity, addiction and depression have in common a down-regulation (reduction in the number or sensitivity) of dopamine receptors. In depression, receptors for other neurotransmitters such as serotonin are also down-regulated, a problem that can actually be made worse by chronic use of SSRI antidepressants.  The article also summarized research indicating that intense exercise, caloric restriction and intermittent fasting can up-regulate dopamine receptors and thereby provide a sustainable treatment for certain types of obesity, addiction and depression.
2. In  ”Obesity starts in the brain“, I outlined the Hypothalamic Hypothesis, a brain-centric analysis of obesity.  I argued that there are two different types of obesity–intra-abdominal and subcutaneous obesity–and that these conditions respectively result from  impairments to the insulin sensitivity or leptin sensitivity of a specific part of the hypothalamus — the arcuate nucleus.  Furthermore, it is the hypothalamic impairments that are primary; for example, insulin resistance starts in the brain and later spreads to the liver and muscles.  The article pointed to specific dietary and inflammatory factors that can improve hypothalamic sensitivity to these hormones and reverse obesity.

I will now build upon the Hypothalamic Hypothesis to account for the influence of the amygdala, to consider how the limbic system governs for drives other than eating, and to propose more generally how we can influence the brain’s control system.

The limbic system. Think about this:  By weight, about 85% of the human brain is the elaborate cerebral cortex, devoted to complex perceptual and conceptual processing and executive function.  In contrast, only a tiny piece of the brain is responsible for the full gamut of motivational drives and emotions, and for maintaining the balance of homeostatic functions like metabolism, body temperature, sleep and energy level.  The simultaneous management of all of these diverse functions is tightly packed into two nut-sized structures–evidently without getting signals crossed! When you think about it, this fact is quite astonishing.  It baffles me that, despite great popular interest in neuroscience, there has been so little commentary about this striking fact.

You can think of the the massive cortex as merely an elaborate pattern recognition system wrapped around the limbic brain.  The cortex’s pattern recognition system has evolved to improve the quality of information being fed to the tiny thermostatic hypothalamus and amygdala.  While the cortex gives us a huge advantage over other animals in analyzing our environment, we seem not to much real control over basic drives like eating and sleeping.  Despite the evolutionary achievement of “rationality”, we humans remain to a large extent at the mercy of our basic animal drives and emotions.

Things are not so bleak, however, once we recognize what makes the limbic brain tick.  While we may not have direct volitional control over the limbic system, there are actions we can take to influence the balance of neural forces within the hypothalamus and amygdala. Over time, we can literally reprogram our psycho-metabolic control systems.

But first a little anatomy.   And I’ll try to keep things simple.  The point of this interlude is not to teach anatomy, but rather to highlight a few key parts of the limbic control system and how they function. I’ve borrowed much of the following discussion from the excellent and incisive monograph, The Limbic System, by Rhawn Joseph, much of which is also contained in Chapter 4 of his online Brain e-book.

The figure below provides a “macro” view of the major parts of the limbic system.  Located at the center of the brain, perched atop the brainstem, the limbic system includes not only the hypothalamus and amygdala, but other structures such as the hippocampus, cingulate gyrus, pituitary gland.  But particularly note that the amygdala is connected tightly by numerous nerve bundles to the hypothalamus.  The amygdala acts directly on the hypothalamus to control hypothalamic drives, and conversely, the hypothalamus “uses” the amygdala (and to some extent the septum) as a window on the world to satisfy its drives by selectively searching out appropriate foods, potential mates, and sleep and exercise opportunities.

Furthermore, notice that the amygdala is closely connected to the olfactory bulb, and mediates its connections to the hypothalamus.  As Joseph notes, “The hypothalamus is exceedingly responsive to olfactory (and pheromonal) input. Perhaps reflecting this partial and putative olfactory origin is the fact that this structure utilizes chemical (hormonal, humoral) molecules to communicate with other areas of the brain, and reacts to these same molecules as well as olfactory cues, including those directly related to sexual status.”  We will come back to the under appreciated importance of olfactory cues in the limbic system’s control of basic drives, particularly appetite and sexual/social attraction.

For present purposes, there are four important points to understand about the actions of the hypothalamus and the amygdala:

1. The hypothalamus is purely reactive. The hypothalamus regulates drives, but is almost totally “blind” to the outside world.  It is inwardly focused and responds reflexively.  It has no memory and acts “in the moment”.   According to Joseph, the hypothalamus is the physical embodiment of the Freudian id:

Emotional functioning at the level of the hypothalamus is not only quite limited and primitive, it is also largely reflexive… Emotions elicited by the hypothalamus are largely undirected, short-lived, being triggered reflexively and without concern or understanding regarding consequences; that is, unless chronically stressed or aroused. Nevertheless, direct contact with the real world is quite limited and almost entirely indirect as the hypothalamus is largely concerned with the internal environment of the organism. Although it receives and responds to light, it cannot “see”. It has no sense of morals, danger, values, logic, etc., and cannot feel or express love or hate. Although quite powerful, hypothalamic emotions are largely undifferentiated, consisting of feelings of pleasure, unpleasure, rage, hunger, thirst, etc….it tends to serve what Freud (1911) has described as the pleasure principle. Functionally isolated, the hypothalamus at birth has no way of reducing tension of mobilizing the organism for any form of effective action. It is helpless. When tensions associated with immediate needs (e.g. hunger or thirst) become unpleasant the only response available to the hypothalamus is to cry and make rage-like vocalization. When satiated, the hypothalamus can only respond with a feeling state suggesting pleasure or at least quiescence.

2. The hypothalamus operates through a hierarchy of channels.  The hypothalamus receives information about the state of the organism, and in turn sends “commands”,  through three main channels:

• The bloodstream. Many signals are exchanged through the relatively porous blood-brain barrier.  For example, as discussed in my previous post on obesity, the hypothalamus receives and integrates a range of signals about short term nutrient status (glucose and fatty acids), gut signals (ghrelin, PYY and CCK) and longer term energy storage  (hormones like insulin, glucagon, leptin and adiponectin).   The blood also carries similar signals regarding body temperature, wakefulness and sleep, and state of readiness for action. And the hypothalamus activates the section of neuroendocrine activators via other glands like the pituitary, thyroid and adrenal glands.
• Nerve fibers –”afferents” and “efferents”.  Certain communication is done via nerve fibers. For example, appetite cues are provided from the nose via the olfactory bulb and from the gut via the vagus nerve.  Body temperature cues are provided from remote thermoreceptors.  The sleep-wake cycle is calibrated by neural inputs from the suprachiasmatic nucleus (SCN), which responds to dark and light cycles.  And conversely, the hypothalamus uses efferent nerves to remotely regulate adrenal glands and digestive organs.
• Higher order inputs.  The above chemical and neural inputs can be modulated or overridden by “emotional” interpretation of perceptual and cognitive inputs.  This is is where the amygdala comes in.

3. The amygdala is the “handmaiden” of the hypothalamus.  It serves as the emotional eyes and ears for the hypothalamus by translating the input of the senses and the great pattern recognition capability of the higher cortex into emotional responses that feed into the hypothalamus.  Going beyond the undifferentiated, spur-of-the moment emotional drives of the hypothalamus, the amygdala provides a highly selective response to specific and often complex sensory stimuli.  As Joseph explains:

In contrast to the primitive hypothalamus, the more recently developed amygdala (the “almond”) is preeminent in the control and mediation of all higher order emotional and motivational activities. Via it’s rich interconnections with various neocortical and subcortical regions, amygdaloid neurons are able to monitor and abstract from the sensory array stimuli that are of motivational significance to the organism. This includes the ability to discern and express even subtle social-emotional nuances such as friendliness, fear, love, affection, distruct, anger, etc., and at a more basic level, determine if something might be good to eat.  In fact, amygdaloid neurons respond selectively to the flavor of certain preferred foods, as well as to the sight or sound of something that might be especially desirable to eat  including even the sight of drugs that induce extreme pleasure…Belying its involvement in emotion, including the pleasure associated with cocaine usage, is the unique chemical anatomy of the amygdala, which is rich in a variety of neuropetides including enkephalins and beta-endorphins as well as opiate receptors. In fact, of all brain regions, the greates concentration of opiate receptors is found within the human amygdala.

Beyond appetite, the amygdala also provides a selective filter on sensory cues related to other drives such as sociality and sexual attractiveness.  Of significant note, the amygdala is the arbiter of very specific social cues such as facial recognition:

The amygdala is exceedingly responsive to social and emotional stimuli as conveyed vocally, through touch, sight, and via the expressions of the face . In fact, the amygdala, as well as the overlying (and partly coextensive) temporal lobe, contains neurons which respond selectively to smiles and to the eyes, and which can differentiate between male and female faces and the emotions they convey. For example, the left amygdala acts to discriminate the direction of another person’s gaze, whereas the right amygdala becomes activated while making eye-to-eye contact …Moreover, the normal human amygdala typically responds to frightened faces by altering its activity, whereas injury to the amygdala disrupts the ability to recognize faces. With bilateral destruction, emotional speech production and the capacity to respond appropriately to social emotionally stimuli is abolished.

Maybe this explains why Seth Roberts observation that looking at faces in the morning makes people happy–a simple anti depression therapy!

Joseph also notes that “The relationship between hypothalamus and amygdala is bidirectional.  The amygdala interprets sensory information and emotions and passes these inputs on to the hypothalamus to initiate drives. And when a drive like hunger or sex emerges, the amygdala helps out by surveying the environment for suitable choices of food or potential sexual partners.”

4. The hypothalamus and amygdala  are composed of opposing sets of neural clusters or “nuclei”.   These pairs of neural clusters act in an oscillating ying-and-yang fashion to achieve homeostasis. In both the hypothalamus and amygdala, the external or lateral nuclei activate the parasympathetic nervous system, associated with hunger and digestion, pleasure, relaxation and sexual arousal.  In the case of appetite, stimulation of neurons in the lateral hypothalamus (LH) increases  appetite, releases serotonin and dopamine, and activates anabolic storage of  glucose and fatty acids,  In opposition to the lateral nuclei, internal or “medial” nuclei activate the sympathetic (“fight or flight”) nervous system, which readies the organism for action, increases heart rate, suppresses appetite and sexual desire, stimulates release of acetylcholine and norepinephrine, and activates catabolic mobilization of nutrients such as fat or glycogen.  Stimulation of the medial nuclei are also associated with “aversive” non-pleasurable sensation.

Similar pairings of opposing limbic nuclei exist for neurons that control thirst, body temperature, the sleep/wake cycle, or activate social or sexual arousal.

The amygdala has a parallel structure to that of the hypothalamus, which allows direct two-way communication between them.   As Joseph notes:

Moreover, through the massive interconnections maintained with the lateral and medial (ventromedial) hypothalamus, the amygdala is able to act directly on this structure, driving the hypothalamus, so to speak, and thus tapping into its emotional reserviour so that its ends may be met. Indeed, it is able to modulate hypothalamic activity through inhibitory and excitatory projections to this structure. Direct stimulation of the basolateral amygdala and the ventral amydalofugal pathway excites the principle neurons of the medial hypothalamus. By contrast, stimulation of the medial (ventro-medial) amygdala and the stria terminalis pathway, inhibits these same hypothalamic neurons. Hence, whereas the lateral amydala exerts excitatory influences on the hypothalamus, the medial amygdala exerts inhibitory influences, and can thus control, or at least exert excitatory/inhibitory and thus modulatory influences on hunger, thirst, sexual arousal, rage, etc., as well as hormonal, endocrine, and other functions associated with the hypothalamic nuclues. Indeed, the amygdala can be likened to the chief executive of the limbic system and weilds enormous power via its control over the hypothalamus.

Similar sets of paired hypothalamic and amydaloid nuclei govern the balances that control thirst, body temperature, sleep and sex drive.  For example, osmoreceptors that monitor the concentration of salt ions in blood control thirst, and respond by adjusting the hormone vasopressin to regulate water retention by the kidney. Thermoceptors in the body and hypothalamus activate different nuclei in the hypothalamus.

Generalized versus conditioned desires. By serving as the “interpreter” that provides higher-level emotive “meaning” to raw sensory inputs, the amygdala plays a prominent role in learning and laying down reward circuitry.  In effect, it turns complex sensory inputs into cues that the hypothalamus can act upon by establishing Pavlovian circuits that automate the way your basic drives respond to the external environment and even your thoughts.  This applies to both attractive (stimulatory) and aversive (inhibitory) stimuli. As mentioned above, the reward circuitry utilizes a high concentration of dopaminergic neurons to reinforce powerful learned responses of the hypothalamus to sensory cues and thought patterns.

While the hypothalamus activates generalized drives and provides hard-wired low-level responses to universal and fairly general cues, the amygdala provides finely tuned and highly specific learned responses that can modify or override these low level cues:

The hypothalamus gets hungry and anything will do…,but the amygdala is picky about which foods it likes or dislikes, to the point of craving a specific type of chocolate with a certain texture, or rejecting a wine with a slight off-note
The hypothalamus wants sex…but the amygdala is selective about what turns it on — down to very fine preferences regarding appearance, aroma, or even sense of humor.  It may be so selective as to be monogamous!
The hypothalamus wants to sleep… but the amygdala picks up cues about danger that can rally your alertness.

The key point is this:   The generic drives of the hypothalamus are equally powerful whether they are activated by low level chemical and nerve inputs from the blood stream or stomach nerves — or rather by higher level perceptual and emotional inputs from the amygdala.  And if the reward circuitry from the amygdala is strong enough, it can override the low level signals.   A Pavlovian response to the aroma of a juicy steak or the sight of a decadent chocolate cake can activate the hunger response and fat storage program initiated in the lateral hypothalamus, regardless of the nutritional state conveyed by blood glucose or leptin and insulin levels.  Conversely, an unappetizing meal, or an emotional shock can quickly suppress appetite or activate a state of arousal and access to energy.

The hypothalamus doesn’t know or care why it is getting hungry, sleepy or sexed up.   It matters not whether the signals are based on blood chemicals or high level emotional perception — the actions taken by the hypothalamus are identical in either case.

An aside on food reward. This dual model of direct hypothalamic regulation versus conditioned amygdaloid regulation of drives like hunger can shed some light on the recent debate about the Food Reward Hypothesis of obesity.  Stephan Guyenet has cited compelling evidence for the FRH, based on the  observation that rats fed a “cafeteria diet” of highly palatable junk food became fatter than rats fed calorically matched standard bland rat chow.  Merely adding flavor or flavor variety to the chow also resulted in fatter rats.

However, in an earlier post, “Does tasty food make us fat?“,  I argued that Guyenet’s version of the FRH suffers from two logical flaws:  First, Guyenet does not take a clear position on whether “reward” is an inherent property of foods, or rather a learned or conditioned property, relative to individual and cultural experience.  Second, while rewarding food is associated with obesity, the causal sequence can be questioned.  I think it is likely food reward is the is the consequence, not the driver of psycho-metabolic dysregulation.  Food becomes rewarding only after primary hypothalamic regulation becomes impaired, for example by the way that the particular fats and sugars in junk food desensitize hypothalamic receptors to insulin or leptin, as I described in “Obesity starts in the brain“.   Of course, once the amygdaloid food reward circuits are established, they can be expected to perpetuate an increased appetite and shift away from fat mobilization to fat storage.  But the amygdaloid reward circuit is not the primary defect — that remains the impairment to the hypothalamus.  The proof is that it is not just appetite that is impaired — it is also the metabolic consequence of a more active lateral hypothalamus and inhibited ventromedial hypothalamus.   If the hypothermic defect is repaired, the food reward circuit should extinguish.

THE BOTTOM LINE

Hormesis and the hypothalamus.   So how do we use this information?  Specifically, how do we “judiciously” apply “stress”s to re-program our limbic control system. What if we are gaining weight due to both a strong appetite and more “efficient” storage. Or what if we have trouble falling and staying asleep?  Or (more speculatively) what if we want to become more or less aggressive, or more or less sexually motivated?

In short, our understanding of the limbic system suggestions two approaches:

1.  Direct reprogramming of the hypothalamus. Every drive is regulated by a balance of stimulatory and inhibitory neurons.  By the logic of hormesis, we can stimulate the growth of one set of neurons or the other by periodically  ”starving” them of their normal stimuli, allowing a compensatory up-regulation of receptor neurons.  Often this process is slow, and the compensating adaptations may take weeks or longer — but with sustainable results. This is the reverse logic illustrated in several posts.

• “Change your receptors, change your set point”  demonstrates how exposure to uncomfortable stresses such as intermittent fasting, strenuous exercise, cold showers and the like can up-regulate dopaminergic neurons and thereby counteract conditions such as obesity, addiction and depression.  While the research cited in that article doesn’t specifically locate the dopamine neurons, , we know they have a high density in the hypothalamus, amygdala and other limbic structures, and the PET scans indicate a brain location consistent with the hypothalamus and amygdala.
• “A cure for insomnia?” describes the use of Sleep Restriction Therapy (SRT).  By forcing extended wake cycles, there is an apparent rebalancing of hypothalamic neurons in the ascending arousal system, thereby activating sleep-active neurons in the ventrolateral preoptic nucleus (VLPO) associated with the  “flip-flop switch” that produces distinct sleep-wake states.  As a result, SRT reduces the  excessive production of corticotropin-releasing factor (CRF) that is associated with many cases of insomnia.

Where does obesity begin?  What drives you to eat too much or expend too little energy, and why has there been such a dramatic increase in obesity since 1980? Some recently popular explanations are the carbohydrate / insulin hypothesis (CIH), singling out the prevalence of carbohydrates in the diet, and the food reward hypothesis (FRH), putting the primary blame on the availability of “hyper-palatable” food.

In this post I will present evidence for new paradigm, which I call the  Hypothalamic Hypothesis (HH).  I think it provides a better explanation for the facts of obesity than the CIH and FRH theories, and leads to some different advice about how best to lose weight.

Some recent research suggests that obesity starts with specific physical changes to the brain. Appetite is regulated by the hypothalamus, particularly the arcuate nucleus (ARC), ventromedial hypothalamus (VMH) and lateral hypothalamus (LH). It turns out that two very specific changes to the brain cause us to get get hungry, overeat, burn less fat, and gain weight. And these changes to particular brain structures come about as a result of what you eat, eating frequency, and to some extent your activity level. The problem of obesity or overweight is often portrayed as a single problem, but it is really two problems, and each type of obesity corresponds to one type of brain alteration. Failure to distinguish these two types of obesity has resulted in much confusion. In part, the confusion comes about because these two types of obesity frequently occur together in the same individual, although one type is usually dominant. If you understand this, and you understand the role your brain plays, you can become more successful at losing excess weight.

I’ll spend a little time explaining the theory, provide some specific suggestions for how it can help you fine tune your weight loss program, and try to point out why I think the Hypothalamic Hypothesis overcomes some weaknesses of the other obesity theories.

Two types of obesity.  One major type of obesity is subcutaneous (SC) obesity.  The man on the right is a Sumo wrestler with subcutaneous obesity,  but you don’t have to be a wrestler to have this type of fat distribution.  It is characterized by lots of looser, softer fat hanging from the torso, arms, legs and even the face.  A double chin and skin folds under the arms are not uncommon for this type.  SC obesity is more common among women than men.

The second major type of obesity is visceral or “intra-abdominal” (IA) obesity. This is depicted by the classic “beer belly” sported by the main in the left photograph, characterized by a protuberant gut, but frequently not a lot of extra fat on the legs or arms. It’s quite prevalent among men, but seen on many women as well.

The above photos show extreme types, but it is common for both types of obesity to coexist in the same person, in varying degrees.  Those with predominant IA obesity are sometimes referred to as “apples”; those with predominant SC obesity are called “pears”.

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Different metabolisms. The difference between subcutaneous and intra-abdominal obesity is not merely a matter of how adipose tissue is distributed on the body, but also about the biological composition of the fat tissue and it’s metabolic activity.  Subcutaneous fat is located just beneath the skin, and on the outside of the muscle tissue, all over the body.  By contrast, intra-abdominal fat– also called visceral fat–is located underneath the visceral muscles, deep within the gut.  It  surrounds the digestive organs — the liver, pancreas, stomach and intestines.  The difference can be seen clearly in the CT scans at the left.  The top image shows a cross-section at mid-belly level of someone with SC obesity, with most of the dark gray fat mass located right under the skin but outside the lighter grey visceral muscles and internal organs.  The bottom image is a similar CT scan of someone with IA obesity, showing much less subcutaneous fat, but considerable fat beneath the walls of the viscera, packed around the intestines.

What is important to realize is that the adipose tissue stored inside the abdomen is biochemically and metabolically very different than the fat stored right under the skin.  Both are called “fat” or “adipose tissue” but they behave as if they were entirely different substances. The image below at left is a micrograph of SC fat; the image at right shows IA fat cells.  Notice the different shape and size, but also the substantial dark “mortar” between the IA fat cell “bricks”.

The adipose tissue in IA fat is not an inert storage tissue.  On the contrary, it is a metabolically active hormonal “organ”: it is infiltrated by macrophages and secretes “adipokines” like interleukin-6, tumor necrosis factor alpha, and C-reactive protein.  These compounds are inflammatory signaling agents, associated with insulin resistance, diabetes, hypertension, and cardiovascular disease characteristic of Metabolic Syndrome.  The health effects of this inflammatory process have been the subject of intense study.  In this article, however, I’ll address only the role that these inflammatory processes have in the development of obesity.

The appetite center.  To understand the dynamics of each type of obesity, it is important to understand how appetite and body fat are governed by the brain. The hypothalamus regulates biological drives, including feeding, sleep and hunger.  As shown in the diagram at right (and also in this video) appetite, feeding behavior and metabolic rate are regulated by two sets of neurons that have opposite effects on appetite and metabolism:

• The  ”anorexigenic” POMC/CART neurons that inhibit appetite and increase the rate of fat oxidation in the body.  In response to nutrients and certain hormones, these neurons produce the appetite-suppressing neuropeptides propio-melanocortin, cocaine-and-amphetamine-regulated transcript and α-melanocyte stimulating hormone (α-MSH). The α-MSH binds to and activates secondary melanocortin-4 (MC-4) neurons in the ventromedial hypothalamus (VHM), causing satiety and increasing energy expenditure and  fat oxidation in the body. Animals with damaged or lesioned POMC/CART neurons eat voraciously and become obese.  Both leptin and insulin are potent hormonal stimulators of the POMC/CART neurons.  These neurons have receptors for appetite suppressing signals like insulin and leptin; low levels of either hormone will increase appetite and reduce metabolic rate. If  a deficiency of leptin or insulin persists, it will lead to obesity.
• The  ”orexigenic” NPY/AgRP neurons that stimulate appetite and slow down fat oxidation in the body.  These neurons produce two neuropeptides — neuropeptide Y (NPY) and agouti-related protein (AgRP) which act to inhibit α-MSH from binding to and activating the MC-4 satiety neurons and stimulates melanin-concentrating hormone (MCH) in the lateral hypothalamus (LH). This inhibition of MC-4 and stimulation of MCH enhances appetite and decreases metabolism and energy expenditure, conserving fat.  Animals in which the NPY/AgRP neurons have been damaged or destroyed by lesions become anorexic and lose weight.  Insulin and leptin inhibit the NPY/AgRP neurons, whereas the “meal timing” hormone ghrelin, which cyclically ebbs and flows, stimulates them.

These two sets of neurons govern fat gain and fat loss.  They effectively sense the energy status of body by centrally integrating inputs from a large number of circulating nutrients, neuropeptides and hormones, and they respond by outputting neuropeptides that drive behavior and peripheral metabolism. When they are in balance, a normal and healthful level of body fat is maintained, but when the balance of  orexigenic or anorexigenic signals shift, this adjusts the body’s fat and activity set points up or down.  As a prime example, if leptin levels in the hypothalamus are low, either because of low body weight or because the leptin is blocked from reaching its receptors in the POMC neurons, appetite will increase, fat oxidation will decrease, and this will lead to an increase in adiposity.

Insulin, leptin and appetite. There are two hormones which predominantly regulate body fat:  insulin and leptin. In healthy individuals, as Byron Richards describes,

Leptin uses adrenaline as a communication signal to fat cells, telling them to release stored fat to be used for fuel. This takes place in the course of a normal day between meals and at night during sleep…A drop in leptin signals hunger. Food intake stimulates insulin release. As a person eats, insulin is always directing some amount of triglycerides to go over to white adipose tissue and enter fat cells….This turns on the production of leptin in fat cells, causing the blood level to rise in response to the meal. As the leptin levels rise high enough, they signal to the brain that enough has been eaten. Leptin now signals the pancreas to stop making insulin…In overweight people, the communications involving insulin and leptin are inefficient. It is like making a phone call where no one answers. Insulin and leptin resistance mean that the hormones don’t communicate efficiently in response to food.” (The Leptin Diet, p. 13, 17, 23, 36)

Increased basal levels of either of these two hormones indicates increased energy stores and adiposity. The hormones have different metabolic effects depending on their site of action.  As Lustig explains, the action of these hormones “centrally” — inside the brain — is entirely different than that in the “periphery” — the rest of the body:

Insulin also plays a pivotal role in the control of appetite and feeding. In addition to its well-defined peripheral role in glucose clearance and utilization, insulin is involved in the afferent (and efferent) hypothalamic pathways governing energy intake, and in the limbic system’s control of pleasurable responses to food. Whereas insulin drives the accumulation of energy stores in liver, fat, and muscle, its role in the CNS tends to decrease energy intake. This is not a paradox, but rather an elegant instance of negative feedback. When energy stores abound, circulating insulin tends to be high; high CNS insulin tends to decrease feeding behaviors, thereby curtailing further accumulation of energy stores. Insulin’s central effects on energy intake are manifested in two complementary ways: first, insulin decreases the drive to eat; second, insulin decreases the pleasurable and motivating aspects of food.

This self-limiting regulatory action of insulin is also noted by Banks:

Insulin plays many roles within the CNS. Several laboratories have shown that some of the CNS effects of insulin are the opposite of those effects mediated through peripheral tissues. In particular, CNS insulin increases glucose and inhibits feeding, whereas serum insulin decreases glucose and increases feeding. Thus, to some extent, insulin acts as its own counterregulatory hormone, with CNS insulin producing features of insulin resistance.

Both insulin and leptin have an appetite suppressing effect when an elevated level of either one reaches the appetite center of the brain, specifically the satiety-inducing POMC/CART neurons within the arcuate nucleus (ARC) of the hypothalamus.  While similar in their appetite suppressing effect, insulin levels fluctuate in response to the ingestion of meals, especially carbohydrate-rich meals, whereas leptin levels generally reflects longer term changes in energy stores.   Most noteworthy for this discussion, however, these two hormones reflect the two different types of fat.  According to Woods et al:

Insulin is secreted in proportion to visceral fat, whereas leptin reflects total fat mass and especially subcutaneous fat. This is an important distinction with regard to the message conveyed to the brain, since visceral fat carries a greater risk factor for the metabolic complications associated with obesity than does subcutaneous fat. Elevated visceral fat carries an increased risk for insulin resistance, type 2 diabetes, hypertension, cardiovascular disease, and certain cancers. Hence, leptin and insulin each convey specific information to the brain regarding the distribution of fat, and the combination of the two additionally conveys information as to the total fat mass of the body.

Interestingly, Woods also reports the brains of females are more sensitive to leptin than insulin, whereas the reverse is true in mails, and that estrogen mediates this difference.   According to  Cnop el at., women on average have three times as much leptin as men, even after controlling for comparable degrees of body mass and insulin resistance. Which explains why there are more male “apples” and more female “pears” — though of course both types of obesity are represented to varying degrees in both genders.

While the appetite regulating actions of insulin and leptin within the brain are well known, what is less well known is that these the two hormones also use “remote control” from within the brain to activate fat loss in the rest of the body.  According to Woods:

As previously mentioned, when leptin is administered into the brains of experimental animals, there is a selective reduction of body fat, with lean body mass being spared. Likewise, when insulin is administered into the brain, there is a reduction of the respiratory quotient, suggesting that the body is oxidizing relatively more fat. These observations suggest that one action of these adipose signals within the brain is to reduce body fat, and a corollary of this is that fat ingestion would be expected to be reduced as well. Consistent with this, we have observed that when insulin is administered into the third cerebral ventricle of rats, fat intake is selectively reduced. Hence, it is reasonable to hypothesize that leptin and insulin, acting in the brain, reduce body fat by increasing lipid mobilization and oxidation and simultaneously by reducing the consumption of dietary fat.

In short, if you want to control your appetite and burn fat faster,  you want leptin and insulin to get inside your brain!  The problem in obesity is that these hormones are not adequately reaching and communicating with the appetite center of the hypothalamus.

Putting up resistance.  So far, I’ve described how leptin and insulin work to homeostatically regulate appetite and body fat in normal individuals.  But this carefully balanced feedback system becomea derailed in obesity.  There are some interesting, but fortunately rare, genetic or disease conditions where the leptin or insulin sensitive receptors in the hypothalamus become defective and insensitive to leptin or insulin. In other words, the “off” switch for appetite stops working correctly.  Or where the leptin or insulin molecules themselves are mutated or damaged and are thus unable to turn off the appetite switch.  Animals or humans with these defects eat voraciously, insatiably and become extremely obese. These rare cases provided some of the initial evidence for the current understanding of how leptin and insulin regulate appetite and body weight.

But defective  hormones and receptors are rare and do not explain the vast majority of cases of obesity. The “normal” cause of obesity involves involves leptin resistance or hypothalamic insulin resistance, whereby there is plenty of leptin or insulin circulating in the bloodstream, and the appetite-suppressing POMC neurons are functional, but not all of the hormone is reaching the receptors in the hypothalamus. The messenger is yelling, but the ears hear the message faintly.  There is a barrier or impediment between messenger and receiver.   The result in each case is that appetite is not getting satisfied, so there is a drive to overeat.  And furthermore, as Woods notes, the “remote control” fat burning functions of the hypothalamus are also reduced.  As a result, with more eating and less fat mobilization and oxidation, you get fatter.

Now, let’s see in more detail what happens to the hypothalamus in each main type of obesity.

Subcutaneous (SC) obesity and the brain.  Leptin is produced in adipose tissue, but specifically in SC fat.  The more SC fat, the more elevated the leptin concentration in the blood.  Normally this would provide a negative feedback signal, inducing satiety in the hypothalamus and increasing the release of fatty acids from fat cells.  In SC obesity, however, only a low level of this leptin is reaching the hypothalamus, so appetite and eating are not inhibited.  But why does this happen?  What is the mechanism?

Some, like Lustig, see insulin resistance in the brain as a likely driver of leptin resistance:

Hyperinsulinemia itself may be a cause of leptin resistance. As described, insulin and leptin use many of the same neurons, the same second messengers, and the same distal efferents to effect induction of satiety….Although confirmation in animal studies is needed…CNS insulin resistance may be a proximate cause of leptin resistance, promoting continued weight gain.

However, it is not plausible to blame leptin resistance on insulin resistance, because many of the obese are insulin sensitive.  For example, Sumo wrestlers notably  can weigh 500 pounds or more,  but they are typically insulin sensitive, and have low cholesterol. According to an study by  Gerald Reaven of Stanford:

The ability of insulin to mediate glucose disposal varies more than six-fold in an apparently healthy population, and approximately one third of the most insulin-resistant of these individuals are at increased risk to develop cardiovascular disease. Differences in degree of adiposity account for approximately 25% of this variability, and another 25% varies as a function of level of physical fitness. The more overweight/obese the person, the more likely they are to be insulin-resistant and at increased risk of cardiovascular disease, but substantial numbers of overweight/obese individuals remain insulin-sensitive, and not all insulin-resistant persons are obese.

Recent evidence suggests that the crux of leptin resistance can be located at the door to the brain:  the blood-brain barrier (BBB).  The BBB is semipermeable along the arcuate nucleus.  This allows for controlled, selective transport of various nutrients and energy signals.  According to Banks,

The blood–brain barrier (BBB) prevents the unrestricted movement of peptides and proteins between the brain and blood. However, some peptides and regulatory proteins can cross the BBB by saturable and non-saturable mechanisms. Leptin and insulin each cross the BBB by their own transporters. Impaired transport of leptin occurs in obesity and accounts for peripheral resistance; that is, the condition wherein an obese animal loses weight when given leptin directly into the brain but not when given leptin peripherally. Leptin transport is also inhibited in starvation and by hypertriglyceridemia. Since hypertriglyceridemia occurs in both starvation and obesity, we have postulated that the peripheral resistance induced by hypertriglyceridemia may have evolved as an adaptive mechanism in response to starvation.

In a study on mice, Banks et al. showed  that triglycerides, but not free fatty acids, induce leptin resistance.  This same study showed that, that fasting for 16 hours reduced triglycerides and increased leptin transport, whereas fasting for 48 hours increased triglycerides and impaired leptin transport. This provides support for intermittent fasting as a strategy to reverse leptin resistance.  Elevated triglycerides also enhance the transport of ghrelin, the hormone responsible for initiating feeding at conditioned meal times, which explains why certain obese people get especially hungry around meal time.

Triglyceride levels tend to increase with your degree of adiposity.  But what causes them to rise in the first place?  The primary culprit seems to be fructose, which is converted to triglycerides if consumed in excess. Of course, fructose is part of sucrose and high fructose corn syrup, so any of these sugars in excess will elevate triglycerides, cause leptin resistance, and SC obesity.  Foods containing high concentrations of sugar include  sodas, candies, breakfast cereal, bread and other baked goods, but also sugary fruits like bananas, mangos and raisins. Michael Eades recognized the connection between triglycerides, the blood brain barrier and appetite in his 2007 blog post “Leptin, low-carb and hunger“. But I suspect that it is specifically the effect of fructose reduction — and not the generalized carbohydrate reduction postulated by Eades– that is the primary explanation for low carb diets work to reduce appetite so well for many people.

Diet, of course, is not the only factor affecting how the blood-brain barrier affect leptin resistance.  For example, Banks also notes that epinephrine enhances leptin transport across the BBB by a factor of 2-3 fold.  This explains why exercise and excitement can act to suppress appetite.

Intra-abdominal (IA) obesity and the brain.  Insulin is produced by the pancreas, when it circulates through most of the body outside the brain and spinal cord — what physiologists call the “periphery” — it’s main function is to regulate the availability and storage of glucose and fatty acids, thus preventing excessive glucose or fatty acid levels in the bloodstream.  When insulin receptors in liver, muscle, and other tissues become less responsive to insulin, the resulting insulin resistance results in hyperinsulinemia and its associated metabolic derangements such as Type 2 diabetes. There has been much investigation regarding what causes insulin resistance, the lead hypothesis being some sort of inflammation due to many suspects, including certain fats.

Unlike leptin, triglycerides do not impair insulin transport into the brain. According to a study by Urama and Banks,

[T]he triglyceride triolein significantly increased the brain uptake of insulin, an effect opposite to that on leptin transport, in starved obese mice….That is, leptin transport across the BBB increased with short-term fasting but decreased with starvation and with administration of triolein. In contrast, insulin transport is decreased by short-term fasting but increased by starvation and by triolein.

So what, if not triglycerides, leads to insulin resistance in the brain?

The answer appears to be: free fatty acids. Certain fatty acids – trans fats, certain long-chain saturated fatty acids, and omega-6 unsaturated fatty acids  – produce an inflammatory response in insulin receptors that blunts insulin sensitivity. By contrast, other fatty acids — principally omega-3 fatty acids (like flax or fish oil) and short or medium chain triglycerides (like coconut oil) — are actually anti-inflammatory).  Certain sugars like fructose also appear to be pro-inflammatory.  But what has not been recognized until recently is that these inflammatory processes occur not just in the liver and muscles, but also within the hypothalamus.

And in fact, inflammation of the hypothalamus may be where insulin resistance starts.

Posey et al found that mice fed a high fat diet, with equal calories to a low fat diet, gained 60% more adipose tissue than those on the low fat diet.  Other experiments by Kaivala et al. showed a high fat diet resulted in a 60% reduction in CNS insulin levels, inversely associated with changes in body weight. Thaler et al. , Schwartz et al and Benoit et al. showed that  one particular long chain saturated fatty acid — palmitic acid — causes inflammation and reduces insulin sensitivity in the hypothalamus, leading to overeating and obesity.  Arruda et al. found that intracerebroventricular  injection of an inflammatory cytokine (TNF-α) or stearic acid (another long chain saturated fatty acid) into lean rats induced insulin and leptin resistance in the hypothalamus and hyperinsulinemia and down regulated thermogenesis and oxygen utilization.  In TNF knockout rats (those missing the TNF receptor), the TNF-α did not produce any of these effects, and the rats were protected.  Furthermore, Araujo et al showed that co-administrering an anti-inflammatory drug (infliximab) restored normal oxygen consumption in the obese rats.  Similar results from other studies have been reviewed by Schwartz et al .

Interestingly, high levels of fructose can also cause inflammation and insulin resistance, leading to IA obesity.  If you are lean and healthy, fructose at reasonable levels is converted to glucose in the liver, and brief excess is then stored as glycogen in the liver and muscles.  But in vast excess, fructose is converted to fat of two types — triglycerides and one particular fatty acid.  Can you guess which fatty acid?  The answer is palmitic acid, the fatty acid associated with brain insulin resistance. The liver begins to accumulate the excess fat – a condition known as steatosis or fatty liver disease — which results in hepatic insulin resistance.   So while high fructose consumption causes elevated triglycerides, those triglycerides cause leptin resistance and are not a direct cause of insulin resistance. do not cause insulin resistance, only So it looks like fructose (and of course sucrose which is 50% fructose) is involved in the genesis of both SC obesity and IA obesity.  The fact  is just one manifestation of how easy it is to get confused about “the cause” of obesity.  Because there are two types of obesity with different but intertwined etiologies, the logic of obesity is not always so easy to sort out.  But the various diveres causal threads always come together in the arcuate nucleus of the hypothalamus

What is most illuminating, however, is research by Ono et al showing that hypothalamic insulin resistance precedes — and probably causes — insulin resistance in other organs and tissues.  Ono found that feeding rats a high fat diet induced insulin resistance in the hypothalamus after only one day, with no concurrent hepatic insulin resistance!  It took a full 3 days on this diet for insulin resistance to show up in the liver, and 7 days for the muscles and peripheral tissues to become insulin resistant.   The mechanism of inflammation was the activation of the mTOR/S6K pathway by exposure to fatty acids.  The S6K protein apparently inhibits insulin signaling in the arcuate nucleus of the hypothalamus, activating the orexigenic NPY/ArGP neurons and inhibiting the POMC neurons.  Similarly, Pagotta has marshalled other evidence suggesting that insulin resistance starts in the brain.  Of particular note is a study by Obici et al, in which central administration of insulin suppressed glucose production by the liver, and blocking insulin signaling in the brain impaired the ability of insulin to inhibit glucose production in the liver. Finally, an excellent post by Stephan Guyenet cites a similar study by Morton and Schwarz showing much the same thing.  As Guyenet notes,

Investigators showed that by inhibiting insulin signaling in the brains of mice, they could diminish insulin’s ability to suppress liver glucose production by 20%, and its ability to promote glucose uptake by muscle tissue by 59%.  In other words, the majority of insulin’s ability to cause muscle to take up glucose is mediated by its effect on the brain.  

In regard to insulin signalling,  the brain seems to be in charge of the liver.  And this plays out in the genesis of insulin resistance.

This raises an interesting question:  why would insulin resistance start in the brain, rather than the liver or the muscles?  When you think about it for a few minutes, it actually makes sense.  The hypothalamus is the ultimate arbiter of whether or not the body has adequate energy intake. It does this by homeostatically regulating energy stores and energy balancing hormones. In the case of leptin resistance, as we’ve already seen, the brain acts to restore homeostasis signaling the peripheral metabolism to “grow” more subcutaneous fat (by increasing appetite and slowing fat oxidation).  If insulin signaling in the brain is blocked or impaired, homeostasis requires the initiation of compensatory processes that will bring more insulin into the brain.  But how to do that?  Insulin is not produced in the fat cells, so growing more fat won’t directly help.  To do this, the periphery must become somehow become hyperinsulinemic, in order to overcompensate so that enough insulin gets into the hypothalamus.  And the best mechanism for this is to induce whole body insulin resistance, primarily in the liver and muscles.

But how does the insulin resistant brain orchestrate insulin resistance in the periphery?  The answer, apparently, is to grow intra-abdominal fat. As Ljung notes, hypothalamic insulin resistance disrupts the hypothalamic-pituitary -adrenal axis (HPA), leading to increased secretion of ACTH and cortisol.  These hormones in turn stimulate the growth of intra-abdominal adipocytes.  The IA fat proliferates macrophages and releases pro-inflammatory  fatty acids and “adipokines” into the bloodstream. (See “Intra-Abodominal Adipose Tissue: The Culprit?“) The portal circulation carries these to the liver where they promote steatosis (fatty liver), insulin resistance, and local inflammation. The systemic circulation further carries these fatty acids and proinflammatory molecules to skeletal muscle where they promote lipid accumulation, insulin resistance, and local inflammation.  As Ross showed,  it is IA fat, not total fat or SC fat, that is associated with whole body insulin resistance.  Insulin resistance in the body causes the pancreas to go into overdrive to supply more insulin, resulting in hyperinsulimia. As basal insulin levels increase, the hypothalamus is now getting its fix of insulin, keeping hunger in check.  Of course, the level of IA obesity and hyperinsulimeia will only be what is required to handle the degree of inflammation experienced by the arcuate nucleus in the brain.  One this inflammation is reduced or removed, and the NPY/AgRP neurons become more sensitive to insulin, the requirement for elevated basal insulin should go down, and with it the need for intra-abodominal fat.

In slogan form, here is the Hypothalamic Hypothesis of Obesity:

If the hypothalamus is deficient in leptin, it directs the body to grows more subcutaneous fat.

If it is deficient in insulin, it directs the body to grow more intra-abdominal fat.

Now for some practical advice:   How can you use the Hypothalamic Hypothesis to lose unwanted fat or better control your weight?

1.  Start by assessing your degree and type of adiposity.  Do you have a waist-to-hip ratio greater than 0.8 (women) or 1.0 (men) and carry your extra weight a belly that sticks out in front? That’s IA fat and you are a probably an  ”apple”. Or do you have a waist-to-hip ratio of less than 0.8 (for women) or 1.0 (for men) and carry most of your extra weight on your butt, your thighs, chest, and possibly also your arms and neck?  That’s SC fat and you are probably a “pear”.   Of course, you may be an “apple-pear” and carry extra fat in both locations, but it is good to know which type of fat is dominant.  If you want a much more precise assessment using specific measurements of body weight, height and other body dimensions, I recommend consulting “Assessing Your Risk”, Chapter 9 in Protein Power, by Eades and Eades.

2.  If you are primarily a “pear”, and particularly if you are significantly overweight, you are leptin-resistant.  Your primary focus should be on reducing triglycerides.  Largely, this means cutting back on carbohydrates with fructose or sucrose (which is a disaccharide of fructose attached to glucose) is readily converted to triglycerides by the liver.  And it is triglycerides that primarily induce leptin-resistant SC obesity.  So of course you want to cut out soft drinks, cookies, cakes, ice cream, candies, most fruits, and most breads (except those with no sugar, which are hard to find). But so long as you are reasonably insulin sensitive, you don’t have to cut out starches.  Potatoes and rice are probably fine if you are insulin-sensitive as long as you avoid any sugar in the same meal.  If you are an “apple-pear” and are resistant to both leptin and insulin, then you can still eat fructose-free starches like potatoes and starch, but you must not add any pro-inflammatory fats. The question of what constitutes a “pro-inflammatory fat” is a controversial one.  Some fats, such as trans fats and high levels of omega-6 fats are clearly pro-inflammatory, while omega-3 fats, mono-unsaturates like olive oil, and medium chain triglycerides like coconut oil are anti-inflammatory.  But for saturated fats, the picture is less clear and the studies are all over the place.  Probably some saturated fats are OK.  But some people have found that cutting back on cheese and nuts help them shed abdominal fat.  Milk and butter from grass fed cows may be preferable to that from grain fed cows.

What about alcohol?  Alcohol is frequently assumed to raise triglyceride levels, but observational studies show this may not necessarily not true.  Moderate alcohol may actually reduce triglyceride levels.

Finally, as the Banks’ fasting study suggests, intermittent fasting (16 hours, but not 48 hours) can reduce triglycerides and restore leptin sensitivity.

3.  If you are primarily an “apple”, pre diabetic, or trying to lose stubborn belly fat — the last 10-20 pounds,  your primary focus should be on eating a non-inflammatory diet.  For the most part, this means cutting back on certain fats — trans fats (anything “partially hydrogenated” on the nutrition label), vegetable fats high in omega-6 oils, and perhaps certain saturated fats like those in meat, milk, butter or cheese from grain-fed cows. As mentioned above, the question of which saturated fats are “pro-inflammatory” is controversial. The strongest evidence that connects saturated fatty acids to brain insulin resistance is for palmitic acid, but that does not mean all saturated fatty acids cause insulin resistance. In any case, don’t shun non-inflammatory fats like fish oil, olive oil, or coconut oil.  Adding these to your meals can help reverse IA obesity.  I’ve personally found coconut oil to be great for energy and weight loss.

Because consuming high levels of sugar in the diet (fructose, sucrose or syrups that contain them) causes output of pro-inflammatory palmitic acid,  foods containing sugar should be restricted.  If you are lean and have a have a healthy liver, I see nothing wrong with fructose in moderate quantitates.  The daily apple will not hurt you, but the excessive amounts of sugar in  sodas, pastries, ice cream, bread (which contains sugar)  sweet fruit — make you (or maintain you as)  both a  ”pear” and an”apple”.

In addition to avoiding high levels of certain fatty acids and sugars, inflammation can also be reversed by a few additional steps:

• ensuring adequate intake anti-inflammatory micronutrients such as Vitamin D and magnesium
• high intensity exercise, intermittent fasting, cold showers and other hormetic stressors which upregulate anti-inflammatory brain compounds such as BDNF

Caveats. In making the above suggestions, I would like to make a disclaimer:  This post is primarily about a new paradigm of obesity, but I realize that people are looking for specific dietary recommendations.  The  above dietary advice is based upon my best attempt to interpret two general principles regarding the effects of triglycerides and inflammation on the appetite center of the hypothalamus.  In doing this, I am relying on a large body of empirical evidence that is sometimes ambiguous or contradictory — for example, regarding which saturated fats are pro-inflammatory, and which are protective.  And so I may be wrong about the hypothalamic effect of this or that specific food.  Despite this uncertainly, the HH provides a test for deciding whether a food or practice is obesogenic and leads to overeating: namely whether it raises triglycerides or inflames the hypothalamus.  And it is also apparent that these guidelines for foods to avoid cut across conventional macronutrient categories like “fat” and “carbohydrate”, since the hypothalamus does not sort things out that way.

…

OTHER THEORIES OF OBESITY.  I would like to close by contrasting the Hypothalamic Hypothesis with two other theories of obesity, showing how it better accounts for certain facts, and leads to perhaps some different recommendations for losing excess body fat.

The Carbohydrate / Insulin Hypothesis (CIH).  Most prominently advocated by Gary Taubes, CIH holds that dietary fat plays no role in obesity.  Rather, dietary carbohydrates, through their stimulation of insulin secretion, result in a greater degree of fat storage. Carbohydrates drive insulin drives net fat storage. Obesity is a disorder of excess fat accumulation, not overeating or inadequate energy expenditure.  In its favor, CIH can account for the close correlation between obesity and hyperinsulinemia, and the success of low carb dieting.  However, it manifestly does not explain why many obese people, like Sumo wrestlers, are insulin sensitive, with normal insulin levels and no indications of diabetes, cardiovascular disease, or other signs of Metabolic Syndrome.  It also does not account for why others, such as the Kitavans and Okinawans, can  eat a diet low in fat but high in certain starchy carbohydrates (polymers of glucose) like root vegetables or rice, and remain lean, with low basal insulin levels.  And it cannot explain why, despite sincere attempts, many people can lose only a certain amount of weight (probably subcutaneous fat) on low carb diets, but often stall and remain insulin resistant when continuing to eat a high fat / low carb diet.  The HH can explain all these facts by carefully distinguishing SC obesity from IA obesity, and by narrowing the cause of type of obesity to very specific types of carbohydrate (fructose and sucrose) and fat (long chain saturates, trans fats and omega-6 fats).  And, perhaps heretically, HH predicts that once you’ve maxed out the benefits of low carb, you can get rid of that paunch and insulin resistance by cutting back on fats– at least the pro-inflammatory fats.

The CIH also cannot explain certain anomalies such that described by Stephan Guyenet and Chris Masterjohn:  the LIRKO mouse which has severe hepatic insulin resistance and hyperinsulinemia — but remains leaner than its normal counterparts.  Guyenet and Masterjohn seem to conclude from this that insulin resistance cannot be a cause of obesity.  The mistake they make, I believe, is overlooking the possibility that only one type of insulin resistance — that of the hypothalamus — leads to obesity.  The LIRKO mouse they discuss had an insulin resistant liver, but apparently a well functioning hypothalamus.  It would have been interesting to feed it some pro-inflammatory fats to see what would happen.

One further aside about the CIH:  I must admit that I was previously persuaded by the orthodox version of CIH and it’s explanation about hunger–which I now suspect is incorrect.  I employed this theory elsewhere in this blog to explain the appetite-suppressing effect of low carb diets, intermittent fasting, and flavor control diets such as the Shangri-La Diet.  The explanation was based on what I thought was a very plausible theory I first encountered in Gary Taubes’ Good Calories, Bad Calories, Chapter 24,”Hunger and Satiety.” .  The insulin-lowering effect of low carb diets is supposed to counteract hunger from hypoglycemia by making glucose and free fatty acids more available.  And the appetite inducing effects of  appetitive flavors or aromas is explained by their action (probably via the vagus nerve, mediated by the brain’s  tractus solitarus) in eliciting a preprandial insulin response.  This preprandial insulin response supposedly causes a sudden drop in  blood glucose, inducing hunger.   I now believe this theory is wrong, or at least incomplete, for several reasons.  Primary among those reasons are my own experience with blood glucose self monitoring, where I noticed that my blood glucose would typically drop after, but not before I would get hungry.  Also, preprandial insulin responses are typically fairly small and unlikely to reduce blood sugar enough to induce hypoglycemic hunger. So the preprandial insulin response seems too little, too late.  It is more likely an effect, not a cause, of hunger.  I now suspect that a more likely explanation would be the direct action of the vagus nerve and tractus solitarus on the orexigenic or anorexigenic neurons in the ARC, or on the permeability of the blood brain barrier.  But that will be a topic for another post.

The Food Reward Hypothesis (FRH).  The most effective advocate for the FRH is Stephan Guyenet, of Whole Health Source.  Guyenet is the first to admit he is not the originator of this theory, which is common among obesity researchers and was prominently featured in David Kessler’s book, The End of Overeating. And Stephan also takes a modest stance in stipulating that he takes “food reward” to a be a major explanatory factor, but not the sole causal factor, for obesity. For example, he mentions exercise, leptin resistance, energy excess and, yes, even hypothalamic inflammation, as “other” contributory causes to obesity. So FRH is not supposed to be a monocausal theory of obesity. But modesty aside, Guyenet has put a stake in the ground and marshaled considerable argument and evidence in support of FRH.  Briefly, FRH holds that feeding people (or animals) foods have a high “reward” level results in overeating and obesity.  Here is how Guyenet defines “food reward”:

I use the term food reward to refer specifically to the motivational value of food, i.e. its ability to reinforce behavior.  For example, acquiring a taste that causes a person to seek out the food in question more often.  This is how some, but not all, researchers define the term.  Others use the term “food reward” to refer to both the motivational and the palatability value of food.  Palatability refers specifically to the enjoyment derived from a food, also called its hedonic value.  Palatability and reward typically travel together, but not always. (“The Case for Food Reward,” Oct, 1, 2011)

The theory is supported by experimental evidence, for example by the rapid weight gain seen with rats switched from ordinary chow to a  high fat, high sugar “cafeteria diet”, and further developed by referring to the effects of such diets on brain opioids, dopamine circuits and other neurochemistry. Guyenet goes on to propose a remedy for the abundance of super palatable food:  just say no.  By avoiding overly rewarding food, our brains can return to sane eating and obesity can be avoided or reversed.

I feel a certain affinity for the FRH theory because, like HH, it is a “brain-centric” theory of obesity.  Guyenet’s self-described field of research is “neurobiology of body fat regulation and obesity”, which I agree is the most promising way to study of obesity.  I’ve been excited to follow his cogent summaries of the most interesting research in this field. However, the FRH seems to have incorrectly formulated the connection between the brain and obesity.  In fact, I’ve already discussed the FRH theory in another post, “Does tasty food make us fat?“.   Here is what I wrote there:

But I think the theory is wrong, for the simple reason that it too blindly takes correlation for causation. And in doing so, it gets the causal direction mostly wrong. We don’t get fat because food has become too tasty. Rather, to a large extent, it is the metabolism and dietary habits of the obese that make food taste too good to resist, leading to insatiable appetites. And the good news is that we are not consigned to blandness.  If we eat and exercise sensibly, we can eat flavorful, delicious foods and enjoy life, without packing on the pounds.

I had not formulated the HH theory when I wrote that post, but it fits the bill of what I said there: it is the metabolic effects of the pertinent foods in “cafeteria” diets that make them “rewarding” and engender the secondary effects on pleasure-related neurotransmitters like beta endorphin, dopamine or serotonin.  What HH does is to more specifically locate the primary metabolic effects within the arcuate nucleus of the hypothalamus, rather than elsewhere in the body.

I think that HH can explain a number of things that FRH cannot.  FRH is a somewhat vague in that it does not go very far to identify what specific attributes of food make them rewarding and what specific mechanism are involved.  Somehow, sugar, fat and salt are involved. It is more like a schema than a full theory, which makes it hard to test or criticize. By contrast, HH is very specific about the mechanisms by which specific food chemistries interact with specific parts of the brain.  HH,  unlike FRH, provides an explanation for why certain “rewarding” foods will eventually lead to  either subcutaneous obesity or rather intra-abdominal obesity.   HH holds that if you are neither leptin resistant or insulin resistant, then no foods will be inherently hyper-rewarding, at least initially.  Foods only become hyper-rewarding once insulin or leptin resistance begins to manifest itself.   HH makes the further prediction that very tasty, palatable foods that contain no fructose or sucrose (or other agents that elevate triglycerides) or pro-inflammatory fats, will not lead to obesity, no matter how good they taste.

A wider perspective: The homeostatic pleasure principle.  Finally, I think that the Hypothalamic Hypothesis provides a way to connect the hormonal regulation of obesity to something overlooked by both CIH and FRH:  the role of emotion and cognition in obesity, and the relation of obesity to our wider sense of well being.  Obesity is often a response to emotional factors like stress and depression, and conversely might be reversed by cognitive techniques such as cognitive reframing and meditation.  By locating the original of obesity within the hypothalamus, it becomes plausible to understand how stress hormones like cortisol and or calming neurotransmitters like serotonin can have a powerful and direct effect on the behavior of hypothalamic neurons and their sensitivity to leptin and insulin, since these neurochemicals are lurking nearby within the “neighborhood” of the brain.  Looked at more broadly, the hypothalamus can be thought of as a homeostatic regulation system that attempts to maintain an internal subjective sense of well-being or pleasure with respect to a broad range of drives, including not just eating, but sleep, sex, aggression, fear and other emotions.   This  homeostatic “pleasure principle” is fundamental — its provides a way to translate objective needs of the organism into conscious desires and emotions.  This fits into a related line of thinking about brain receptor sensitivity that I wrote about in my post “Change your receptors, change your set point“.  Whenever there is a dysregulation of the pleasure principle, such as occurs in the appetite drive of obesity, but also in conditions such as depression or addiction, we should look within the control system itself to find out what is going wrong. And that is what the HH does, by looking for specific brain mechanisms that explain not only our subjective experience, but the way the rest of the body responds objectively in homeostatic response to physiological disturbances.

Like this article or disagree with it?  Add you comments below, or join the more extended discussion in the Discussion Forum.

But one can come away from the study of hormesis with the misleading impression that it’s all about adjusting the level and timing of stressors to induce an appropriate adaptive or defensive response.  In this article, I would like to focus on a frequently overlooked ingredient in hormesis:  the role of intention, attitude and voluntary choice.  If you omit this ingredient, you are leaving out an important element of the way that stress helps you become stronger.

Voluntary, deliberate exposure to stress can be particularly effective in providing psychological benefits, including overcoming anxieties, obsessions and phobias, and vanquishing appetite cravings, addictions. Beyond overcoming such self-defeating tendencies, deliberate exposure works to unleash confidence and generate a sense of joy and accomplishment.

Hans Selye

General Adaptation Syndrome. Our modern understanding of stress can be traced in large part to Hans Selye, the Hungarian-born endocrinologist whose detailed studies of animals and humans under stress led to a model of stress as a generalizable force capable of causing disease.  Selye distinguished between good  stress, which he called “eustress”, and bad stress, which he called “distress”.  While acknowledging that some stress is good because it is energizing and activates our defenses, Selye spent most of his career studying the negative effects of exposure to stress, which he fit into a pattern called GAS or General Adaptation Syndrome.  Selye claimed that GAS proceeds through three stages:

• Stage 1: Alarm reaction is what is often called “flight or fight” syndrome — a quickening of the heartbeat, tensing of the muscles, release of adrenaline and a cascade of other neurochemicals.  This is typically a short term galvanizing response, reversible once the source of stress is removed.
• Stage 2: Resistance or adaptation occurs when the stressor is sustained.  Glucocorticoid hormones and catecholamines are ramped up to maintain alertness and provide a continued supply of blood glucose, and blood pressure increases to sustain tonicity of the muscles and other organs.  Positive coping and adaptation during this stage can increase resistance and immunity, although not indefinitely. With time, and if continued unimpeded without periods or rest and relaxation, this stage leads to mental fatigue, overtaxing of the adrenal glands and immune system, and vulnerability to disease
• Stage 3: Exhaustion, in which the organism becomes depleted of energy energy reserves and immunity. Mentally, it leads to emotional withdrawal and depression.  If sustained, this third stage leads to grave illness and eventual death.

While Selye did acknowledge some positive aspects of stress during Stage 1 and the Stage 2, he did not leave much room in his model to account for the beneficial biological aspects of stress. Looked at this way, only relatively mild and short-term stresses can be considered useful and positive, insofar as they activate readiness and resistance.  But even here, Selye held that repetition of Stage 1 and Stage 2 stresses can weaken and degrade resilience.  He saw chronic, repetitive, and sustained stress as uniformly damaging to both the psyche and the body. The possibility that routine or frequent stress could significantly and sustainably build resilience was something he did not address.

Learned helplessness. Angela Patmore, in her illuminating book, The Truth About Stress, points out that Selye’s model has led to an emphasis on “stress management”, which is largely about stress prevention and strategies for coping and relaxation.  While acknowledging Selye’s contributions, Patmore believes that he overlooked a key factor which can make a very big difference in whether stress is beneficial or detrimental:

In animal experiments using inescapable threat (prolonged and repeated tail shock, forced swim, water restraint, hot plate contact and other ordeals dreamed up by researchers), long-term inability to respond to perceived danger results in a syndrome that is the biological opposite of the galvanizing stress response. In this quite different response, which has nothing at all to do with survival, the subject gives up the struggle for its life and resigns itself to its fate. This is the so-called ‘third phase’ of Selye’s GAS, but it is important to realize, as Selye evidently did not, that the animal may do this in return for a degree of neural tranquilization, and that its brain may now release pentapeptides and other opiate-like substances to dull the pain and horror of its situation. The resigned animal then succumbs to morbid physiological changes…Giving up may buffer you from reality, but at considerable cost. Resignation causes the suppression or shutting down of the immune system.  If you’ve given up, why would you need an immune system anyway? (TTAS, pp. 110-111)

The act of “giving up” or resignation literally turns a switch and redirects the entire physiology of the animal’s response into a downward spiral of depression and failing health.  This is seen not only with animals, but also in human studies.  Patmore describes experiments by Martin Seligman that demonstrate much the same phenomenon:

…Seligman and his colleagues turned their attention to students, shutting them in a room with loud unpleasant noise, and various knobs that might or might not control the volume. Some continued to alter the sound levels. Others gave up. By now Seligman had developed a model of depression based on his experimental work. His concept of learned helplessness — resigned failure to act in the face of threat — has become of fulcrum of psychological research. (TTAS, p. 113)

The concept of learned helpless highlights the importance of looking beyond the type and extent of stress alone, to consider the internal mental state of the subject.  The essential factor is the perception of control and self-determination:

A number of key studies in the stress literature have highlighted the importance of control in the vulnerability to illness from distressing experiences. Here we plainly see why this is so. Those who act to help themselves assume control. Those who fail to act requlinquish it…Viktor Frankl studied [first hand] the behavior and susceptibilities of the victims of Auschwitz and Dachau, and formulated a theory of survival that he called the ‘will to meaning’. Of immense significance was self-determination. As Frankl observes: ‘Everything can be take from a man but one thing: the last of the human freedoms – to choose one’s own way.’  Taking action based on personal choice..may also send vital messages from the brain to the body to keep fighting and not fall sick. (TTAS p. 116)

Countering Selye’s GAS theory, Patmore puts forward an alternative theory of stress:

The distress-disease link that he formulated was not the direct, simple bond that he envisaged, but a complex sequence of events dependent on each individual’s psychological make-up, courage and coping skills. According to this alternative theory, disease strikes not a direct result of the response to threat, but as a result of resignation, helplessness and failure to act.  (TTAS, p. 118)

Learned control and mastery. We can take these learnings about the negative effects of learned helplessness and turn them around:  Perhaps we can enhance the effectiveness of adaptation and resistance to stress by enhancing our sense of intentionality or deliberate control when we are exposed to stress.    One way to do this is to train ourselves to become more resilient to stress by deliberately exposing ourselves.  This is well recognized in the case weight lifting or athletic training to become physically stronger and more skilled.  But I’m talking here about something more fundamental: our attitude towards facing life’s challenges and hardships.

In contrast to the modern ideology of stress management, which teaches us to avoid stress in order to stay healthy and sane, Patmore recalls that

…there was a far different school of thought, dating back to the Romans, based not on avoiding negative emotions such as fear and tension, but on rehearsing them.  Children were taught resourcefulness and mental strength by ‘character-forming pursuits’ that developed fortitude and self-mastery. By using the opposite of stress management – emotional rehearsal…our ancestors made themselves psychologically more robust….Childhood dares, games and contests, sport and adventure activities — all provide emotionally challenging experiences that help people to understand and season their own sensations and feelings, and take them through unpleasant emotions in order to achieve a resolution…

This attitude goes back at least to the Stoic philosophers such as Epictetus, Seneca and Marcus Aurelius. William Irvine, in his excellent modern reinterpretation of Stoicism, A Guide to the Good Life, notes:

Indeed, by practicing Stoic self-denial techniques over a long period, Stoics can transform themselves into individuals remarkable for their courage and self-control. They will be able to do things that others dread doing, and they will be able to refrain from things that others cannot resist doing. They will, as a result, be thoroughly in control of themselves.

By rehearsing or training techniques such as these, you can substantially improve your resilience in handling everyday stressors, whether they be physical or social and emotional.   But what about situations in which we actually have no real control, or where the outcome is highly uncertain?  Perhaps ironically, I think that fostering a sense of control can be helpful even when we may not or do not actually have much control over the situation.  By “making the involuntary voluntary”, we can transform the way the way we respond to stress at the deepest levels of both our biology and our psyche.

I think this attitude of voluntarily embracing unavoidable stress is most articulately expressed by Epictetus, the Greek Stoic and slave whose teachings have inspired two millennia of philosophical and religious thought.  Epictetus distinguished between externals — the events and actions of others which we cannot control — and internals — our values and attitudes.  A slave for much of his life, Epictetus realized how much freedom he nevertheless retained in choosing how to react to his fate. A Stoic “sage”, he said,  never finds life intolerable, but sees in every challenge as an opportunity to test and improve oneself:

You should look to the faculties that you have, and say as you behold them, ‘Bring on me now, O Zeus, whatever difficulties you will, for I have the means and the resources granted to me by yourself to bring honour to myself through whatever may come to pass.’ (TD, Book One, Ch. 6, p. 18).

Furthermore, it is by how we handle the challenges in life that our character is revealed and built:

Difficulties are the things that show what men are. Henceforth, when some difficulty befalls you, remember that god, like a wrestling-master, has matched you with a rough young man.  (TD, Book One, Ch. 24, p. 53).

By deciding to accept the hardships that come your way, as if you had deliberately chosen them, your reactions are transformed.  What may otherwise have been a stress that leads to resignation, giving up, and Selye’s third phase of exhaustion, now becomes a challenge deliberately embraced.  This does not mean deceiving oneself and pretending that you can control the uncontrollable.  Rather, it means embracing the challenge as an opportunity to demonstrate your ability to handle a physically or emotionally difficult situation with courage and grace, to grow from it, and to actually become stronger, not weaker.  Whether or not the stressor eventually diminishes or resolves, with or without your intervention, you are left more resilient as a result.

For a more detailed discussion of Stoicism and its similarity to Hormetism, the philosophy advocated in this blog, I would encourage you to read my page on Stoicism.

Real world applications.   Many of you who have read this far may be wondering: “Interesting philosophy, but how do I actually apply this to my life?”.   I’d like to answer that by illustrating with three very different examples.  Cold showers, intermittent fasting, and exposure therapy for anxiety and phobias.

Cold showers.  The single most popular page on this blog is the March 2010 article on Cold Showers. Initially, it surprised me that so many people would show an interest in something that is without any question uncomfortable. And for some people: terrifying. The article recites a number of health benefits that have been shown or claimed to result from taking cold showers or baths.  

But the article goes beyond the objective physical health benefits to describe my subjective experience of taking cold showers.  In particular, I noted that cold showers are initially quite uncomfortable, provoking an involuntary reactions like rapid breathing, a pumping heart and even laughing. While the shock and discomfort becomes less the more cold showers you take, my experience is that–unless the weather outside is hot–there is almost always hesitation and discomfort when first stepping into the cold shower. It takes an act of will to force myself to do this.  But I do it willingly because I’ve come to understand the benefits that result.  Beyond that initial hesitation upon jumping into the cold shower each morning, I embrace it and enjoy it.

The intentional, voluntary attitude makes a big difference to the experience.  Consider the case of those who must take cold showers unwillingly, perhaps because they have no hot water for a period of their lives, or perhaps were forced to take cold showers at camp or school dormitories.  I get comments from such people, and their attitude towards cold showers is typically very negative.  It is likely that they did not receive much physical or psychological benefit from taking cold showers.  Perhaps the experience even had an adverse effect on them, at least psychologically.

Intermittent fasting.  Going without food some days, or eating only one meal per day is the involuntary fate of millions of people living in poverty or near-poverty.  It can also happen to you if you become lost, stranded or trapped in a place without ready access to food.  This experience of hunger can be quite uncomfortable, even painful.

It’s entirely different matter, however, to abstain from eating periodically for 12-24 hours as a deliberate, voluntary practice.  I’m not talking about eating disorders hear, but rather the practice of intermittent fasting (IF), undertaken to achieve not merely for healthful weight management, but for the well-documented health and longevity benefits, which I’ve discussed in my video article, Intermittent fasting for health and longevity.   When you engage in IF voluntarily, you’ll surely experience moments and periods of hunger cravings.  But in just knowing that hunger cravings are expected and are possible to
“ride out” without adverse effects, you gain a sense of control over your urges. You soon come to recognize the difference between a conditioned craving that can be extinguished by training, and true biological hunger that deserves attention.  The sense of achievement in mastering your appetite, rather than being its slave, can be empowering.  

I’ve found that intermittent fasting works best for me when I am the one who controls the eating schedule. Rather than follow someone  else’s rigidly prescribed diet or eating schedule, I like the flexibility that IF affords.  I can choose which days to fast and which meals to skip, adapting the schedule to the demands of my week.  But once I make a decision, for example to skip breakfast and lunch tomorrow, I am very disciplined about sticking to my plan.  Here again, I believe that feeling “in control” plays an important role in the outcome. A prisoner forced to follow a fasting regimen against his would be much less likely to reap the benefits — unless perhaps he decided to “own” the imposed diet in the manner of Epictetus.

Exposure therapy for anxiety, obsessions, and phobias.  One of the most common and successful approaches to treating anxiety, fear and obsessive-compulsive disorder (OCD) is the use of exposure therapy.   Often this involves both a cognitive and a behavioral component, in which a therapist works with the patient to identify beliefs, emotions and responses relating to stimuli that provoke anxiety, fear, obsessive thoughts and compulsive behaviors.  Cognitive Behavioral Therapy (CBT) emphasizes the cognitive component and proceeds by demonstrating that the underlying beliefs are false or irrational.

My personal view is that the changing the behavioral component by controlled exposure to the problematic stimulus is the most important aspect of exposure therapy, and may be sufficient even without examining your beliefs. The essential element of treatment is progressive exposure to stronger stimuli until habituation or extinction occurs.  The theory of Pavlovian extinction and deconditioning is discussed in more detail on the Psychology page of this blog.

So if you have a fear of height, snakes, or social situations, you should progressively–and very gradually–expose yourself to tougher situations.  To counteract acrophobia, you could start by ascending very small elevations.  Walk to a height that just begins to make you anxious and hold there for a while, but retreat before it becomes too uncomfortable. If you fear snakes, start by looking at photographs of snakes, then handle fake rubber snakes, or observe real snakes cages at zoos.  Eventually, work on handling real, but harmless snakes for increasing amounts of time  For social situations, start with small groups of friends, and build from there.  A related version of this exposure therapy, called exposure and response prevention, has been found useful in treating OCD.  The key is to recognize the obsessive thoughts or compulsive behaviors as “escape responses” or “safety behaviors” in response to stressful stimuli, while learning to prevent the escape response to progressively stronger stimuli.

It is especially important with exposure therapies that you stay in control of the situation at all times.  There must always be an “exit hatch” that allows you to back down and escape or stop the stressful stimulus before real panic sets in.  Being forced by a therapist or third party to go beyond the edge of your comfort zone can be extremely counterproductive and anxiety-inducing.  The therapist, if any, should be at best a “guide” or coach.  If you are strongly motivated to succeed, exposure therapy may be quite effective if you do it yourself, without a therapist.

Psychology and hormesis. What all the above practices and treatments have in common is an important psychological dimension. In each situation, the extent to which the exposure process is voluntary is the key to successful hormesis.  When stress exposure is voluntary, the gains in resilience can be substantial, even when the stress faced is sustained or repeated over the long term.  Contrary to Selye, chronic and repeated exposure to stress does not invariably lead to impaired health and depression.  What is perceived as stress can be turned into an energizing stimulus, when it is approached with a willing and inviting attitude.  Just as you can decide to “give up” in the face of stress, you can make the opposite choice: to persevere and embrace mastering what challenges you.

Voluntariness is not an essential component of all types of hormesis.  For example, it is likely that low level exposures to radiation, chemical toxins and allergens build biological resilience by activating DNA and mitochondrial repair mechanisms, endogenous antioxidant enzymes, and immune responses that involve no psychological or neurological mediation.  But a surprisingly large realm of human biology, including digestive, metabolic, immune processes — has a significant psychological or neurological dimension.  An entire field — psychoneuroimmunology — has been laboring to elucidate the mechanisms of such neurologically-mediated processes.  Human intentionality — or what is sometimes called “will”– must be considered a key factor in the successful application of hormesis to improve your health.

At points, paradoxically in spite of his focus on the detrimental aspects of stress, Selye himself came close to appreciating the importance of  this.  I was particularly struck by one statement attributed to Han Selye, that succinctly crystallizes the essential insight of this entire article:

“Adopting the right attitude can convert a negative stress into a positive one.”

That theory has been around the block but it is in fashion again.   In 2009, David Kessler’s book, “The End of Overeating” put forward the thesis that food in contemporary American food has been deliberately engineered–by adding fat, sugar and salt–to exploit our neurochemistry and hijack our free will.

More recently, one of the luminaries of the Paleo movement, Stephan Guyenet, has formulated his own version of this theory, in a compelling series on his Whole Health Source blog, arguing that  ”food reward” is a main driver of obesity. His prescription:  eat a bland diet. Guyenet’s talk about this at the Ancestral Health Symposium last month is the buzz of the paleosphere.

But I think the theory is wrong, for the simple reason that it too blindly takes correlation for causation. And in doing so, it gets the causal direction mostly wrong. We don’t get fat because food has become too tasty. Rather, to a large extent, it is the metabolism and dietary habits of the obese that make food taste too good to resist, leading to insatiable appetites. And the good news is that we are not consigned to blandness.  If we eat and exercise sensibly, we can eat flavorful, delicious foods and enjoy life, without packing on the pounds.

Brain chemistry. Stephan Guyenet’s series on food reward, like Kessler’s book, pins the blame for obesity largely on the increased availability of more palatable “high reward” food.

According to USDA data, Americans today eat an astonishing 425 more calories per day than they did in 1970.  That is the reason for the obesity epidemic, plain and simple.  However, that fact doesn’t tell us why we’re eating more calories, so its usefulness is limited. The increase in calorie intake has come primarily from refined carbohydrate, but even that doesn’t get us very far, because why did we decide to eat more refined carbohydrate?  Probably because of the systematic efforts of commercial food manufacturers to increase the palatability/reward value and availability of processed food.  In the last four decades, the US has become saturated with hyperpalatable/rewarding commercial and restaurant foods including fast food, soda, french fries, chips, candy and other industrial products.  I’ve seen people claim that they ate these things just as much in the 1960s and 70s, but the USDA and National Restaurant Association data show otherwise.  The qualitative changes in the US diet have been swift and profound… (A Roadmap to Obesity, August 25, 2011)

But what is it about food that makes it rewarding or not?  Guyenet suggests that food reward relates to opioid and dopamine signaling:

Feeling satisfied after eating something is not reward. If you keep eating a starch food beyond what’s appropriate, that is probably because it has too much reward/hedonic value for you. Opioid signaling, implicated in hedonic processing, shuts off satiation signals in the brain and may also increase the setpoint. Dopamine signaling, implicated in reward, can strongly influence food intake and also seems to be able to increase the set point.

In “The End of Overeating”, Kessler also emphasizes the way that “hyperpalatable” foods stimulate dopamine, opioids and other reward neurotransmitters.  To be fair, both Guyenet and Kessler acknowledge that food reward is not the only explanation for obesity.  They acknowledge the role of genetics, exercise and other factors.  But for both of them too-tasty food is the leading culprit.

The relativity of taste.  But is it really that simple?  Are some foods inherently and invariably rewarding? Do our taste buds and noses directly respond to tasty foods or foods high in fat, sugar or salt by stimulating the secretion of dopamine and opioids in the brain, turning us into addicts? Somehow, it must be more complex than that.

Seth Roberts has postulated a different explanation, in which learning plays a role. His Shangri-La Diet was derived from observations that tasty foods lead to weight gain only after repeatedly encountering the flavor and the calories together. Roberts calls this process “flavor-calorie association”.  It’s a Pavlovian conditioning process: the more habitual the association, the greater the obesogenic potential of the food or beverage.  So his diet involves regular doses of “flavorless calories” in the form of bland oils, sugars or proteins.  Alternative strategies include consuming foods with unfamiliar flavors or “crazy spices”, or flavored noncaloric beverages like herb teas. (For more on flavor-calorie association, see my post on Flavor Control Diets).

Some foods and flavors may be naturally appealing to infants and children, but there is strong evidence that food preferences vary considerably among individuals and cultures.  ”One man’s food is another man’s poison”. Roberts describes the interesting story of a Gaku Homma, Japanese cookbook author whose initial impression of Coke was  that it tasted “like medicine” and was repulsed by it. Similarly, Westerners are often repulsed by Asian fermented foods, or delicacies like dog or snake. Certain cultures find insects and grubs to be delectable, but most of us would probably pass, even knowing that such foods represent a nutritious source of calories.  There are many unfamiliar foods, rich in fat, sugar, salt or flavor, that the average fan of potato chips and ice cream would reject, even if hungry. For an interesting discussion of the cultural relativity of food acceptance and rejection of unfamiliar or novel foods, see the article by  John Prescott in the Encyclopedia of Food and Culture.

Likewise, over time we can learn to like flavors and tastes that were once unappealing.  Roberts cites experiments where rats that do not like the taste of saccharine, grow to like it when they are intravenously fed glucose.  There are many “acquired tastes” that we come to like only after repeated exposures.  Our palates are changeable.

If you think that food aromas are naturally or inherently appetizing, rather than relative, ask yourself: Why do we respond to food odors differently than other evocative and pleasant odors – flowers and plants, soil, sea, even pleasant or sensual human scents?  Smelling a rose does not make you hungry. Could we be conditioned to salivate and secrete insulin in response to the smell of a rose if we always sniffed a rose before gulping down a sweet drink? I think so. Pleasant aromas or tastes don’t necessarily generate a drive to eat.  The association between sensation and the drive to eat must be learned.

In fact, both Guyenet and Kessler appear to acknowledge the relativity of taste at certain points in their accounts.  For example, Guyenet notes that taste preferences towards beer or vegetables change as we transition from childhood to adulthood.  It is instructive that Guyenet defines “food reward” in a surprisingly  broad way:

Food reward is the process by which eating specific foods reinforces behaviors that favor the acquisition and consumption of the food in question.  You could also call rewarding food “reinforcing” or “habit-forming”, although not necessarily in an addictive sense.  Food reward is a perfectly normal and healthy part of life, although I believe it can be harmful if it exceeds the bounds of what we’re adapted to.  Food reward is essential for survival in a natural environment, because it teaches you what to eat and how to get it through a trial-and-error process. (Food reward, May 26, 2011)

In this definition of reward, Guyenet seems to move away from the idea that “reward” is an inherent property of food (i.e. fat, sugar, salt) in triggering opioids and dopamine, but rather is a result of conditioning. Sounding very similar to Roberts, Guyenet notes that

Researchers have demonstrated in rodents and humans that pairing a flavor with a source of calories makes us gradually enjoy the flavor more, whether or not it remains paired to calories afterward.  That’s called a “conditioned flavor preference”, and it’s a simple demonstration of food reward in action.  The brain senses the ingested calories and assigns a positive reward value to the cues (flavor, location, etc.) associated with the calories, after which we’ll be more likely to eat something that contains the preferred flavor.

As another example, rats prefer to hang around a place where they have repeatedly received rewarding food.  Have you ever seen a child run after an ice cream truck?  After a certain time, our motivation to obtain a food that we perceive as rewarding increases, and so does our consumption of it.  Rats accustomed to eating human junk food will endure foot shocks and extreme temperatures to obtain it, even when much healthier unprocessed rodent chow is freely available

Put another way:

It doesn’t matter whether or not you like the Little Debbie cake once it’s in your mouth.  It doesn’t matter how you feel afterward.  The only thing that matters is whether or not you’ll buy another one tomorrow.  That’s food reward.

Kessler also acknowledges the role of Pavlovian conditioning in appetite, recognizing that not just flavors, but any cues can serve as reinforcers.  In Chapter 10 of his book, he cites Pavlov’s success in training dogs to salivate in response to the ringing of a bell, even after it is no longer accompanied by food. Kessler discusses Kent Berridge’s related concept of “incentive salience” :

Simply put, incentive salience is the desire, activated by cues, for something that predicts reward.  It’s a learned association — we learn to want a food or some other substance we once liked…Cue-induced wanting, said Berridge is “triggered by the sight of a cookie or someone lighting up a cigarette nearby or clinking the ice cubes in the glass of alcohol…Those kinds of cues have the power to evoke the desire to take that thing again.” Experience imbues the cue with incentive salience. Positive emotions become embedded in cues, which then develop a force of their own. (The End of Overeating, Ch. 10)

So the door has been opened here to the idea that “reward” is not an inherent property of food but rather the consequence of a conditioned association or “pairing” between the calories in the food and a sensible signal or cue.  The cue could be a flavor, but it could just as well be a visual or auditory cue,  a familiar location or a social context.  In this understanding, “reward” not an inherent property of the food, but is rather a learned response to perceptual cues associated with the food.  These cues need only at some point to have become associated with a conditioned expectation of caloric value.

But now we come to the internal contradiction in the Kessler-Guyenet theory of food reward:  Is “reward” objective and invariant — or relative, subjective and variable?  It cannot be both. To say that reward is “relative” means that it varies markedly among individuals and across cultures, but that does not make it any less real.  It can be a powerfully motivating force, driving the obese to overeat and even binge to unhealthful extremes.  But to acknowledge the subjectivity and relativity of food reward is at odds with the idea that there is such thing as inherently “hyperpalatable” food that is irresistibly obesogenic in and of itself.

An alternative explanation: impaired metabolism.  I’m not denying here that people crave or get addicted to foods like potato chips, cookies and ice cream.  No doubt these people find the flavors salient and compelling, even to the point of addiction. But it’s not the flavor that causes the behavior in the first place. The flavor only becomes a strong cue under certain conditions.  That’s obvious from the simple fact that many people, eating the very same foods, do not find them to be addictive.  While I occasionally enjoy a cookie or some ice cream, I actually find it repulsive to eat more than a modest amount.  While I used to like soda, I now experience Coke as sickly sweet.  And I think I’m not alone in that reaction.

A more likely explanation is that food addicts have altered, perhaps even damaged, their metabolisms.   They are most likely insulin-resistant and leptin-resistant as a result of many possible factors, including obesity, stress and inflammation of their insulin receptors and glucose transporters.   Guyenet aptly describes how inflammation and lipotoxicity damage the hypothalamus:

There’s an additional factor that I’ve come to believe may be an “elephant in the room” when it comes to insulin/leptin resistance and chronic inflammation, and that is, ironically, energy excess.  Glucose and fatty acids, the body’s main two fuels, are toxic when present in the bloodstream in excess.  When someone eats too many calories, his body has to deal with the excess.  The healthiest way of doing this is actually to shunt the excess energy into fat tissue where it is inert.  If the fat tissue does not have a sufficient affinity for the excess fat, free fatty acid levels in the circulation may rise, and tissues and cells may accumulate fat and fat metabolites…if fat mass increases enough, fat cells become insulin resistant, release more fatty acids into the circulation and fail to clear fatty acids from the circulation after a mixed meal.  Essentially, fat tissue loses its formerly high affinity for excess fat, and these undesirable fat metabolites accumulate in lean tissues in a manner reminiscent of lipodystrophy.  This contributes to insulin resistance and glucose intolerance by the same mechanism described above, creating an excess of circulating glucose as well, which together with the excess of fatty acids can enhance chronic inflammation, further insulin resistance and damage the insulin-secreting pancreas.

…Therefore, it’s possible that an excess of circulating fatty acids (and perhaps glucose) itself acts to raise the setpoint through the gradual accumulation of fatty acid metabolites and inflammation in the hypothalamus, promoting leptin resistance and creating a “cascading failure” of energy balance regulation, glucose metabolism and inflammatory signaling.  This would explain why people in affluent societies have trouble staying lean as they age, as well as why obesity is so difficult to treat.  I think this is likely to be a late stage process, occurring after significant body fat accumulation and essentially “cementing” the increase in body fatness.  The early stage that causes the initial rise in body fatness probably has more to do with food reward/palatability/availability, although that should remain a factor even after obesity is well established…The basic idea is that in genetically susceptible people, excessive food reward/palatability/availability and inactivity cause overconsumption and an increase in the body fat setpoint, followed by the eventual accumulation of fat metabolites and inflammation in the hypothalamus, which exacerbate the problem and make it more difficult to treat.  Other factors, such as micronutrients, gut flora, fiber, fat quality, polyphenols, sleep and stress, may also play a role.  I think this is a reasonable working hypothesis of why obesity has increased so rapidly in the last 30 years, and is so difficult to treat once established.  I believe these ideas are broadly consistent with the research and opinions of senior obesity researchers I respect. (Roadmap to Obesity, August 25, 2011)

Cause and effect. Where I believe Guyenet goes wrong in the above passage is in postulating that “the early stage” of obesity is driven by primarily by food reward causing overconsumption, which then leads to obesity and leptin resistance.  I think the cause and effect relationship is reversed. Certainly “normal” reward is part of a healthy appetite, but that doesn’t lead to obesity.  It is the leptin resistance of obesity that sets one up for food reward to become pathogenic.   According to Robert Lustig, the normal satiating effect of insulin within the brain (CNS) becomes impaired in those with insulin and leptin resistance:

Although CNS insulin levels tend to reflect serum insulin levels, the relationship breaks down in obesity states. In obesity, there is proportionally less CNS insulin; the expression of the CNS insulin transporter is decreased in several obesity models. This paucity of insulin available for satiety signaling may represent a form of CNS insulin resistance. (Lustig, Fast Food, Central Nervous System Insulin Resistance, and Obesity)

Put simply, it takes more time and larger quantities food or beverage for insulin-resistant individuals to become sated, because the appetite-suppressing or “shut off” effect of insulin in the hypothalamus is impaired.  Added to this is the fact that obese, insulin-resistant individuals typically have a grossly amplified preprandial insulin response, which means that blood glucose is more easily stoked by mere appetite cues like the sight, aroma, or even thought of food.  Frequent, regular and familiar eating of these reward foods further strengthens the reinforcement.  Even stress can trigger this hunger cycle.  This leads to a very strong drive to start eating and great difficulty in shutting off the eating.  And with more overconsumption of food and the resultant obesity, a vicious cycle sets in, leading to heightened insulin-resistance and leptin-resistance.  Once this vicious cycle begins, the psychological component of food cravings and addictions is enhanced.  The association between flavor cues — or any cues — and consumption of the food is strengthened.  And the food becomes more and more palatable, even “hyperpalatable”.  But it is the impaired metabolism of obesity and the reinforcing eating patterns that make these foods hyperpalatable to the individual, not the other way around.

Foods are not inherently hyper-rewarding.  Rather, an impaired metabolism, combined with reinforcing eating patterns  lead to food becoming hyper-rewarding. 

I can anticipate the following objection to my argument:  Am I saying that any food can become hyperpalatable or addictive?  If so, why are foods like french fries, bread, cookies, chocolate and ice cream craved more than celery, cucumbers and lamb chops?   The answer, I think, is that if you are leptin-resistant and insulin-resistant, these high calorie foods provide a sufficiently rapid “bolus” injection of calories into the bloodstream to overcome any initial preprandial drop in blood glucose, and to spike insulin sufficiently high to overcome the CNS insulin resistance and thus satisfy appetite.  However–and this is a key point–not everyone finds junk foods to be irresistable.  Most insulin sensitive individuals are readily sated on pizza or dessert.  And not everyone even finds these foods to be enjoyable.

Another important factor in the addictiveness of food is the reduction or impairment in dopamine receptors in the brains of the obese, as documented by PET scans. Interestingly, a similar reduction in dopamine receptors is seen in drug addicts and depressed individuals.  This could be a result of the overstimulation by raised levels of dopamine from the “bolus” of large meals or binges. resulting in a homeostatic downregulation of receptors.  I’ve discussed this in more detail in my post Change your receptors, change your set point. Probably any large amount of calories, even with unfamiliar, less palatable, or weaker flavors would do the same trick.  For a short time, there would be frustration due to reduced dopamine signaling  — until the brain learned the new flavor-calorie association.

Bland food diet.   From his theory of food reward, Guyenet proposes a way out:  Eat bland foods.  He supports this by citing evidence that pre-industrial cultures such as the Kitavans eat a diet that is quite bland, despite being high in carbohydrates, and thereby they remain lean and healthy.  He references studies on the effects of bland food diets in lean and obese humans (by Hashim and Van Italie, and by Michael Cabanac) to support his thesis.

Investigators have known for decades that the cafeteria diet is a highly effective way of producing obesity in rodents, but what was interesting about this particular study from my perspective is that it compared the cafeteria diet to three other commonly used rodent diets: 1) standard, unpurified chow; 2) a purified/refined high-fat diet; 3) a purified/refined low-fat diet designed as a comparator for the high-fat diet. All three of these diets were given as homogeneous pellets, and the textures range from hard and fibrous (chow) to soft and oily like cookie dough (high-fat). The low-fat diet contains a lot of sugar, the high-fat diet contains a modest amount of sugar, and the chow diet contains virtually none. The particular high-fat diet in this paper  (45% fat, which is high for a rat) is commonly used to produce obesity in rats, although it’s not always very effective. The 60% fat version is more effective.

Consistent with previous findings, rats on every diet consumed the same number of calories over time… except the cafeteria diet-fed rats, which ate 30% more than any of the other groups. Rats on every diet gained fat compared to the unpurified chow group, but the cafeteria diet group gained much more than any of the others. There was no difference in fat gain between the purified high-fat and low-fat diets.

So in this paper, they compared two refined diets with vastly different carb:fat ratios and different sugar contents, and yet neither equaled the cafeteria diet in its ability to increase food intake and cause fat gain. The fat, starch and sugar content of the cafeteria diet was not able to fully explain its effect on fat gain. However, each diets’ ability to cause fat gain correlated with its respective food reward qualities. Refined diets high in fat or sugar caused fat gain in rats relative to unpurified chow, but were surpassed by a diet containing a combination of fat, sugar, starch, salt, free glutamate (umami), interesting textures and pleasant and invariant aromas.

Guyenet’s interpretation is that the rats ate more of the “cafeteria diet” because it was more palatable, presumably due to the higher fat, starch and sugar content, than the equally calorie dense blander diets. But this is not proven.  How do we know it was more “palatable”, if this is a subjective quality?  All we know is that more of the cafeteria diet was consumed.  We can of course define that as palatability, but that would make the argument circular.  The real question is:  Do we eat more calories because inherent “palatability” or taste characteristics?  Or do foods become  perceived as more palatable because of prior food experience, eating patterns and associations that modify neural circuitry and the drive to eat?  Palatability appears not to be something inherent in food, but rather something changeable. We do not know what diets or reinforcement schedules the rats were raised on before Cabanac’s conducted his experiments.

From these and other observations, Guyenet concludes:

Some people may be inclined to think “well, if food tastes bad, you eat less of it; so what!” Although that may be true to some extent, I don’t think it can explain the fact that bland diets affect the calorie intake of lean and obese people differently. To me, that implies that highly rewarding food increases the body fat setpoint in susceptible people, and that food with few rewarding properties allows them to return to a lean state. (Food Reward, A Dominant Factor in Obesity, Part II)

In recognizing that bland diets have different effects on the lean and the obese, Guyenet here seems to made a full retreat from asserting the explanatory power of food reward as a primary driver. The relativity of taste here reveals that it must be a consequence, not a determinant, of metabolism and neural conditioning.

What can we do?  If you believe that tasty food is inherently addictive, it is reasonable to seek out bland food, and avoid strong flavors, fat, sugar and salt.  But is this necessary?  Do we have to give up not just “junk foods” like Big Macs, french fries and ice cream — but also more healthful foods that are flavorful, fatty, sweet or salty? What about lamb curry (fatty and flavored), berries and cream (sweet and fatty) or salted steak?  I think not. Flavor, fat, salt and even a modest amount of sugar is not the seed of obesity.  Rather, it is the effect that foods have on our hormones and receptors that we should think about.  To avoid obesity, we should strive to maximize our insulin sensitivity and leptin sensitivity. This can be done by a variety of measures, discussed elsewhere on this blog, including:

• weight loss, particularly abdominal fat
• intermittent fasting
• avoiding inflammatory foods and toxins that impair receptor sensitivity
• supplementing with fish oil, magnesium and vitamin D for receptor health
• avoiding chronic stress, but pursuing intermittent, intense “good” stress, such as:
• > high intensity exercise
• > cold showers
• > brief thrills and unpleasant challenges

…

Bon apetit.

We start off the day with a list of things that need to get done, and by the end of the day those plans are often hijacked and many tasks remain untouched. To some extent, that’s understandable and normal. We can always point to legitimate interruptions — an urgent assignment from the boss, a sick kid, an unexpected visitor. And of course there’s ultimate excuse:  In the complex new business environment, you have to stay flexible and go with the flow!  Can’t be rigid!

But be honest:  a lot of the time, it’s just because we prefer to procrastinate.

For those with office jobs or self-employed knowlege workers, connectivity is the norm. But this comes with a new kind of temptation: cyberslacking. It’s so easy to take a peek at an interesting blog, check your Twitter or Facebook, play a quick online game between phone calls.  Before you know it, you’re wasting a lot of time.

There are a lot of tasks that we tend to put off at work.  Difficult, undefined tasks like planning or starting a writing project. Boring or mind-numbing tasks like tabulating numbers. Stressful tasks the require us to deal with unpleasant people or situations.

Think about phone calls. There’s that phone call you’ve been meaning to make to resolve an issue you just don’t want to deal with. Or that client, associate or relative who likes to boast, berate you, or bore you with infinite detail. That call is just not going to be any fun. Easier to put it off.

At home, that storage room or garage stuffed full of old junk just sits there all year. There are all the little projects you dread doing–like bills, taxes, repairs, or organizing the closet.

I think you get the picture.  If your life is perfect and you can’t relate to any of this, just stop reading here.

There is a simple change you can implement today, that will help you stop procrastinating. Won’t cure it, but I think it will help. It’s called the Premack Principle, named after David Premack, a behavioral psychologist. He studied the reinforcement of behavior. Here is what his principle says:

A high probability behavior can serve as reinforcement for a low probability behavior.

What that means, in plain English, is that something you really like doing (playing games, relaxing with a drink or good book, calling a friend) can make it easier to do an unpleasant activity — if you put the pleasant activity after the unpleasant one. What David Premack understood is that pleasant tasks are reinforcing tasks, and when we put reinforcing tasks after something, we get more of that something. So put the pleasant tasks last in the sequence! Sometimes this is called Grandma’s Rule, because your grandmother told you to eat your spinach first and then you can have your dessert.

Aubrey Daniels realized that this concept can be turned into a great way to overcome procrastination:

The Premack Principle also provides us with the most effective time-management system known. Make a list of the things your have to do. Rank them from the thing you most like to do to the thing that you least like to do and then start at the bottom. If you start at the bottom, a curious thing happens. When you complete the last item on the list, the more reinforcing the tasks become.  If you are like most people, you will start at the top, but look what happens then. When you complete the first task, the next one is less desireable. The farther you go, the more punishing the tasks become. Is it any wonder that people who start at the bottom get two or three times more done than do those who start at the top? (“Other People’s Habits, p. 86)

Daniels used this technique to overcome his own writers’ block and finish his Ph.D. dissertation on time. I think this method is sheer genius and it has helped me fight procrastination. One specific change I’ve made is to no longer start my day by checking e-mail. I find reading e-mail very “reinforcing”, so I do it twice a day now: right before noon and again at the end of the day.

A surprising side effect of using the Premack Principle is that unpleasant activities eventually become more tolerable, or even pleasant!  This follows from the principle of reinforcement. I didn’t believe it at first, but it has been validated by my experience.

I’ve made one small adjustment to Daniel’s method which helps if you find his “reverse to do list” too hard to do. Use this approach if you are dealing with very unpleasant or difficult tasks, or as a way to get started if you have a serious procrastination problem:  If you have a short tolerance for drudgery or unpleasantness, put a pleasant reinforcing task as every third or fourth task. In the extreme, you can even do “task pairs” of unpleasant and pleasant tasks. The downside of this approach is that you risk getting sidetracked early in the day on something very reinforcing. You can’t be playing an Internet game every hour. So in most cases, it’s best to withhold the super pleasant, highly reinforcing tasks until later in the day when you’ve accomplished something.

Another suggestion for dealing with unpleasant, difficult or ill-defined projects comes from the GTD (Getting Things Done) methodology:  Determine just the very Next Action, the first concrete step needed to get things moving for your procrastinated projects.  It could be making a first phone call to get some information, or buying needed supplies.  Put these Next Actions ahead of the more pleasant tasks in your “reverse to do list”

Procrastination is not the only problem than can be attacked using the Premack Principle. Here are a few other applications I’ve come up with myself.  Perhaps you can think of your own:

1. Workouts. For a more effective workout at the gym, start with the more difficult exercises or the ones you dislike, and save those that are more relaxing or enjoyable for the end of the workout. When going for an outdoor run, do the steepest uphill section first and end with the downhill.
2. Dieting. To cut back on calorie intake,  start your meal with low-calorie appetizers and end with a small calorie-dense dessert. This is much better than starting out with calorie dense appetizers. If you practice intermittent fasting, do the fasting in the beginning of the day and break your fast as late in the day as possible. That gives you something to look forward to as a reward for your discipline.  This may be why most people who practice fast-5 break their fasts in the late afternoon or early evening, rather than in the morning.
3. Phone calls. When making phone calls, make the one you don’t want to make first, end with the people you like talking to.
4. Space organizing. When re-organizing a cluttered house or work area, start with the worst or most visible area first. You’ll notice the impact immediately and it will give you the energy to continue.

The Premack Principle can be thought of as yet another application of Hormetism, the application of a controlled stress to build your adaptive strength and resilience.  With the Premack Principle, you are actively reshaping the way you respond to unpleasant or challenging tasks. The more you apply it, the more you will lower the barrier to doing these difficult tasks the next time around.

Try it today (don’t procrastinate) and let me know if it helps your day go a little smoother.

This week I wrote a guest post about willpower for Julien Smith’s blog.  It synthesizes a number of the ideas on this blog about deconditioning urges and emotions that tend to undermine our resolve to make significant changes in life.

And then…progress stalls. You’re still eating the same foods, faithfully completing your workouts, but your weight loss stalls, perhaps the scale even goes up a few pounds. The progress you make at the gym similarly maxes out…you can’t lift any more weight, your running speed or distance maxes out…maybe even some soreness or injury sets you back a bit. You’ve hit the dreaded plateau.  Sometimes it lasts a few weeks and progress resumes. But it can last months. And it saps your morale because you are not getting any more return on your invested effort. In all likelihood, you give up or cut back, your discipline withers. Your weight goes back up, maybe adding a few pounds on top of where you started, and you cut back on or cut out your exercise program. The genie is back in the bottle.

What causes plateaus?  Are they inevitable endpoints in any effort to make progress? Or are they at best temporary way-posts or resting points that you can move beyond with the right approach?  The school of thought that says that plateaus are unavoidable indicators of biological limits is called the Set Point theory. I think that the Set Point theory is wrong, and that there is a reliable way to push past plateaus to bring about substantial weight loss and improved fitness.

Conventional plateau busting suggestions. Before we get into the Set Point theory, let’s take a look some typical suggestions you’ll get if you google “plateau busting” or “break through plateau”:

To break through exercise plateaus:

1. Increase exercise intensity
2. Take a break – don’t overtrain
3. Try new exercises
4. Mix up your routine, change the order of exercises
5. Wait out the plateau

To break through diet plateaus:

1. Eat more frequently, don’t skip meals
2. Eat different foods
3. Drink more water
4. Wait it out

Many of these are good suggestions, and they can work to jump start progress. But I suspect that more often than not, these approaches at best result in temporary progress, lasting perhaps a few days or weeks. Progress is soon reversed and you are right back on the original plateau. Eating more frequent small meals might lead to a temporary boost in metabolism and better blood glucose control, but it is unlikely to result in any permanent weight loss, once the body adapts. The least effective of the above suggestions is to wait it out. If you don’t change the input, you can’t expect the output to change. So while these recommendations might help get you started, they are unlikely to lead to permanent, long term change.  But where does that leave us?  Are we doomed to stay on the plateau forever?

The ‘Set Point’ theory. I discussed the Set Point theory in a previous post on the Shangri-La Diet, just one of many diets based upon the set point theory. (See:  Flavor Control Diets). Set point theories trace back to the lipostatic (“constant fat”) weight control theory of Gordon C. Kennedy, based upon research he did on rats in the 1950s. Kennedy found that when he varied the caloric density of rat chow, his rats initially gained or lost weight, but they eventually adjusted how much food they ate, or their physical activity levels, so as to re-establish their original weight. Kennedy took this to be evidence that rats have an internal set point, a “natural weight” which their physiology acts to maintain against external changes to environment. The set point concept was later extended to explain the persistence of stable weights in human, in the face of variation in dietary intake and energy expenditure. The physiological explanation is that your metabolism slows when you attempt to diet and your weight drops below its set point; this also typically makes you less inclined to be active.  Conversely, overeating leads to a ramped up metabolism, which puts the brakes on weight gain; it also often gives you the extra energy to be active and burn off calories.  In the end, try as you might, you just can’t budge your set point weight.

The set point theory is ultimately a rather pessimistic view. (For a typical popular portrayal of the theory, take a look at this discussion of set point theory in the context of eating disorders). The underlying assumption is that each of us is born with a natural weight (or more accurately, a weight “program” that specifies a weight set point that changes as a function of age).  We can temporarily deviate from our pre-programmed set point weight by extreme diets, intense exercise, emotional events or illness, but eventually we will return to equilibrium, to our intrinsic, biologically predestined set point weight.  We best off not to fight our set point, but to accept it. Some adherents of the Set Point theory believe that the set point can be changed, but only by means of a sustained intervention.  For example, Seth Roberts, in his Shangri-La Diet, prescribes the use of “flavorless calories” (such as oil or sugar water) to break associations between flavor and calories and trick the metabolism into lowering set point.  Set point can also be changed by other interventions such as diet pills or special appetite suppressing foods.  However, once the dietary or medical intervention is stopped, the set point will return to its “natural” level, and the weight will creep back on.  Permanent, lasting change is impossible without the intervention, according to this Set Point theory, since progress requires lifelong dependence on some external crutch, some substance which hopefully is healthful, but nevertheless which we can never afford to go without for very long.

If you think about it and look around, it soon becomes clear that the Set Point theory can’t be right, or at least it is too simple, because it can’t explain certain undeniable facts.  Despite the numerous people who have failed to keep the weight off, we all know people who have lost huge amounts of weight — and kept it off. One of the most remarkable stories is that of Jon Gabriel, who dropped from 400 pounds to a very muscular 189 pounds and published his story and his insights in a best-seller called The Gabriel Method. Many people have replicated Gabriel’s type of “non-dieting” weight loss, to varying degrees.  We also know that various ethnic populations, such as Pacific Islanders and the Pima, who are healthy and trim on their native foods and in their native environment, frequently become morbidly obese and diabetic when they transition to a Western diet and lifestyle. And the American population as a whole is experiencing skyrocketing rates of obesity since the 1970s, which cannot be explained in terms of genetic programs. So the experience of both individuals and populations testifies against the Set Point theory.

And yet, there is at least some plausibility to the Set Point theory, or it would never have taken hold so strongly.  There are undoubtedly periods in our lives where our weight is remarkably stable, and where we experience resistance at our efforts to lose weight or get fit. Even outside of weight control and fitness, whenever we try to change ingrained habitual behaviors, there is a strong tendency to return to where we started.  In both physiological and psychological terms this is called “homeostasis” — the strong tendency of an organism to resist change. Homeostasis is generally beneficial because it helps us to maintain a healthy stability in the face of environmental changes that could be potentially detrimental or even lethal, if not resisted.  But at the same time, homeostasis can sometimes be the enemy of positive changes, such as losing excess weight, or becoming more fit.

If the Set Point theory is based upon a recognition of homeostasis, a well established biological reality, what could possibly be wrong with it?  Well, upon looking more closely, it turns out that the Set Point theory is based upon a serious misunderstanding of homeostasis.

What homeostasis really is and how it really works.  The big mistake in the Set Point theory is that it fails to realize that homeostasis applies only to our internal environment, not to our external physical condition. The organism does not inherently defend any particular macroscopic bodily features such as total fat or muscle mass, or external fitness. What the organism defends is the internal environment, the so-called “milieu interieur“, as Claude Bernard called it in the nineteenth century. Homeostasis appropriately applies to certain essential internal physiological variables, at the level of the cell or the bloodstream:  pH, the concentration of glucose (or more accurately, glucose+fatty acids+ ketones), electrolytes, and certain other essential physiological metabolites. These essential physiological parameters must be tightly controlled within narrow bounds — not as a constant, but as a range — in order to support cellular function. For example, blood glucose should be kept within the range of about 70-150 mg/dL; if it drifts outside of this range, hormones like insulin, glucagon or epinephrine will normally act to bring it back within range. If the body is unable to successfully regulate these key parameters, it may enter a state of shock and tissue damage, loss of consciousness, or death may ensue.

So if there is a “set point”, it applies not to body weight, fat, muscle, conditioning, or other outward characteristics; rather, it applies only to the inner environment of our cells and the bloodstream that nourishes them and supplies their energy.  Our brain and endocrine systems don’t directly detect our weight or muscularity — they sense only what is present in the immediate cellular environment.  There are certain hormones, such as leptin, which do to some extent vary as a function of body composition, but they do not do so in an absolute way, and can alter their response over time in a dynamic fashion. Body weight and fitness tend to act “as if” there is a set point only because they are influenced strongly by energy metabolism, and are linked to them in the short term. So in the short term, weight loss does tend to produce an energy deficit that is reflected by blood metabolites, cellular response, and even hunger. And in the short term, if nothing is done to change this connection, the set point theory seems to work. However, this is at best a temporary type of stability which is not centrally controlled, but rather results from a “balance of forces” that can be dynamically altered over time. Gary Taubes expressed this point well in his critique of the lipostatic set point theory:

Life is dependent on homeostatic systems that exhibit the same relative constancy as body weight, and none of them require a set point, like the temperature setting on a thermostat, to do so. Moreover, it is always possible to create a system that exhibits set-point-like behavior or a settling point, without actually having a set-point mechanism involved. The classic example is the water level in a lake, which might, to the naive, appear to be regulated from day to day or year to year, but is just the end result of a balance between the flow of water into the lake and the flow out. When Claude Bernard discussed the stability of the milieu interieur, and Walter Cannon the notion of homeostasis, it was this kind of dynamic equilibrium they had in mind, not a central thermostatlike regulator in the brain that would do the job rather than the body itself.  (Good Calories, Bad Calories, p. 428).

Once you grasp this point, it becomes obvious that you can have a stable, sustainable inner environment whether you are fat or skinny, fit or flabby.  On the other hand, the good news is that you can significantly change your body composition and fitness — and maintain the new state — so long as you can do so while maintaining internal homeostasis.  In fact, you can make major, lasting changes to your body and fitness by understanding how homeostasis works.

A stepwise evolutionary model of plateau busting. So if we are not constrained by arbitrary set points, if our body weight, fat, and muscle composition are not predetermined at birth, why is it so hard to make progress, and how can we progress to a new state? I think the best way to answer this question is to think about how systems evolve and adapt.  Adaptation is typically not a smooth, continuous process, but moves from one relatively stable state to another through a series of discrete, quantum steps.  Mathematical analysis of complex adaptive systems — such as cells, individual organisms, biological species, and human organizations and economies–shows that they typically display stable “nodes” or “attractors”– states which tend to resist change — until the change is big enough, and in the right direction, to move them to a new stable state or “orbit”.

A useful analogue for how this works comes from the Darwinian explanation of how biological species evolve.  Species are typically very stable in the short term (which can be thousands or millions of years on the timescale of evolution).  Species resist genetic change because a common breeding population exerts conservative forces that tend to keep variation within a limited range, so the population traits remain stable.  But every so often, new or divergent traits appear within sub-populations in response to environmental pressures.  If such a sub-population becomes reproductively isolated for long enough, perhaps by due to geographic separation, it can continue to grow far enough apart genetically that the new sub-population can no longer interbreed with the original breeding population.  In this way, a new differentiated species is born, with no “bridge” back to the original species.

Individual adaptation is of course not the same thing as species adaptation. But there is at least this much similarity:  if the adaptation is large enough, and if there arise new forces which act to stabilize the adaptation, then a stable change is possible.  If the stability persists long enough for the balance of forces to change, the adaptation will be “permanent”, with no easy reversion to the original state.  However, some sort of “separation”, analagous to geographic isolation, is needed to prevent reversion or “backsliding” to the original state.  Just as a river or ocean separating two islands can keep two sub-species from rejoining, there needs to be some type of “habit separation” between new and old patterns to prevent us from going back to where we started.

A good mental model for this is crossing a stream which is broken up by a series of large boulders. Getting from one side to the other may seem like an impossible task. It certainly cannot be done with a single bounding leap.  But if the task is broken down into a series of small steps, each of which is a stable “boulder”, then it can be done.  If the boulders are far apart, you may hang out for quite a while on each boulder, getting your footing and balance. But then at the right time, with enough confidence, you decide to make your move to the next boulder. Each step is still a challenge and takes some preparation, but with preparation and sufficient strength, it is within your reach.  By the time you are to the other side, it is equally hard to return to where you started. Just as biological evolution proceeds stepwise, and generally without reversion, to a new space, so can individual adaptation evolve to a new stable state through a series of intermediate “resting points”, each stable in their own right. And if these resting points are far enough apart, it will be hard to return to the original place you started.  But, applying this to “plateau evolution”,  a stream with well spaced boulders is preferable to a stream crossed by a continuous foot bridge, because the bridge makes it too easy to re-cross the river back to where you started.

How does this look in practice? The stepwise evolutionary model is not mere theory, but something I have experienced myself. And I think it may provide a more general model of how we can adapt and bust out of plateaus that appear (but only appear) to be holding us back.  The figure below shows the most recent 8 months of my weight loss.  I started out at 185 pounds several years ago and just recently reached my goal of 150 pounds.  But only since February 2010 did I keep an almost daily record of weights. I annotated my weight log with comments regarding various changes I made to my eating or habits, including both sustained and individual events:

When you look closely at the day by day weight measurement in any period of a few weeks, you tend to see only a lot of fluctuation over a range of about 4-6 pounds.  These are plateaus.  A plateau does not mean a constant weight, but rather what stock investors might call a “trading range” — a normal range of variation around some average weight.  But periodically there is a move of 3-4 pounds that seems to endure, to “take”.  And then there is a new average weight with a range of variation around it. These shifts may not become apparent immediately as permanent shifts in the average, because the magnitude of the shift (3-4 pounds in my case) can actually be smaller than the “trading range” variation around the old average (4-6 pounds in my case).  Only after several weeks have passed, does it become clear that a new “plateau” has been established, because the weight is not going back up.

What causes the shifts? The key question is how to explain the moves to the new plateaus.  From my limited analysis, I think I have an answer:

1. Single, unique events are incapable of establishing new plateaus.
2. Gradual, continuous changes are generally not likely to lead to new plateaus.
3. Step changes in behavior are the main driver in new plateaus.

So, to look at my example, preparing for (and running) a challenging two-day relay race in late April did cause a brief and significant loss in weight, but the pounds came back quickly over the following week, even exceeding the starting point. What did cause a lasting shift to the first new plateau was permanently cutting back my consumption of alcohol from 5 times to 2 times a week. Eating a big birthday dinner in June spiked my weight, during that phase, but the effect was transient. But what had a significant and lasting effect in July was increasing the frequency of my intermittent fasting from once a week (on average) to about 2-3 times a week. Most recently, I used an extended fast of between 2 1/2 to 3 days to reach my goal weight of 150 pounds, dropping 4 pounds from my last plateau of 154 pounds. I now realize that a single big move like that will not by itself produce a permanent change.  So my plan is to further extend my use of intermittent fasting so that I limit my eating to only 1 or 2 meals per day, going forward. So I will simply give up eating 3 meals a day; it will be either 1 or 2 meals (still giving me some freedom).  That may have seemed extreme several months ago.  But because I have approached this gradually, in small increments, I believe it will not be difficult at all.

The secret to plateau busting. To summarize, I think there are three important principles to keep in mind:

1. Make a deliberate, discrete step–and write it down! One of the most important aspects of this strategy is to define permanent changes based upon discrete quantum steps, not tiny moves along a continuum. For example, rather than gradually increasing the intervals between meals, make a one-time decision to cut out afternoon snacks. Or to skip lunches on certain days. Or add an extra workout each week. Write down the change on paper in clear language.  The value of doing this is that the change is conscious and deliberate, not something you slide into without awareness. Just as you pause on each boulder when crossing a stream and carefully plan your hop to the next boulder, be sure to deliberately and carefully plan each move to a new plateau, to be sure it is a step you think you can commit to. Look before you leap!
2. Keep records and establish a range of variation for each plateau. Any step to a new stable plateau is not a step to a fixed and unvarying behavior. There should be a certain range of “freedom”, allowing for natural variation. You will first need a little time after each change to “discover” what the new range of variation is. And the change will be more apparent if you are keeping good records of your weight, your speed, or whatever you are trying to change. (If you see no change within a week, you probably did not make a significant change). It’s best to chart the results graphically so that you can see the plateaus and the shifts. But once you see some results, it is equally important to establish firm limits to this range and stay within them.  In my last plateau, where my average weight dropped from 158 to 154 pounds, I was careful to stay in the range between 152 and 156 pounds.  Whenever I got close to the high end of the range, I consciously cut back on my eating to allow the weight to drift lower. I had just enough freedom to make this new plateau comfortable, but not enough to make it meaningless. Likewise I never pushed hard to get below 152 pounds during this period. These limits or bounds provide essential “habit separation” to isolate the new plateau or habit from backsliding into a previous plateau range.  Enjoy the freedom of the range, but strictly enforce the limits!
3. Allow yourself adequate time on each plateau. It is very important to allow yourself enough time to “get comfortable” at each new step. Don’t push too hard or move too quickly to the next step.  Habits take time to consolidate, both physiologically and psychologically. In the case of weight loss, what is really happening is that your hormones, enzymes, and other modulators of metabolism need time to re-balance, to provide the same level of homeostatic control of key energetic variables such blood glucose and fats as they did on the previous plateau.  If you are using intermittent fasting to lose weight, you must allow time to up-regulate the catabolic hormones and enzymes so that they can more readily mobilize fatty acids and glucose from storage, keeping your cells and your brain happy. This adaptation can take weeks, and you might be wise to stay on the new plateau for a few months!  Similarly, if you are adapting to lifting heavier weights or running faster miles, your body needs time to grow muscle tissue or increase aerobic capacity in response to the newly added stress. These changes are often imperceptible to you, but they are going on “behind the scenes”. To use the river-crossing analogy, allow time to catch your balance before you make the jump to the next boulder!  But don’t stay there forever…keep your ultimate goal in mind and make the next move when you feel ready.

Understanding that it takes time to adjust to a new plateau is, I think, a key point to being psychologically prepared to handle the inevitable resistance to change that is experienced whenever we “stretch” ourselves in the effort to grow physically, mentally or spiritually. Learning to appreciate your time on the plateau — even to love it — was one of George Leonard’s great insights that can help all of us who are on the path of change, as I discussed in another post about his book, “Mastery”. But the good news is that we don’t have to stay on a plateau forever, if we understand how it works. Armed with this knowledge, we can judiciously make our move to the next plateau in the right way and at the right time.

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Consider the following ten situations:

1. Drug addicts, before becoming addicted, experience the euphoria of a drug with few negative consequences. Over time, however, they develop a tolerance for the drug, requiring increasing doses to get the same high.  At the same time, their cravings and distressful feelings increase when going without the drug, leading to increased in withdrawal symptoms and a cycle of increasing drug use.
2. Firefighters and emergency room doctors have stressful jobs, but many find themselves experiencing an irresistible rush and heart-throbbing exhilaration from these fast-paced occupations.
3. New lovers, after a honeymoon period of initial infatuation, often experience a drop-off in affection, leading to dissatisfaction, fights, and sometimes breakups.  When reconciling after the breakup, they experience renewed closeness for a period of time. Typically, the more intense the infatuation, the greater the strife and negativity during the falling out periods.
4. Marathoners and other runners often experience a “runner’s high” which builds up during longer, more strenuous runs, and can extend for hours or even days after a run. Runner’s high has been associated with release of endorphins, a natural “opiate” produced by the body.
5. Infants who are given a bottle and start sucking on it experience pleasure.  But if the bottles are removed before the infants have finished feeding, they universally cry.  And yet they would not have cried if the bottle had never been given.
6. Depressed adolescents often resort to “cutting”, a form of self-mutilation that introduces some pleasure or even a high into their otherwise sad or pleasureless day.  They often find the need to increase the cutting to maintain the pleasure.
7. Scratching an itch generally relieves the itch and can be pleasurable, but often this ends up making the itch more intense and, after repeated itching, even painful.
8. Horror movies, which initially are disturbing or even terrifying, can become addictive
9. Politicians and executives in positions of power come to crave the power.  When they are out of the limelight, they experience a letdown, boredom, or even depression.  Upon retirement, this depression can lead to poor health or shortened longevity.
10. People who donate blood frequently report a sense of well being and pleasure that cannot be explained in terms of the blood removal itself.

Can you see the pattern?  In the odd-numbered examples above, pleasure turns to pain; in the even numbered examples, pain becomes pleasure. And in all cases, the effect intensifies with repetition. But why does this occur?  One possible explanation for these types of situation is described in William Irvine in his book “A Guide to the Good Life”:

The psychologists Shane Frederick and George Loewenstein have studied this phenomenon and given it a name: hedonic adaptation. To illustrate the adaptation process, they point to studies of lottery winners. Winning a lottery ticket typically allows someone to live the life of his dreams. It turns out, though, that after an initial period of exhilaration, lottery winners end up about as happy as they previously were. They start taking their new Ferrari and mansion for granted, the way they previously took their rusted-out pickup and cramped apartment for granted. (Irvine, p. 66).

Hedonic adaptation is the experience of “getting used to” a good or pleasurable thing until one returns to a state of relative indifference or equilibrium, feeling about the same as one did beforehand. As I describe in more detail on the Stoicism page of this blog, Irvine goes on to point out how the Greek and Roman Stoics were able to combat hedonic adaptation by practicing techniques such as “negative visualization”, in which they regularly took time to vividly imagine loss of people, relationships and possessions they held dear, so they could better appreciate what they had.

Hedonic reversal and habituation. While hedonic adaptation of this sort certainly exists, the ten situations I listed above are quite different than than that of the lottery winner that Irvine describes. My ten situations do not involve a return to homeostasis or equilibrium. They involve a total switch, what I will call hedonic reversal. Pleasure becomes pain; pain turns to pleasure. This is the phenomenon that Richard Solomon tries to explain in his paper.  Solomon quotes Plato, who may been the first to describe true hedonic reversal and puzzle over it:

How strange would appear to be this thing that men call pleasure! And how curiously it is related to what is thought to be its opposite, pain! The two will never be found together in a man, and yet if you seek the one and obtain it, you are almost bound always to get the other as well, just as though they were both attached to one and the same head….Wherever the one is found, the other follows up behind. So, in my case, since I had pain in my leg as a result of the fetters, pleasure seems to have come to follow it up.

In hedonic reversal, a stimulus that initially causes a pleasant or unpleasant response does not just dissipate or fade away, as Irvine describes, but rather the initial feeling leads to an opposite secondary emotion or sensation. Remarkably, the secondary reaction is often deeper or longer lasting than the initial reaction.  And what is more, when the stimulus is repeated many times, the initial response becomes weaker and the secondary response becomes stronger and lasts longer. This is what happens quite clearly in the case of addiction. After repeated administration, the original dose no longer gives the same high, so it must be increased to achieve that effect. In addition, as time goes on, abstaining from the addictive dose becomes more difficult, while cravings, anxiety and depressive feelings increase. The mirror image of this addictive pattern is apparent in the case of endorphin-producing athletic activities like running, or thrill-seeking pasttimes like parachuting. Solomon reports on a study of the emotional reactions of military parachutists:

During the first free-fall, before the parachute opens, military parachutists may experience terror: They may yell, pupils dilated, eyes bulging, bodies curled forward and stiff, heart racing and breathing irregular. After they land safely, they may walk around with a stunned and stony-faced expression for a few minutes, and then they usually smile, chatter, and gesticulate, being very socially active and appearing to be elated….The after-reaction appears to last about 10 minutes…After many parachute jumps, the signs of affective habituation are clear, and the fearful reaction is usually undetectable. Instead, the parachutists look tense, eager or excited, and during the free-fall they experience a “thrill”. After a safe landing, there is evidence of a withdrawal syndrome. The activity level is very high, with leaping, shouting…and general euphoria. This period, often described as exhilaration, decreases slowly in time, but often lasts for 2-3 hours. Indeed, I was once told by a sport parachutist…that his “high” lasted 8 hours. A new, positive source of reinforcement is now available, one that could never have eventuated without repeated self-exposures to an initially frightening situation to which the subject then becomes accustomed. (Solomon, pp. 693-8)

Thus, both the addictive pattern and the thrill pattern share the features of hedonic habituation (reduced intensity of the primary response) and hedonic withdrawal (heightened intensity of the secondary, opposite response). In surveying and studying a wide range of such experiences, Solomon found a common pattern of hedonic contrast, which he represented as follows:

baseline state → State A → State B

State A is the initial emotional or “affective” response to a stimulus, which can be either pleasant or unpleasant.  Typically, the first time a novel stimulus is applied, the primary or State A response is most pronounced at the outset and then tapers to steady level as long as the stimulus is maintained, as shown below in Figure 4.  For example, exposure to the heat of a sauna or hot tub may cause an initially hot or burning sensation, which diminishes somewhat over time. Once the stimulus is removed, the sensation is replaced by a contrasting sensation or affective state, the after-reaction, or State B.  State B is opposite in hedonic character to State A. If one is pleasant, the other is unpleasant, and vice versa. Initially, and after the first few stimulations, State B typically has a much lower intensity than State A, but often lasts longer in duration, before it eventually decays and returns to the baseline state.

What Solomon noticed is that after many repeated stimulations, the intensity of State A typically diminishes, both in peak intensity and steady state intensity. This is the hedonic habituation effect, also called “tolerance”, and it is seen with both pleasant and unpleasant affective reactions. The only way to increase the intensity of State A is to increase the magnitude of the stimulus. At the same time, with repeated exposures, the secondary affective State B often intensifies and lasts longer. This is the hedonic withdrawal effect. This combination of habituation and withdrawal effects is shown in Figure 5:  For addictions, the pleasurability of the stimulus diminishes with time and the unpleasant withdrawal grows in both intensity and duration. For the thrill-seeking or excitatory pattern, the stressfulness or unpleasantness of the stimulus is reduced with repetition, while the  ”withdrawal” becomes more pleasant and lasts longer, before returning to baseline.

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The opponent-process theory. So far, all we have presented is a qualitative description of some common patterns of sensory or emotional response, without any real explanation for why these patterns occur as they do. But Solomon’s real innovation is that he can explain these patterns by decomposing them into more elemental underlying biological processes. His central insight is that the nervous system is organized in such a way that any sensory or emotional response can be decomposed into two concurrent processes. The State A response diagrammed in Figures 4 and 5 above is in reality a composite of two complementary physiological processes:

• a primary process “a”, which is the direct observable response to the stimulus; and
• an opponent process “b”, which acts to inhibit or counteract the primary process.  It occurs at the same time as the primary process, but is not always evident or easy to perceive.

To understand how these processes actually work in practice, let’s look more closely at Figure 7 below. The opponent process “b” actually begins shortly after the initiation of the primary process “a” and acts to dampen it during what we observe as State A. Because “b” is both smaller and opposite in effect to “a”, it acts to reduce the net impact of “a”.  That explains why the intensity of the A process is greatest at the outset, but drops as the stimulus in continued.   According to Solomon, for a novel stimulus the “b” process is smaller and more sluggish than the “a” process.  It is slower to built to its steady state level (asymptote) and slower to decay after the stimulus stops.  This is shown in Panel A of Figure 7:

So what happens to bring about habituation after many repetitions of the stimulus, when the stimulus is no longer novel? According to Solomon, the primary “a” process remains unchanged in response to the stimulus.  What changes with repetition is the opponent process “b”.  As depicted in Panel B of Figure 7, after many stimulations:

• it intensifies
• it starts earlier (reduced latency period)
• it decays more slowly

The net impact of these changes in the opponent process is to progressively dampen the magnitude of State A and increase the speed, magnitude and duration of State B.  Thus, without any changes in the primary process, these changes in the opponent process can fully explain the increase in both tolerance and withdrawal, as shown in Figure 7.

Biological basis. Opponent processes are not just some clever hypothetical construct that Solomon came up with out of thin air. These kinds of inhibitory processes are common in biological systems.  For example, many or perhaps most neurotransmitters, hormones, and biological receptors have corresponding opposites, which act to inhibit or moderate the primary response. These inhibitory processes serve a useful biological control functions by preventing over-reactions to environmental disturbances. They form the the biological basis of systems of homeostasis, systems that enable organisms to resist or adapt to disturbances to their steady functioning.

Solomon’s opponent-process theory also identifies several key factors that can strengthen or weaken the opponent “b” process.  His paper summarizes some very clever animal research on distress behavior in ducklings, from which he deduced that the opponent process can be strengthened in three primary ways:

• increasing the intensity of the initial stimulus exposure
• increasing the duration of the stimulus
• shortening the interstimulus interval (the time between stimulus exposures)

Interestingly, merely repeating the stimulus, in and of itself, had no effect on strengthening of the opponent process if the stimulus was too weak or too short, or if the interstimulus interval was too long.  In particular, he found that, depending on the inherent duration of the opponent process, the interstimulus interval had a major effect on whether or not the opponent process will increase in strength.  According to Solomon

The critical decay duration is that disuse time just adequate to allow the weakening of the opponent process to its original, innate reaction level. If reinforcing stimuli are presented at interstimulus intervals greater than the decay duration, then the opponent process will fail to grow. (Solomon, p. 703)

Each opponent process has an inherent decay behavior, that is, a rate at which it fades away.  This will depend on the specific physiological and biological underpinnings of that process.  On a biochemical level, for example, this decay duration may depend on the half-life of the neurotransmitters, hormones, or receptor behavior involved.  It will surely also involve higher order processes which relate to the nervous system and psychological conditioning of the individual.  Figuring out the decay duration of various opponent processes should be a matter open to empirical determination.  It can be approached both by psychological investigations on others (or on oneself), and also by looking into the underlying physiological and biochemical mechanisms.

The final element of Solomon’s theory is a phenomenon he calls “savings”.  Although opponent processes can be weakened or faded away by avoiding the stimulus for an extended period of time, that does not mean they leave no memory traces. Studies show that these opponent processes are more quickly reactivated the next time they are re-stimulated. Reflexes and emotional reactions build up more quickly when reactivated than they did with the initial stimulation. According to Solomon,

Such a phenomenon is not unexpected. In alcohol addiction, for example, the abstainer is warned that one drink may be disastrous, and the reason is the savings principle. The reexercise of alcohol’s opponent-process system strengthens the withdrawal syndrome very rapidly and sets up the special conditions for resumption of the addictive cycle. Cigarette smokers report the same phenomenon: Readdiction to nicotine takes place much more rapidly than does the initial addiction. (Solomon, p. 703)

This savings effect also applies to positive opponent effects, such as the exhilaration experienced by skydivers or runners when resuming their thrilling or strenuous activities after a hiatus.  Understanding this effect is important in designing strategies for avoiding or minimizing the negative effects of relapse, as will be discussed below.

Put into simplest terms, the opponent-process theory explains the psychology of addiction and thrill-seeking in terms of the strengthening of inhibitory processes.  These inhibitory processes  get stronger when stimulation of a primary emotional response is sufficiently intense, sustained and frequent.  They become evident only when there stimulus and the primary processes are not present, and typically last for some time afterwards.   On subsequent re-exposure the stimulus, opponent processes often reactivated more quickly.

Is this a biologically realistic explanation?  Perhaps Solomon has not generated a broad enough set of hard physiological data to conclusively prove his hypothesis.  However, there is still a strong case in favor of it. First, his hypothesis provides a model which offers a coherent and consistent explanation for a wide range of  sensory and emotional behaviors for which there are few other good explanations. Second, there one application of the Opponent-Process theory–to an area unrelated to emotions–which has already been empirically verified:  the explanation of color perception. It is worth spending a paragraph on this because it provides some insights into the biological reality of this theory.

The opponent-process theory of color vision. Until the late nineteenth century, the primary theory of color vision was the trichromatic theory, which held that color perception was the result of the stimulation of three different types of cone receptors in the retina of the eye.  In 1892, Ewald Hering first proposed the opponent-process theory of color vision. He observed that any color can be uniquely analyzed in terms of the colors red, yellow, green, and blue, and noted that these four primary colors exist as the complementary pairs red-green and yellow-blue. Hering’s theory accounts for how the brain receives signals from different kinds of cone cells and processes and combines these signals in real time. The opponent-process theory of color vision received further support in 1957 in studies by Hurvich and Jameson, and in 2006 by Liapidevskii. Some of the most compelling evidence for the theory is the phenomenon of complementary color after-images, which cannot be explained by the tricolor theory.  You can demonstrate this for yourself by staring at the red dot in the middle of the image below for 30 seconds without letting your eyes drift from the center; then look at a blank white sheet and you will see the image with a more familiar set of colors. (It may take a while for the image to develop).

Looking at the colors under bright light and for longer periods enhances the opponent (inhibitory) processes in the receptors, which intensifies the after-images, just as one would predict based on the principles Solomon found for sensation and emotion.

Consider the similarity between this contrasting after-image response to visual stimuli and the emotional or affective responses that that Solomon found in his animal studies.  The sensory after-images may be less intense and of shorter duration, but the principle is the same, and both phenomena illustrate how opponent processes can arise within our nervous systems. Beyond the processing of simple nerve signals, such as those involved in visual sensory perception, the opponent process theory can account for psychological processes of increasing complexity and at multiple levels, based on the well established fact that the brain is able to integrate sensory information by adding and subtracting different excitatory and inhibitory inputs from different receptors and neurotransmitters.

Practical applications.  Besides explaining common sensory and emotional reactions, I believe the opponent-process provides some very practical guidance for how we can use pleasant and unpleasant experiences to our advantage.  This guidance can be boiled down to seven basic insights:

1. Be aware of hidden processes! The most important insight is to be aware that any primary sensory or emotional stimulus, whether pleasurable or unpleasant, will give rise to opponent processes of an contrasting nature.  Even though you most likely cannot directly perceive them, these opponent processes are happening–and even growing in strength–at the very same time as the primary emotions and sensations that you do perceive.  When the primary emotions and sensations stop or pause, these contrasting processes emerge into consciousness!  For example if you put your hand in cold water, a “warm” opponent processes is being stimulated, but you feel that warmth only once you withdraw your hand from the water. And the pleasure of overindulging in sweet desserts is likely to be followed by an unpleasant reaction that arises some time after you stop eating.
2. Avoid overexposure to pleasurable stimuli. This does not mean that you should minimize or avoid direct pleasure! Just be aware that too much of a good thing too often can backfire — and be aware WHY that is so. By remaining vigilant, you need only to moderate the intensity and frequency of pleasant stimuli to ensure that the opponent processes do not build up. For example, eating small portions of delicious foods, and spacing out meals — or even individual bites — will tend to reduce the level the opponent processes (cravings) that would otherwise reinforce appetite and cravings. When you go for that second cup of coffee, you may marginally increase your alertness in the short term, but realize that you are at the same time continuing to stimulate a reactive opponent process, counteracting the caffeine high, that may lead to increased tiredness later on.  There is a biological argument for moderation!
3. Use unpleasant and stressful stimuli to indirectly build pleasure. This is one of the most powerful insights of the opponent-process theory. By judiciously exposing ourselves to intermittent stresses, of sufficient intensity and frequency, we activate in our bodies and psyches some powerful opponent processes, which in turn result in heightened pleasure and satisfaction. Depending on the type of stimulus, these indirect pleasures can be short-lived or more sustained. Stressful or unpleasant stimuli can therefore be thought of as a form of “psychological hormesis”:  The nervous systems is activating certain pleasurable inhibitory processes in order to defend against and build tolerance to stress. These pleasure-generating defense mechanisms are real, biological processes which operate in our nervous systems. One well known example is the production of endorphins, our natural opiates, which can be produced by engaging in strenuous exercise. Endorphins literally help us to endure the pain of exercise by providing a counteracting pleasure. So by increasing the intensity and frequency of stress exposures, we are not just building tolerance–we are actively building up a sustained background “tone” of pleasurable emotions. This is very much in line with what the Stoics called “tranquility”. As explained on the Stoicism page, Stoic tranquility is not apathy or a lack of feeling!  On the contrary, it is a positive sense of equanimity, contentment, and happiness that endures and supports us.  It is the opposite of depression; you might even call it “elevation”.
4. Indirect pleasure is superior to direct pleasure. So we have learned that we can paradoxically use pain or discomfort to indirectly cause pleasure.  But is there any reason to think that the pleasure resulting from running, hard work, cold showers, or skydiving is superior to the pleasure from sweet desserts or scratching an itch? Aren’t they equivalent? Doesn’t any pleasure, whether direct or indirect, nevertheless have the potential to lead to addiction?  This is an interesting question, but I think the opponent-process theory makes the case that indirect pleasures — those that results as reactions to stress — are superior. There are two main reasons for this:  First, according to Solomon, opponent-processes are “sluggish”; they take time to build, and decay more slowly. They continue even when the stimulus stops. And unlike direct pleasures, which may be more intense, there is no sudden withdrawal reaction when they stop, hence no “craving”. They tend to fade slowly. Second, the initial unpleasant stimulus — exercise, work, cold sensations — must be sufficiently unpleasant to be effective. This initial unpleasantness will always be a “barrier” that requires conscious effort to face and overcome. If it starts to become “addictive”, it is easier to let this unpleasant barrier stand in the way. It is easy to decide not to go running or take a cold shower if one becomes concerned it is becoming too habit-forming or detrimental to one’s health.
5. Use unpleasant stimuli to counteract addictive pleasures. This is one of the most interesting, and I think unexplored, applications of the opponent-process theory. Addictions are characterized by increased cravings. These arise when opponent process build up in reaction to pleasurable primary stimuli that are too intense and frequent. The craving can become a sustained background “tone” that is always there when the pleasurable stimulus is absent. And the “savings” effect makes the opponent cravings come back more easily. But we can overpower these cravings by deliberately introducing unpleasant stimuli at the same time as the addictive cravings, in order to generate new pleasurable opponent processes. The key is to time the unpleasant stimuli to coincide with cravings or withdrawal, and make them sufficiently intense and frequent, that one builds up sufficient background pleasure tone to counteract the unpleasant anxiety that typically accompanies addictions. So fight cravings by adding a new stressful activity like high intensity exercise, cold showers, or intermittent fasting! It may also help explain why cue exposure therapy — exposing oneself to the forbidden fruit without partaking — can often be more effective in extinguishing addictions than merely abstaining or avoiding the addictive stimulus. It is possible that active cue exposure might generate a type of acute “stress” that “burns out “the original craving with an opposing pleasure. This is like fighting fire with fire!
6. Don’t abuse pain and stress. Despite the potential benefits of controlled stress and unpleasant stimuli to indirectly induce sustained pleasure or “elevation”, this approach is easy to misinterpret or apply incorrectly. Some might take this to be a justification for masochism or self-harm, but it is not. The key here is to carefully think through the consequences of one’s actions. Does the application of the stress or unpleasantness result in an objective strengthening of your body and mind — or does it lead to physical or psychological harm?  Depressed teens sometimes engage in a practice called “cutting” to relieve their depression and apathy, because it can actually reactivate pleasure or a rush that fills a gap and can become addictive. Most likely, this pleasure can be explained in terms of opponent processes that release some of the same endorphins or other neurotransmitters as exercise does. But one needs to distinguish between objectively harmful activities like cutting and beneficial habits like exercise or cold showers. Far from injuring oneself, these beneficial uses of stress and “pain” act to act to build strength, resilience, and long-term happiness.
7. Optimize your stimulation schedule. Be aware of critical decay durations and savings effects of opponent processes, for both pleasant and unpleasant stimuli. Addictions and cravings can be minimized by reducing the frequency of exposure to pleasure-triggers to allow enough time for any cravings to decay. The next time you are mindlessly wolfing down bite after bite of an addictive snack like popcorn or candy, try spacing out bites to allow the craving sensations to die off between bites and see whether you end up satisfied with fewer bites. On the flip side, if you are finding it hard to get started on a healthy habit like strenuous exercise, cold showers, or fasting, it may be that you need to increase the frequency and intensity of the new habit until it takes. According to Solomon, it will become increasingly pleasant if you do this.

Since becoming aware of the opponent-process theory, I applied it to myself in two instances recently:

• On the pleasure side, I reduced my craving for alcohol by drinking less frequently, and limiting the amount that I drink.   The pleasure remains, but the daily cravings have disappeared. I’ve documented this on the Discussion Forum of this blog.
• On the pain side, I have increased my enjoyment of cold showers by never missing a day, by lengthening the showers, and by making sure to expose my most sensitive body parts to the coldness.  This has significantly increased the pleasure I feel, and it comes on more quickly while in the shower (within 10-15 seconds, versus previously more than a minute) and the warm, exhilarating post-shower feeling lasts all morning.  I’m happy all the time, and I definitely feel less stress.

Think about how this might apply to your own situation. Are there pleasures in your life that tend to result in cravings when they are absent? Can you think of ways to introduce healthful but somewhat unpleasant stress into your life in a way that builds your resilience and at the same time a deeper level of satisfaction and sustained pleasure?  Can you use this indirect pleasure to displace cravings or dissatisfaction? And in both cases, how aware are you of the relationship between the intensity and frequency of the stimuli, and the tendency to foster opposing processes that turn pleasures into pains, and pains into pleasures?

The potential applications are infinite!

Models of addiction. There are a number of different views of what addiction is. The medical model views addiction as a disease, focusing on the biological aspects of physical or psychological dependency. This view typically confines the idea of addiction to cases of substance abuse and dependency, and attempts to pinpoint the basis for addiction in terms of changes in brain circuitry and the chemical action of reward neurotransmitters such as dopamine and serotonin. The medical model also highlights the biological reality of withdrawal symptoms when the addictive substance is removed. A second model, the psychiatric model, looks at addiction somewhat more broadly as a manifestation of unresolved psychosocial or emotional conflicts that lead to compulsions or poor impulse control; often this is broadened to include the family, social or cultural context. A third model, which we might call the autonomy model, rejects the medical and psychiatric models as too deterministic and incompatible with the existence of free will.  This model takes addiction to be fundamentally a question of personal responsibility and choice. Finally, behavioral models do not necessarily take a position on the origins of addiction, but look instead at how addictive behaviors can be modified and eliminated. Of course, there are many variations and combinations of these models of addiction.

Varieties of treatment. Depending on which model is favored, different treatments variously emphasize medical detoxification and the use of pharmaceuticals; individual, family, group or residential rehabilitation counseling; recognition of personal responsibility; or various modalities of behavior modification. Under the medical model, pharmaceuticals are often prescribed for detoxification and the relief of cravings.  While drugs may in fact help reduce cravings in the short term, they can create their own problems of side effects and substitute addictions. Antagonist drugs, which block receptors for “reward” transmitters such as dopamine, are often unpleasant and create incentives to quit or circumvent treatment, and they invite relapse once they are discontinued. Typical success rates for drug and alcohol detox rehab programs, which combine medical detox and psychological or psychiatric treatment, have been cited to be as low as 2-20 percent. One such program, Narconon, claims a success rate of 76%, but this figure has been challenged as being vastly overinflated and based upon methodologically flawed statistics. As with many similar programs, Narconon insists on the importance of getting treatment away from the normal work-home environment: :

One thing is for sure if you are trying to break a habit such as drug addiction, a change of environment should be at the top of the list as far as solutions. Due to these factors, attending a drug rehab close to home is seldom the correct treatment option for chronic drug abusers. It is extremely therapeutic to be distanced from the people they used drugs with, drug dealers, and the surroundings that can continue to stimulate their past addictive behaviors.

As we’ll see shortly, it is precisely this key assumption that is questioned by cue exposure therapies.

Behavioral therapies. In essence, behavioral approaches look at addictions primarily as conditioned behavioral patterns that are strongly reinforced, but from which the addict nevertheless still has some motivation to escape. Behavioral therapies tend to divide into two camps: those which employ classical and operant conditioning to directly modify behavior by changing the reinforcement patterns; and those which supplement the conditioning techniques, or replace them entirely, with a cognitive element, following the model of Cognitive Behavioral Therapy (CBT).  The cognitive element typically involves actively thinking about ones behavior, and reflecting on whether or not it is based upon rational or empirically valid assumptions. For example, CBT may treat depression, anxiety, or phobias by challenging an individual to consider whether one’s worst fears are in fact likely to happen, what one is giving up by maintaining the present behavior, and what one stands to gain by stopping it.  Often meditation, mindfulness, and notions of self-efficacy are involved in these cognitive approaches. Examples of the application of CBT to addiction are Alan Marlatt’s Relapse Prevention Therapy and also his Mindfulness therapy; and Aaron Beck’s Cognitive Therapy of Substance Abuse.

However, overcoming addiction may not be all that susceptible to “reasoning” and reflection. Addictive cravings are often incredibly powerful and tend to overwhelm rational thinking.

Cue exposure therapies. There are two very different approaches to treating addiction by behavior modification:  stimulus avoidance and cue-exposure therapies. While they are both considered “behavioral” treatments, they are in fact polar opposites! The stimulus avoidance therapies involve training the individual to avoid exposure to the stimulus. In practical terms, this means abstinence. It  is the approach taken, for example, by Alcoholics Anonymous. A core assumption of AA is: “Once an alcoholic, always an alcoholic”.  Those who take this view claim that it is impossible, or highly risky, for an alcoholic ever to return to moderate drinking. AA has a good success rate, but it tends to require a strong “spiritual” commitment, and can be sabotaged by relapse if the recovering alcoholic or addicts takes even a single drink.

There is an emerging area of research, however, which takes issue with the stimulus avoidance school of thought, and supports the idea that addictions can be replaced by normal responses to behavioral cues, using cue exposure therapy, sometimes called response prevention therapy.  And even more radically, the treatment works best if carried out in the most realistic context of the daily life patterns of the addict.  This completely contradicts the central assumption of Narconon in the above quote!

For a full explanation of the psychological basis and technical terminology of reinforcement theory, I would recommend reading the Psychology page of this blog, which provides useful background on the work of Pavlov and current applications by behaviorists such as Daniels and Pryor in the use of cue exposure as a general method for extinguishing behaviors.  In short, the essence of cue exposure therapy is to extinguish the addictive behavior by allowing the addict to be exposed to normal cues or stimuli that typically precede the addictive behavior, but preventing that behavior from getting underway. This clearly leads to significant discomfort and even withdrawal symptoms in serious cases.  However if repeated frequently enough, and in the presence of a sufficient variety of cues and contexts, cue exposure therapy can be very successful in extinguishing addiction.  Even more importantly, there is evidence that is is successful in preventing relapse over the longer term.

Furthermore, cue exposure therapy is a general approach to addiction treatment. It works not only in treating “chemical” addictions of substance abuse, but addictive behaviors more generally.  There are studies showing its effectiveness with treatment of drug and alcohol addiction, tobacco addiction, and eating disorders. For example, using cue exposure and response prevention, combined with gradualism may be more effective than going “cold turkey” for learning to permanently stop smoking. Other studies show that cue exposure therapy is more effective than a “self control” based cognitive behavioral approach in treating bulimia.

What makes cue exposure succeed? Despite encouraging data of the effectiveness of cue exposure therapies in both addiction cessation and relapse prevention, it is not always successful. A recent review article in the journal Addiction, by Conklin and Tiffany of Purdue, provides an excellent meta-analysis of 18 cue exposure therapy for treating a range of addictions–including treatments for addiction to alcohol (N=5), nicotine (N=5), cocaine (N=1), and opiates (N=6).  The review includes a careful analysis of why cue exposure therapies in many cases fail, why they often succeed, and what specific factors determine their degree success. Conklin and Tiffany not only review the clinical and field studies with human subjects, but also cite the most current animal research on addiction extinguish to buttress their analysis. This is an academic paper, but clearly written and accessible to the intelligent layperson. For anyone struggling with addiction and willing to consider cue exposure therapy, I highly recommend reading this paper carefully to absorb its many insightful lessons.

The cue exposure treatment studies varied considerably in their design and execution. In about half of them (mainly the drug studies), the participants were abstinent during cue exposure.  In one study (with alcohol dependence),  a moderate drinking goal was encouraged by providing “priming” doses of alcohol, with the the prevention of drinking more than one drink, and this behavior was practiced both “inpatient” and as outpatient “homework”.  Cue exposure varied from real “in vivo” cues to surrogate video, audio, and even “imaginal” cues just pictured in the mind.  The frequency of cue exposure varied greatly — from a single cue exposure (e.g. smelling a glass of alcohol for 3 minutes) within a single session, to multiple, frequent exposures per session over 10 consecutive days of cue exposure sessions, to periodic exposure sessions spaced in time over weeks, with follow up over 6-12 months.

In their review article, Conklin and Tiffany identify 4 main “threats to success” (and corresponding success factors) that explain both why cue exposure did not work well in some cases and where it either was, or could be made, more effective.  Before summarizing these success factors, I think it is important to note one key insight they highlight regarding recent learnings from animal research:

Rather than simply trying new things in an effort to discover the optimal parameters for use in cue-exposure addiction treatment, ideas for improving treatment can be directly informed by recent animal learning research focusing on extinguishing learned behavior…ideas about extinction have changed considerably since cue exposure was first introduced as a treatment for addiction. For many years, extinction training was believed to lead to a weakening of the initially condition CS-US association…However current concepts about extinction resemble more closely the original ideas of Pavlov (1927), who postulated that repeated unreinforced exposure to the CS does not break the original CS-US learning, but rather serves to mask it…Therefore, the conventional notion that extinction is unlearning has been replaced with the position that extinction is new learning, that is, during extinction, CS-US learning remains intact, but new associations develop to the original CS. (p. 159)

This is a crucial insight!  The original addictive response to stimulating cues will never die by itself, merely by not reinforcing those stimuli.  Rather, it is important to learn new behavioral responses to those old cues which come to “mask” or dominate the the old responses.  Cue extinction is an active process, not a passive one!

Now let’s turn to the specific threats to the success of cue extinction which have been identified by Conklin and Tiffany:

1. The renewal effect occurs when a behavior is successfully extinguished in one limited context or set of cues, but re-emerges in response to a different context or cues. This is a common problem in treatment, because the treatment context often differs in significant ways from the “real world”.  Conklin and Tiffany give the example of a heroin addict who gets inpatient extinction treatment in a hospital room, but resumes shooting up at home–a different context, with different cues. The same conditioned stimulus (CS)– for example seeing or handling drug paraphernalia, or being stressed–can acquire a different “meaning” in the two different settings. Cues can be rich, subtle and varied: the action of lighting a cigarette with a match, handling of drug equipment, or the smell, the size and feel of surroundings, people, and the time of day. There are a number of important ways to deal with this problem.  First, the extinction training should as much as possible occur in the “original conditioning context”, that is the real-world context in which the addiction was acquired and has been developed.  Second, given the fact that most addictions are reinforced by a rich set of cues and multiple contexts, the extinction training should occur in several distinct contexts, and then re-tested in the original context.  According to the authors, “Apparently, whereas conditioning generalizes readily, extinction is largely context-dependent”. (p. 160).
2. Spontaneous recovery occurs merely with the passage of time, even when a behavior is initially extinguished successfully.  The addiction can re-emerge by itself days, weeks, or months after being apparently terminated. Dealing with spontaneous recovery requires consideration of the “temporal spacing” of cue-exposures. Here, the authors cite a number of animal studies for guidance. In one such study, extinction occurred more rapidly and successfully when the cues were given as a series of short exposures over time instead of as a single “massed” presentation. Other studies found that extinction success was optimized by allowing longer intervals of time between exposure sessions, combined with more frequent in-session exposures. This was also reflected in the human studies. Based on this research, Conklin and Tiffany give the following guidelines:
   • Within each session, the cue should be presented several times to ensure complete extinction of “responding”, defined as as subjective desire or objective physiological or behavioral response
   • Within-session exposures should be separated by enough time to allow some recovery of responding between exposures
   • Enough time should be allowed between sessions to allow for spontaneous recovery of responding, and therefore further extinction at each session
   • The number of extinction sessions needed depends on the individual’s pattern of responding, which can vary considerably among individual subjects
3. Reinstatement occurs after a conditioned stimulus (CS) has been extinguished, by presenting the unconditioned stimulus (US) alone.  For those not familiar with this terminology (which is described in more detail on the Psychology page of this blog), the US is the immediate agent that produces the addictive “high”, e.g. the drug, tobacco, alcohol or food itself, whereas the CS is any cue which becomes associated with it, e.g. seeing or handling a bottle or cigarette, or visiting a bar or drug dealer. So in reinstatement, the former addict has learned not to respond to the environmental context and cues, but for one reason or another encounters the addictive substance in a new context, re-igniting the addiction anew and leading to potential relapse after even a single new exposure.  Here, the research on prevention is very interesting. Relapse in such situations can apparently be prevented or quickly cut off by immediately exposing the lapsed addict to unreinforced exposure to the new context alone (without the US).  So if your addiction to sugar or alcohol is re-ignited by inadvertently or unwittingly consuming a food that stealthily contains this offending substance, expose yourself to eating other foods (without the addictive substance) in the same place and with the same cues, on more than one occasion, and the relapse will be forestalled.
4. Behavioral cue conditioning is one of the more subtle, but insidious threats to successful extinction. If the addiction is based upon classical conditioning (that is the addictive behavior is a direct “conditioned response” (CR) to one or more conditioned stimuli (CS), then deconditioning by extinction training has an excellent chance of success.  However, in many cases of addiction the CS indirectly elicits behaviors that precede the direct addictive response, and these behaviors themselves act as secondary “discriminant stimuli” which provoke the addictive response independently of the CS.  For example, for an alcoholic, the CS may be a bottle of booze. By the principles of classical conditioning, the appearance of the bottle can be extinguished as a cue for the urge to drink (the CR or conditioned response), by exposing the alcoholic to the bottle and not allowing drinking. However, in the normal context, the alcoholic engages in certain active routines or behaviors, such as pouring the alcohol into a glass, handling the glass, drinking from the glass, etc. These behaviors in themselves serve as independent cues, beyond appearance of the bottle itself, that stimulate the desire for the alcohol.  So it is not just the sensory stimuli that need to be extinguished, it is also the behavioral cues.  Overlooking this reality turns out to be a major flaw of many of the less successful treatments reviewed by Conklin & Tiffany. In these flawed treatments, the cue exposure sessions dealt with sensory cues alone. The authors found the best treatments involve extinction of active behaviors.  For example, one study had smokers actually light cigarettes and take non-inhaled puffs.  Another study had heroin addicts go through an actual cook-up procedure and handle all their paraphernalia, without allowing follow-through to actually administering the drug. While to an adherent of the “abstinence” approach such therapies may seem unduly risky, the science actually supports such realism as being the most effective way to immunize an addict against relapse.

There is some recent evidence from a study by researchers at McMaster University and the University of California at San Francisco that takes this approach even further.  In cases where the goal is moderation and not abstinence, it is important the the cue exposure involve actually take small doses (e.g. one drink), while preventing any follow up drinks, to re-train the response.  This is based on observations that addicts or alcoholics respond to a small dose as a cue that “more is coming”. Without this type of conditioning, there may be increased risk of relapse.  Again, “you get what  you train for”.

Conclusions. In short, cue exposure therapies will not work if they are confined to small number of artificial exposures within a single limited context, especially if it is significantly different from the context where the addictive behavior was “learned”.  The exposure should be rich and varied, repeated both within a cue exposure session and at subsequent sessions while allowing an adequate time interval both between in-session exposures and between separate sessions to allow “responding” or partial re-emergence of the desire or craving. Cue exposure therapy should not involve mere passive exposure to sensory cues but should  include a realistic “behavioral” component which is practiced without allowing the reinforcement itself to occur. Finally, it is important to keep in mind that extinction is not a matter of passively “unlearning” an old behavior by just not responding, but actively learning new substitute behaviors for responding to the original cues and contexts; adding a degree of “counter-conditioning” is useful here (see the discussion of counter-conditioning on the Psychology page of this blog.

What does this mean for you? Is there an addictive behavior or a bad habit you would like to overcome?  Are you willing to try cue exposure therapy.  If so, observe and think about the sensory and behavioral cues that precede your behavior and how you could design your own cue exposure sessions to help extinguish the behavior.

What does this mean for me? I stated at the beginning of this post that I would do something unusual. Rather than writing this post purely as a scientific report or as an “advice column” to others, I am going to put it to the test on myself.  In the tradition of self-experimentation inspired by Seth Roberts, I am going to put my money where my mouth is and try it on myself.  I have used cue extinction already as the basis for deconditioning myself from having a strong appetite for food (at certain times of day), for cutting back significantly on certain favorite desserts (such as ice cream), and for giving up caffeinated coffee (but still enjoying the occasional cup of decaf).  However, I retain a certain fondness for alcohol.  I’m not an alcoholic and and don’t believe I have a drinking problem, but I drink more than I would like to and find myself craving certain drinks before dinner almost nightly. My favorite drinks, in order, are: (#1) B&B cognac liquor on the rocks; (#2) Manhattan cocktail; (#3) beer; (#4) red wines, especially Pinot Noir.   About a year ago, I cut back to a frequency of 1-2 drinks per week, but recently this has crept up to a nightly drink, and I find myself really looking forward to it after work.  It is a real pleasure and stress reliever, and I don’t want to cut back, but I know I should.

So you’ll find a record of my experiment, starting today (Thursday, April 14), on my personal page on the Discussion Forum.  At this point, my goal is not total abstinence, but cutting down to a maximum of 1-2 drinks on 1-2 nights per week. Wish me luck!