and then there is the mental illness portion of the obesity issue

ADD, ADHD, OCD, and obesity: what doe these have in common?

Is there a "mental illness" component to obesity? or is it just that anyone who cannot eat a restrictive diet, remain hungry for life is "not normal" hence becomes over weight.

It is much more like the excess and crap in the modern diet causes us to be hungry all the time. Abundance makes food always available. We get fat due to both, and it is all natural. Remove either one, and the problem goes away.

ADD, ADHD, OCD may contribute, as depression, boredom, and other emotions, but is this just one more reason the medical profession can use to describe there inability to provide workable free living solution to the desire to eat obesity problem?

http://www.drsharma.ca/all-obese-patients-should-be-screened-for-adhd.html   so sharma, now that you screen and find ADD, it is not obesity that you cannot treat, it is ADD that is the issue, so you are not a failure, it is the psychiatrists fault for not being able to treat ADD? And the patients for not thinking right, and CBT has a bit of the solution? Yah sure.

Background

Here is a beautiful little summary via  http://www.gnolls.org/ahs-2012-bibliography/
 at
http://onlinelibrary.wiley.com/doi/10.1111/j.1467-3010.2009.01753.x/abstract

Summary

In the context of the rising prevalence of obesity around the world, it is vital to understand how energy balance and bodyweight are controlled. The ability to balance energy intake and expenditure is critical to survival, and sophisticated physiological mechanisms have developed in order to do this, including the control of appetite. Satiation and satiety are part of the body's appetite control system and are involved in limiting energy intake. Satiation is the process that causes one to stop eating; satiety is the feeling of fullness that persists after eating, suppressing further consumption, and both are important in determining total energy intake.

Satiation and satiety are controlled by a cascade of factors that begin when a food or drink is consumed and continues as it enters the gastrointestinal tract and is digested and absorbed. Signals about the ingestion of energy feed into specific areas of the brain that are involved in the regulation of energy intake, in response to the sensory and cognitive perceptions of the food or drink consumed, and distension of the stomach. These signals are integrated by the brain, and satiation is stimulated. When nutrients reach the intestine and are absorbed, a number of hormonal signals that are again integrated in the brain to induce satiety are released. In addition to these episodic signals, satiety is also affected by fluctuations in hormones, such as leptin and insulin, which indicate the level of fat storage in the body.

Satiation and satiety can be measured directly via food intake or indirectly via ratings of subjective sensations of appetite. The most common study design when measuring satiation or satiety over a short period is using a test preload in which the variables of interest are carefully controlled. This is followed by subjects rating aspects of their appetite sensations, such as fullness or hunger, at intervals and then, after a predetermined time interval, a test meal at which energy intake is measured. Longer-term studies may provide foods or drinks of known composition to be consumed ad libitum and use measures of energy intake and/or appetite ratings as indicators of satiety. The measurement of satiation and satiety is complicated by the fact that many factors besides these internal signals may influence appetite and energy intake, for example, physical factors such as bodyweight, age or gender, or behavioural factors such as diet or the influence of other people present. For this reason, the majority of studies on satiation and satiety take place in a laboratory, where confounders can be controlled as much as possible, and are, therefore, of short duration.

It is possible for any food or drink to affect appetite, and so it is important to determine whether, for a given amount of energy, particular variables have the potential to enhance or reduce satiation or satiety. A great deal of research has been conducted to investigate the effect of different foods, drinks, food components and nutrients on satiety. Overall, the characteristic of a food or drink that appears to have the most impact on satiety is its energy density. That is the amount of energy it contains per unit weight (kJ/g, kcal/g). When energy density is controlled, the macronutrient composition of foods does not appear to have a major impact on satiety. In practice, high-fat foods tend to have a higher energy density than high-protein or high-carbohydrate foods, and foods with the highest water content tend to have the lowest energy density. Some studies have shown that energy from protein is more satiating than energy from carbohydrate or fat. In addition, certain types of fibre have been shown to enhance satiation and satiety. It has been suggested that energy from liquids is less satiating then energy from solids. However, evidence for this is inconsistent, and it may be the mode of consumption (i.e. whether the liquid is perceived to be a food or drink) that influences its effect on satiety. Alcohol appears to stimulate energy intake in the short-term, and consuming energy from alcohol does not appear to lead to a subsequent compensatory reduction in energy intake.

The consumption of food and drink to provide energy is a voluntary behaviour, and, despite the existence of sophisticated physiological mechanisms to match intake to requirements, humans often eat when sated and sometimes refrain from eating when hungry. Thus, there are numerous influences on eating behaviour beyond satiation and satiety. These include: the portion size, appeal, palatability and variety of foods and drinks available; the physiological impact on the body of physical activity and sleep; and other external influences such as television viewing and the effect of social situations.

Because satiation and satiety are key to controlling energy intake, inter-individual differences in the strength of these signals and responsiveness to their effects could affect risk of obesity. Such differences have been observed at a genetic, physiological and behavioural level and may be important to consider in strategies to prevent or treat obesity.

Overall, it is clear that, although the processes of satiation and satiety have the potential to control energy intake, many individuals override the signals generated. Hence, in such people, satiation and satiety alone are not sufficient to prevent weight gain in the current obesogenic environment. Knowledge about foods, ingredients and dietary patterns that can enhance satiation and satiety is potentially useful for controlling bodyweight. However, this must be coupled with an understanding of the myriad of other factors that influence eating behaviour, in order to help people to control their energy intake.

Yoni got me thinking

Yoni got me thinking about the way I was raised, the way the nieces  raise their children and the way I see kids generally being raised. The interesting is the default condition, minimal involvement, as long as the marks are good, the child is well behaved, not in trouble, responsible about informing the parents of there whereabouts and minimally demanding.

There was no money for junk food. It was the parents that bought it, had it in the house "for the kids", but we never got any. I now understand what shrinkage is really about, the junk food addiction. Reward driven, or energy partitioning, or pure addiction, it does not matter.

Those of us who grew up obese had access to lots of food, much of it good food, but we had addiction to wheat, sugar, or fruit to deal with as well. Addiction is dose dependent and availability dependent in the development stage. If it is not available, we do not become addicted. Real addiction or addiction like, I do not know.

Now there are great numbers that are dealing with this problem, and the none addicted do not accept the issues of overcoming addiction to food. There is no good solution. 12 steps help those who with believe base personalities. The rest of us... well rational recovery... is a crock, chemistry explains it... but recovery is elusive... but many do get it... if they try long enough... and do not die first.

There are always pushers at every door... from grand mothers, mother, and the corner stores. Drug pushers all. But they do not see themselves as the problem. But they are. It is no wonder that many of us like to hang with those who understand, even if we are not "belief driven personalities".

Almonds?

Are almonds addicting, just like wheat? Do these, along with oats contain gliadin? Is glutamic acid the same stuff, or the courser division? Gliadin runs with glutin, but does it also come separately?


from http://www.celiac.com/articles/8/1/What-is-gluten-What-is-gliadin/Page1.html

There are two main groups of proteins in gluten, called thegliadins and the glutenins. Upon digestion, the gluten proteins break down into smaller units, calledpeptides (also, polypeptides or peptide chains) that are made up of strings of amino acids--almost like beads on a string. The parent proteins have polypeptide chains that include hundreds of amino acids. One particular peptide has been shown to be harmful to celiac patients when instilled directly into the small intestine of several patients. This peptide includes 19 amino acids strung together in a specific sequence. Although the likelihood that this particular peptide is harmful is strong, other peptides may be harmful, as well, including some derived from the glutenin fraction.

From Wheat Belly:

It’s the gliadin opiate at work again, stimulating appetite throughout the day. Lose the wheat, lose the gliadin protein, lose the abnormally stimulated appetite that impairs our impulse control.

Are there other sources of gliadin beyond Gluten rich foods (wheat, barley,rye)?

,"I'd rather enjoy my food and die early than eat healthfully and live long"?

,"I'd rather enjoy my food and die early than eat healthfully and live long"? This is not for me any longer. Enjoyment of food is a concept that has crept in, likely from TV or completive cooking. OK, there is nothing wrong with enjoying food, but it is not essential, and necessary. The purpose of food is just energy. That it, that all. Enjoyment of food as an requirement will just lead to more problems.

insulin

It is clear now. Satiation, after a meal, the stop eating signal may be influenced by insulin rise in the brain. OK, that is the stop eating signal.

Satiety, the stay stopped signal, the antagonist of hunger, is controlled by available energy.

Insulin is the storage hormone, as in Volek's xy=c curve, x being fat release rate, y the blood insulin concentration.

So what does this all mean? Low carb is the default diet, but protein and carbohydrates must both be low.

Then there is the first pass gut hunger, the gut eats first, then the liver, then the energy gets to blood flow and circulates.

Omega 3 as Shangra la oil?  

hunger

Woo notes :  

I tried a lower protein diet, for the benefit of more stable blood sugar and lower hunger.

Any truth or just another story?

Can you tell what is in the fridge by looking in the garbage? --- This was a statement about urine ketone testing. But is the shopping cart better? It tells what the family want's now. Wants not needs. There is the change since I was young. Affluence. As a youth, if we did not grow it, we did not eat it. No money. Simple.