How to Stay on a Diet and Finally Lose Weight Using the Outer Child Program

© Susan Anderson 2010

Stick to your diet? Have trouble with it?  Taming Your Outer Child Slims You Right Down

Outer Child is always trying to get immediate gratification, and the most immediately gratifying experience is popping a piece of food in your mouth – you taste and feel it instantly. Taming Your Outer Child has a truly effective program for overcoming Outer Child resistance to your diet.

But not all weight control problems are caused by an overactive Outer Child. Out of compassion for those whose bodies tend to stockpile fat (regardless of how much they eat), I want to list some of the biological factors that can increase your appetite, promote excessive fat storage, and-or slow metabolism. These factors remain unknown to many dieters who are left to suffer their weight problems in shame and frustration. I present the following tidbits to give them, you, and ME both validation and hope: Science may soon be closing in on our problem.

White versus brown fat cells

Your weight can be affected by the proportion of your white to brown fat cells. White cells (whitish yellow) are known to lower your metabolic rate whereas brown (brownish) burn more calories (i.e. to keep you warm in a cold climate). AP, “Focus on ‘good’ body fat in battle against weight gain,” Newsday, April 9, 2009.

Infectious (Ad-36) and fat storage

A number of infectious viruses are implicated in obesity. A high percentage of a fat-associated virus, Ad-36 (also in pink-eye), is found in obese populations as compared with non-obese populations. Laboratory studies show that stem cells exposed to Ad-36 turn into fat cells. Twin studies: Identical twins who’d had the Ad-36 virus (as shown by antibodies) weigh significantly more than other twin who never had the virus (Nikhil Dhurandhur 2004 and others ___). Epidemiological studies show obesity distribution across geographic regions to be similar to the way viral infections distribute (independent of variations in regional dietary habits). Robin Marantz Henig, “Fat Factors,” New York Times, Aug 13 2006. AP, “More Evidence of Virus Link to Obesity,” New York Times August 20 2007.

Microbes and fat storage

Microbes: Trillions of microbes colonize the gut – bacteria, fungi, protozoa, and archaea – and depending on their composition, can promote fat stockpiling. Mice raised in sterile lab to prevent microbe colonization, do not lay down fat unless they are transplanted with microbes from “normally exposed” mice. Microbes can be harmful or helpful, and depending on proportions of certain bacteria (i.e. B. Theta and M. Smithii bacteria) in the gut, your body either has tendency to either lay down fat or slough it off. Bryan, Jenny, “Could fat be catching?”

 

Biochemistry and fat storage

Some elements in the biochemistry of appetite/fat storage/metabolism have been identified, i.e. leptin, ghrelin, NPY, insulin, etc. Chemistry involved in countering the urge to eat includes obestatin (Matthias Tschop, U of Cincinnati 2005__________), MPH, and PYY (found in some high fiber foods), etc.

Leptin (appetite shut off switch) and fat storage

Leptin, a neuropeptide, is involved in appetite shutoff switch. Leptin is made by fat cells; one of its roles is to signal the brain to know when you’re full. Research shows that adding leptin after weight loss helps people keep weight off, because it tricks the brain into believing your fat cells are full (Dr. Jeffrey Friedman, Jeffrey DeFalco, at Rockefeller University August 21 2001. Rudolph Leibel at Columbia 2000___).

 

Ghrelin and fat storage

Ghrelin is made in gut and intestines and slows metabolism, promotes fat storage, and increases your urge to eat. Researchers at U. of Washington, New England Journal of Medicine, May 23 2002.

History of dieting and fat storage

Fat cells are particularly resistant in people who have dieted. Fat cells shrink but fight back by storing lipids or by stimulating appetite through certain hormones (leptin, ghrelin). There are different types of fat cells; one is the precursor fat cell which creates new fat cells that are highly resistant to giving up their fat stores. Extensive research shows that two non-obese people of same weight require different amounts of calories to stay thin; a formerly fat person has to eat fewer calories. Furthermore, people with history of obesity have more fat cells, so even when they’re thin (which means their fat cells are deflated versus engorged) they look heavier than naturally thin people (who have fewer fat cells) (Susan Fried, Rutgers 2007).

 

Set point and fat storage

Set point refers to the self-regulating range of an individual’s weight, above which and below which an individual’s metabolism works automatically to return to this average weight. Each person’s set point is well established and varies greatly from person to person. Some peoples’ range gets established at a high a set point and their metabolism adjusts downward to keep them within that higher range (fatter) (Dr. Rudolph Leibel at Columbia 2000).

 

Genes and fat storage

Some people are genetically predisposed to stockpile fat, particularly if their genes originated from famine-prone geographic areas which would have selected for ‘thrifty genes’ (capable of lowering metabolism and resisting fat burning during famine, i.e. Pima Indians). Conversely, populations from the food-abundant ‘Fertile Crescent’ selected for genes for sloughing off excess fat, since obesity would make people slower, easier prey (Jeffrey Friedman 2004). There are up to 1000 genes implicated in metabolism and weight.

Hypothalamus and fat storage

An important site for weight control is the hypothalamus, as evidenced by a 9 year old boy with injury to his hypothalamus who rapidly grew to 400 pounds (work of Dr. Jeffrey Flier (2000). Research: if hypothalamus is destroyed in rats, they grow massively obese.

Prenatal and fat storage

Obesity can develop in utero. For instance, in a pregnant woman with high blood sugar, glucose levels build and can cross over to fetus, causing fetus’ pancreas to secrete high levels of insulin which promotes fat storage. Rabin, Roni, “Obesity begins in utero,” Newsday, Nov 7 2005.

Estrogen and progesterone and fat storage

These hormones which spike to overcompensate at onset of menopause), can cause women (and men on hormone therapy for prostate cancer) to lay down significant fat in lower body where it resists weight loss.

Stress and fat storage

Having discussed the chronic release of cortisol’s potential to interfere in hippocampal memory, here it is again interfering in our diets. Although extreme stress initially reduces your appetite, the longer acting stress hormones like cortisol increase our appetites to get us to regain our fat stores. Sapolsky, Why Zebras pages 74-78. See “Stress linked to obesity: Hormone triggers growth of fat cells.” Bloomberg News in Newsday July 3 2007.

Neuropeptide Y and fat storage

Another stress hormone, neuropeptide Y (NPY) causes fat cells to double in size and multiply. In rats, if receptors for NPY are blocked, they stop laying down fat, no matter how much they eat (Herbert Herzog of Sydney Australia 2007).

Sleep and fat storage

The ‘clock gene’ is implicated in disturbances in circadian rhythm – a sleep / appetite self-adjusting system that varies according to position of sun to earth based on shifting light-darkness patterns. Another factor involves stress hormones (i.e. cortisol) that interrupt sleep, slow metabolism, and increase urge to eat (Joseph Takahashi, et al, published online in Science Express, May (2), 2005.

 

Gastric bypass and fat storage

Dieter’s bodies produce more Ghrelin to restore their fat stores. Gastric bypass reduces ghrelin by reducing its production-site – the gut. It is believed that weight loss from bypass surgery is due not to people’s reduced food intake, but to reduced ghrelin production; less ghrelin means increased metabolism and reduced eating urge (Dr. Cummings, University of Washington 2002).

Liposuction and fat storage

Liposuction removes belly-type of fat, but it can leave precursor fat cells (which recruit other cells into fat) or visceral fat (known to resist weight loss).

Insulin and fat storage

Insulin is a fat-mobilizing hormone. If you’re insulin resistant, it means that the more you gain weight, the more insulin you pump out of your pancreas. As mega doses of insulin bombard your cells, they become insensitive to insulin, so you pump out more insulin to compensate with the result that you store more fat.

Magic weight loss remedies

Science hasn’t yet found magic pills to eliminate the need for dieting and exercising; yet research continues exploring these remedies:

Built in evolutionary mechanisms and fat storage

I believe there is a built-in evolutionary mechanism that makes us (perhaps women more than men) hyper-vigilant toward something that potentially causes us to be deemed visually unattractive. On an evolutionary level, in parts of the world where food supply is scarce and people die of starvation, being heavier is deemed attractive for a woman. But in parts of the world where food is abundant, eating too much food (evolutionarily speaking) could be seen as a potential threat to survival in that weight gain could limit our desirability as a mate and therefore threaten the survival of our genes. The female body shape considered unattractive varies from society to society, but in today’s mainstream America of overabundant food (witness the enormous portions served in American restaurants), being overweight is considered unattractive. Our idealization of ‘skinny’ has heightened our collective amygdalal response to food.

 

New remedies under study

Rimonabant and Acomplia, two drugs that block cannabis (marijuana) receptors in the brain to block appetite (reducing the ‘munchies’) and increase metabolism. See Talan, Jamie, “New weight-loss drug works in trial, Newsday, Feb 14 2006; and Kolata, Gina, “Will a New Drug Melt the Pounds?” New York times Dec 5 2004. Obese people have more receptors for these endo-cannabinoids.

 

Mesotherapy, injections containing various agents reportedly make “fat and cellulite melt away” in specific areas of the body, according to Dr. Marion Shapiro (2002) who trained in Europe where Mesotherapy has been practiced.

 

The “exercise pill” increases mitochondria in muscles that burn fat (transforming sugar burning switches into fat burning switches), as if you’d strenuously exercised. Zarembo, Alan, “No, exercise in a pi8ll form?” Newsday, August 1 2008.

 

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