Avoid Milk and Sugar for a Clear Complexion

Acne sucks and no one likes it….

Why is it so prevalent in our present times and how can we rectify this current epidemic? 

Well, an interesting, yet alarming tidbit is that currently 85% of our adolescents are experiencing acne as well as men and women in their twenties. It is common knowledge to assume the main culprit of this problematic condition is hormone related, and pubescent teens are pulsing the greatest hormone production of their lives during these times. Fluctuating hormone levels do elicit side effects such as acne, BUT there might be some environmental factors that are magnifying these effects.

Let's face it, our current nutritional guidelines that are being recommended is insanity. High carbohydrates, low fat and low protein based nutrition. Also, how many teenagers do you know that adhere to meticulous nutritional regimens and properly stay hydrated and avoid excessive empty calories and other "anti-nutritious" foods?

I would guess your answer is "not many." 

Recent research has demonstrated that the consumption of milk and dairy-based products are major players in contributing to the acne epidemic we currently face. Milk is loaded with hormones and growth factor's such as; bGH (bovine growth-hormone) IGF-1 and also trigger's insulin release. Elevated plasma IGF-1 levels from milk further exacerbate endogenous production of hormones that are already high during puberty. The presence of 5a-pregnanedione, 5a-androstanedione and other precursors of 5a-dihydrotestosterone add to the potency of milk to increase the formation of acne. 

Most cheaper milk products currently available derive milk from prenatal cows, which are jacked full of hormones from the pregnancy. DHT is then transferred into the milk product and then consumed by adolescents and young adults in conjunction with their sugary morning cereal!

(High consumption of milk & high glycemic carbs like French fries can trigger acne)

 Let's consider the role DHT plays on the production of sebum. As DHT gets elevated from milk consumption, new sebocytes are produced which ignite more sebum production, which trigger more acne. This vicious cycle is even further magnified by a diet rich in sugar and high-glycemic carbohydrates. Sugary foods with high glycemic loads will induce abrupt pulses of insulin production by the pancreas. The bolus amount of insulin will also spike IGF-1 levels, which are already high in teens and young adults to begin with. 

IGF-1 is a mitogen and after IGF-1 attaches to its receptor sites in various tissues, it induces cell division, cell proliferation, and prevents cell apoptosis (which is the death of cells) Keratinocytes (epidermis cells), sebocytes (epithelial cells) as well as the adrenals and gonads, which get stimulated by IGF-1 production.

Here is something to think about – 

Notice how you will occasionally see what appears to be a young women, meaning fully developed and looks "of age,' then your jaw drops when you realize that this young female is 12 or 13 years old…..

There is sound reasoning for this mind-boggling occurrence. It would be unethical and twisted to inject 8-9 year old females with several hormones such as; estrogen, progesterone, prolactin, testosterone, IGF-1, rHGH and various other growth factors right? Well drinking milk in high amounts is doing just that – saturating their endocrine system with a multitude of growth spurting, powerful hormones. There is research indicating that average height's and body weights of young females have increased dramatically in the last 50 years. I suppose drinking a substance that contains over 59 bio-active hormones can have such an affect.

Back to the subject at hand pertaining to dairy & sugar promoting a greater incidence of acne.

What can be done?

Well, for starters stay away from milk or dramatically decrease its consumption. I would suggest exchanging milk for Almond Milk or Coconut Milk. These 2 substitutes are low in calories and do not contain unpredictable hormonal fluctuations and contain MCT fatty acids (coconut milk) & Monounsaturated fatty acids (almond milk). Trust me – YOU CAN STILL ENJOY CEREAL! Of course to keep insulin under control and igf-1 levels stable, the cereal selection should be scored low on the glycemic index and be enriched with dietary fiber

Some useful herbal based supplements to take for insulin control would be gymnema sylvestre, banaba leaf, bitter melon and cinnamon. For pharmaceuticals Metformin also known as Glucophage would lower IGF-1 levels and keep insulin and blood sugar at low baseline levels.

If persistent acne stays with you well into adulthood, you need to take charge immediately and get your IGF-1 levels down. As adulthood acne may be considered a health risk factor for increased risk of cancer, which will require dietary modifications and proper natural or pharmaceutical treatment of insulin-sensitizing agents.

As always, I write these articles to give you (the reader) something to think about and consider. Do I personally stay away from all dairy products? I would be a liar if I said yes. I eat cottage cheese, low-fat mozzarella cheese, Greek yogurt (occasionally), and as a competitive Bodybuilder, various forms of dairy protein in powder form is consumed at key times of the day. I do however; avoid milk consumption and use almond & coconut milk instead. 

If you suffer with mild to severe acne, try eliminating the consumption of dairy products and also monitor your carbohydrate intake, namely simple sugars. I personally adhere to high fluid intake to constantly stay hydrated and to flush toxins out of the body. I find when I drink 2 gallons of water per day, my complexion improves dramatically.

 

References:

1.)Danby FW.Nutrition and acne.Clin Dermatol. 2010 Nov-Dec;28(6):598-604.

2.)Melnik BC, Schmitz G.Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris.Exp Dermatol. 2009 Oct;18(10):833-41. Epub 2009 Aug 25.

3.)Melnik BC.Evidence for acne-promoting effects of milk and other insulinotropic dairy products.Nestle Nutr Workshop Ser Pediatr Program. 2011;67:131-45. Epub 2011 Feb 16.

4.)Melnik B.[Acne vulgaris. Role of diet].Hautarzt. 2010 Feb;61(2):115-25. 

5.)Melnik B.Milk consumption: aggravating factor of acne and promoter of chronic diseases of Western societies.J Dtsch Dermatol Ges. 2009 Apr;7(4):364-70. Epub 2008 Feb 20.

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Opioid Modulation for Preventing AAS Induced HPTA Suppression.

Suppression of the HPTA (Hypothalamus, Pituitary, Testicular Axis) is seemingly unavoidable during a steroid cycle. What I will be presenting in this article is a new idea to the world of AAS users. This exciting new concept addresses the possibility of limiting and possibly preventing suppression of the (HPTA) during cycle. More specifically, I will show you how to actively modulate the hypothalamus & pituitary pulse generator during cycle and how this can prime our endocrine system for a quicker, smarter, and healthier recovery from anabolic androgenic steroids (AAS).

For a moment, let’s forget the concept of “post cycle therapy”, and embrace the idea of “on cycle therapy” – active therapy throughout a steroid cycle. The HPTA involves a constant biological interplay of responses and feedback loops that can ultimately become shutdown and degraded during AAS administration. However, research suggests suppression of the hypothalamus and pituitary may be preventable during steroid use. Before we delve into the details, lets first take a quick recap on the HTPA and how it responses to AAS.

HPTA ñ The basics

When the hypothalamus senses low hormone levels, it secretes gonandotropin releasing hormone (GnRH). This GnRH then travels a short distance to the nearby pituitary gland to stimulate the release of the gonadotrophins — luteinizing hormone (LH) and follicle stimulating hormone (FSH). These gonadotrophins travel all the way down to the testes, to activate their respective leydig and seritoli cells. LH initiates testosterone production by stimulating the leydig cell receptor (steroidogenesis), while FSH initiates sperm production by stimulating the sertoli cell receptor (spermatogenesis).

AAS’s inhibit hormone production just as your body’s own hormones do. Testosterone interacts with the androgen receptor (AR) and estrogen interacts with the estrogen receptor (ER). When these hormones are in high concentration, they cause the hypothalamus to decrease its release of GnRH, which decreases LH and FSH production from the pituitary. (1) This cuts off the signal to the testis and halts all hormone production. This process is a daily event for the rhythmic endocrine system. Spikes in LH & FSH are followed by spikes in testosterone, and spikes in testosterone result in a reduction of LH & FSH release until testosterone levels decline and LH & FSH is released again. The caveat with most steroids, is that hormone levels remain chronically high (24/7) and do not allow release of LH or FSH, thus leaving the pituitary and testis in a dormant state for as long as the steroids are administered.

While low-dose on-cycle hCG is a good protocol to mimic LH and keep the testes from atrophy, (discussed here) it won’t help prevent pituitary atrophy. We forget that the pituitary is susceptible to the same degradation and atrophy as the testes. That is, when the GnRH secretion from the hypothalamus stops (during a steroid cycle), the pituitary reduces its number of GnRH receptors and becomes less and less responsive to GnRH stimulation as time goes on. (11) This is analogous to atrophy of the testis, during absence of an LH or FSH signal. On the other hand, both the pituitary and testis will decrease receptor concentration during over stimulation as well, as its been found from too much hCG use or too much GnRH stimulation.(12,13) The point here, is that only minor stimulus is required for the preservation of sensitivity in the endocrine organs. Perhaps a completely neglected and suppressed pituitary (or testes) may explain the lack of full and prompt recovery for many steroid users, despite adherence to a “tried and true” PCT regimen. So the question is ñ How can we prevent suppression of the testes, and better yet, how can we prevent suppression of the pituitary?

A closer look ñ

There are several ways that steroids can inhibit LH & FSH release from the pituitary based on the receptors they occupy, and this is important to understand if you plan on blocking AAS induced suppression. For instance, it appears that AAS which bind strictly to the AR only inhibit LH & FSH release by suppressing GnRH release from the hypothalamus (ie Primobolan, Proviron, Anavar or Masteron). (34,37,39) However, AAS which possess estrogenic (ER) or progestogenic (PR) activity inhibit LH & FSH by directly down-regulating the GnRH receptors on the pituitary, while also reducing GnRH release from the hypothalamus. (35,38) Therefore, progestin based AAS such as trenbolone and nandrolone are “double suppressive” because they are binding to the AR and PR and suppressing LH & FSH by two different mechanisms. (36) The same can be said for steroids that aromatize, such as testosterone or methandrostenolone since they can activate both AR and ER receptors.

Evidence suggests that estradiol is about 200x more suppressive than testosterone on a molar basis (37), and that administration of Arimidex can greatly reduce testosterone’s suppression of LH release. (42) However, since progesterone based AAS’s such as nandrolone and trenbolone are inherently progestogenic based on their hormone structure, there is no way to prevent them from activating the PR. Therefore, it’s virtually pointless to try to block the suppression from progestin based anabolics. However, we can block suppression from the ER by using either non-aromatizing AAS’s or aromatase inhibitors. So this now leaves us with suppression of LH & FSH via the AR, but this suppression can be blocked, and that’s exactly what I’m going to show you.

When it comes to suppression of the hypothalamus, there is more than a simple on/off switch for the hypothalamus control center. Evidence suggests that there isn’t even a direct AR or ER receptor on GnRH secreting neurons. (2-6) Meaning, steroid hormones do not directly influence GnRH release from the hypothalamus, but actually communicate through an intermediary. (7)

It was well summarized here by A. J Tilbrook et al,

“It follows, that the actions of testicular steroids on GnRH neurons must be mediated via neuronal systems that are responsive to steroids and influence the activity of GnRH neurons.”

And again here by FJ Hayes et al,

“It was thus postulated that estrogen-receptive neurons were acting as intermediaries in the non-genomic regulation of GnRH by estrogen”

There is a network of neurogenic intermediaries in the hypothalamus governing GnRH release from steroid hormone influence. More specifically, it is the combined efforts of neuro-active peptides and catecholamines which send the message of “suppression” to the GnRH neurons once activated by steroid hormones. (16) These primary messengers are known as a group of neuro-active peptides called endogenous opioid peptides (EOP’s). (7,16) The EOP’s consist of the three main peptides — b-endorphin, dynorphin, and enkephalins, which act upon their respective u-opioid, k-opioid, and s-opioid receptors. It appears that the most influential EOP in GnRH modulation is b-endorphin, acting upon the u-opioid receptor. (8-10) For this reason, b-endorphin will be the main focus of the article (although there are other minor intermediates involved.)

When steroid hormones reach the hypophysial portal, they activate the EOP’s, which suppress GnRH and consequently suppress LH & FSH. We know that steroid hormones must communicate with these opioid receptors in order for them to inhibit the release of GnRH from the GnRH neurons, since the GnRH neurons do not have their own AR or ER receptors. What’s most interesting here is that the suppression on GnRH neurons can actually be intercepted by a u-opioid receptor antagonist ñ such as naloxone, and the orally active congers naltrexone, and nalmefene.

This is accomplished by blocking the u-opioid receptor and preventing the inhibitory effects of b-endorphin upon the GnRH releasing neuron. It should be noted that this “antagonism” of suppression is not due to antagonism of the AR or ER itself, since u-opioid antagonists to not bind to hormone receptors. (15,32)

The effect of a u-opioid receptor antagonist on the HPTA is demonstrated here —

Essentially, a u-opioid antagonist such as naloxone takes the brakes off of GnRH release and allows pulses of GnRH to occur as if no steroid hormones are present. (17) Naloxone, and related u-opioid antagonists have consistently proven to block the suppressive effects of testosterone, DHT, and estrogen administration in both animals and humans. (18-25) It also appears that these drugs have the ability to increase pituitary sensitivity to GnRH. (26,27)

U-opioid antagonists have long been used for treatment of opioid dependence; not only to control cravings of narcotics, but to restore a suppressed endocrine system. (28,29) It’s well known that strong opioid based drugs such as methadone, cocaine, heroin and alcohol can suppress GnRH and therefore suppress LH & FSH. It seems that this decease of GnRH, LH & FSH is due to the same EOP mechanisms seen with AAS induced suppression. (33) In alcoholics, cocaine and heroin users, naltrexone and naloxone have been used to restore LH and testosterone levels. (28,29) Naltrexone has even been proposed as a treatment for male impotence and erectile dysfunction. (30,31)

Naloxone, naltrexone and nalmefene seem progressively more powerful in their potency to block b-endorphin, respectively. (14,18) Naloxone lacks oral bioavailability therefore injection is required. An injectable preparation could easily be made with BA water due to the water solubility of the compound. A 40mg subcutaneous injection would be a typical dose of naloxone. Naltrexone is orally active, with a safe and effective oral dose being about 100mg for a 220lb male. (18) While a lower dose of about 25-50mg of nalmefene would seemingly have the same benefit. (20,24) Increasing the dose of these drugs will surely increase the likelihood of side-effects without notably increasing the benefit. A twice a week dosing protocol would seem appropriate with these drugs, as only to increase GnRH and LH release enough to prevent pituitary and testicular shutdown ñ Just enough to keep them in the “ball game” so to speak. Also, a twice a week dosing protocol would most likely limit the increased opioid sensitivity induced by the long-term use of the drugs.

A word of caution: The opioid antagonists mentioned in this article are recognized as safe and non-toxic at the given dosages; however they can cause severe withdrawal symptoms in opiate users (methadone, morphine, cocaine, and heroin addicts.) Caution is also advised when using opioid antagonists prior to sedation or surgery as they can reduce effectiveness of anesthetics. Temporary nausea, headache or fatigue, are occasional side-effects associated with the use of these drugs. Naltrexone has been reported to heighten liver enzymes, while naloxone and nalmefene do not appear to have this issue. At any rate, a twice a week protocol for 4-16 weeks is unlikely to cause any liver issues that may be associated with naltrexone. Contrary to popular believe, opioid antagonists do NOT have any addictive properties.

A few points to consider –

For those who choose to embark on an opioid antagonist protocol several things should be considered.

  1. Remember, progestin based anabolics such as trenbolone and nandrolone are “double suppressive” because they desensitize the pituitary directly by PR activation. It also appears that no opioid receptor antagonist or aromatase inhibitor can prevent suppression via the PR. Therefore, trenbolone or nandrolone are going to cause unavoidable inhibition of HTPA function by causing suppression via the ER, AR and PR. (40,41) If one hopes for a prompt and full recovery post cycle, perhaps progestin based anabolics are better avoided, or at least limited in duration of use.
  2. As it was pointed out earlier in this article, estrogen has a markedly stronger effect on suppression of LH release compared to androgens since estrogen suppresses the hypothalamus and pituitary. Usage of an AI such as anastrozole, letrozole, or exemestane (Aromasin) can reduce estrogen and greatly reduce suppression on GnRH, LH and FSH release by preventing excessive ER activation in the hypothalamus and desensitization of the pituitary GnRH receptors. (35,37,38) Anastrozole has ~50% maximal total estrogen suppression at 1mg/day. Exemestane has ~50% maximal total estrogen suppression at 25mg/day. While letrozole has ~60% at 1mg/day. These are averages based on compiled data from several studies. Similar estrogen suppression can also been seen from only twice a week administration of these AI’s. (43-47)

References

1. Hypothalamic Gonadotropin-Releasing Hormone: Basic and Clinical Aspects.
Yen SSC
Raven Press, New York, pp 245ñ280 (1991)

2. Absence of androgen receptors in LHRH immunoreactive neurons.
Huang X, Harlan RE.
Brain Res 1993; 624:309ñ311

3. Augmented hypothalamic proopiomelanocortin gene expression with pubertal development in the male rat: evidence for an androgen receptor-independent action.
Kerrigan JR, et al.
Endocrinology.128:1029-1035. (1991)

4. Distribution of estrogen receptorimmunoreactive cells in the preoptic area of the ewe: co-localisation with glutamic acid decarboxylase but not luteinizing hormone-releasing hormone.
Herbison AE, et al.
Neuroendocrinology 1993; 57:751ñ759.

5. Unmasking the neural progesterone receptor in the preoptic area and hypothalamus of the ewe: no colocalization with gonadotropin-releasing neurons.
Skinner DC, at el.
Endocrinology 2001; 142:573ñ579.

6. Multimodal influences of estrogen upon gonadotropin releasing
hormone neurons.
Herbison AE.
Endocrine Reviews 1998; 19:302ñ330.

7. Negative Feedback Regulation of the Secretion and Actions of Gonadotropin-Releasing Hormone in Males
A.J. Tilbrook and I.J. Clarke
Biol Reprod, Mar 2001; 64: 735

8. Steroid Control of Gonadotropin-Releasing Hormone Secretion: Associated Changes in Pro-Opiomelanocortin and Preproenkephalin Messenger RNA Expression in the Ovine Hypothalamus
James A. Taylor, et al.
Biol Reprod, Mar 2007; 76: 524

9. Do gonadotropin-releasing hormone, tyrosine hydroxylase-, and ?-endorphin-immunoreactive neurons contain oestrogen receptors? A double-label immunocytochemical study in the Suffolk ewe
Lehman MN, Karsch FJ.
Endocrinology 1993; 133:887ñ895

10. ?-Endorphin blocks luteinizing hormone-releasing hormone release by inhibiting the nitricoxidergic pathway controlling its release
Alicia G. Faletti, et al.
PNAS, Feb 1999; 96: 1722.

11. The frequency of gonadotropin-releasing hormone stimulation determines the number of pituitary gonadotropin-releasing hormone receptors.
Katt JA, et al.
Endocrinology. 116:2113ñ2115. (1985)

12. Exogenous gonadotrophin-releasing hormone (GnRH) stimulates LH secretion in male monkeys (Macaca fascicularis) treated chronically with high doses of a GnRH-antagonist.
Weinbauer GF, et al.
J Endocrinol. 133:439ñ445. (1992)

13. Chronic administration of the luteinizing hormone-releasing hormone (LHRH) antagonist cetrorelix decreases gonadotrope responsiveness and pituitary LHRH receptor messenger ribonucleic acid levels in rats.
Pinski J, Lamharzi N, Halmos G, et al. 1996
Endocrinology. 137:3430ñ3436.

14. Acute effects of testosterone infusion and naloxone on luteinizing hormone secretion in normal men.
GB Kletter, et al.
J. Clin. Endocrinol. Metab., Nov 1992; 75: 1215 – 1219.

15. Naloxone-induced increases in serum luteinizing hormone in the male: mechanisms of action
TJ Cicero, et al.
J. Pharmacol. Exp. Ther., Mar 1980; 212: 573.

16. Endogenous opioids participate in the regulation of the hypothalamic-pituitary-luteinizing hormone axis and testosterone’s negative feedback control of luteinizing hormone.
CICERO, T. J., et al.
Endocrinology 104: 1286-1291, (1979)

17. Opiatergic control of LH secretion is eliminated by gonadectomy.
BHANOT, R. et al.
Endocrinology 112: 399-401, (1983)

18. Role of endogenous opiates in the expression of negative feedback actions of androgens and estrogen on pulsatile properties of luteinizing-hormone secretion in man.
Veldhuis JD, et al..
J Clin Invest. 74:47ñ55 (1984)

19. Counteraction of gonadal steroid inhibition of luteinizing hormone release by naloxone.
VAN VUGT, et al.
J. Chro- naloxone. Endocrinology 34: 274-278, 1982

20. Unexpected effects of nalmefene, a new opiate antagonist, on the hypothalamic-pituitary-gonadal axis in the male rat.
P Limonta, et al.
Steroids, Dec 1985; 46(6): 955-65.

21. In vivo evidence for a direct effect of naloxone on testicular steroidogenesis in the male rat
TJ Cicero, et al.
Endocrinology, Aug 1989; 125: 957

22. Endogenous opioids participate in the regulation of the hypothalamus- pituitary-luteinizing hormone axis and testosterone’s negative feedback control of luteinizing hormone
TJ Cicero, et al.
Endocrinology, May 1979; 104: 1286

23. Effect of naloxone on the plasma levels of LH, FSH, prolactin and testosterone in Beetal bucks.
Singh B, et al.
Department of Animal Production Physiology, CCS Haryana Agricultural University, 125004, Hisar, India

24. Endocrinology: The effect of nalmefene on pulsatile secretion of luteinizing hormone and prolactin in men
G.R. Graves, et al.
Hum. Reprod., Oct 1993; 8: 1598 – 1603.

25. Effects of the novel opiate antagonist, SDZ 210-096, on luteinizing hormone secretion in the rat
RA Siegel et al.
J. Pharmacol. Exp. Ther., Apr 1989; 249: 264.

26. Effect of antagonists of dopamine and opiates on the basal and GnRH-induced secretion of luteinizing hormone, follicle stimulating hormone and prolactin during lactational amenorrhoea in breastfeeding women
C.C.K. Tay, et al.
Hum. Reprod., Apr 1993; 8: 532 – 539.

27. Naltrexone administration modulates the neuroendocrine control of luteinizing hormone secretion in hypothalamic amenorrhoea
Alessandro D. et al.
Hum. Reprod., Nov 1995; 10: 2868 – 2871.

28. Heroin and naltrexone effects on pituitary-gonadal hormones in man: interaction of steroid feedback effects, tolerance and supersensitivity
JH Mendelson, et al.
J. Pharmacol. Exp. Ther., Sep 1980; 214: 503.

29. Alcohol effects on luteinizing hormone and testosterone in male macaque monkeys
NK Mello, et al.
J. Pharmacol. Exp. Ther., Jun 1985; 233: 588.

30. Erectile function and naltrexone
Goldstein JA
Ann Intern Med 105:799 (1986)

31. Opiate antagonists in erectile dysfunction: a possible new treatment option? Results of a pilot study with naltrexone
van Ahlen H, et al.
Eur Urol 28:246ñ250 (1995)

32. The effects of opiates on androgen binding in the forebrain of the rat.
PJ Sheridan and JM Buchanan
Int J Fertil, January 1, 1980; 25(1): 36-43.

33. Morphine exerts testosterone-like effects in the hypothalamus of the castrated
male rat.
CICERO, T. J., et al.
Brain Rae. 202: 151-164, (1980)

34. Studies of gonadotropin-releasing hormone (GnRH) action using GnRH receptor-expressing pituitary cell lines.
Kaiser UB, Conn PM, Chin WW.
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35. Patterns of LH secretion in castrated bulls during intravenous infusion of androgenic and estrogenic steroids: Pituitary response to exogenous luteinizing hormone-releasing hormone
M.J. D’occhio et al.
Biology of reproduction 26, 249-257 (1982)

36. Demonstration of progesterone receptor mediated gonadotrophin suppression in men.
Brady B, Anderson RA, Kinniburgh D, Baird DT 2002
J Endocrinol 3(Suppl):OC37

37. The direct pituitary effect of testosterone to inhibit gonadotropin secretion in men is partially mediated by aromatization to estradiol.
Bagatell CJ, Dahl KD, Bremner WJ. 1994
J Androl. 15:15ñ21.

38. Studies on the role of sex steroids in the feedback control of FSH concentrations in men.
Sherins RJ, Loriaux DL. 1973
J Clin Endocrinol Metab. 36:886ñ893

39. Is aromatization of testosterone to estradiol required for inhibition of luteinizing hormone secretion in men?
Santen RJ. 1975
J Clin Invest. 56:1555ñ1563

40. Influence of nandrolondecanoate on the pituitary-gonadal axis in males.
JW Bijlsma, et al.
Acta Endocrinol (Copenh), September 1, 1982; 101(1): 108-12.

41. Endocrine approaches to male fertility control.
UA Knuth et al.
Baillieres Clin Endocrinol Metab, February 1, 1987; 1(1): 113-31.

42. Aromatization Mediates Testosterone’s Short-Term Feedback Restraint of 24-Hour Endogenously Driven and Acute Exogenous Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone and Follicle-Stimulating Hormone Secretion in Young Men
J. A. Schnorr, et al.
J. Clin. Endocrinol. Metab., June?1,?2001; 86(6): 2600 – 2606.

43. Short-Term Aromatase-Enzyme Blockade Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and Testosterone Secretion in Older Men
Johannes D. Veldhuis et al.
J. Clin. Endocrinol. Metab., Jan 2005; 90: 211 ñ 218

44. Effects of Aromatase Inhibition in Elderly Men with Low or Borderline-Low Serum Testosterone Levels
Benjamin Z. Leder, et al.
J. Clin. Endocrinol. Metab., Mar 2004; 89: 1174 – 1180.

45. Comparative Assessment in Young and Elderly Men of the Gonadotropin Response to Aromatase Inhibition
Guy G. T’Sjoen, et al
J. Clin. Endocrinol. Metab., Oct 2005; 90: 5717 – 5722.

46. Pharmacokinetics and Dose Finding of a Potent Aromatase Inhibitor, Aromasin (Exemestane), in Young Males
Nelly Mauras, et al.
J. Clin. Endocrinol. Metab., Dec 2003; 88: 5951 – 5956.

47. Differential Regulation of Gonadotropin Secretion by Testosterone in the Human Male: Absence of a Negative Feedback Effect of Testosterone on Follicle-Stimulating Hormone Secretion
Frances J. Hayes, et al
J. Clin. Endocrinol. Metab., Jan 2001; 86: 53 – 58.

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