More on Morbid Obesity in Kids

fixing-a-car

The photographer titled this “Talk about junk in the trunk!”

Food addiction has been discussed here many times. Like other popular expressions, it is an incomplete shorthand term for something that takes more than a few syllables to say.

The addiction to overeating is more of a behavioral addiction than a substance addiction. Even that simplification has to be qualified, by admitting that quite a few foods and pseudo-foods do cause the same reactions as hard drugs.

Among many similar studies, the extensive European project NeuroFAST found that people diagnosed as morbidly obese “show changes in their dopamine systems which are similar to the changes in a person who is addicted to drugs or alcohol.”

In the course of creating Weigh2Rock and developing W8Loss2Go, Dr. Pretlow became familiar with the health journeys of thousands of children and teens. He observes:

Dependence on the pleasure of food may be on a continuum: overweight children may be only partially dependent (addicted); obese children may be fully dependent (addicted); and morbidly obese children may be in addictive tolerance mode.

This is explained further in Dr. Pretlow’s book Overweight: What Kids Say:
Overweight: What Kids Say:

Chapter 9 describes “tolerance,” which is a characteristic of addictive behaviors, where an individual must use more and more of a substance or behavior, or worse substances, to obtain the same pleasurable effect. If the childhood obesity epidemic is due in part to an addiction to highly pleasurable foods, then tolerance might be a factor that is worsening the epidemic and contributing to development of severe or “morbid” obesity in some kids.

If overweight kids need progressively larger amounts of pleasurable food or higher pleasure-level foods to feel satisfied or comforted, this would certainly worsen the childhood obesity epidemic and contribute to morbid obesity.

Morbid obesity is skyrocketing because cheap, high pleasure, high calorie food is becoming even more widely available, in the face of ever increasing tolerance. Furthermore, the stress of morbid obesity continually stokes the vicious cycle of spiraling comfort eating.

Last time, we spoke of how some individuals who suffer from morbid obesity may, either knowingly or unconsciously, derive some type of reward from their condition. No doubt in many cases it is the same reward that all addicts partake of. To be hooked on anything is to inhabit a life where all complications are removed and all answers are simple, because all decisions boil down to one question: Will this action get me more of my addictor?

If an eating addiction leads to morbid obesity, the trouble is doubled. Consider this: Many substance-addicted people are able to maintain a normal appearance. Their addiction disease is not readily discernible, but the person addicted to overeating can’t fool anybody.

Psychotherapist Mary Jo Rapini has learned the importance of helping a morbidly obese person identify what benefits they might be reaping from morbid obesity. What does the extra weight allow the person to protect or avoid? When the “condishun” fills a need, therapy can help to reduce that need or find another way to satisfy it.

When a person no longer benefits from old behaviors, Rapini says, those behaviors can be left behind. She adds:

It is also important to look at obese children’s homes especially if there is a substantial weight gain. Many times, something is going on at home that is causing this child to medicate their anxiety with food.

Dr. Pretlow is concerned by the number of children who are homeschooled so they can avoid the embarrassments and threats posed by public school. It is possible that their isolation and lack of socialization opportunities combine to encourage even more “comfort eating,” which in turn leads to more obesity. Dr. Pretlow writes:

We once had a weekly parents chat on our website hosted by a nurse. Mostly it was attended by parents, who were desperate for help, in regard to their morbidly obese homeschooled kids. Typically, they were single parents with no recourse.

Your responses and feedback are welcome!

Source: “Food addiction: know the facts,” Food.UK.MSN.com, 01/05/2013 10:15
Source: “Addiction to Highly Pleasurable Food as a Cause of the Childhood Obesity Epidemic: A Qualitative Internet Study,” Tandfonline.com, 06/21/11
Source: “What is Being Morbidly Obese Protecting You From?,” Chron.com, 09/27/11
Photo credit: kennethkonica via VisualHunt/CC BY-ND

Rewards of Morbid Obesity

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The term “treatment resistant” has a couple of different meanings, one of which is a major cause of compassion fatigue and social worker burnout. Every now and then, someone in a helping profession encounters a patient or client who is, for all intents and purposes, un-helpable. An example that is seen too often is the abused woman who can’t be persuaded to leave the abuser.

The condition of treatment resistance has been described as a determination not to get well. It amounts to a low-grade and sometimes decades-long case of Munchausen Syndrome. To those in more robust mental and emotional health, treatment resistance is incomprehensible. A fellow named William Tell wrote:

Practitioners will meet no end of frustration until they accept that such patients exist. No amount of time, energy or resources will bring about a change that the patient doesn’t want.

In fact, the same dynamic plays out anytime one person seeks to impose on another person goals that aren’t congruent with that person’s own. Free will wins out every time.

Free will conquers all, even when that will is utilized to a self-destructive end. But why, why, why, would anyone choose to spend their free will in this counterproductive way? Escaping morbid obesity is such a worthy goal, what competing ambitions could possibly override it? In the same way that social workers can’t understand why leaving a brutal spouse might not be the highest priority, doctors can’t understand why losing dangerous and potentially deadly weight is not at the top of a patient’s to-do list.

Because of her wide acquaintance with morbidly obese people, psychotherapist and relationship specialist Mary Jo Rapini has been consulted by many bariatric surgeons. She writes:

The genetic role helps explain the body type; the way food may be processed, stored, and proportioned. It cannot explain what keeps the person from changing the behavior that contributes to obesity… These patients have a story to tell, but we aren’t listening and we continue asking the wrong questions.

It is easy to categorize patients as living on the legendary Egyptian river, “de Nile,” but Rapini reminds health professionals that they too can slide into denial, and warns them against it. She emphasizes a point that Dr. Pretlow has made, time and again. Most people know exactly what a healthful diet consists of. It simply doesn’t work for them.

Rapini pilots 12-step groups that address food addiction, and as part of the “amends” step of the program, she asks, “How do you benefit from being obese?” If a comedian asked some version of that question in a club, half the audience would probably walk. In these groups, however, the members are committed to rigorous self-examination.

It turns out that a large proportion of morbidly obese patients were indecently interfered with in childhood, and have built around themselves fortresses of fat designed to discourage any repetition of that trauma. Some are in marriages that never were good, or that started out happy and went off the rails. They wouldn’t cheat with an actual human, but food can make a satisfactory replacement.

Other reasons are less intense. Morbid obesity provides people with an excuse to not do things they don’t want to do. The rest of the world may often be persuaded to abandon its expectations and lower the bar. And this is too big a subject to be contained in one post.

(To be continued…)

Your responses and feedback are welcome!

Source: “Treatment resistant,” The Homeless Blogger, 07/05/16
Source: “What is Being Morbidly Obese Protecting You From?,” Chron.com, 09/27/11
Image by Roundhouse

A Special Kind of Globesity

tunisia-bedouin

Man in Search of a Morbidly Obese Bride.

Strangely, there have been cultures in which morbid obesity was highly valued, and at least one such culture still exists. Author Rebecca Popenoe studied the Azawagh Arabs, among whom feminine obesity is so self-evidently, obviously desirable that her interview subjects didn’t even understand why she asked questions. She writes:

Girls are fattened on milk and porridge for several years leading up to puberty to attain the full, abundant, luscious look that is admired by men and women alike, and that is considered sexually desirable. Women work to maintain the folds of fat around their stomach, fleshy behinds, and stretchmarks on every limb…

The Azawagh diet consists of milk, grain, millet, and sorghum. Fruits and vegetables are unknown. The sociologist connects desirable obesity to the value of milk. The whole family achieves high status when a man’s livestock can provide enough milk to keep his wife in a state of “voluptuous immobility.” Her physical bulk will be converted back into milk to feed their children. Fat on a woman is like money in the bank.

An undated essay by Samiha Fariha adds more details to the picture by describing the life of a 10-year-old named Parveen, who is being fattened according to custom. The traditional way involves tough love from her aunt Nusrat, because after all, it’s for her own good, to obtain the right kind of husband.

When before Nusrat used to indulgently feed Parveen porridge, now she yells at her or sometimes hits her to eat the porridge. Furthermore when before Nusrat used to encourage Parveen to go out and play with her friends, now she restricted her from completely going and mixing with her friends.

The Azawagh Arab society is Muslim, like the Islamic Republic of Mauritania, another place where big is still beautiful. The fattening of girls begins when they are eight years old, and when they are old enough to marry, they are sent to a kind of finishing school, a “fat camp” that is the exact opposite of the American understanding of the term.

How does 15,000 calories per day sound? At least their diet is a bit more varied, with the addition of olive oil and figs. Modern science aids in the process by providing steroids, and girls are made to eat veterinary-grade growth hormone pills.

The preference for morbidly obese women has never been limited to one religion. There is a book called Goddesses of Flesh and Metal: Gazes on the Tradition of Fattening Jewish Brides in Tunisia, whose title says it all. As soon as a girl was engaged to be married, the extreme fattening program began.

Supposedly, in Tunisia, the preference for obesity was mainly prevalent in the 19th and early 20th centuries, but who knows? Needless to say, these practices are horrendously destructive to women’s health, and even inimical to their fertility, which is especially incomprehensible, since the whole custom is supposedly built around the sanctity of family and childbearing.

Rebecca Popenoe says that worldwide, about 80% of societies prefer plump women, though they don’t all go to such lengths to promote excess flesh. If reincarnation is how things actually work, maybe some obesogenic parents can not help valuing bodily abundance, because in a past life they belonged to a society where that is the norm.

Your responses and feedback are welcome!

Source: “Feeding Desire: Fatness, Beauty and Sexuality Among a Saharan People,” Google Books, 2004
Source: “Feeding Desire: Parveen’s Glorious Future,” Wattpad.com, undated
Source: “Force fed to find a husband,” DailyMail.com, 07/15/13
Photo via Visualhunt.com

Let’s Get Morbid About Childhood Obesity

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Terrible title, right? But posts about morbid obesity are read, and that is statistical reality. Morbid means unhealthy or unwholesome, and the Latin root meant disease.

To be morbidly obese is to be fat to the point where fatness itself is a disease. For any obesity specialist, the bottom line is saving lives. Sure, it’s also about improving quality of life for millions of people. But saving lives is the main thing.

About 5% of children and teens in America qualify as morbidly obese, a term which is being replaced by “severely obese,” but morbid tells the story better because it is associated with death and that’s what we’re talking about here. Twenty-year-olds develop medical conditions that used to be the exclusive property of the middle-aged. People who start out obese in childhood, and remain obese, die 10 to 20 years sooner than their normal-weight age peers.

The situation is so weird, there are even people who gain as much weight as possible on purpose, to satisfy an inner compulsion not merely to eat, but to actually be morbidly obese. This is one good reason for the earliest possible intervention, because the drive to obesity is exponential, like the proverbial snowball rolling down a hill.

The earlier obesity sets in, the more of a foothold it gains in the body. The body’s structures and processes make adjustments to accommodate the fat, and then if weight-loss efforts are made, the body seems to resent the necessity to change back, and it resists. The weight becomes self-perpetuating, and the longer it sticks around, the harder it is to get rid of.

Morbid obesity’s posse

The other diseases that tend to come along with morbid obesity are co-morbidities — diabetes, bone and teeth problems, heart disease, fatty liver disease, metabolic syndrome, high blood pressure, asthma, obstructive sleep apnea, and more.

A co-morbidity may cause obesity, or be caused by it, or both may result from a third condition, or they might originate from different causes altogether. The point is, they feed into and worsen each other.

Obesity might cause a broken bone, then the forced immobility necessary to heal the bone will cause more obesity. In many situations, obese kids are more accident-prone, although that may be compensated for, mathematically, by fewer obese kids putting themselves into accident-prone situations.

This insight comes from UCLA’s Dr. Neal Halfon:

An understanding of the association of obesity with other co-morbidities may provide important information about causal pathways to obesity and more effective ways to prevent it.

Other posts

What Exactly Is Morbid Obesity?” gave some definitions and referred to an authority who called morbid obesity an addiction disorder, a term familiar to readers of Childhood Obesity News. Some define morbid obesity as when the person exceeds ideal body weight by 100 pounds or more, and others have mapped out the Body Mass Index ranges that are acceptable, versus those that are not.

Morbid Obesity in Children and Teens” mentions a study showing that extreme obesity has been increasing much more than moderate obesity.

Childhood Obesity, Co-Morbidities and Surgery” mentions how the options for treatment of severely obese kids are rather limited, which leads to recommendations for bariatric surgery that are perhaps premature. Young people are not in a position to appreciate how such a step will change their lives forever, and how difficult it will be to maintain the necessary lifestyle to make the surgery effective. People can die as a direct result of bariatric surgery complications, but they can also die from complications of other types of surgery undertaken on an obese body.

Morbid Obesity and Motivation” looks at how some individuals have found the strength and determination to remove themselves from a state of morbid obesity. Another relationship between morbid obesity and death is the possibility of self-destruction. No one wants to see children abused or bullied for being overweight, and if even one child commits suicide for that reason, it’s too many.

Your responses and feedback are welcome!

Source: “Childhood obesity linked to more immediate health problems than previously thought,” UCLA.edu, 01/14/13
Image by Eksley

Where Did the World’s Biggest Boy Go?

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What happens when a mother hopes her son will be named the world’s heaviest child in the Guinness Book of Records? In the case of Jambik (his Anglicized nickname) the four-year-old achieved this goal in 2003. But a followup article published 10 years later, asking, “Whatever happened to Dzhambulat Khatokhov, the World’s Heaviest Child?” came up empty. Although he would have been 14 at the time, no news of him had been heard for three years.

Jambik was born in 1999 in the rugged Caucasus mountains of Russia to a mother abandoned when she was seven months pregnant, which she attributes to witchcraft that was used to lure her husband away. Nelya Kabardarkova also shared with her compatriots some old-fashioned beliefs about overweight kids:

In this poor and superstitious corner of the world being big is not seen as a problem. Local people do not think he is sick, they spoil him and feed him… Jambik’s size has earned him the nickname Sosruko after an ancient hero from local mythology. Sosruko was a giant, a fierce warrior who protected his people. He embodies qualities people in the Caucasus greatly respect; strength and size.

Jambik was normal weight at birth, but after his first year weighed as much as an average six-year-old, and by age three, his weight matched that of a typical 12-year-old. He started wrestling and lifting weights, and formed the ambition to become a sumo wrestler, a goal that his mother shared and encouraged.

At a very young age, Jambik appeared on television in Russia and Germany, and was even flown to Japan to visit a sumo school and be on TV. At age four, he had been referred to a specialist hospital in Moscow, but somehow his mother ended up taking him to a different hospital, where she was apparently reassured.

Jambik’s notoriety piqued the curiosity of Dr. Campbell, founder of Britain’s National Obesity Forum, and inspired a National Geographic documentary. A film crew recorded the expert’s trip to visit Jambik, who was then seven years old and weighed more than 220 pounds.

Dr. Campbell stayed for a week, part of which he spent observing Jambik in his natural environment with his non-obese mother and two brothers. Supposedly, the boy was consuming only 2,000 calories per day, and the local medical establishment was unable to find anything wrong with him.

Dr. Campbell saw that, unlike many obese children Jambik was not shunned, but admired. In a part of the world with 90% unemployment, celebrity was brought benefits, and Nelya freely admitted that she counted on Jambik to provide for the family’s future. But old records showed ominous warning signs, like four year’s worth of bone-age development within six months. Dr. Campbell began to suspect that at some point, probably before he was three, Jambik had been dosed with anabolic steroids.

Followed by the film crew, Dr. Campbell took Jambik to Moscow for consultation with a pediatric geneticist, who agreed that steroid use was not unheard of among ambitious Russians. Leaving Jambik with Dr. Natalia Belova at a state-of-the-art clinic, Dr. Campbell returned to his job in England. While in Moscow, and against the advice of Dr. Campbell, who was worried about the boy’s heart, Nelya took advantage of the chance to introduce her son to the exclusive sumo club, to seek sponsorship for his future career.

The results from this new testing showed that Jambik’s bone development was now equivalent to that of a 13-year-old, although no evidence could be found of a genetic problem or steroid abuse. Nelya steadfastly denied ever giving her son anything other than cough medicine.

Dr. Campbell returned to Moscow and tried once more to convince Nelya that her son’s condition was dangerously unhealthy, and that training as a sumo wrestler could be fatal, but was unable to make much of an impression. Nelya referred again to the legendary heroes of ancient times who “lived long and healthy lives” and never had to listen to doctors.

When Jambik was nine, a news story reported that he was 5’2” tall and weighed 23 stone (or 322 pounds). He has a Facebook page, supposedly begun by him in 2013, but it contains only one entry, made in that year. Jambik would be 17 now, but the all-seeing Internet appears to know nothing of his fate.

Your responses and feedback are welcome!

Source: “Whatever happened to Dzhambulat, Khatokhov, the World’s Heaviest Child?,” DangerousMinds.net, 09/18/13
Source: “Dzhambulat (Jambik) Khatokhov The World’s Biggest Boy,” MyMultipleSclerosis.co.uk, 07/02/15
Source: “23 stone aged nine,” The Sun.co.uk, 07/19/09
Image by Facebook

Always More Dots to Connect

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If there is any doubt about the far-reaching influence exerted by the microbiome, check out these typical titles from the website cell.com:

  • Effects of the gut microbiota on obesity and glucose homeostasis
  • Interactions between Gut Microbiota, Host Genetics and Diet Modulate the Predisposition to Obesity and Metabolic Syndrome
  • Pathways in Microbe-Induced Obesity
  • The gut microbiota in human energy homeostasis and obesity
  • Bile Acid-Activated Receptors, Intestinal Microbiota, and the Treatment of Metabolic Disorders

Speaking of bile acids (BA), this much is known about them:

A dynamic equilibrium is evident between diet, the gut microbiome, and the size and composition of the BA pool. A dysbiotic gut microbiome arising from diet, antibiotic therapy, or disease results in disrupted intestinal homeostasis.

The host and presence of the gut microbiome appear to regulate the BA pool size… [M]icrobes in the gut are proficient in producing secondary BAs that bind to and activate a number of host nuclear receptors, affecting host physiology.

The “host” being referenced here is us, and our guests are trillions of tiny beings who have inveigled their way into becoming the show-runners. Some scientists call the microbiome our second brain, or our second genome.

Some even call the microbiome an organ, just like the heart, liver or skin. Its residents manufacture chemicals that we need and use, that “affect host physiology” — in other words, they change our bodies, sometimes in ways that happen to be beneficial to us, but always according to their own agendas and rules.

Per study referenced above:

These recognized roles include metabolic functions such as vitamin synthesis, regulating the uptake and deposition of dietary lipids, absorbing indigestible carbohydrates, and modulating the intestinal epithelium’s absorptive capacity for optimum nutrient metabolism.

The millions of tiny bugs do many things that can influence our size and weight. Just to give a hint of some processes that take place unknown to us, these excerpts are from the Abstract of a study titled “Nutrient-Sensing Mechanisms in the Gut as Therapeutic Targets for Diabetes,” which is ultimately about reversing insulin resistance.

It describes the duodenum’s talent for sensing nutrient influx and passing the message on, which is supposed to curtail further eating so everything stays in balance. But…

In diabetes and obesity, intestinal nutrient-sensing mechanisms fail to lower food intake and glucose production, leading to a disruption in metabolic homeostasis.

And now here they come, the miniature tenants who are all up in our business:

[G]ut microbiota composition may alter intestinal nutrient-sensing mechanisms to regain better control of glucose homeostasis in diabetes and obesity in the long term… High-fat feeding induces obesogenic microbiota…

Obesogenic microbiota (translation: tiny fat-causing critters) are exactly what we don’t want! This is not the job we pay them to do. How do we ensure that we and they are on the same page?

Your responses and feedback are welcome!

Source: “The Interplay of the Gut Microbiome, Bile Acids, and Volatile Organic Compounds,” NIH.gov, 2015
Source: “Nutrient-Sensing Mechanisms in the Gut as Therapeutic Targets for Diabetes…,” DiabetesJournals.org, September 2013
Photo credit: Matthew Bernhardt

The Appetite Dot

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Yesterday we reviewed some characteristics of leptin, a hormone associated with satiety. We also looked at the “hunger hormone” ghrelin. When the brain and the digestive organs communicate about appetite, these chemicals and many more are involved, and the gut microbiome also intervenes. The general theme of this group of posts is the notion of “connecting the dots” which will reveal the effect the intestinal fauna have on our obesity or lack thereof.

Speaking of leptin, here is an example. A study is titled, “The gut microbiota reduces leptin sensitivity and the expression of the obesity-suppressing neuropeptides proglucagon (Gcg) and brain-derived neurotrophic factor (Bdnf) in the central nervous system.” It suggests that our inner bacteria have the ability to thwart what our bodies attempt to do.

How? According to the study:

[T]he gut microbiota reduces the expression of 2 genes coding for body fat-suppressing neuropeptides… Moreover, the presence of body fat-inducing gut microbiota is associated with hypothalamic signs of Socs-3-mediated leptin resistance, which may be linked to failed compensatory body fat reduction.

The bugs can mess with our genes. They can set up resistance to an old-fashioned, basic hormone like leptin. They are tagged as body fat-inducing microbiota, which is the same as calling them obesity villains. These are serious charges!

And they are not the only critters at play in our innards. Clinical nutritionist Mike Mutzel notes that “We have parasites, viruses, and things that we really cannot quantify as readily as we can the bacteria at this point.” He goes on to say:

If you have imbalances in these bacteria, they can extract more energy from the food that you eat. And that energy can form or trigger the body to undergo adipogenesis or the formation of new fat cells. It can inhibit lipolysis or the release of stored fat.

It seems that the microbiota can really sabotage us in a big way. Clues are scattered everywhere, but no one is quite sure, yet, how they fit together or what they all add up to. For instance, this single sentence, from a study titled “Gut-brain axis: how the microbiome influences anxiety and depression,” is fraught with implication:

New studies show that bacteria, including commensal, probiotic, and pathogenic bacteria, in the gastrointestinal (GI) tract can activate neural pathways and central nervous system (CNS) signaling systems.

Our tiny residents do not just sit around, sopping up our leftover nutrients and byproducts. They do things, all the time, without our knowledge, that affect us in more ways than we have begun to realize.

For instance, the mitochondria that provide our cells with energy used to be bacteria, hitchhiking a ride in us (just like the gut fauna do now). Then, around a billion years ago, they became part of us. But their homies, the gut fauna, help them out in various ways, like switching them on and facilitating their reproduction.

The microbiome has a lot of chutzpah, taking over like this. Mutzel says:

Everything you put in your mouth, your thoughts, how you think, how you feel, how you sleep, whether you are grateful or you are mad at the world, all these different things impact the composition of these bugs.

And it goes even further. Quite possibly, everything is reciprocal and the bugs influence our decisions about what to eat, and our sleep patterns, and moods, and attitudes. In the words of the philosopher Voltaire, “The fate of a nation has often depended upon the good or bad digestion of a prime minister.”

These quotations are also apt:

“Unquiet meals make ill digestions.” — William Shakespeare

“Happiness for me is largely a matter of digestion.” — Lin Yutang

“Happiness: a good bank account, a good cook, and a good digestion.” — Jean-Jacques Rousseau

Your responses and feedback are welcome!

Source: “The gut microbiota reduces leptin sensitivity and the expression of the obesity-suppressing neuropeptides proglucagon (Gcg) and brain-derived neurotrophic factor (Bdnf) in the central nervous system,” NIH.gov, 2013
Source: “Episode 31 with Mike Mutzel,” SigmaNutrition.com, 2014
Source: “Gut-brain axis: how the microbiome influences anxiety and depression,” Cell.com, 2013
Photo credit: pilllpat (agence eureka) via VisualHunt.com/CC BY-SA

Meet Leptin

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The subject of the most recent Childhood Obesity News post was ghrelin, a hormone connected with hunger and food cravings. There is also a hormone called leptin, connected with satiety, which originates in the stomach and in adipose tissue (fat). Despite their seemingly opposite natures, Dr. Billi Gordon draws some parallels between them.

He notes that both of these signaling hormones are able to cross the blood-brain barrier in order to bind to receptors that are mostly located in the hypothalamus. Also, both can enter the brain by way of the vagal nerve and a structure in the medulla oblongata known as the nucleus solitarius, which collects sensory information from many organs.

Additionally, both can either stimulate or suppress neurons in the hypothalamus, resulting in more or less appetite. Gordon describes the hypothalamus as the key brain structure in homeostatic maintenance, and points out that, unfortunately, it may be remodeled by a horrendous childhood, known in the profession as “early life trauma.”

In consequence:

[W]hen persistent stress, emotional and psychological factors are present, the hedonic factors will override the homeostatic control of food intake… When this occurs the brain utilizes dopamine derived from food’s hedonic value as a drug to intervene on the pathophysiology of stress. Hence, food goes from being a fuel to being an opiate to intervene on suffering…

Dr. Gordon includes a very elaborate explanation of the relationship of leptin to overeating, and the bottom line is this:

In a healthy individual, the body is able to communicate effectively with the brain via hormones such as leptin, ghrelin, insulin and other informational substances. In the obese individual’s unhealthy body, converging reasons breach communication between the brain and the body.

He lists five of those reasons, and the end result of it all is that “you overfeed your body because your brain believes you are starving.”

In a previous post we mentioned the work done by neuroscientists from the Children’s Hospital of Los Angeles among adults who do not have Prader-Willi syndrome, but who show the same behavior of unappeasable hunger, because “their ghrelin-producing mechanism was somehow damaged in infancy.” This discovery strikes another blow against the calories in — calories out paradigm, showing that:

Unstable levels of the hunger hormone ghrelin in infancy may pose lifelong risks for obesity, a new study finds. The results suggest a departure from the will power-focused ideas of the past, where obesity is a simple and direct result of eating right and exercising often.

Vancomycin is an antibiotic used to kill various bacteria, including the ferocious C. difficile. For just a hint of the complexity of these matters, consider this description of lab research in the field:

This novel paper demonstrated that alteration of the gut microbiome by vancomycin significantly reduced leptin levels and subsequently led to an increased myocardial ischemia tolerance. They confirmed that leptin was directly involved in myocardial ischemia tolerance by demonstrating that pretreatment with leptin abolished the cardioprotection seen with vancomycin treatment.

The short version is, a lot more goes on inside us than even the most advanced thinkers have previously guessed. Mainly, it begins to become apparent that no body system can be adequately described without taking into account the gut microbiome.

Your responses and feedback are welcome!

Source: “The Fatter the Body, the Hungrier the Brain,” PsychologyToday.com, 02/21/14
Source: “Ghrelin Hunger Hormone Poses Obesity Risk For Life When Imbalanced In Infants,”
MedicalDaily.com, 01/20/15
Source: “Intestinal Microbiota Determine Severity of Myocardial Infarction in Rats,” fasebj.org, 2012
Photo credit: Digital Shotgun via Visual Hunt/CC BY-ND

Clues to an Elusive Ghrelin-Microbiome Tie

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Incredibly, there are still more dots to connect in the microbiome story, because the colonies of bacteria that live inside us seem to stick their meddling fingers into every aspect of our lives. Yesterday, we talked about the cravings dot. Granted, a craving can be positive, like when a person craves a tuna sandwich because the body needs a dose of protein. But unfortunately, cravings are often for things we really shouldn’t eat at all, ranging from doughnuts to burnt matches, and usually lead to grief.

Then, there is appetite, which is similar to craving but not the same. Appetite is generally considered a desirable thing to possess. If an endogenous chemical did not remind us to eat, we might forget and starve. Appetite is what people lose when taking certain medications and undergoing certain treatments, and medical science strives to restore appetite to them because a sick person needs good nutrition.

We know that upset feelings often result in the urge to comfort-eat, or binge-eat. An important question is whether bacteria are involved in that transaction. Apparently the bugs that compose the microbiome can influence the happiness hormones.

Presumably, corralling the bugs into good order could change a person’s emotional landscape enough that they no longer eat to “stuff their feelings” down. What else might the microbiota do?

Weird ghrelin

Childhood Obesity News has spoken before of ghrelin, the “hunger hormone.” It originates mainly in the stomach and small intestine (where most of our native bacteria hang out) and in several other bodily locations as well. The substance is produced by “specialized cells,” and it would be interesting to know whether anyone suspects that those cells might be not our own. It’s not impossible that this chemical comes from one of the many species of bacteria that inhabit us.

Some people are positive they know what ghrelin is all about, and that it increases when the body is in negative energy balance and decreases when the energy balance is positive. Others wish that it could be so simple. There is little certainty about this substance, except that it appears to be reduced when the body is overwhelmed by too many H. pylori, an organism that is, like ghrelin, little understood and much reviled. Paradoxically, an overgrowth of candida albicans appears to increase ghrelin, and so does the chronic digestive tract inflammation called celiac disease.

An overabundance of ghrelin flips the switch from “eating to live” to “living to eat,” but that is not the reason why a previous post labeled it as weird. (Look for the sentence that reads, “Then, they measured the levels of ghrelin in the participants’ bodies — which reacted exactly as if those pretend calorie counts had been real.”)

In other words, psychosomatic ghrelin fabrication. Also, any interested party may follow up on a report titled “Ghrelin fluctuation, what determines its production?,” which contains this fascinating tidbit:

The pre-prandial surge of ghrelin may be induced largely by the expectation of food. The signal is discharged from the central nervous system and transmitted to stomach through the efferent fiber of vagus nerve…

As with Pavlov’s salivating dogs, the body can apparently be induced to generate ghrelin through mind power alone. The same journal article also says:

However, the current understanding about the regulation of ghrelin level, especially its mechanism, is far from satisfaction, with much discrepancy among studies. Unanimous conclusion on some critical topics is still lacking, reflecting the remarkable complexity in the regulation system…

In addition, many previous reports identify only correlation between ghrelin and a certain agent, but cannot distinguish whether the change in ghrelin level is the cause or effect, or they are actually independent. Thus, future works need to discover agents that have more direct and significant effect on ghrelin secretion, confirm the causality, and elucidate the underlying mechanism of its regulation.

That last part, about how science needs to discover “agents that have more direct and significant effect on ghrelin secretion,” and the parts about causality and the underlying mechanism of its regulation, leave open the possibility that the intestinal bacteria are up to something. Here is a sentence that might be very significant in this regard:

New studies show that bacteria, including commensal, probiotic, and pathogenic bacteria, in the gastrointestinal (GI) tract can activate neural pathways and central nervous system (CNS) signaling systems.

Is that sinking in? The critters that live in our intestines, amongst all the ghrelin and other interesting chemicals, also have the ability to “activate neural pathways and central nervous system signaling systems.”

Ghrelin is only a small part of the mystery. Science at the moment quite frankly does not know what is going on. Science is like the baffled husband in an old-time detective movie, pretty sure his wife is stepping out. But when, and where, and why, and how long has this been going on? And who is the low-down son of a gun, anyway?

Your responses and feedback are welcome!

Source: “Ghrelin fluctuation, what determines its production?,” OxfordJournals.org, 2009
Source: “Gut–brain axis: how the microbiome influences anxiety and depression,” Cell.com, 2013
Image by: Jessy Rone

The Cravings Dot

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Lately, Childhood Obesity News has been connecting the dots between scattered bits of evidence about the role of the gut microbiome in obesity or the absence thereof. In his Psychology Today column titled “Obesely Speaking,” Billi Gordon, Ph.D., reflected on the power of food cravings.

Why do we seek out and consume foods we know are bad for us? He blames this unfortunate tendency on the “micro-thugs,” the populations of bacteria that live inside us and pretty much call the shots — in other words, the residents of the microbiome.

Sure, the gut fauna perform a lot of beneficial services for us. But their essential nature, Gordon argues, is straight outta Compton. He calls them “microscopic thugs that hijack our bodies and behaviors for personal gain.” They do this by creating cravings, to encourage us to eat the things they like, and, if necessary, they will manipulate our moods to achieve this goal.

The bugs even convince us to eat the things that will destroy their fellow bacteria that are competing for space and resources. Killing for turf — how gangster is that?

Shockingly, gut microbes have the ability to rewire our reward systems, and even mess with our taste receptors. Gordon says:

Taste buds exist to detect toxins and identify nutrient value. Hence, altering taste buds results in changed eating behaviors, cravings, and conceivably reward values of food because dopamine is involved in the rewarding aspects of taste, which evolution uses to ensure we seek proper nutrients.

Intuitively, it makes sense that the gut bugs could cause cravings. They are in the position of hotel guests who can’t leave. All they can do is call for room service. In their primal yet effective way, they connive do what’s necessary to get what they want put on the tray and delivered to their door.

Do micro-thugs make us fat?

It has long been part of folklore that pregnant women who experience cravings are actually acting out the body’s very real need for potassium, protein, or some other constituent element of the food they feel a strong desire for. A non-pregnant person can also experience the need for a certain food, so strongly that from outside it looks like a mental disorder. What might actually be happening is that a certain clan of microbes are sending out chemical signals demanding whatever it is that they want.

Dr. Pretlow notes that it is productive to learn techniques to quell cravings, regardless of the cause of the cravings. With the help of, for instance, W8Loss2Go, we are entirely capable of learning methods to control and quell cravings. If the ornery bugs don’t get what they want, perhaps they die off and make room for more peaceful and cooperative bugs. So, for a person to learn techniques for craving resistance is totally helpful — bugs or no bugs.

Diet can definitely reshape the gut microbiome, but apparently not in such a crudely direct manner as we might wish. Apparently, just the fact of eating spoonfuls of yogurt, even the brands with the best live culture count, is not the whole story. The secret is in supplying the existing bugs with probiotics, the right raw materials for them to survive and thrive.

Is this how it works? If we can convince ourselves to eat leeks instead of potato chips, it would make sense that doing so would cultivate more leek-loving bugs and suppress the population of grease-loving bugs. A lot of different things can be true, valid, useful, etc., but maybe not for the exact reasons that people have been assuming.

It’s incontestable that diet and exercise make a difference in people’s health — but maybe not for the blatantly obvious reason of energy exchange or “calories in — calories out.” More subtle mechanisms seem to be at work also. Maybe diet and exercise are both incredibly important, but indirectly.

Concerning both diet and exercise, maybe the influence is wielded through the bugs, encouraging some and restraining others. Then it just might be that the messages the bugs send out, that influence the metabolism, are the indirect means of healing the mind and emotions. In this roundabout way, a person could arrive at the happy condition of using food for nutrition, rather than whatever compensatory reward they have previously been using food for.

Your responses and feedback are welcome!

Source: “A Hijacked Brain and a Tongue Held Hostage,” PsychologyToday.com, 08/07/14
Photo credit: VegaTeam via Visualhunt.com/CC BY

Childhood Obesity News | OVERWEIGHT: What Kids Say | Dr. Robert A. Pretlow
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