Thyroid hormones are derivatives of the amino acid tyrosine bound covalently to iodine. The thyroid gland secretes two principle thyroid hormones thyroxine (T4) and the more physiologically active triiodothyronine (T3). A healthy thyroid is intimately linked to a balanced endocrine system. The health of the endocrine system will reflect our overall health. The thyroid is a major player when it comes to hormonal health since it stimulates and synchronizes all metabolic cellular functions. All tissues in the body are stimulated by the thyroid and the level of cortisol at the cell level controls thyroid hormone production.
What is burning in Kundalini? Glucose mainly, but also fat...in ones first awakening it appears that a lot of muscle is burnt...that is converted to fuel...I lost 30 lbs my first awakening. The second one I didn't really burn body tissue like that, the mix of thyroid to growth hormone must have been different...I was "hotter" in the second awakening but the increased growth hormone/sex hormones made the second awakening more conservative/regenerative than the first.
In my experience kundalini awakenings can disrupt menstruation. Especially during the first awakening when we have no knowledge of what is happening to us, the stress hormones will essentially cease menses by lowering progesterone and thyroid. Perhaps after the shock of the initiation and the boost of hyperthyroid activity the thyroid simply burns out from the stress. The first awakening represents more of a shock as our thyroid, adrenals and nervous system go from an uninitiated to an initiated state. Thus the first awakening is more on-edge, wildly swinging, unintegrated and extreme, even if subsequent awakenings are actually more intense. The shift from the uninitiated to the initiated poses the largest jump for both the body and the mind.
In addition to T3, there are two additional active metabolites of T3: 3,5 and 3,3' diiodothyronines, which they collectively call T2. T2 acts on the mitochondria directly, immediately increasing the rate of mitochondrial respiration, with a consequent increase in ATP production. T3 on the other hand requires a day or longer to increase metabolic rate by acting at the nuclear level, inducing the transcription of genes controlling energy metabolism, primarily the genes for uncoupling proteins.
There are a number of supposed mechanisms whereby T2 is believed to increase mitochondrial energy production rates, resulting in increased ATP levels. These include an increased influx of Ca++ into the mitochondria, with a resulting increase in mitochondrial dehydrogenases. This leads to an increase in reduced substrates available for oxidation. Also if there is an increase in cytochrome oxidase activity this would hastens the reduction of O2, speeding up respiration. Scientists looking for the mechanism of increased ATP production in kundalini might like to consider the influence of T2.
Catabolic--During fasting or when carbohydrate intake is reduced the conversion of T4 to the physiologically active T3 is reduced in order to lower the basal metabolic rate to preserve fat and muscle. Long-term hyperthyroidism with excessive T3 production is catabolic to bone as well as muscle.
Overworked heart--The increased work of the heart puts the greatest single demand on ATP usage, with increased heart rate and force of contraction accounting for up to 30% to 40% of ATP usage in hyperthyroidism.
Increased Oxidative Energy Metabolism--T3 and T2 increase the flux of nutrients into the mitochondria as well as the rate at which they are oxidized, by increasing the activities of the enzymes involved in the oxidative metabolic pathway. The increased rate of oxidation is reflected by an increase in oxygen consumption by the body.
Hyperthyroidism increases ATP production and thereby increases metabolic activity in the following ways:
Increased Na+/K+ATPase: This is the enzyme responsible for controlling the Na/K pump, which regulates the relative intracellular and extracellular concentrations of these ions, maintaining the normal transmembrane ion gradient. It has been estimated this effect may account for up to to 10% of the increased ATP usage.
Increased Ca++-dependent ATPase: The intracellular concentration of calcium must be kept lower than that outside the cell to maintain normal cellular function. ATP is required to pump out excess calcium. It has been estimated that 10% of a cell's energy expenditure is used just to maintain Ca++ homeostasis.
Futile cycling: Hyperthyroidism induces a futile cycle of lipogenesis/lipolysis in fat cells. The stored triglycerides are broken down into free fatty acids and glycerol, then reformed back into triglycerides again. This is an energy dependent process that utilizes some of the excess ATP produced in the hyperthyroid state. Futile cycling has been estimated to use approximately 15% of the excess ATP created during hyperthyroidism.
Heat Production: T3, has the ability to uncouple oxidation of substrates from ATP production. Resulting in reduced ATP production and an astounding production of heat. Such uncoupling occurs in skeletal muscle, contributing to T3 induced thermogenesis, with a resulting increase in basal metabolic rate. To make up for the deficit in ATP production "more" substrates (fat and muscle protein) are burned for fuel, resulting in weight loss. Muscle glycogen is also more rapidly depleted, and less efficiently stored during hyperthyroidism, which may create muscle weakness.
Increased Lipolysis: The catecholamines, epinephrine and norepinephrine, bind to the beta 2 adrenergic receptor in fat tissue and activate Hormone Sensitive Lipase (HSL). T3 results in an increased ability of catecholamines to activate HSL, leading to increased lipolysis or fat mobilization. Besides increasing beta 2 receptor density in adipose tissue, T3 upregulates this receptor in human skeletal muscle. Due to excessive T3 in more catabolic awakenings such as the first one, supplemental growth hormone might be necessary to avoid loss of fat and muscle.
The exhaustion phase of the stress response and kundalini awakenings occurs when the body's ability to cope with stress becomes depleted. At this point, adrenal hormones plummet, from excessively high to excessively low. It is this latter phase of adrenal exhaustion that sometimes accompanies, or is mistaken for low thyroid. Some scientists believe that even the entrance of thyroid hormone into our cells is under the influence of adrenal hormones. Thus, if your adrenals are exhausted, you might do well to take both adrenal and thyroid hormone together.
Where do low thyroid and adrenal stress intersect? If you find yourself in the alarm phase of adrenal stress (high levels of ACTH and high levels of cortisol), one result might be altered conversion of T-4 into T-3, or thyronine.
The level of cortisol at the cell level controls thyroid hormone production. The enzyme that is used to convert T4 to T3 is inhibited by stress, acute and chronic illness, fasting and the stress hormone cortisol. Thus a hyper-adrenal situation can reduce the availability of biologically active thyroid hormone.
When the thyroid hormone is deficient, the body is generally exposed to increased levels of estrogen. The thyroid hormone is essential for making the 'protective hormones' progesterone and pregnenolone, so these hormones are lowered when anything interferes with the function of the thyroid. The thyroid hormone is required for using and eliminating cholesterol, so cholesterol is likely to be raised by anything which blocks the thyroid function.
Thyroid disorders are more common in women than men. In women, adequate binding of T3 is dependent upon sufficient progesterone. A low level of progesterone is a common experience in both young and older women. When women stop ovulating (anovulation) this means they are not producing adequate progesterone each month, leading to progesterone deficiency. This is also a similar condition that occurs for perimenopausal women. The main causes of the cessation of ovulation include an poor diet, nutritional deficiencies, skipping meals, emotional and physical stress, and over-exercising. Thus low progesterone levels in young women interferes with thyroid efficiency and is also one of the most frequent causes of infertility. One study showed that 94% of women with PMS were hypothyroid. Progesterone deficiency in perimenopause or menopausal years can predispose a woman to hypothyroidism during this time of her life.
Estrogen dominance, that is an excess of estrogen in relation to progesterone, inhibits thyroid function and can result from taking birth control pills, hormone replacement therapy, or exposure to environmental estrogens. A poorly functioning liver, exhausted adrenal glands, insulin resistance, compromised digestion and candida can also contribute to estrogen dominance. There are receptor sites for estrogen and progesterone in every cell throughout the body. Thus the immune system, the nervous system, the circulatory system, the digestive system the vascular system, the respiratory system all are effected by the flow and proper balance between these two hormones. Thyroid hormone is required to convert cholesterol into the vital anti-aging steroid hormones, pregnenolone, progesterone, and DHEA. Pregnenolone converts to progesterone and DHEA in the body. Progesterone and DHEA are precursors for more specialized hormones, including estrogen, testosterone, and cortisol.
Heat shock proteins (HSPs), or stress proteins, are a group of proteins that are present in all cells in all life forms. They are induced when a cell undergoes various types of environmental stress like heat, cold, oxygen deprivation, poisons or signals from nerves or hormones. These heat shock proteins are sometimes called molecular chaperones, because they protect and usher other protein molecules around in the cell. They play an essential role in regulating normal protein equilibrium, that is the balance between synthesis and degradation.
Research has demonstrated that prior heat shock protects the nervous system at the functional level of neurotransmission and that specific stress-induced heat shock proteins are created tailored to elements of the synapse. This might suggest that the heat of kundalini actually protects synapses whose functionality must be preserved during stressful conditions to prevent breakdown of communication in the nervous system.
The heating of the nervous system by kundalini could increase the production of "heat shock proteins" which would protect the nerves and protein synthesis. Heat shock proteins are also present in cells under perfectly normal conditions. They act like 'chaperones,' making sure that the cell's proteins are in the right shape and in the right place at the right time. They also shuttle proteins from one compartment to another inside the cell, and transport old proteins to 'garbage disposals' inside the cell. Cells produce high levels of chaperones only briefly, even if stressful conditions persist, because too much HSP can straightjacket the cell into necrosis or cell death.
Inside the cell, heat shock proteins take the peptides and hand them over to another group of molecules. These other molecules take the abnormal peptides that are found only in sick cells and move them from inside the cell to outside on the cell's surface to help the immune system recognize diseased cells. These abnormal peptides are called antigens -- a term that describes any substance capable of triggering an immune response.
As cells age, the heat shock response doesn't function properly, just when it needs to be most efficient, but inducing extra heat shock protein has a neuroprotective effect. Stimulation of various repair pathways by mild stress has significant effects on delaying the onset of various age-associated alterations in cells, tissues and organisms. Spice and herbs contain phenolic substances which have potent antioxidative and chemopreventive properties. In particular, curcumin, a powerful antioxidant derived from turmeric, is a strong inducer of the heat shock response.
Oxidative stress has been implicated in mechanisms leading to neuronal cell injury in various pathological states of the brain. Brain seizures start cascades of cell death as the nerve cells in that area release toxic chemicals, including oxygen radicals and excitatory amino acids such as glutamate. Seizures no doubt induce a heat shock response to protect neurons from glutamate-induced excitotoxicity. Studies show protection due to heat shock requires "new" protein synthesis, since it did not occur when protein or RNA synthesis inhibitors were added.
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