There is a powerful way to re-program your brain that has been largely overlooked. A way to change your relationship with eating, sleep, sex and basic emotions like fear, love and aggression. While cognitive therapies can modify behavior, they are of questionable help in altering these basic drives.
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:
The third category is perhaps a less well recognized form of hormesis:
- 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:
- 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.
- 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 exert 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 greatest 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.
- Flores et al have found that extended exercise can directly improve insulin and leptin sensitivity in the hypothalamus, based upon IL-6 signaling.
- Marnia Robinson and her husband Gary Wilson have developed a therapeutic method to “reboot” sex drive and romantic interest, based upon deliberate restriction of sexual stimulation for several weeks, combined with alternate forms of intimacy. Their rebooting method can even reverse problems such as erectile dysfunction and has been found useful in combatting addiction to pornography. They cite evidence that dopamine and prolactin circuitry is at work with both the problem and the solution. Both the hypothalamus and amygdala regulate sex drive, so it would be interesting to know exactly how “rebooting” affects the relevant neural nuclei.
- Extinction. An addictive response becomes weaker and eventually dies out when you stop responding to a triggering cue. This approach works, but can take a long time and requires patience and discipline.
- Cue exposure or deconditioning. This involves deliberate, repeated and provocative exposure to the triggering cue, withholding the response. After some initial discomfort, this approach proceeds rapidly and can be quite effective. Success is improved the more realistic and varied the presentation of the cue.
- Putting on cue. A new cue is developed and the behavior is only allowed in the presence of this cue. It could be a special sound, or a location. Then the special cue is withheld and the behavior disappears.
- Counter conditioning. This involves the substitution of an alternative behavior to actively displace the old reward circuitry. It can be very effective.
- The general psychology of deconditioning
- The Deconditioning Diet
- Overcoming addictions using cue exposure therapy
The anatomy of the limbic system offers one other strong leverage point into reprogramming the amygdala-hypothalamus axis: namely, the prominence of the olfactory bulb. The olfactory bulb directly innervates the amygdala, and there is ample support that smell and taste are powerful triggering cues for the appetitive and sex drives.
Several diets are based on control of this powerful trigger, as I have argued in my post on Flavor control diets. Flavor and flavor variety tend to stoke appetite, due to direct classical conditioning of the amygdala (and without the hypothesized intermediation of a preprandial insulin and blood glucose mechanism, as I erroneously speculated in my original article, which I intend to re-write based on my current understanding). While some diets work by either suppressing flavor (Shangri-la Diet) or limit flavor variety to induce sensory-specific satiety (Flavor Point Diet), these approaches don’t reprogram the amygdaloid flavor-appetite reward circuit. They merely avoid appetitive triggers, which remain intact until re-activated. I think the most effective way to change your appetite is via the above-mentioned Deconditioning Diet, which directly modifies reward circuitry, presumably within the amygdala.
The use of olfactory cue conditioning to modulate other hypothermic drives is worthy of exploration.
A final speculation. Admittedly, this is one of my more speculative articles. While I have started out in the known physiology of the limbic system, I am to some extent going beyond proven data in my judgements and recommendations. So I’ll continue one step further down the path with a parting thought. At the beginning of this article, I expressed my astonishment that the control of so many apparently distinct drives — eating, sleeping, body temperature, aggression, sex drive and sociality — are all packed into two structures the size of a pea and an almond. It seems quite remarkable the the neurons and circuitry for these different drives remain distinct and do not interfere with one another. But perhaps they are not so distinct. In fact there is some evidence that they interact. For example, many have reported that fasting makes them feel colder and may depress thyroid function, at least in the short term. Fasting also may result in reduced sex drive and changes to the sleep cycle. So the hypothalamic control of feeding, body temperature, sleep and sex drive may interact. To some extent, these effects may be compensated for by actively exercising, which appears to increase body temperature. In addition, these short term interactions may or may not persist during longer term adaptations.
I take cold showers every day and have found they raise my energy level and mood and help me to stay lean. In his book, The Four Hour Body, Tim Ferriss correctly rejects the thermodynamic argument of Ray Cronise that cold showers and baths promote weight loss based because shivering involves significant energy expenditure. Not only do the energy calculations fail to add up, but this explanation would defy the principle of homeostasis: If we lose weight by shivering, and nothing else changed, our hypothalamus and leptin accounting system should compensate by driving us to increase appetite to restore the lost weight. Ferriss proposes what I think is a more plausible explanation, namely that cold exposure induces metabolic changes that cause a replacement of white adipose tissue (WAT) with more metabolically active brown adipose tissue (BAT). Interestingly, work by Cao et al at Ohio State recently found that the conversion of WAT to thermogenic BAT is triggered by the the action of BDNF in the hypothalamus. Interestingly, BDNF is a stress response hormone that is also up-regulated by intermittent fasting or calorie restriction. Furthermore, it is is known that the hypothalamus responds to cold exposure by up regulating the production of thyroid stimulating hormone (TSH) which directs the thyroid gland to output thyroid hormones T3 and T4, increasing basal metabolic rate. That alone could explain increased energy levels and weight loss, which may be sustained so long as the cold stimulus is provided at a certain frequency. There are likely many other examples cross talk” between temperature regulation, eating behavior and hypothalamic regulation of other drives.
More needs to be explored on how control of our apparently distinct drives interact with each other. This can be helpful in designing strategies for effective diet and exercise, and for addressing sleep and sexual problems.
Given the speculative nature of this article, I would be more than interested in feedback and suggestions for further investigation or development of the ideas presented here.