According to Mr. Rea, biochemist
THYROID HORMONES
Thyroid hormones were most likely one of the most misunderstood and underrated drug groups in the bodybuilder’s so-called arsenal. Based upon personal experiences, they certainly increased the rate and efficiency of fat loss during diet periods. And they acted synergistically to increase the rate of lean tissue growth during mass gaining periods….if used correctly.
The noted positive physiological effects of reasonable dosages of thyroid hormones included:
*Increased protein synthesis rate.
*Increased rate of fat oxidation.
*Increased sensitivity of receptors for androgens, Insulin, GH, IGF-1, PGE-1, PGF-2, Clenbuterol, Ephedrine, Creatine, and others.
*Increased metabolization of proteins, carbohydrates, fats and micronutrients.
*Increased metabolic rate and calories expenditure.
*Enhanced oxygen consumption by most body tissues
*Improved recovery time.
The noted negative physiological effects of excessive dosages of thyroid hormones included:
*Loss of lean mass tissue.
*Increased heart rate and palpitations.
*Insomnia.
*Diarrhea.
*Vomiting.
Thyroid hormones govern the body’s metabolic rate. This means that the metabolism of nutrients and subsequent cellular utilization or storage rate is dependent upon blood circulatory thyroid hormone levels. Higher levels result in elevated over all metabolic rate providing that other metabolic factors are accommodated also.
THYROID HORMONES AND CALORIE EXPENDITURE
Those who are familiar with, or have read the section on DNP are aware of the term “oxidative phosphorylation”. This is a process by which cells/mitochondria convert ADP (Adenosine Diphosphate) into ATP (Adenosine Triphosphate). Basically this means adding another phosphate molecule to ADP so that it can be converted back into the body’s energy /ATP. But the term keeps kids flunking biology anyway. DNP makes cells waste calories and burn fat by “uncoupling” the oxidative phosphorylation process and making it less efficient, even when at rest.
Thyroid hormones are powerful uncouplers of oxidative phosphorylation. However this is a different method of action than that induced by DNP. Thyroid
hormones increase cell/mitochondrial substrate oxidation by effecting both cytochrome-C reducers and cytochrome-C oxidizers. This increases metabolic rate and substrate (nutrient/food) use as fuel for either ATP or heat production. Heat production by a cell is referred to as thermalgenesis, in this case the conversion of fat into heat. Though other substrates such as glucose /glycogen can be used for heat production also under adverse conditions.
THYROID HORMONES AND FAT OXIDATION
Fat oxidation or thermalgenesis involves the conversion of fat calories into heat. In the case of thermalgenesis caused by thyroid hormones it is due to “special uncoupling proteins” found in fat, muscle, and organs called UCP-3. Two things before we continue here. First UCP-3 stands for uncoupling protein -3 (big deal) and “special” refers to “specific”, not “special” like the weirdo we all dated once and tried to explain later. When UCP-3 is increased, the calorie expenditure through thermalgenesis increases. But decreases will result in an increase in fat stores. As example, supraphysiological T-3 levels increase UCP-3 600 % and below normal levels results in a 300 % decrease. This is why calorie restricted diets significantly decrease in results after 2-4 weeks. The body down-regulates thyroid hormone production to save calories and reduce calorie expenditure as heat. The result is less UCP-3 and slower metabolism.
Thermalgenesis and oxidative phosphorylation uncoupling is the reason athletes used synthetic thyroid hormones during calorie restricted or diet phases. The individuals were able to ingest more calories than normal while still burning fat. It should be noted that a minimum of 2 grams of protein per pound of body weight was ingested daily during exogenous thyroid hormone use to prevent excessive muscle catabolism or loss. Athletes commonly stacked adrenalgenic beta-agonist drugs like Clenbuterol, Ephedrine/Norephedrine, or Fenoterol to increase UCP-3 levels and act synergistically with thyroid hormones to favor fat oxidation and reduce muscle loss. DNP was another option commonly used as well. Obviously, anabolic/androgenic steroids, Insulin, GH, and other growth enhancement drugs were commonly stacked with thyroid hormones too.
THYROID HORMONES ARE ANABOLIC
Many athletes were not aware of the fact that thyroid hormones are a true form of absolute anabolic. The usual method of employment for thyroid hormones was during pre-contest periods. Obviously, this is because increased thyroid hormone levels means elevated metabolic rate and resulting increased calorie expenditure or use. This explanation itself suggests the noted anabolic potential.
Thyroid hormones govern or regulate our metabolic-rate or metabolism. Metabolic rate is the speed or rate at which all chemical and physical processes occur. This is true of every living cell in our bodies. This means that the rate of nutrient metabolism, absorption, and utilization is vastly dependent upon thyroid hormones. In
fact the levels of thyroid hormones in our body determines if the food we eat is stored as adipose (fat) tissue, utilized for regeneration and building, or burned as heat /energy. How often have you heard some whale claim “it’s glandular” as they stuff another box of donuts in their mouth? In some cases it is actually the truth. So fix it!! Low thyroid hormone levels slow the healing / growth process while increasing fat stores. Overly high thyroid hormone level results in tissue catabolism or wasting. But thyroid hormone levels matched to nutrient supply and demand were commonly considered to be seriously anabolic. Remember, training and chemical muscle enhancement protocols created a massive nutrient demand. If thyroid hormone levels are too low, no amount of calories will be an adequate supply simply because they are not metabolized at the necessary rate. This is why athletes often got needlessly big-time fat. They ate to keep up with major muscle chemistry, but failed to provide a metabolic rate to match.
*The administration of thyroid hormones should be under a doctors care only.
WHY ARE THYROID HORMONES ANABOLIC?
Thyroid hormones trigger the release of fat stores so other cells can convert the long chain triglycerides (fat) into heat, energy, ATP. By increasing ATP, muscle cells are better able to regenerate, and do so at an increased rate. Thyroid hormones increase creatine transport and increase androgen/GH/IGF-1/IGF-2 receptor-site sensitivity. Thyroid hormones increase the rate of nutrient metabolism, absorption, and utilization. Gee, sounds like the perfect growth environment to me when considering the fact that growing children do this naturally so well. It also meant major chemical muscle enhancement synergy for those whom reported use.
Many would be surprised to realize how many top bodybuilders remained “on cycle” with thyroid hormones all year long. This allowed maximum growth and recovery rates while preventing excessive fat accumulation even in the very brief “off season”.
The difference in diet and mass phases was dosage, though some altered the term dosage to mean “available”. Why did they include thyroid hormones in their mass stacks?
Thyroid hormones can have a re-partitioning effect upon body composition or muscle-to-fat ratio. As example were the many athletes whose weight was 250 LBS but only 10% bodyfat when total daily circulating thyroid hormone levels were elevated 10- 50%. This would be due to thyroid hormone activity inducing improved nutrient metabolization and cellular efficiency combined with other hormone synergy. Of course, this is what “Absolute Anabolic Phases” were all about. But those who read about” Frank
N. Steroid” already know about this effect and how it was created.
NATURAL THYROID HORMONE PRODUCTION IN HUMANS
The thyroid is a part of the endocrine system. The endocrine system monitors and manufactures or synthesizes many hormones and hormone-like substances. For this reason, the endocrine system and its sub-systems have many built in “checks and balances” to assure proper substance ratio or synergy. It is no surprise that thyroid functions are no exception.
*Endogenous thyroid hormone production begins when neuro-input tells the hypothalamus to synthesize an release Thyroptropin -Releasing -Hormone. (TRH)
*TRH stimulates the anterior pituitary gland to release or secrete Thyroid-Stimulating- Hormone (TSH) (also referred to as Thyrotropin on some lab chem. Panels)
*When TSH contacts its receptor-sites located throughout the thyroid gland a series of enzymic reactions occur using tyrosine and iodine as substrates or raw materials to produce and/or release L-Thyroxine (T-4). This is then released into the vascular system so it can circulate. It should be noted that T-4 is an active form of thyroid hormone.
*The active T-4 circulating in the vascular system merges with receptors and triggers metabolic activity; but when it reaches the liver it is changed into the more active thyroid hormone L-Triiodothyronine (T-3) by an enzyme called 5-deiodinase. T-3 is about 5 times more active than T-4. The newly formed T-3 is released into the vascular system where it may contact and merge with cellular receptors which initiates all the metabolic activity discussed earlier.
FEED-BACK MECHANISMS and FEED-BACK LOOPS
Of course the thyroid does not simply produce T-4 continuously. This is due to the “checks and balances” nature included called “feedback-mechanisms”. In the care of thyroid function the feedback-mechanism or loop involves the hypothalamus (secretes TRH), pituitary gland (secretes TSH), thyroid gland (secretes T-4), and the liver (converts T-4 into T-3). A feedback-mechanism or loop can trigger the release of another hormone (positive feed-back), or inhibit its release (negative feed-back) thus maintaining that balance. This means high levels of T-4 or T-3 initiate a negative feed-back loop that tells the hypothalamus to produce less TRH, and low levels of T-4 or T-3 initiate a positive feed-back loop that tells the hypothalamus to produce more TRH.
*Individuals reported the utilization of doctor prescribed blood tests for their personal average thyroid hormone levels before, during, and after thyroid drug administration as a means of base line dosage requirements and assessment.
*Thyroid gland function also regulates calcitonin which combats elevated levels of calcium.
*The normal thyroid gland (human) contains about 200 MCG of T-4, and 15 MCG of T-3 per gram)
*About 80% of circulatory T-3 comes from Monodeiodination (T-4 to T-3 liver conversion) of T-4.
*It should be noted that only “free” or unbound thyroid hormones are active and the bound form is not. When reviewing blood test results and reference ranges this is an important factor to assess. The human body normally produces about 76 MCG/daily of T- 4 and 26 MCG/daily of T-3. A mid range test result/reference would express these approximate averages. Over 99% circulating hormones are bound. Thyroid Binding Globulin (TBg) Thyroid binding pre albumin (TBPA) and albumin (TBA) .
HEALTHY THYROID HORMONE REFERENCE RANGES
TSH (Thyroid Stimulating Hormone Serum/Plasma 2-10 M U/L T-4 (L-Thyroxine) Total serum 65-155 NMOL/L
T-4 (L-Thyroxine) Free Serum 0.8-2.4 NG/DL (or) 10-31 PMOL/L TBG (Thyroxine Binding Globulin ) Serum 15.0-34.0 MG/L
- (L-Triiodothyronine) Serum 100-200 NG/DL (or) 1.54-3.08 MMOL/L T-3 (L-Triiodothyronine) Serum 260-480 PG/DL (or) 4.0-7.4 PMOL/4L
NOTES OF INTERESTS
*According to researchers, calorie restricted periods that provide less than 2 grams of complete protein per pound of bodyweight daily during thyroid drug administration usually resulted in weight loss consisting of 75% fat and 25 % muscle in most cases.
*The 5-deiodinase enzyme activity necessary for liver conversion of T-4 into T-3 requires adequate levels of zinc and selenium. During calorie restricted periods lasting more than 2-3 weeks T-4 conversion to the more active T-3 decreases dramatically greatly reducing fat loss. Adequate zinc intake and absorption prevents the decline in 5- deiodinase that causes this negative by about 67% and adequate selenium levels prevents the decline by about 47%. Obviously both in sufficient amounts are best.
*Thyroid hormones were commonly cycled with Insulin, AAS, GH, IGF-1, PGF-2, Ephedrine, Clenbuterol, and other drugs by athletes.
