A Special Kind of Globesity


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

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?

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

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

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

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

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

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

The Antibiotic Dot

In the past, Childhood Obesity News posted a general overview of the research about antibiotics, babies and obesity, and took a closer look at a five-way link between antibiotics, premature births, ototoxicity (or hearing loss), obesity, and epigenetics (the passing along of somatic liabilities to descendants). Well, let’s call that instead a six-way network of links, because, as it turns out, the microbiome adds itself to the mix and complicates the game of connect-the-dots.

We may wish out colonies of interior bugs would chill out once in a while, but no. Everything about us is their business. One characteristic of the microbiome is stubbornness.

Michael Pollan charmingly explains:

Your microbial community seems to stabilize by age 3, by which time most of the various niches in the gut ecosystem are occupied. That doesn’t mean it can’t change after that; it can, but not as readily… Just like any other mature ecosystem, the one in our gut tends to resist invasion by newcomers.

However, the microbiome of a child is vulnerable to change from antibiotics, of which the average beneficiary of western civilization is treated at least a dozen times before the age of 18. Even if it were possible to keep a child healthy without any doctor visits, the antibiotic residue ingested through water, milk, and meat is unavoidable.

It should come as no surprise that the unintended consequences are serious. The gut fauna are bacteria, after all, and bacteria are what antibiotics are designed to kill. Even when we take a course of antibiotics for the most legitimate reason, there is always collateral damage. Our good bugs, our allies and comrades-at-arms, die by the millions as a result of “friendly fire.”

We have catalogued extensively the characteristics and habits of the bacterium Helicobacter pylori, which lives in the human stomach. Researcher Martin Blaser discovered that H. pylori aids in appetite regulation, by controlling the level of the “hunger hormone” ghrelin.

Strangely, this bug used to be much more prevalent, and it may be coincidence, but when H. pylori started to disappear from the American gut, the obesity epidemic really got underway. In the words of Scientific American writer Claudia Wallis:

Blaser […] notes that antibiotic use varies greatly from state to state in the U.S., as does the prevalence of obesity, and intriguingly, the two maps line up — with both rates highest in parts of the South.

Researchers from Johns Hopkins found that antibiotic use can permanently change the microbiota, affecting they ways in which food is broken down, and even increasing the absorbed calories. They wrote “Antibiotic Use and Childhood Body Mass Index Trajectory,” which shows that children who receive antibiotics tend to gain weight in a very noticeable way, when compared to other kids.

Worse, there is what they term a “compounding effect.” In other words, weight gain accelerates with age. The study leader, Dr. Brian S. Schwartz, told a reporter:

Our data suggest that every time we give an antibiotic to kids they gain weight faster over time… [O]ur finding that the effects are cumulative raises the possibility that these effects continue and are compounded into adulthood.

Just to round things out, here is a tidbit of information about zero-calorie artificial sweeteners, reported by Jason Best:

When researchers used antibiotics to wipe out the gut bacteria of mice, it completely reversed the effects of the artificial sweeteners on the mice’s glucose metabolism. Likewise, when scientists took the gut bacteria from glucose-intolerant mice and transferred it to mice that had had their gut bacteria eradicated, the recipients became glucose intolerant.

Glucose tolerance is not something you want to mess around with. Altogether, there seems to be more and more reason to employ caution in dealing with the microbiome.

Your responses and feedback are welcome!

Source: “Some of My Best Friends Are Germs,” MichaelPollan.com, 05/15/13
Source: “How Gut Bacteria Help Make Us Fat and Thin,” ScientificAmerican.com, 06/01/14
Source: “Children Who Take Antibiotics Gain Weight Faster Than Kids Who Don’t,” Jhsph.edu, 10/21/15
Source: “Drinking Diet Soda and Not Losing Weight? Blame Your Gut Bacteria,” Takepart.com, 09/18/14
Photo credit: Andres Rueda via VisualHunt.com/CC BY

The Autism Dot

Anyone not up to date on the wide-ranging microbiome discussion is invited to catch up by revisiting “Connecting the Universe of Dots” and “The Microbiome — More Dots to Connect.” The photo on this page is a reminder of how the ancients sought patterns in the skyful of stars.

The basic theory of the microbiome is, the bacteria that make their home inside of us probably do a lot more than is suspected by even their most enthusiastic proponents. We have been looking at their relationship to allergies and addiction. What other kinds of mischief can the gut bacteria get up to?

The neurodevelopmental problem known as Autism Spectrum Disorder resides in the brain and/or central nervous system, yet somehow also influences body size and weight. A typical reference says:

The investigators also found lesser but significant increases in obesity rates among teens with autism and among children whose autism was complicated by sleep and mood problems, the latter including depression and anxiety.

A while back, we mentioned an article from the journal Pediatrics that spoke of a link between obesity and autism, and a report in Current Biology that drew lines between previously isolated dots. Obesity and autism are connected. Autism and the neurotransmitter GABA are connected. GABA has a close relationship with at least two kinds of gut bacteria, Flavonifractor sp. and Bacteroides fragilis, that seem to be linked somehow to autism.

And then, there is Clostridia. An essay from Economist.com reminds us that the link between autism and intestinal problems has long been recognized. Investigation has shown that the microbiomes of people afflicted with autism contain large populations of this organism. No one has proven that Clostridia actually causes autism, but the link is definitely present. In its effort to kill off competing bacteria, Clostridia produces phenols, which are poisonous to human cells.

So the body neutralizes phenols with sulphate. Interestingly, a lot of autistic people have a genetic defect that prevents them from metabolizing sulphur properly. This report says:

So having too many Clostridia, producing too many phenols, will deplete the body’s reserves of sulphur. And sulphur is needed for other things — including brain development. If an unusual microbiome leads to the gut needing extra sulphur, the brain may pay the price by developing abnormally.

Like any other creatures, the bacteria that live inside us need to excrete, and they also produce poisons to defeat their bacterial rivals who compete for space and food. Just on their own, bacterial toxins cause inflammation.

Additionally, fat cells or adipocytes enter the picture and interact with bacterial byproducts, such as the lipopolysaccharide that oozes out of yet another species of gut bacteria, E.coli. Perturbed by these intrusions, the fat cells get busy producing cytokines, molecules that incite even more trouble, and pretty soon you’ve got a chronic inflammatory process with no end in sight.

“Autism: Inflammatory cytokines induce autoimmune reactions in the brain arresting right hemisphere development.” That sentence is from Dr. David M. Marquis, who goes on to say:

When antibodies combine with our structural proteins, specific genes are turned on in a special type of immune cell in the body. Inflammatory chemicals are created called cytokines, which are strongly damaging to brain function. In fact, elevated cytokines are seen in such devastating conditions as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and even autism.

A report on the impact of microbiota on the brain and behavior notes the increasing evidence that changes in the populations of gut microbes are associated with behaviors associated with cognition, pain, and even mood.

Dysfunction of the microbiome-brain-gut axis has been implicated in stress-related disorders such as depression, anxiety and irritable bowel syndrome; and neurodevelopmental disorders such as autism.

The controversial fecal transplant treatment is being tried on autistic kids in Arizona. It has also been suggested that microbes might some day be used to diagnose neurodevelopmental diseases. To finish up with, here is another autism-related quotation:

Although communication between gut microbiota and the CNS are not fully elucidated, neural, hormonal, immune and metabolic pathways have been suggested. Thus, the concept of a microbiome-brain-gut axis is emerging, suggesting microbiota-modulating strategies may be a tractable therapeutic approach for developing novel treatments for CNS disorders.

Your responses and feedback are welcome!

Source: “Seeking solutions, study explores autism-obesity link,” AutismSpeaks.org, 11/02/15
Source: “Me, myself, us,” Economist.com, 08/18/12
Source: “A ‘perfect storm’ for inflammation – bacteria and fat — may promote diabetes,” MedicalNewsToday.com, 11/04/13
Source: “How Inflammation Affects Every Aspect of Your Health,” Reset.me, 12/08/15
Source: “The impact of microbiota on brain and behavior: mechanisms & therapeutic potential,” NIH.gov, 2014
Photo credit: mikecogh via Visual Hunt/CC BY

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