Why Counting Calories Doesn't Work

The argument that all a person needs to do to lose weight is to obey the First Law of Thermodynamics (calories in vs. calories out) is wrong. Just eating less and exercise more, and the fat pounds will fall off, isn’t working for most people. This argument assumes that the human body functions like a simple mechanical machine, and if you wish to lose weight, just burn more calories then you consume, end of story.

If it were that simple the obesity epidemic would be easy to solve. The size, efficiency and speed of a woman’s metabolic engine are estrogen dependent. The tendency to gain weight, no matter how well you watch your diet and exercise, may be the first clue that your estrogen levels are declining. A woman’s weight and how she looks has more to do with her estrogen production than calories in versus calories out. Many women never experience a problem with weight until they reach age 35 or 40 just at the time when her estrogen levels begin to decline. This drop in estrogen has a slowing effect on her metabolism, decreasing the efficiency of her metabolic engine to burn fat. Eventually, the scales turn in favor of relentless weight gain.

Primitive agriculturalists recognized the relationship between the ovaries and obesity. They observed that the spayed female tends to grow fat, her metabolism altered. In Aristotle’s day, farmers were accustomed to spay the females of domestic animals. The ovaries of sows were excised with the view of quenching their sexual appetites, and stimulating growth in size and fatness. In spite of the widespread practice of female castration by farmers throughout history, modern medicine continues to ignore the metabolic impact of ovarian function on a woman’s physiology.[i]

The size and efficiency of a woman’s metabolic engine correlates with the size and efficiency of her lean body mass, which is dependent on her estrogen levels. This is why diets don’t work. When you restrict your calories in order to lose weight, you can reduce your muscle mass (metabolic engine) by as much as 30%. Every time you restrict your caloric intake you deprive the endocrine system of the very calories and nutrients it needs to produce hormones. Every attempt to lose weight through calorie deprivation renders your endocrine system less capable of growth, healing and repair.

Estrogen promotes a pro-anabolic effect (muscle building and repair) on skeletal muscle and increases muscle mass.[ii] Skeletal muscle is loaded with estrogen receptors found on the muscle cell membrane, in its cytoplasm, on its nuclear membrane, on the surface and within the mitochondria (where fat is burned in the cells of our body) as well. Muscle strength and mass is highest when estrogen levels are at their peak throughout a young woman’s menstrual cycle.

Burning the fat through oxidative phosphorylation (final metabolic pathway for energy transfer from oxygen) occurs in the mitochondria. In order to live, survive and reproduce, our bodies need energy. It is within the mitochondria where we burn fat (and produce energy). Promoting the health of the mitochondria is key. Energy is stored in the food that we eat. Food is analogous to the crude oil that is drilled from oil wells. It is the job of the mitochondria to convert the energy from the food that we eat into the energy signature used by our bodies called ATP that drives the biochemical reactions that permit our cells and tissues to function normally. ATP is analogous to the gasoline that fuels our cars. Mitochondria are analogous to the oil refineries. The number and size of the mitochondria are not fixed and can be increased by exercise.[iii] Furthermore, the number of mitochondria, the size of the mitochondria, and rate at which mitochondria burn fat are all estrogen dependent functions.[iv] [v] [vi] When estrogen levels decrease, so does the rate at which a woman burns fat.

When estrogen is present in adequate amounts it blocks the deposition of fat in the fat cells of the abdomen and trunk, while at the same time signaling the muscles to become more efficient at burning fat.[vii] Estrogen regulates fat burning in a woman’s body. It has a direct insulin sensitizing effect while at the same time regulating the expression of lipoprotein lipase (the enzyme factor that bridges lipoprotein uptake into cells), inhibiting absorption of fat at the fat cell while increasing the release of fat out of the fat cell. Additionally, it promotes activation of lipoprotein lipase at the muscle, increasing the absorption of fat and the rate of fat burning by the muscles, literally priming the pump for maintaining fat burning and weight loss.

This important role of estrogen in determining regional body fat distribution not only results in the pleasing physical confirmation of the healthy female body, but also has health promoting effects, placing her at one-tenth the risk as her male counterparts for developing cardiovascular disease.

Many factors contribute to the obesity epidemic. The environment we find ourselves in does not foster optimal estrogen production by the ovaries. We were designed to consume nutritionally dense foods, not the cheap and unhealthy junk foods that comprise the staple of modern society. School, work environments and leisure pastime promote physical inactivity and sedentary behavior. Most of our time is spent indoors sequestered away from sunlight, fresh air and energetic connection to the planet. Stress hormones transform our metabolism into rapid fat storage mode. Chronic sleep deprivation promotes insulin resistance and intense carbohydrate cravings. 

To be barefoot and fancy free, working or having fun in the sun, are powerful inducers of estrogen production. It doesn’t matter if you’re spending your time doing Aerobic gardening in the backyard or playing volleyball on the beach; the end result is the same: the optimal production of estrogen. In the case of vitamin D, its receptors are strategically expressed in the ovaries setting the stage that begins a cascade of biologic events designed to foster biosynthesis of estrogen.[viii]

If your ovaries are to generate sufficient estrogen to support fat burning, they require the best nutrition possible. Your ovaries will fail you in an environment of sugar, processed food and soda.

The Standard American Diet (SAD) doesn’t possess the nutritional horsepower essential to support optimal ovarian function.

In addition to the malnutrition imposed by our diet (SAD), other environmental endocrine disruptors found in the plastics and fertilizers, and pollution all around us, sabotage ovarian function. Endocrine disrupting chemicals, such as dioxins and PCBs, act in a number of ways to reduce the production and release of hormones from endocrine glands, counteracting the action of hormones at target tissues, or speeding up the metabolism of hormones while reducing their action.

An unintended consequence of inadequate estrogen is sugar and carbohydrate cravings. Not only is estrogen an important neurotransmitter in the brain, but it regulates the synthesis of serotonin, dopamine and other neurotransmitters. As estrogen levels decline, so does our sense of wellbeing, creating the need for comfort foods. Something sweet is a symbol of love and nurturance. Our first food as infants is lactose or milk sugar. Well-intentioned parents reward their children with sugary snacks, giving them a treat, turning a biochemically harmful substance into a comfort food. This conditions us to need something sweet to feel complete or satisfied. We continue to self-medicate with sugar as adults. This quick fix gives a temporary boost in our mood or energy. One quick fix soon leaves you looking for another. Each hit of momentary satisfaction comes with a long-term price. Once insulin resistance sets in, it becomes possible to gain weight on a Tic Tac, a phenomenon independent of its calorie content.

Sugar, the enemy of the ovaries, is a major factor contributing to chronic decreased estrogen production and its resultant health consequences. It turns out that sugar is a potent inhibitor of estradiol production by the ovaries. Chronic sugar intake and reduced estrogen levels result in insulin resistance, a condition where the body does not respond to insulin in normal ways. Other factors, such as excess body weight and lack of exercise, result in the body becoming insulin resistant. Insulin resistance has been responsible for ailments such as heart disease, diabetes, hypertension, high cholesterol, cancer, depression, chronic fatigue and premature aging. Insulin’s job is to create insulation. It does this by permanently inducing lipoprotein lipase (enzyme responsible for uptake of fat) at the fat cell, converting one’s physiology into an efficient fat-storing machine.

Insulin resistance is a pro-inflammatory condition; the more weight you gain the more inflammation you generate. This is what links obesity to increased risk of heart disease, cancer, diabetes and Alzheimer’s. Estrogen’s anti-inflammatory and insulin sensitizing effect protects a woman from cardiovascular and other diseases. .

Recent evidence shows that the gut microbial ecology is a major determinant of body weight and plays a far more important role in the development of obesity then has previously been recognized. We are a walking mountain of microbes that inhabit our gastrointestinal tract. These microbes are directly or indirectly driving the metabolic bus. Put simply, metabolism, inflammation, insulin resistance, and ones risk for developing scores of metabolic diseases—hinges on the state of the gut microbial ecology.

Diet plays a central role in shaping the gut microbial ecology. The character of the bacteria, and their products, may be modified to an astonishing degree by changes in food (pre-biotic). Gut microbial composition depends on dietary habits just as health depends on microbial metabolism. A diet rich in starch, fiber, fermented foods and plant polysaccharides, is best for reprograming the gut microbial ecology for optimal sustainable weight control.

The success of sustainable weight loss hinges on the state of your hormones, mitochondrial health, microbial ecology, and the quality of the food choices you make, and has nothing to do with counting calories.

[i] Corner GW. 1965 The Early History Of The Oestrogenic Hormones. The Journal of Endocrinology. 31:111

[ii] Tiidus PM. 2009 Estrogen and HRT promote a pro-anabolic skeletal muscle environment in older women. Journal of Applied Physiology. 107(5):1367-1370

[iii] Evens JL. 2010 Secret Life of Mitochondria: Your cells microscopic power house for longevity, appearance and performance. Xymogen EP.

[iv] Klinge CM. 2008 Estrogenic control of mitochondrial function and biogenesis. J Cell Biochem. 105(6):1342-1351

[v] Burris TP, Krishnan V. 2005 Estrogen: a mitochondrial energizer that keeps on going. Mol Pharmacol. 68(4):956-8

[vi] Rodriguez-Cuenca S, Monjo M, Gianotti M, Proenza AM, Roca P. 2007 Expression of mitochondrial biogenesis-signaling factors in brown adipocytes is influenced specifically by 17 beta-estradiol, testosterone, and progesterone. Am J Physiol Endocrinol Metab. 292(1):340-6

[vii] Mayes JS, Watson GH. 2004 Direct effects of sex steroid hormones on adipose tissue and obesity. Obes Rev. 5:197-216

[viii] Harkness LS, Bonny AE. 2005 Calcium and vitamin D status: key roles for bone, body weight, glucose tolerance, and estrogen biosynthesis. J Pediatr Adolesc Gynecol. 18(5): 305-3111