If It Isn’t Addiction, What Is It?

In the light of how much attention has been paid to addiction over the last few decades, the amount of mystery that still surrounds the subject is considerable. As a small example, take Dr. Vera Tarman’s words about weighing and measuring portions:

A food addiction treatment plan may also include ample amounts of food so that the person does not over/under eat. To this end, it may even be necessary to weigh and measure foods. This is not about calorie counting or food restriction, it is about keeping the food addict safe by controlling the amount and type of food choices.

But if you can put a leash on it, is it really an addiction? Or just a bad habit? And, is the problem in the substance, or the person? Prof. Bruce Alexander, of Rat Park fame, says research has confirmed that “the great majority of individuals in reasonably healthy social environments who use the so-called ‘addictive drugs’ do not become addicted.”

Is addiction forever?

Even long-term users, like surgical patients, Vietnam veterans, and others, have shown that the inescapable addiction trope is not accurate. So, if drugs with proven addictive potential don’t necessarily hook everybody who tries them, isn’t it overly dramatic and even silly to talk about being addicted to potato chips or cookies?

A phrase that lurks in many minds is, “Once a junkie always a junkie.” In other words, even if someone is not currently using, and has not used for years, they are still just as much an addict as the on the long-ago day when an ambulance picked them up from the gutter and took them to a hospital. Another way of expressing the notion is, “Never recovered, always recovering.” Even within Alcoholics Anonymous, the granddaddy of all programs, the controversy continues, as shown by a lengthy collection of opinions from AA members.

The BED conundrum

We have been talking about the concepts of food addiction (FA) and eating addiction (EA), and also about what a person’s own body and/or psyche might contribute to the likelihood that they will become addicted, obese, neither, or both. In “Is food addiction a valid and useful concept?,” H. Ziauddeen and P. C. Fletcher discussed “the possible validity of a FA model in the context of a subgroup of individuals in whom obesity is prevalent: specifically those who suffer from binge eating disorder (BED).” They wrote,

In BED, we have a phenotype that goes beyond obesity with a behavioral profile of disordered and compulsive eating, and this is critical to begin an evaluation of the underlying processes and neural circuitry.

The NeuroFAST research organization has made an interesting statement about obesity: that in most types of it, food addiction is “unlikely to be relevant.” While FA may exist, most weight accumulation results from “marginal overconsumption of calories over long periods of time,” a slow process that is unlikely to be noticed in the short term, somewhat like facial wrinkles. Instead, they see the FA concept as more likely to apply to regular and significant overeating “within the context of a clinical eating disorder resembling an addiction.”

According to the research brief,

Patients with drug addiction or eating disorders that mimic food addiction (such as BED) do share some character-traits, such as impulsivity. In particular, it will be important to establish how comparable the behavioral and neurobiological processes in chemical and food addiction really are, and whether similarities and differences can be exploited to benefit.

Your responses and feedback are welcome!

Source: “Guest Post: Food Abstinence for Food Addicts: Deprivation or a New Freedom?,” DrSharma.ca, February 2015
Source: “Addiction: The View from Rat Park,” BruceKAlexander.com, 2010
Source: “Recovered versus Recovering — What’s your position?,” BigBookSponsorship.org, undated
Source: “Is food addiction a valid and useful concept?,” NIH.gov, January 2013
Source: “The Biology Behind ‘Food Addiction,” Europa.eu, undated
Image by Fabio Venni/CC BY-SA 2.0

Feel-Good Genes and Addiction, Continued

Heredity influences the body and brain to have certain attitudes and behaviors around food and eating. This is significant for many reasons. It could influence the effectiveness of any program designed to alleviate the problems that are called, for lack of better terms, food addiction or eating addiction.

The more positive a person feels in general, the more likely they are to participate in the program with a hopeful and cooperative attitude. The paradox here is that, if their baseline emotional state was pretty good in the first place, they might not have been drawn into harmful eating habits, and the whole question of their joining and participating in a program would be moot.

In a previous post, we mentioned that about one out of five people apparently experience natural happiness because of their genetic makeup. In many instances, this tends to line up with nationality, and the next post will go into more detail about the reasons for that. Researchers Michael Minkov in Bulgaria and Michael Bond in Hong Kong looked into the situation and wrote it up for the Journal of Happiness Studies. The article begins with a definition:

Anandamide is a neurotransmitter that binds to cannabinoid receptors in the brain and body, stimulating a sense of happiness and mental wellness. It works by binding to the same receptors in the brain as the main psychoactive compound in marijuana.

This may seem counterintuitive, but Dr. Richard A Friedman in his very thorough article “The Feel-Good Gene,” wrote:

Thus, it is possible that a medication that targets the endocannabinoid system could be beneficial in treating addiction to cannabis, and other drugs, too.

And could such medication also help to pry people away from their attachment to food and overeating? That is one of the many questions inspired by such chemical explorations.

Wellness writer and biologist Deane Alban helped explain these concepts to a larger public, with the addition of information about how to increase the body’s supply of anandamide. For instance, people do not eat chocolate just because of candy’s delicious sweetness. It turns out that basic unsweetened chocolate is the chief food source from which a human can derive anandamide. Chocolate also contains caffeine, serotonin, tryptophan, and other biochemicals that possess mood-elevating effects, as well as ingredients that delay the breakdown of anandamide.

As we have seen, anandamide gets broken down by an enzyme known as FAAH, which comes from the gene that keeps four-fifth of the people less happy than the fortunate one-fifth. The bounty of nature has also provided another chemical that helps protect the “bliss molecule” by inhibiting FAAH. Known as kaempferol, it is found in green tea, some fruits, and several vegetables including — yes — broccoli, the comical opposite of chocolate. Strange as it seems, they all share this very important trait of fostering anandamide’s presence in the body.

Back to Dr. Friedman again for a moment:

The fact is that we are all walking around with a random and totally unfair assortment of genetic variants that make us more or less content, anxious, depressed or prone to use drugs… What we really need is a drug that can boost anandamide — our bliss molecule — for those who are genetically disadvantaged.

Your responses and feedback are welcome!

Source: “’Genes may contribute to making some nations happier than others,’ First study to show link between genetic make-up and perceived national happiness,” ScienceDaily.com, 01/14/16
Source: “The Feel-Good Gene,” Archive.ph, 03/06/15
Source: “Anandamide: Bliss Molecule for Happiness & Mental Balance,” BeBrainFit.com, 09/01/21
Images by sjephoto and Richard North/CC BY 2.0

What Goes On In There?

As outlined in the previous post, anandamide (AEA) makes us happy, but for four-fifths of people, FAAH steps up and says, “But just hold on there… Not too happy.” What other substances and processes can influence our moods and cravings?

The types of food that people eat, and how much of it, depends mainly on two types of appetite. Homeostatic is the healthy kind, triggered by a decrease of available energy, where the body is legit saying, “Hey, send some calories, or else.” A 2013 paper on fatty acid modulation and the endocannabinoid system by authors from three institutions in Melbourne, Australia, adds that, conversely, “hedonic food intake is triggered by appetite in response to endogenous and exogenous stimuli and often occurs in satiated or postprandial states.” In other words, even when they have just finished a meal and are stuffed, a disordered person will keep shoveling it in.

As it turns out, the endocannabinoid system “is implicated in both homeostatic and hedonic food intakes, with activation of the system resulting in an increase in hunger.” AEA and another molecule, 2-AG, bind to the two main cannabinoid receptors (CB1 and CB2)…

[…] leading to activation of pathways to initiate food intake in the limbic system, hypothalamus and hindbrain.

What brings on the inappropriate and harmful hunger? Quite often, it is stress, which as we have seen, some people are genetically wired to cope with, although most are not. Dr. Pretlow has written,

Understanding and targeting the behavioral and psychological precursors to compulsive eating behaviors is essential as a means of facilitating control over food intake to mitigate obesity. Stress is a precursor that is common both to compulsive eating behavior and alcohol/drug use.

In 2015, Dr. Richard A. Friedman made waves with an article called “The Feel-Good Gene,” in which he discussed “intriguing new therapeutic targets for drug abuse in general.” He referred to tinkering with the cannabinoid circuit, which “directly influences the dopamine reward pathway, which is the shared target of commonly abused drugs, like cocaine, opiates and alcohol.”

And food. As the Australian research on fatty acid modulation and the endocannabinoid system had found,

Endocannabinoids are products of dietary fatty acids (FA) and… modulation of cannabinoid receptor function can occur via modification of dietary FA intake.

A 2018 paper added,

Obesity is associated with chronic low-grade inflammation and metabolic disturbances, including insulin resistance and type 2 diabetes. One of the major drivers of the obesity epidemic is the consumption of an energy-dense high-fat diet…

Interest in the endocannabinoid system as a target for obesity therapy has re-emerged since rodent studies demonstrated that obesity-associated changes in the gut microbiota activated the intestinal endocannabinoid system…

Now, back to Dr. Pretlow, who writes that displacement behavior is an innate, biobehavioral mechanism in the brains of all animals, which…

[…] functions as a response to situations that the animal cannot readily face, yet cannot avoid — situations involving uncertainty, confusion, conflict, or a feeling of being trapped, threatened, or frustrated.

Resembling addiction, displacement behavior is irrepressible behavior that is contextually inappropriate, […] e.g., an animal that sleeps or feeds when threatened by a predator, or an individual who drinks to intoxication or binge eats after encountering a stressor in the workplace.

Displacement behavior bears a striking resemblance to addictive behavior.

Your responses and feedback are welcome!

Source: “Fatty Acid Modulation of the Endocannabinoid System and the Effect on Food Intake and Metabolism,” Hindawi.com 05/26/13
Source: “The Feel-Good Gene,” Archive.ph, 03/06/15
Source: “Plasma endocannabinoid levels in lean, overweight, and obese humans: relationships to intestinal permeability markers, inflammation, and incretin secretion,” Physiology.org, 02/13/18
Image by Donald Lee Pardue/CC BY 2.0

Feel-Good Genes and Addiction

Here is a story from a 5’2″ elementary school teacher, 24 years of age, who described her life as “miserable” because of disordered eating:

[A]fter one personal trainer, over two years of therapy, three juice cleanses, four gym memberships, 20 pounds lost, 30 pounds gained back, and thousands of dollars spent on healthy groceries and high-end cookware, I am […] spending another night, like so many nights before, eating a bowl of last-minute, mediocre cookie dough alone in my apartment at 11 p.m. And I hate myself for it.

Anita Badejo saw a therapist who diagnosed “a low-grade, chronic form of depression” called dysthymia, along with generalized anxiety disorder. But why do so many millions of people fall prey to these gloomy mental states with equivocal boundaries and no clear causes? Are they all psychiatrically or psychologically impaired? As it turns out, the topic of genetics and the long-cherished hope of discovering “the” obesity gene might throw some light on this puzzle from another angle.

The road to bliss

In 2015, Dr. Richard A. Friedman wrote for The New York Times about the endocannabinoid system and specifically about anandamide (AEA), which some have called the “bliss molecule.” It binds to cannabinoid receptors and exerts a calming effect, in both mice and humans, by reducing fear and anxiety.

A gene called FAAH regulates the production of AEA by producing an enzyme that de-activates it. When the FAAH gene has a certain mutation, it does not keep such a tight leash on AEA, and consequently more “bliss molecule” is available to make the person happy. Since fear and anxiety lead a lot of people along the path of drug abuse, it looked like finding a way to regulate the relationship between AEA and FAAH could allow people to be naturally happier, and less likely to take up with dangerous drugs.

By 2018, it was known that “anandamide exerts an overall modulatory effect on the brain reward circuitry,” and some reports seemed to indicate its involvement somehow in the addiction-producing effects of drugs of abuse:

AEA and drugs that modulate its circulating brain levels have been shown not only to be involved in mediating the effects of several drugs of abuse but also, in many circumstances, to create potential positive interference with the dependence-producing actions of several drugs of abuse… suggesting potential therapeutic activity against substance use disorders.

Anandamide affects not only happiness, but memory, sleep, pain relief, and appetite. The cannabinoid receptors that welcome it are located not only in the brain but, writes wellness writer and biologist Deane Alban, “are widespread throughout the body occurring in the central nervous system, spleen, lungs, liver, kidneys, white blood cells, reproductive organs, and in the gastrointestinal and urinary tracts.”

These discoveries were then connected with data from surveys that measure the happiness rates of people in different countries — which may have something to do with the genes that regulate the level of AEA. Alban wrote, “Countries where citizens generally rate themselves as ‘very happy’ have a higher instance of this gene.”

To be continued…

Your responses and feedback are welcome!

Source: “I’m Mending My Broken Relationship With Food,” BuzzFeedNews.com, 02/26/15
Source: “The Feel-Good Gene,” NYTimes.com, 03/06/15
Source: “Brain activity of anandamide: a rewarding bliss?,” Nature.com, 07/26/18
Source: “Anandamide: Bliss Molecule for Happiness & Mental Balance,” BeBrainFit.com, 09/01/21
Image by Elijah van der Giessen/CC BY 2.0

Inherency, Addiction, and People

This discussion has been about which substances in foods may or may not be dangerously attractive. Now, it is about which qualities in humans can, or might, increase their susceptibility to obesity caused by addictive-like eating behavior. What makes a “prone subject?” We have frequently quoted the 2014 paper by authors from Germany, The Netherlands, Spain, the United Kingdom, and Sweden, which said,

We perceive the necessity, and at the same time the difficulty, to clearly separate known causes of overeating, which without knowledge of the underlying process (e.g. leptin deficiency, hypothalamic tumor) could be labeled as an addictive behavior.

So there is the whole question of the physical characteristics present in the individual, that either potentially or demonstrably exert influence on eating patterns. Dr. Pretlow recently wrote,

In a lecture on addiction by a professor at Columbia, he stated that tolerance develops to the addictive substance (pleasure high). But what causes the addiction is development of hypersensitivity to the cues, i.e. cravings and the drug pushers and paraphernalia. Hypersensitivity to and seeking tempting foods similarly develops, which are likewise needed to trigger the displacement mechanism to get rid of excess brain energy.

How genes complicate matters

The obesity gene was eagerly sought for a while, but of course nothing can be simple. It turned out to be one of those multifactorial cases. The same internationally-authored paper mentioned above, “‘Eating addiction’, rather than ‘food addiction’, better captures addictive-like eating behavior,” said,

Given the increasing number of gene variants known to contribute to the variance in body mass index in the general population, it will be of interest to genotype normal weight and obese subjects with and without “eating addiction…”

In light of the polygenic basis of BMI variance in the general population, we need studies to address if addictive overeating (and obesity) can occur independently of a genetic predisposition to an elevated body weight.

In other words, maybe people who self-identify or qualify as food addicts under various criteria would not be in the same condition if only their genetic inheritance had been different.

We perceive the need to disentangle the mechanisms underlying an “eating addiction” with and without obesity. The differentiation of subjects who overeat due to increased hunger and/or a reduced satiety from those with an “eating addiction” appears difficult…

So, there can be several kinds of people: addicted but not obese; addicted and obese; obese but not addicted; neither obese and nor addicted. This is a lot to think about.

[R]esearch is required to uncover biological, physiological, and psychological differences. Obviously, twin and family studies are required to assess heritability of “eating addiction” (or different subgroups of “eating addiction”)…

As progress is made in uncovering alleles predisposing to diverse substance use disorders or addictive disorders, the overlap with “eating addiction” can be assessed.

Your responses and feedback are welcome!

Source: “’Eating addiction’, rather than ‘food addiction’, better captures addictive-like eating behavior,” ScienceDirect.com, November 2014
Image by Rutger Tuller/CC BY 2.0

Inherency and Food Addiction — Some Thoughts

We have quoted before from a landmark 2014 paper with a dozen authors, titled “‘Eating addiction’, rather than ‘food addiction’, better captures addictive-like eating behavior.”

Humans who overeat usually do not restrict their diets to specific nutrients; instead the availability of a wider range of palatable foods appears to render prone subjects vulnerable to overeating…

It can be argued that access to a diversity of foods, especially a diverse range of palatable foods, may be a pre-requisite for the development of addictive-like eating behavior.

In other words, while it is pretty clear that manufacturers are at fault for messing around with the ingredients of processed foods, something else is going on too. Why might it be suspected that the problem is inherent in or intrinsic to the human being who eats too much and becomes too large? This is not a “blame the victim” move, but an acknowledgment that some of the causality might originate with the individual, whether they had any control over it or not.

Why would they not? Maybe because of their chromosomes. Maybe because of societal forces, whether blunt or casual. What makes a “prone subject”?

Psychology professor Bruce Alexander (of Rat Park fame) has noted the importance of the discovery that many medical patients who have been prescribed opiates for months at a time are able to quit very successfully — no muss, no fuss.

As writer Johann Hari phrased it,

The same drug, used for the same length of time, turns street-users into desperate addicts — and leaves medical patients unaffected… Professor Alexander argues this discovery is a profound challenge both to the right-wing view that addiction is a moral failing caused by too much hedonistic partying, and the liberal view that addiction is a disease taking place in a chemically hijacked brain.

On the social front, Dr. David Kessler has called food addiction “the most socially acceptable fix in our society,” which seems fair in the realm of substances, anyway. It is true that unlike alcohol abusers and hard drug addicts, people whose lives are dominated by food and eating never go to jail for it. The downside is, whether it is called food addiction or eating addiction, the concept is treated like a joke, which it most certainly is not, when a person is helplessly caught in its trap.

Political journalist George Monbiot went so far as to say,

When alcoholism and drug addiction are discussed, the tone tends to be sympathetic. When obesity is discussed, the conversation is dominated by mockery and blame, though the evidence suggests that it may be driven by similar forms of addiction.

There was a time, before all this complicated stuff was discovered, when people didn’t even know there was such a thing as drug dependence or addiction, and simply concluded that their obstreperous relatives were possessed by demons, or whatever. Could it be that our current suppositions will turn out to be equally fanciful?

What if, for instance, reincarnation were to be proven as the mechanism behind human life? What if some people cannot stop eating because in their last lifetime they were starved? Or conversely, because in a previous life they were a powerful, wealthy and enormous person in the HenryVIII mold, who feels entitled to consume every deer and partridge in the kingdom? While that may seem improbable, it is possible that while scientists argue the fine points, some new discovery could come out of the left field and render all previous theories moot.

Even as the various food addiction and eating addiction points are being made, empirically there does seem to be some benefit in treating compulsive overeating with the programs and protocols designed to help addicts. If treating it according to an addiction model is effective, it seems sensible to do that while still figuring out the big picture.

Your responses and feedback are welcome!

Source: “’Eating addiction’, rather than ‘food addiction’, better captures addictive-like eating behavior,” ScienceDirect.com, November 2014
Source: “The Likely Cause of Addiction Has Been Discovered, and It Is Not What You Think,” HuffiPost.com, 01/20/15
Source: “Alzheimer’s could be the most catastrophic impact of junk food,” Guardian.co.uk, 09/10/12
Image by Ann Longmore-Etheridge/Public Domain

Inherency and Food Addiction and Factors

Food Addiction (FA) causality will probably never be a settled matter because, in matters like this, various factors can change. It is difficult, in other words, to do any kind of deliberate study in the real world because we cannot set hard rules about what the conditions will be.

One part of the multi-faceted conversation says that all or some foods can contain substances that act like hard drugs in the human body. Here is an example of how controlled experiments are not compatible with life in the wild. Just when that issue was starting to be explored, the food processing corporations were seriously ramping up their efforts to prove that there is indeed such a thing as FA, and a whole industry eager to sell it to us.

More data, more problems

The multidisciplinary NeuroFAST program was designed to figure out whether FA exists, and in the course of about five years compiled a massive archive of findings. Not surprisingly, the more deeply researchers look into these issues, the more complicated everything becomes. One conclusion contains a lesson in the futility of making generalizations:

Our epidemiological studies have identified risk factors for the onset of substance use and eating disorders and have found these to differ widely depending on age, gender, sample and individual diagnoses.

The relationship between eating and addiction problems differs by age and gender.

As befits a multifactorial problem,

This multidisciplinary project explored the neurobiology of addiction and eating behaviour and the complex socio-psychological forces that can lead to its dysregulation.

And get this:

Food addiction-related overweight/obesity cannot be identified using anthropometric, metabolic, biochemical or adrenal hormonal parameters… These forces include dietary components (e.g. highly palatable foods and alcohol), some of which may have addictive properties, but also cultural and social pressures and cognitive-affective factors (perceived stress and stress regulation, anxiety and depression), and family-genetic influences on these.

Under the “Limits to Our Understanding” subhead, one of the limits is,

[W]e do not know the importance of ”food addiction” as an obesity factor in women, or what mechanisms underlie gender differences in eating behaviour…

While the hormones ghrelin and leptin have been intensely scrutinized because of their influence over the presence or absence of eating urges, little attention has been paid to what the female hormones can accomplish in this regard. An interesting discovery has been made about obese and overweight women. A cerebral positron emission tomography test can tell the difference between an addicted woman and a non-addicted one. And let us never forget,

In rodents, females are more vulnerable than males to weight gain in response to intermittent sweet treats.

Your responses and feedback are welcome!

Image by madaise/CC BY-ND 2.0