Friday, September 20, 2013

The link between food addiction and obesity. Part Two

Courtesy of Yum9me-Flickr Photostream
A study published on PLOSOne on September 4, 2013 conducted on a sample of the general population in Newfoundland in Canada suggests afood addiction’ prevalence of 5.4% (6.7% in females and 3.0% in males) and closely linked to obesity. For the BMI scale 11.4% of normal weight individuals were addicted to food but 88.6% of obese/ overweight populations was found to be addicted. Compared to controls food addicts were 4.6 BMI units higher 11.7 kg heavier, and had 8.2% more body fat and 8.5% more trunk fat. For those identified as food addicts there consumed more calories from fat and protein compared with controls.
It is not clear how much of Newfoundlanders diet is similar to neighbors south of the border but it cannot be too different unless compared to certain high risk States such as, Mississippi,
Alabama, West Viriginia, Tennessee, and South Carolina. The study analyzed macronutrients in the diet of the subjects but did not indicate food preferences of the addicted population.
In the south “ everything fried” appears to be not only popular but gaining ground. Fried chicken, and French fries and donuts are perennial favorites but new ‘delicacies’ are
Courtesy of Bionicgrrrl-Flickr Photostream
becoming available such as fried Oreos, fried ice cream, fried mozzarella and fried bananas. Much of this was popularized by Paula Deen, perhaps the high priestess of southern fried foods. One can imagine how food toxicities can become compounded when preservatives, sugars and stabilizers are fried in the same batch of oil, over and over again. As we will see below, something happens when plain old food is fried. It gets worse when refined white flour and sugar are thrown in the mix. It is no wonder based on current trends it is believed 100 % of Americans will be overweight or obese by the year 2050.
How can one get addicted to food?
After all addiction is a term used for psychoactive drugs, narcotics and illicit substances. Still it means dependence on a substance or behavior without being able to exert self control. Addiction is also the term applied to uncontrollable gambling, exercise, and of course, food.
Scientists see a common thread in addiction, and much of that connection involves the brain, and to be more precise, neural circuits. The very same pathways that provide a high with the use of a drug and subsequent dependence are involved in food addiction.
One such mechanism is the endocannabinoid-dopamine connection.

(The following section is an excerpt from Knee Deep in Pain book. Amazon.)
Endocannabinoids (ECs) are lipids that are made by the body in metabolizing arachidonic acid. They are capable of mimicking the pharmacological actions of hashish, marijuana, and bind to two types of cannabinoid receptors. These receptors are expressed in the brain, mostly CB1, and CB2 mostly in the viscera, and gastrointestinal tract, adrenal glands, liver, and adipose tissue, and the heart.
Endocannabinoids (endogenous cannabis-like substances) are small molecules derived from arachidonic acid. The endogenous cannabinoid system controls the motivation for appetite stimuli, including food and drugs.
The endocannabinoid system participates in the rewarding and addiction of substances such as cocaine and amphetamines, opioids, nicotine, alcohol, and food. This is pretty much the same pathway employed by endorphins which are released after sustained vigorous exercise and rewards those poor souls with unparalleled happiness. The abundance of instantly released dopamine is what gives us the high.
Lipids are a family of fats that include oils, waxes, phospholipids, steroids (like cholesterol), and others such as monoglycerides, diglycerides, triglycerides, phospholipids. They do not mix with water.
Receptors are proteins that reside on membranes of neurons. Neurons are nerve cells. Neurotransmitters bind to receptors to propagate or attenuate neural signals.
Endorphins are neurotransmitters found in the pituitary gland, and other parts of the brain, as well as in the nervous system. Working with opiate receptors they mitigate perceptions of pain with actions similar to pain killers.
Dopamine is a neurotransmitter that helps control the brain's reward and pleasure centers. It is involved with feelings of euphoria and with seeking more pleasurable sensations.
But how does the brain make the connection between a stimulus and creation of feelings of euphoria?

To answer that let us talk about bliss.

When Whitney Stalker, a pretty university educated Chicago girl, visited India in 2009 she may have been looking for Anand but found Harish Kumar instead, the rickshaw driver who showed her around the historic sites of the beautiful city of Jaipur and won her heart in the process. They married four days later and she ultimately found Anand. This (Anand male, female Ananda) is a common name in the country and in Sanskrit means blissful happiness. Given its reference to this emotion, anand-amide became the name given by the scientific community to a messenger molecule arachidonyl ethanolamide (AEA), isolated by an Israeli scientist Raphael Mechoulam in 1992.
AEA Anandamide happens to be the body’s natural molecular key that locks into nerve receptor sites that have a role in pain, depression and appetite, as well as memory and fertility. Where keys open locks in our traditional world, molecular keys do the opposite. They close the receptor mechanisms by locking them, in the case in point, preventing the nerve cell from carrying on its normal function; that of firing rapidly and alerting the body of noxious stimuli. With time natural system enzymes eat away at the key, eventually unlocking the cell, and allowing it to start firing again.
And once again; Hello pain!
The difference between the natural molecules and substances like THC, a forged key, is that THC is harder to pry loose while anandamide and 2-AG are relatively easily unglued by enzymes, hence the longer lasting and higher highs associated with marijuana.
In a way we can thank marijuana for efforts that led to Anandamide’s discovery. The cannabis plant’s principal psychoactive compound, THC ( tetrahydrocannibol), latches onto the receptors of the nerve cells and dulls pain and creates feelings of happiness as well disallowing the nerve cell to fire.
When scientists found the lock that is keyed with marijuana they obviously had to go looking for a natural key, since the lock receptor could not have existed without a key. The search for that natural key led to the discovery of anandamides. Soon enough another natural sister key was discovered, 2 arachidonylglycerol (2-AG) by Dr Mechoulam and his colleagues. It is not clear why 2-AG was not given an Indian name as well; perhaps shanti-jee, meaning respected peaceful lady. This cannabinoid is believed to be 200 times greater in concentration in the brain than anandamide.
Both endogenous AEA and 2-AG, and exogenous THC have a similar role; that of addiction. Elevated levels of endogenous cannabinoids indicate the presence of addictive, habit forming agents. In this context; more EC activity means more cravings. Dopamine resulting from excess, sudden happiness, release ECs. These endocannabinoids seek out CB1 receptors and quickly lock them up. At this point of no pain, all gain, the affected person has a few simple wishes:
Get me more dope, and (in case of food addiction) get me more food, I don’t care!”
More cravings mean eating more bad food. More bad food leads to more cravings. One would be tempted to characterize this as a vicious cycle.
It is not that these cannabinoids are bad for us; it is when exogenous factors trigger too many of them, creating conditions that the body is not equipped to handle.
Both AEA and 2-AG are synthesized from arachidonic acid,
(Chapter: “Veni, Vidi, Vici” in Knee Deep in Pain book) itself a metabolite of linoleic acid which, downstream, leads to production of endocannabinoids. And what fatty acid are most vegetable oils rich in….?

Quick! Where did you see LA?

For people like Gus on an 8 to 1 diet ratio of omega-6 to omega-3, there is plenty of linoleic acid. For those who have more in common with Jaq, or even Ringo, the amount available to enzymes that break down the fatty acids, is limited in presence of less linoleic acid and more alpha-linolenic acid, the substrate that helps produce long chain omega-3 fatty acids, like EPA and DHA.
Why do we find fresh hot french fries irresistibly enticing; much more so than boiled, or baked potatoes?

Neither, potatoes nor chicken, if baked or boiled, can be considered to drive people to eat more, and more. You probably never hear anyone say: “I just can’t resist it. If I have one baked potato, I want to have three more”. But cut that one potato into thin strip slices so it can soak up the goodness of oil, and deep fry it, and some people will eat twice their body weight in potatoes.
Well, not exactly, but close. Why is that?
Hello! It is not the potato that is addictive.
It is the oil it is fried in.
How about sugary foods, or meats? Apparently at least rats do not crave either one. Researchers at the University of California, Irvine, sham fed rats on different diets and found ECs spiked in the small intestines of rodents that received corn oil rations, or a nutritionally complete diet, but not those who were given sugar or protein solutions. The mouth being the first point of contact sends impulses to the brain which sends signals to the intestines to stimulate EC production, making the rat crave for more.
But we were talking about mice and rats here. How about Mice and Men? Are humans just as discriminating? Here is an experiment you can conduct on your own.
Buy a quarter pound of your favorite chocolate. Then go to your favorite fast food place and order a half pound of french fries and make sure they are prepared fresh on demand.
Sit down and put both the chocolate and the fries in front of you, and remove the wrapper from the chocolate.
Here is the particularly trying part of this test.
Eat a small bite of the chocolate, the size of a french fry. Then eat one single french fry.
Now you have to decide which one you will want to eat more of. You can only continue to eat one of the two. Not both. What will you pick?
Tormented yet?
Here is where we are probably different from rats. If we were to accept the findings of the UIC study it would be a no brainer for the rat. At this point it would give up the chocolate in favor of the fries. We can try the same experiment with donuts and chocolate. Let’s face it. We just don’t crave only the fried food. We want it all.
The endocannabinoid system has been intriguing scientists for the last several decades. One European company took a stab at it to curb people’s appetites. They figured if they can whack the CB1 receptor hard enough it would close to any incoming impulses. Sanofi-Aventis introduced its drug called Rimonabant with great fanfare and met with early success.Who wouldn’t want to eat endlessly and not put an ounce of fat on?
However, within a few months, the company started getting complaints about nausea, depression and suicidal thoughts. Not only did they lose their appetite, many patients taking the drug also stopped smiling at the sight of beautiful bouncing babies. Playful puppies jumping up and down could not get them to respond. Laughter, smelling of roses, romance, desires, happy thoughts, all went out the window.
Making CB1 receptors invisible was like letting dopamine cause a lot of little endocannabinoids released and run loose, and all dressed up, but nowhere to go. This in turn may be signaling to dopamine neurons to take it down a notch, or two, or maybe a lot. Their only answer to “if you could do one thing today what would it be?” was “I would like to kill myself.” In December 2008, the company withdrew Rimonabant from the European market. It never made it to the U.S. At least not legally!
Meanwhile research continues on brother receptor CB2 more heavily expressed in the gut, which if whacked could presumably ratchet down dopamine release without affecting the brain. So they say!
PLOS ONE : accelerating the publication of peer-reviewed science. "PLOS ONE: Food Addiction: Its Prevalence and Significant Association with Obesity in the General Population." Accessed September 20, 2013.
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Barbara Batetta, Mikko Griinari, Gianfranca Carta 4 , Elisabetta Murru, Alessia Ligresti, Lina Cordeddu, Elena Giordano, Francesca Sanna, Tiziana Bisogno, Sabrina Uda, Maria Collu, Inge Bruheim, Vincenzo Di Marzo, and Sebastiano Banni."Journal of Nutrition." Endocannabinoids May Mediate the Ability of (n-3) Fatty Acids to Reduce Ectopic Fat and Inflammatory Mediators in Obese Zucker Rats. .
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Senese, Fred. "General Chemistry Online: The Bliss Molecule." General Chemistry Online: The Bliss Molecule. Fred Senese, Frostburg State University Department of Chemistry,
Endocannabinoids Shape Accumbal Encoding of Cue-Motivated Behavior via CB1 Receptor Activation in the Ventral Tegmentum
Erik B. Oleson, Michael V. Beckert, Joshua T. Morra, Carien S. Lansink, Roger Cachope, Rehab A. Abdullah, Amy L. Loriaux, Dustin Schetters, Tommy Pattij, Mitchell F. Roitman, Aron H. Lichtman, Joseph F.
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Mone, Gregory. "Mind & Brain / Pharmaceuticals." How Pot, Cocaine, and Hunger Intersect in the Brain. N.p., 1 Dec. 2011. .
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yum9me Flickr photostream.
Flickr Photostream of Bionicgrrrl

#food addiction #obesity #overweight #BMI #BF #Paula Dean #Fried food #endocannabinoids #anandamide #AEA #2-AG
The link between food addiction and obesity. Part Two



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