In our last discussion we looked briefly at basic lifestyle principles underlying our systems of metabolic regulation. As we continue this journey exploring healthy weight management we will move on now to an overview of endocrine regulation of metabolic rate. This is not just a sight-seeing excursion; we need to understand that the endocrine system is central to managing metabolic function and that unless we achieve balance between the actions of the various endocrine hormones we will be inefficient at burning calories and thus find it very difficult to lose weight regardless of the method we choose.
The endocrine system consists of a series of glands that secrete hormones, biochemical messengers that serve as controllers and regulators of various aspects of metabolic function within cells. These glands include the hypothalamus, pituitary, adrenals, thyroid, ovaries and testes, and islet cells of the pancreas. Through an intricate feedback system the hormones secreted by these glands serve to regulate each other in addition to the effect they have on the body as a whole. For the purpose of this discussion we will consider the hypothalamus and pituitary primarily as regulators; our discussion will focus primarily on the hormone actions precipitated by the adrenals, thyroid, sex glands, and islet cells.
We’ll look first at thyroid issues since thyroid hormone is the primary controller of metabolic rate within the cell. The thyroid gland produces thyroid hormone in two forms; thyroxine (T4) represents the bulk of thyroid gland output and serves as a storage or precursor hormone for l-thyronine (T3) which is the active form. T4 is converted to T3 in the thyroid gland, in the liver, and in peripheral tissues as needed. The majority of T4 and T3 in circulation is bound to thyroid binding globulin; the bound portion is not active. The pituitary measures circulating T4 and sends messages back to the thyroid gland to increase or decrease production based on that evaluation. When we look at metabolic rate, however, the critical issue is activity of T3 in the cells, and we must remember that production of T4 is merely the first step. Of equal importance are three additional factors: the degree of binding, the extent of conversion to free T3, and the availability of receptors on the cell wall.
Adrenal glands are our stress response managers, producing adrenalin, cortisol, and DHEA along with other hormonal agents. Increases in stress, whether mental, emotional, or physical (including dietary) cause increased release of adrenalin and cortisol to enable us to deal with danger. Direct effects may include increased heart rate and blood pressure, increased glucose levels, and reduced digestive secretion. Cortisol’s primary activity is to release blood glucose; under acute stress challenge this would provide energy for escape, but when chronic stressors lead to chronic elevation it leads more directly to weight gain. Conversely, low cortisol leads to hypoglycemic issues (low blood sugar). Adequate cortisol is necessary for conversion of T4 to T3; excessive cortisol reduces the activity of thyroid receptors on the cell wall. DHEA, another of the primary adrenal hormones, has direct androgenic activity, helping maintain muscle mass, bone mass, and energy processes. DHEA is a precursor hormone as well; we convert it to testosterone (and testosterone to estradiol), both highly active hormones. DHEA also is a determining factor in the conversion of T4 to T3 and thus helps in controlling metabolic rate.
We’ll look at ovarian and testicular hormones together since men and women both produce the same hormones, just in different balances.
Testosterone is our primary androgen, responsible for maintaining muscle mass and bone mass as well as masculine sex characteristics. Androgens (DHEA and testosterone) are anabolic (muscle building) hormones- and remember, muscle is our primary calorie burning tissue. Testosterone is converted by enzymes called aromatases into estradiol, our primary estrogen. Estrogens increase fat deposition and are responsible for feminizing sex characteristics. Progesterone helps regulate estrogen responses throughout the body; inadequate progesterone to balance estrogens leads to a broad pattern of symptoms that includes weight gain. Excessive estrogenic activity (estrogen dominance or oral estrogen supplementation) has also been shown to increase thyroid binding globulin, which reduces the amount of active thyroid hormone, further slowing metabolic rate.
Islet cells of the pancreas produce insulin and glucagon, which are designed to work together (along with cortisol) to regulate blood glucose levels (immediate cellular energy). Carbohydrates (and to a lesser degree proteins) stimulate insulin release to enable the cellular uptake of rising glucose levels. Fats, in the absence of sugars, trigger glucagon release to stimulate fat burning for energy (including stored body fat). Excessive intake of refined carbohydrates leads to the development of insulin resistance, a process characterized by elevated insulin levels coupled with poor cellular insulin response. Insulin resistance is the underlying causal factor for metabolic syndrome (hypertension, high triglycerides and LDL, lower HDL, increased cardiac risk, type II diabetes, and obesity). Elevated insulin levels not only lead to direct weight gain but also decrease thyroid receptor response as well.
Got it? Good! The hard part is behind us, now that we have an understanding of basic metabolic issues and the integral role our endocrine system plays in the direct control of cellular energy. In the next installment we’ll get to the fun part- how we can use nutritional agents to improve metabolic function and speed weight loss. We will conclude with discussion of specific dietary patterns that can help us reverse metabolic inefficiencies and restore optimum health. When we put it all together, we’ll find we’re well on our way to a healthy weight, and more importantly, a healthy life.