"Keep More Hair AAS, but HPTA Function is Nice Too Protocol"; Insulin and Carbohydrates
by Author L. Rea
Publication Date: October 7, 2003 Nothing in this article is intended to take the place of advice from a licensed health professional. Consult a physician before taking any medication. Q1: Hello Mr. Rea. I have a question I'd like your big brain to answer. If one uses an 8 weeks protocol of 200mg week of Deca and 15 mg day of Dianabol in the morning, of what degree is the HTPA shut-down? A1: My "big brain" is at your service, Lad! As most are aware, many AAS (Anabolic-Androgenic Steroids) aromatize or convert to estrogens to some degree and estrogens shut down male androgen production by way of the HPTA. HPTA refers to the Hypothalamus-Pituitary-Testes-Axis, which is our body’s androgen regulatory system. The use of nandrolone decanoate alone can shut-down HPTA (Hypothalamus-Pituitary-Testes Axis) function even though it aromatizes at a reasonably low rate. It simply requires a longer time of activity in the system to do so when compared to most other aromatizing AAS. Interesting is that after a maximum of 28 days of nandrolone decanoate administration, at a dosage of 200-400mg/w, there is about a 40-50% average decrease in HPTA activity and its markers (FSH, LH and LHRH). But when testosterone cypionate is employed alone, 28 days of administration results in near total HPTA shut-down. The inclusion of methandrostenolone in an AAS protocol, regardless of the daily administration pattern, has severe HPTA suppressive potential. Alone and administered once daily does still result in a slightly limited degree of HPTA inhibition...though still significant. So the issue becomes what drug has been effectively used as the base and could another be added. When it comes to hair loss some men feel that, though natural, it is near comparable to castration, while others seem to care not at all. Each of us carries a genetic encoding for hair loss. Our hormone profiles dictate the rate and degree of loss. The three primary hormones having the greatest effect upon hair loss are DHT, estrogen and IGF-1. Each plays a role and must act in symphony to trigger an increased rate of drain clogging hair suicide. When DHT is blocked, but estrogen and IGF-1 are present, hair expenditure is slowed...but not stopped. If IGF-1 is blocked, or estrogen, the same is true again. *An interesting fact is that I have noted that many who use 500mg of Cytadren and 20mg of Tamoxifen daily in divided doses tend to retain hair better than those who opt for other off-cycle estrogen/cortisol suppression protocols. The answer may be in that Tamoxifen inhibits IGF-1 activity while it blocks estrogen receptors and Cytadren inhibits cortisol formation and acts as an estrogen biosynthesis inhibitor. The key may be additional control of stress hormones as well as one of the evil three. So the basis for a reasonably successful "Keep More Hair AAS, but HPTA Function is Nice Too Protocol" has been a 28 day structure alternating nandrolone decanoate and methenolone enanthate. The intent being to decrease DHT and estrogen activity while exiting at a point of reasonable HPTA function. The aromatization product of nandrolone is nor-17b-estradiol, which is much weaker than the aromatization by-product of testosterone (17b-estradiol). This means less of an HPTA negative feed-back loop and less negative hair follicle activity. Methenolone is a DHT derivative but the drug itself is less active upon hair follicles than DHT itself. This oddly enough has a "short term" anti-DHT effect. Since DHT derivatives are not affected by the 5-alpha-reductase or aromatase enzymes there is no resulting increase in DHT itself or estrogen. Alternating these drugs appears to allow for the best of both worlds with a decrease in potential hair loss. The addition of 12.5-25mg 2xd of Oxandrolone has also been noted to result in some very high quality lean tissue growth. Warning: This is an example intended for discussion purposes only. The use of any drug must be under the guidance of a licensed health care professional only. "Keep More Hair AAS, but HPTA Function is Nice Too Protocol Example" Day
| 1. Nandrolone Decanoate 400mg | | 2. | | 3. | | 4. | | 5. | | 6. | | 7. | | 8. Methenolone Enanthate 200mg | | 9. | | 10. | | 11. | | 12. Methenolone Enanthate 200mg | | 13. | | 14. | | 15. | | 16. Nandrolone Decanoate 400mg | | 17. | | 18. | | 19. | | 20. | | 21. | | 22. | | 23. Methenolone Enanthate 200mg | | 24. | | 25. | | 26. | | 27. Methenolone Enanthate 200mg | | 28. |
*Any of the many HPTA stimulation protocols I have written in the past would layer well over this example…obviously. Q2: Hey, I have just started taking Humulin-R (about 3-4 days ago/once in the morning and once after I workout. I take 5 iu's in the morning and 10iu's after my workout. My question is this (since this is the first time using insulin.) Am I taking in carbohydrates too early if I am consuming them about 15-20 minutes after the humulin shot? The reason I ask this is because I have not noticed any signs (and not that I want to) of low blood sugar levels. Everything seems exactly the same as when I never used insulin. I know this can be dangerous but one morning (not after a workout) I drank a protein/carb drink consisting of 40grams of whey protein isolate and only 25 grams of carbs from 1% milk (no dextrose, glucose, sucrose, etc. I know milk is definetely not a good source to raise blood sugar levels but I have read that it is high on the insulin index. Anyways, with that low of carbs with a 10 iu insulin injection I was sure that better be prepared for the effects of low blood sugar in a few hours. But guess what - nothing, nada. No low blood sugar levels, no feeling bad, no headaches, no hunger and no disorientation. Believe me I know how it feels to have low blood sugar levels because I would get them when I was playing basketball at the age of 13-14 years old. I would begin to sweat a lot, my hands would slightly tremble, I would get dizzy and I would have a strong craving for chocolate and potatoe chips (the potatoe chips I never understood). I think I may switch to just using the humulin after my workout but should I use it on my days off from weight training and cardio. A2: The average accepted amount of "necessary carbohydrates" to ingested per iu of insulin administered is 10g. This was originally coined by the late and great Dan Duchaine…with no medical or physiological basis for reasoning. Like most, I liked Dan when he would let us, and commonly refer to his near genius insights. But he was sometimes wrong or had simply errored to the side of safety. Those who have read "Big Fat Bastard and Insulin" are well aware of a few protocols that include moderate dosages of insulin yet require no carbohydrates whatsoever. This is due to the fact that the body does have pathways for making necessary blood glucose, in moderate amounts, other than from carbohydrates. GLUCOSE Glucose is the body’s preferred energy substrate. Though the brain’s nutrient make-up is nearly 1/3 omega-3 fatty acids, it is glucose that is without fail mandatory for continued sentience. So carb up a little and read closely as we learn a few things about the body we have been entrusted to play nice with. When we ingest food stuffs in the form of the three macronutrients protein, carbohydrates, and fats the GI track introduces a series of chemical Action/Reaction Factors that result in the break-down of these nutrients to metabolic substrates. Proteins = amino acids Carbohydrates = glucose Fats = fatty acids It appears simple on the surface but in fact glucose can be converted to triglycerides and adipose tissue or lean tissue glycogen stores and toilet tinkle. Like wise fatty acids can be stored as fat or utilized as an energy substrate by the body’s tissues but it cannot be converted to glucose. This is interesting when one considers the fact that carbohydrates can become glucose or fat, but fat cannot become glucose (though the cellular mitochondria can use fatty acids as an energy substrate as a keto response). Protein is ultimately destined to become amino acids employed for cellular repair and growth or intimate moments with the bathroom. But certain amino acids called gluconeogenic amino acids can be converted to glucose too. This can be disastrous for a bodybuilder who hopes to be a beast one day since lean muscle mass is predominantly made up of protein in the form of amino acids and a complete spectrum is necessary. We will get to this later. For now simply accept that glucose is necessary for life and bodybuilding progress alike. The average circulatory value for glucose allows for about only 4 grams of glucose. It is actually uncommon for blood glucose levels to rise beyond an additional 1.5-2.0 grams or to drop below the 4 gram mark. A healthy individual who ingests a meal containing 50-150g of mixed carbohydrates will realize the normal increase in circulatory glucose for only about an hour. Interesting thing here is that endogenous (made by the body) insulin secretion will remain elevated for an additional 2 hours after glucose clearing. When the same individual ingests 300g of carbs (Fat Bastard) at one time the resulting insulin secretion levels will be 300% above normal for an additional 7 hours after blood glucose clearing. This is clearly a highly anabolic environment, but after tissue glycogen stores reach maximum levels a grotesque amount of the excess glucose finds its way to adipose tissue. And don’t worry. If all of the existing fat cells are full, the body is way to happy to make new ones to secrete lots of aromatase enzyme. And herein awaits the key to greater lean mass tissue and a decrease in adipose tissue. GLUCONEOGENESIS Gluconeogenesis is the biosynthesis of new glucose. This means that glucose is synthesized from substrates other than carbohydrates or glycogen stores. Obviously since the only source of fuel for the brain, testes, kidneys, and erythrocytes is glucose the body in its amazing adaptive manner can manufacture glucose from other materials. Those who are up on keto diets are aware of the fact that the body can derive energy from ketone bodies (which are converted into acetyl-CoA). But that is an entire different topic for now. In short the body utilizes the carbon structures within substrates to create energy in the eventual form of ATP (adenosine triphosphate). ATP is cellular energy that, as readers are aware, is the body’s only energy currency. In the case of gluconeogenesis the carbon structures can come from other sources. Triglycerides Too? Triglycerides are structures consisting of three fatty acids adjoined by a glycerol molecule. By cleaving the fatty acids away from the glycerol molecule the body can utilize the freed glycerol molecule to make glucose through a series of conversions and subsequent carbon utilization. Back To Amino Acids With the exception of lysine and leucine all 20 (or 22 if you are of that school of thought) amino acids can be turned into TCA cycle intermediates which in turn allows for the carbon skeletons of the amino acids to be converted to pyruvate. The newly formed pyruvate can then be utilized by the gluconeogenic pathway to create glucose by way of another series of metabolic pathways. Let me explain that a little better. When glycogen stores in the liver and muscle are depleted the working/recovering muscles, brain and organs need another energy source. Catabolism of muscle tissue proteins to amino acids becomes the main source of carbon skeletons for the maintenance of mandatory blood glucose. As you will recall the body can clear 50 –150 grams of carbohydrates in only a few hours. So how much muscle do you think the gluconeogenic adaptive process can munch in the same period of inadequate nutrient supply from diet? By the way, the amino acid Alanine is the favorite gluconeogenic snack with Arginine and Glutamine coming in as close seconds. THINK ABOUT IT In the presence of circulatory insulin elevation gluconeogenesis in the liver and muscle tissue decreases. During periods of circulating supraphysiological levels of amino acid muscle catabolism decreases. In the presence of both protein synthesis occurs. So it would seem that the two choices a wanna-be beast faces is 300 grams of carbohydrates to induce a sufficient prolonged insulin spike and a Big Fat Bastard pose down or non-stop keto diets and declarations of "Hey, I may look like a weenie but I am really cut" for life. *The obvious solution is an elevation in both circulatory insulin and a corrected amino acid pool rendered highly efficient by design and not by chance. One Sentence Summery In summary it is the use of the fast acting whey protein that is preventing hypoglycemia during insulin administration…and the accumulative fat that normally comes with it for many. |
