by Cat, June 2007; updated May 2019
Do you cringe when your doctor casually describes you as obese? You object, “But I’m only 35 pounds overweight! I’m just a little plump!”
The doc responds, “You’re 30% overweight and your BMI* is over 30. You need to lose weight to avoid type 2 diabetes!” He wheels around in his office chair and searches for something in his files, then hands you a pamphlet on weight loss. “Try this diet for 2 months. You should lose 5 – 10 pounds in that time.” *[BMI is Body Mass Index]
You scan through the pamphlet: Calorie restriction; tips on reducing the fat content of your meals; advice on eating low-glycemic foods. Nothing new here.
“But, Doc, I’m already doing all these things,” you protest.
He looks at you like you’re a 3 year old. “Are you being honest?” he asks, and you can tell he doesn’t believe you. You stare at your toes. “I am being honest! I haven’t been cheating!” you think to yourself; the shame of his disbelief is just too much. You don’t have the energy to argue.
- Includes: 1. “It’s a Lifestyle Problem;” 2. The Low Fat Myth; 3. A Metabolic Problem
- See also: 1. Diet & Health Menu; 2. Obesity 102
“It’s a Lifestyle Problem”
A large percentage of our American population is overweight. A national tragedy. Most so-called experts believe this problem is “brought on by lifestyle choices;” their euphemism for overeating and sedentary behavior.
Humph! Those experts should try carrying around a 30 pound sack of flour day in, day out, and see just how much energy they have at the end of a long working day. They should try resisting the cravings for sweets that are more urgent, more demanding than a heroin addiction. They should walk a mile in my shoes.
Could these symptoms be a consequence of some underlying metabolic problem, rather than a weakness of personality? I think so. And so do many emerging experts.
The Low-Fat Myth
The myth states:
- “Fat provides twice as many calories per gram as carbs or proteins, so when you are trying to cut calories, limiting fats gets you the biggest bang for your caloric buck.
- Dietary fats just turn into body fat.”
But while there is a small amount of truth to each of these beliefs, they are, for the most part, diet myths.
The Truth: Low fat diets promote weight gain, not weight loss.
Most dietary fat is not converted to body fat, but rather is required on a daily basis for many cellular and physiological functions; fatty acids are the main constituent of cell and mitochondrial membranes.
- Dietary fat and cholesterol are also required to regulate insulin levels and trigger enzymes that convert food into energy. They are also required for assimilation of dietary minerals from the intestines, to keep our bones healthy.
- Consuming fat with carbs slows down digestion, creating a sensation of fullness, and thus keeping you from overeating (and gaining weight). (6) So, go ahead, enjoy a pat or two of butter or sour cream with your baked potato.
- Body fat is made from excess dietary carbs, which are converted to palmitic acid (a fat) in the liver and then transported for storage in fat (adipose) tissues.
While your body can make many of the fats it needs from sugar or protein, it prefers to get it from the diet. And there are two types of fat the body cannot make; these are the essential fatty acids, Omega-3 and Omega-6. These fats MUST be present in the diet to prevent disease and degeneration of the body’s tissues. Generally we get sufficient Omega-6 fats in our American diet (present in canola, corn, soy, and sunflower oils; vegetables; and meats – especially those not raised in pasture). But many of us do not get enough Omega-3 fats (present in nuts and seeds, and deep water fish such as wild salmon, halibut and tuna).
A Metabolic Problem
When you lower your caloric intake, your body down-regulates your metabolism, so that you do not expend energy at the same level as you did before you changed your diet. (6) If you lower your calories significantly, your body goes into famine mode, conserving energy production and converting as much of your food intake as possible into stored fat. When your caloric intake is restored, your body may not correspondingly up-regulate your metabolism, and instead continue to store your food intake as fat. What could cause this?
Fact: If you are obese, with most of your excess weight around your middle, you likely have elevated blood insulin, and altered fat metabolism in the liver (see fatty liver for more). You may also have problems with cortisol and other hormone levels. < link is to my old iWeb site, Disease section. Update link when I’ve moved that article to a new blog.
Emerging research notes a connection between the balance of gut bacteria and fat metabolism (see Obesity 102 for more).
Many people now believe the underlying problem behind obesity is a metabolic condition called Insulin Resistance (aka Metabolic Syndrome or Syndrome-X), exacerbated by subclinical, underactive thyroid.
Insulin resistance is diagnosed by elevated blood insulin, and possibly also elevated blood glucose. Insulin is the hormone secreted by the pancreas that triggers entry of sugar (glucose) into the cells, where it can be burned as fuel for energy. Insulin also causes the cells to favor burning sugar over stored fat, for energy. In the case of insulin resistance, it is postulated that the cells stop responding when insulin knocks (the insulin receptors are either turned off, or have been eliminated), even though those same cells are starving for more sugar. The pancreas pumps out more insulin until the cells are bathed in it, and yet they do not respond.
Insulin acts as a double-edged sword when its levels are too high. In the words of Dr. Mercola, “Insulin, secreted in response to excess dietary carbohydrates promotes fat, and then wards off the body’s ability to lose that fat.” (2B)
- When glucose isn’t being taken up by the cells (due to insulin resistance), it builds up in the blood until the liver turns it into fat, for storage in the fat cells concentrated around the body’s middle.
- The increased level of insulin also keeps the body from breaking down stored fat (by inhibiting the secretion of the hormone glucagon, which stimulates the burning of fat, and the enzyme lipase, which breaks down fat), so the end result is that the cells become starved.
I know a lot about this metabolic problem because I have had it since my early 20s. The following describes my own experience and that of others who have this problem:
Early on, people with insulin resistance tend to experience hypoglycemia (low blood sugar). They can be light headed, edgy, moody, irritable. And they crave sugary foods. While they are young, they may have enough energy to work off the extra calories, but as they reach middle age, they accumulate fat in the abdomen and buttocks. They feel a lack of energy and complain of fatigue. With time, as the pancreas wears out, the problem shifts to the other extreme: hyperglycemia, otherwise known as type-II diabetes.
Type-II diabetes is reaching epidemic proportions. Even pets are developing the problem. Can we all just be lazy, undisciplined overeaters? What about those of us who do not overeat, get daily exercise, and are still overweight? Are we really cheaters and liars about our diet and exercise levels? Or is something else going on?
Could the sedentary behavior, and indulgence in sweets and other simple carbs, be a consequence of a metabolic problem, rather than the cause? Could our cell’s resistance to insulin be causing the body to crave (and do anything to get) sugar, because the cells need sugar for energy, and are not getting it? Even though it may be plentiful in the diet? Could this lack of sugar at the cellular level be responsible for the overwhelming fatigue that makes even light exercise more than some can handle? Yes, YES, YES!
(I don’t intend to minimize the importance of exercise in controlling elevated insulin, but it is a cyclic situation: the less exercise, the more insulin resistant; the more insulin resistance, the less energy to exercise. For more on this, refer to Dr. Mercola’s article “Exercise Reduces Diabetes by Reducing Insulin Resistance” (2C)
You have now completed Obesity 101. Interested in more? Check out Obesity 102.
Note: the numbers in parenthesis are the reference numbers in my original article (on old iWeb site). When I moved and updated the article to this Cat’s Kitchen version, I reorganized references on the same site (such as Mercola) to be together (as 2A, 2B, etc.. Those added since that reorganization say “new” in the parenthesis.
- content.nejm.org/cgi/content/short/354/15/1601 (Trans Fatty Acids and Cardiovascular Disease by D. Mozaffarian, M.D., et. al; New England Journal of Medicine, Volume 354 (15):1601-1613, April 13, 2006)
- dartmouth.edu/~toxmetal/RSCRge.shtml (link no longer valid)