> What is psychotropic about organic raw cacao?

"One of the best effects of eating chocolate is the 'good feeling' or moderate high that many people experience after consuming it. Researchers have developed different hypotheses of how chocolate affects the central nervous system to cause the high that people report. These hypotheses have focused separately on cannabinoid systems and opioid systems, although these two systems may be tied together to form a unitary mechanism of chocolate effects and to form a basis for chocolate craving....

It is believed that the cacao bean was first transformed into chocolate by the Olmec people of Mexico as early as 400 B.C., and by around 500 A.D. the Mayans of Central America and Mexico systematically planted cacao crops (WWW 2)....

By the 17th century, the drink was common among European nobility, especially in England (WWW 2)....

Cravings may be a moderate form of addiction in that craving symptoms mimic minor symptoms of withdrawal....

One of the largest obstacles to determining the basis for the chemical effects and the craving mechanisms for chocolate is that chocolate contains over three-hundred known chemicals (WWW 2). The effects of chocolate may be associated with a single chemical, isolated actions of multiple chemicals, combined actions of multiple chemicals working together, or all three....

The amount of phenethylamine in chocolate is very high compared to other foods. Phenethylamine is similar to amphetamine in its structure and rewarding properties in the central nervous system (WWW 1). It may act by increasing attention and alertness mechanisms in the brain, by raising blood pressure and blood glucose levels (WWW 1; WWW 2). It may also act by potentiating dopamine and norepinephrine, which have connections to the reward pathway of the limbic system. Some reports have stated that an antidepressant drug, with a structure similar to phenethylamine, abolishes chocolate craving (WWW 2). 

Another main component of chocolate is methylxanthines, such as caffeine and theobromine, which act as antagonists at inhibitory adenosine receptors. Caffeine is known to have addictive properties, but caffeine is present in chocolate in much lower concentrations than theobromine. There is a possibility that theobromine may also have addictive properties, and thus chocolate craving may represent an attempt to alleviate withdrawal from either of the methylxanthines (Michener and Rozin 1994). Researchers have also found tyramine in chocolate, which is known to have varied effects throughout the menstrual cycle (Michener and Rozin 1994). This may help to explain why women's chocolate craving increases around the menstrual cycle. 

The latest breakthrough in chocolate research comes from Emmanualle di Tomaso et al. who have found that chocolate contains pharmacologically active substances that mimic the effects of marijuana on the brain (Di Tomasso et al. 1996). The pursuit of this line of research came from the observations that chocolate cravings were associated with psychoses induced by certain drugs, such as MDMA (Chianese 1992; Di Tomasso et al. 1996). This suggested that chocolate cravings and effects are more than a sensory experience of the nervous system they involve some sort of pharmacologically active substance. Even though earlier research had focused on methylxanthines (caffeine and theobromine), these scientists focused on another substance, anandamide. Anandamide is a member of a family of fatty acid ethanolamides composed of arachidonic acid coupled to ethanolamine through an amide linkage (Devane et al. 1992). 

Within the last couple of years, anandamide has been recognized as an endogenous cannabimimetic, meaning that it a substance produced in the body that binds to cannabinoid receptors with high affinity and mimics the effects of plant-derived cannabinoids on established behavioral patterns (Di Tomasso et al. 1996; Axelrod and Felder 1998). Anandamide is not a classical neurotransmitter in the sense that its hydrophobicity allows it to easily pass through plasma membranes limiting its ability to be stored in synaptic vesicles. Instead, it may be synthesized when needed at the plasma membrane (Axelrod and Felder 1998). The cannabinoid receptor that anandamide acts on is a G protein-coupled plasma membrane receptor (Axelrod and Felder 1998). The primary effect of this receptor is to inhibit adenylyl cyclase activity, which occurs in a dose-dependent and stereoselective manner. 

Cannabinoid receptors are present in many locations in the brain, such as the cerebellum, hippocampus, basal ganglia, cortex, and striatum (Herkeham et al. 1990), which explains the fact that cannabinoids have varying effects. The actual reward and reinforcing effects of cannabinoids that may explain the effects and chocolate craving may be mediated through the mesolimbic dopamine system. This system projects from the ventral tegmentum to the nucleus accumbens of the limbic system, and is often referred to as the "reward circuit" (Tanda et al. 1997). In a study of the effects of cannabinoid activation on dopamine transmission, Gianluigi Tanda, et al. found that THC (the active ingredient of Cannabis) significantly increased dopamine in the nucleus acumbens (NAc). These researchers also found that naloxone and naloxohazine, both opioid antagonists, prevented the effects of THC on dopamine, demonstrating that cannabinoid receptors activate dopamine transmission through opioid receptors on the ventral tegmentum (Tanda et al. 1997). Because of the connections of the NAc with the limbic system areas involved in emotions, it is likely that the activation of dopamine transmission in the NAc is involved in the affective and motivational properties of THC (Tanda et al. 1997). These findings provide an interesting tie in with research on opioid involvement in preferences for sweet high-fat foods such as chocolate (Drewnowski et al. 1992). 

It has also been found that the cannabinoid receptors are more responsive to psychoactive than non-psychoactive cannabinoids (Matsuda et al. 1990). Because cannabinoid drugs are known to produce euphoric effects, anandamide may "intensify the sensory properties of chocolate thought to be essential to craving (Di Tomasso et al. 1996)." It is also possible that the feeling of well-being associated with chocolate could be due to the interaction of elevated anandamide levels and the many other pharmacological compounds present in chocolate (Di Tomasso et al. 1996). 

Di Tomasso et al. did isolate small amounts of anandamide in samples of chocolate, but they also isolated larger amounts of two other anandamide-like compounds, N-oleoylethanolamine and N-linoleoylethanolamine. Neither of these anandamide-like compounds activate brain cannabinoid receptors, but they were shown to inhibit anandamide hydrolysis in rat brain microsomes and intact cells (Di Tomasso et al. 1996). The resulting effect of this inhibition is an increased amount of residual anandamide. Therefore, the ethanolamine compounds found in chocolate could act on the body by one of two mechanisms either directly activating cannabinoid receptors or by indirectly increasing anandamide levels (Di Tomasso et al. 1996). It is yet to be determined whether the concentrations of these ethanolamides exist in chocolate in high enough concentrations to actually produce significant effects in humans. 

The best sources for anandamide and the other ethanolamides, such as N-oleoylethanolamine and N-linoleoylethanolamine, are cocoa and dark chocolate. In fact, dark chocolate contains as much as three times the amount of ethanolamides as does milk chocolate (Chianese 1997). Increased anandamide levels in the brain do not mean that people experience a marijuana-like high after eating chocolate they only experience a mild euphoria, if anything at all. One reason for this may be that anandamide only binds to a portion of the available cannabinoid receptors, while marijuana activates every cannabinoid receptor simultaneously. The fact that anandamide only selectively activates receptors may have benefits in a therapeutic sense. Marijuana is an effective therapy for soothing side effects of chemotherapy in cancer patients and for stimulating appetites in AIDS patients, but its use is limited because of its psychotropic effects (Chianese 1997). The actions of anandamide or the other ethanolamides in chocolate may provide researchers with a mechanism to create the same therapeutic effects of marijuana while eliminating the psychotropic high (Chianese 1997). These findings could even have implications for diseases such as depression, which could be caused by a rapid breakdown of euphoria causing chemicals, such as anandamide. Potentially, a disorder caused by rapid chemical breakdown could be treated by inhibiting the breakdown of the chemical as the ethanolamides do (WWW 3). 

The hypotheses formed by Tomaso, et al. regarding chocolate and anandamide have not gone without criticism. Di Marzo, et al. argue that the endocannabinoids in chocolate are not present in high enough quantities to produce any euphoric effects in humans (Di Marzo et al. 1998). This group of researchers tested, through oral administration in rats, how anandamide could survive passage through the digestive system. They found that endocannabinoid substances were active in behavioral tests of cannabimimetic activity, but only at concentrations much higher than that which is present in foods such as chocolate (Di Marzo et al. 1998). They concluded that enzymes in the gastrointestinal tract limit the amount of endocannabinoid reaching the bloodstream to only 1.6-50f the compound that was administered orally. They also noted that much smaller doses of THC were sufficient to produce strong effects in all of the behavioral tests (Di Marzo et al. 1998). From their data, they argue that the amount of anandamide in food is not nearly enough to produce the noticeable psychotropic effects that THC causes. 

Massimiliano Beltramo and Daniele Piomelli, two of the authors of the original article, responded to the criticism by noting that, in their original article, they formulated two hypotheses about the euphoric effects of chocolate. While there may not be enough anandamide in chocolate to directly produce an effect, levels of N-oleoylethanolamine and N-linoleoylethanolamine may be adequate to inhibit anandamide degradation in vivo, indirectly increasing anandamide levels (Di Marzo et al. 1998). Di Marzo et al. did not investigate the effects of either of these two compounds. Beltramo and Piomelli also aimed their criticism at the fact that Di Marzo et al. expect the ethanolamines in chocolate to display a "pharmacological profile similar to cannabis (Di Marzo et al. 1998)." In their original article, Beltramo and Piomelli only said that chocolate acts through the same receptors as marijuana, not that as many receptors are activated or that they are activated to the same degree by chocolate (Di Marzo et al. 1998). They did concede, however, that much research still needs to be done before any true conclusions can be reached. 

Other groups of researchers have focused less on the specific compounds in chocolate and more on the effects of chocolate on the central nervous system. Drewnowski et al. hypothesize that chocolate normally triggers the production of opioids. When the opioid receptors are blocked by antagonists, the craving for high sugar and fat foods declines (Drewnowski et al. 1992). Past research has shown that regulation of energy intake in humans is mediated by endogenous opioid peptides. Opioid antagonists, such as naloxone, reduce intakes of 
carbohydrates and fats, while opioid agonists, such as morphine, increase fat consumption. Because opioids are linked to reward pathways in the nervous system, researchers have hypothesized that opioids effect caloric intake by mediating pleasure responses to food (Drewnowski et al. 1992). In particular, it appears that preferences for sweet tastes may be under opioid control, leading to the hypothesis that opioid blockers cause appetizing food to be less rewarding (Drewnowski et al. 1992). The foods that are usually considered appetizing are sweet, high-fat foods that are frequently craved, especially chocolate. 

In the study by Drewnowski et al., researchers examined the effects of naloxone on reduction in caloric intake. The study showed that the opioid antagonist reduced the caloric intake of sweet high fat foods 54ompared to the levels consumed by control samples, although the effect was only significant in the group of binge eaters (Drewnowski et al. 1992). The study also examined changes in taste preferences and reward values of food and found that naloxone significantly reduced taste preferences for sugar and high-fat sensory stimuli in all subjects. It is interesting to note that the effect was especially large in female binge eaters, which is a group that consistently shows high cravings for chocolate (Drewnowski et al. 1992). The strongest effects of naloxone were for the food group composed of M&M candies, Snickers bars, and Oreo and chocolate chip cookies, which is consistent with the hypothesis that chocolate acts through opioid pathways. 

Other studies have also shown connections between opioids and chocolate. In one study, beta-endorphin release was caused in rats by consumption of chocolate milk or chocolate candy, which provides direct evidence of chocolate effects in the central nervous system (Drewnowski et al. 1992; Dum et al. 1983). Some researchers have also concluded that opioid release plays a role in development of food preferences, which is clearly consistent with chocolate cravings. Further evidence comes from studies showing that sweet cravings are often associated with opiate addiction and opiate withdrawal is sometimes eased by sweets (Drewnowski et al. 1992). While this data does not imply that chocolate has the same effects on the body as opiates, it provides strong evidence for a role of the endogenous opioid peptide system in chocolate effects. 

While there has been a good deal of research focused on effects of chocolate, there has been very little investigation into the actual craving aspects of chocolate. Good evidence for a physiological basis of chocolate craving comes from the finding that, in many females, cravings are especially strong around the onset of menstruation, which is consistent with the idea that ovarian hormones influence cravings (Michener and Rozin 1994). Further evidence for the role of ovarian hormones comes from evidence that men and elderly women, who experience a decline in the effects of ovarian hormones, experience cravings to a much lesser degree than young women. These cravings tend to be for high fat, high carbohydrate mixtures, especially chocolate (Michener and Rozin 1994). Chocolate cravings have also been observed in many different populations such as in people with obesity and eating disorders, seasonal affective disorder, and in the course of antidepressant treatment (Drewnowski et al. 1992). 

Scientists have considered that cravings may be conditioned responses to environmental conditions when a food was eaten, but this view fails to explain the consistency of chocolate craving in the population (Pelchat 1997). Cravings could also arise from monotonous diets and, therefore would serve to create dietary variety, which could improve someone's nutritional status. Again, though, this fails to explain why chocolate is craved more than other substances that may be lacking in a diet (Pelchat 1997). 

Some studies have pointed to the rewarding effects of phenethylamines, magnesium, opiates, and, more recently, anandamide, but Michener and Rozin have questioned the existence of a pharmacological component of chocolate craving (Michener and Rozin 1994). They developed three hypotheses that may account for the initiation and termination of carvings. The first hypothesis is that cravings begin from a desire for the sensory properties (i.e. smell, taste) of chocolate and are satisfied by the sensory properties. Another hypothesis is that cravings stem from an internal physiological factor, such as a deficit of endogenous ethanolamides, and are satisfied by ingesting chocolate to compensate for the deficit of the internal factor. A third hypothesis is that the cravings stem from an internal physiological factor, but are not directly terminated by chocolate consumption, instead terminating from natural physiological changes (Michener & Rozin 1994). Michener and Rozin tested these hypotheses by administering chocolate to chocolate cravers at the beginning of their craving. The cravers were given either a chocolate bar, white chocolate, which contains none of the pharmacological components of chocolate, cocoa capsules, or a placebo. They found that the chocolate bar and the white chocolate reduced cravings, while the cocoa capsules, which contained the same compounds as the chocolate bar, had very little effect on the cravings (Michener & Rozin 1994). 

Clearly, these results support the view that chocolate cravings are satisfied by sensory experiences, such as aroma, sweetness, and texture (Michener & Rozin 1994). However the results do not imply that the initiation of a chocolate craving is due to sensory factors. Therefore, these findings are still consistent with the relationship between chocolate and substances involved in reward pathways of the brain. It is very possible that the cravings may be initiated by an internal pharmacological deficiency, while the satisfaction only depends on a particular sensory experience (Pelchat 1997). This research, along with all the research discussed previously, provides an interesting beginning into the discovery of the neurochemical effects of chocolate and the basis for chocolate craving, although there are still many unanswered questions."

Source: http://sulcus.berkeley.edu/mcb/165_001/papers/manuscripts/_303.html