How your lifestyle influences your Testosterone levels
by John M. Berardi




Like it or not Testosterone is the hormone of the decade. The granddaddy of the male hormones has gotten more media attention over the last few years than any other hormone around. Heck, I even heard a rumor that some crazy bodybuilding media guys were thinking of naming a magazine after it. Can you imagine that?

While Testosterone (the hormone, of course) has been the target of much bad press, I think that if you asked this big dog of hormones what he thought of all of this, he would bark out something to the effect of "What of it? I must be doing something right if they keep talking about me! Now can't you see I'm trying to work this shaved little poodle over here?"

Although the popular media has made Testosterone out to be a destructive bad guy, researchers have been slowly but surely embracing its use. Clinical trials have been conducted in diverse groups of individuals from HIV wasting patients and burn victims to people with compromised immunity, along with older men whose "Testosterone" hasn't been up in years. There have even been a number of recent trials investigating the use of Testosterone in healthy weight trained men. So where do I sign up?

The results of these investigations have shown that Testosterone is not the demon the medical community once thought it to be and that it actually can be of great benefit to certain individuals and, in certain patients, possesses very few risks.

I'm pretty positive though, that the use of Testosterone will never be condoned for use in healthy weight trained males. To this end, us law abiding citizens have to do the best we can with what we've got to work with. So let's talk about how our own body provides us with the big T and what we can do, both naturally and with dietary supplements, to maximize our T levels.

When most people think of steroids, they tend only to think of Testosterone. This, my friends, is yet another fact which tends to make me believe that T is the hormone of the decade. Testosterone, however, is only one member of the steroid family. Some of the other steroids in this family include cholesterol, progesterone, the estrogens, cortisol, and aldosterone.

Although these molecules are part of the same family and have strikingly similar structures, their functions differ like night and day. This is important to recognize because although the steroids tend to act very differently, they are subject to similar rules with respect to biochemistry and metabolism.

For a simplified view of steroid metabolism in the body, you can assume that all steroid hormones begin with cholesterol. From cholesterol, steroid metabolites are formed in various tissues of the body. For example, enzymes in the adrenal glands are responsible for converting cholesterol into cortisol, while enzymes in the gonads are responsible for converting cholesterol to Testosterone.

With this simplified view, it's easy to make the mistake of thinking that by simply providing the body with more cholesterol (make that two large fries, please), we can make more Testosterone. This is a mistake because the body has regulatory mechanisms that control hormone production. These regulatory mechanisms, not your bedtime prayers to the iron gods, are what determine which steroid metabolites will ultimately be formed.

So the next important questions are, what magic does it take to make Testosterone out of cholesterol (now don't get too excited, you can't do this in your bath tub), what regulates this conversion, and ultimately, what regulates Testosterone production? In order to get the gonads to produce T, the body has a chain of command that must be dealt with just like any smooth running business.

In business, the action plan comes down from the CEO to upper management, the plan is solidified and delegated to the production team, and the production team gets the job done. Well, in the body, a portion of the brain called the hypothalamus is the CEO, the pituitary gland is the upper management, and the testes are the production team members.

As in business, the buck stops with the CEO/hypothalamus, which is known as a "pulse generator," because during the day it sends out pulses of hormones that are designed to stimulate other organs. With respect to T, the hypothalamus sends out numerous daily pulses of GNRH (gonadotropin releasing hormone) through the blood stream. These pulses are designed to stimulate the pituitary gland to get to work.

The pituitary gland then senses the pulses of GNRH and sends out a work order of its own, consisting of LH (leutinizing hormone) pulses. The LH message travels down to the leydig cells of the testis to stimulate the enzymatic conversion of cholesterol to Testosterone.

Cholesterol conversion to T is no easy process and I'm not going to go into all of the details (partly because no one really knows them all). One fact that you should understand, though, is that there's a high level of complexity to this pathway and that there are many enzymes and intermediates that cholesterol has to encounter before forming T.

Some of these intermediates include pregnenolone, DHEA, androstenedione, and other well-known androgens. So, although the hypothalamus might be functioning well, the pituitary might be doing the right thing, and the testis are getting the "ball" in motion, ultimately the enzymes in the leydig cells determine whether you're pumping out loads of muscle building T or simply forming other intermediates at the expense of the top dog.

As a result of the process I mentioned above, T levels fluctuate wildly. If you were to measure your Testosterone levels throughout the day, you'd likely be amazed. One minute you have the hormonal profile of a hyper-muscular bull ready to "fertilize" an entire herd of cattle� and the next minute your blood profile is that of a fully menstruating Martha Stewart intent on color coordinating your powder room.

These odd fluctuations occur as a result of the pulsatile nature of hormone secretion. Again, this begins with the hypothalamic pulse generator's release of GNRH. Incidentally, researchers now believe that it is this physiologic pulsatility of Testosterone that makes it anabolic. So if you can mimic this pattern of hormone release, you can stimulate muscle growth.

With this hormonal cascade in mind, it's important to realize that each step in the pathway has a regulation point designed to either stimulate or inhibit pulse release. In this respect, the body is a bit of a control freak as it tends to like many control points rather than just one.

In this particular case there are three main control points; the hypothalamus, the pituitary, and the testis. With this type of control, the body can maintain the Testosterone homeostasis (a sort of hormonal status quo) and prevent us from any abnormal changes in muscle development and strength. For example, if our Testosterone levels go way up, the body senses this and the hypothalamus and the pituitary produce less GNRH and LH in order to slow down T production. This, of course, is the famous negative feedback. Damn that homeostasis!

Now that I'm certain you're all experts in Testosterone production (and there will be a test at the end � I'm serious!), I'd like to address one more important issue that will come up later in the article with regard to Testosterone in the body. When Testosterone is converted from cholesterol in the leydig cells of the testis, it's released into the blood stream where it embarks on an anabolic adventure.

However, when in the blood, 60% of the big T released from the boys down below is bound up by a protein known as SHBG, or sex-hormone binding globulin. SHBG is produced and released by the liver. The important point is that the Testosterone bound to SHBG is biologically inactive and this is why there's an important distinction between total T and bioavailable T.

Total T represents all the Testosterone in the blood, while bioavailable T represents the non SHBG bound Testosterone. There are other proteins in the blood that bind Testosterone, too, but their binding is rather weak, so this T is bioavailable and these proteins can still enter the cells to produce and effect all the things we're interested in.

As I said, bioavailable T represents the Testosterone that is not SHBG bound, while free T represents the Testosterone that's not bound to any blood proteins at all. It's tricky, I know, but I hope that it's now evident that although only about 2% of the T in blood is technically considered free T, there is a larger percentage of T (about 40% or so) that is bioavailable because it's only weakly bound to non SHBG blood proteins.

I'm taking you through this complex path for good reason. When trying to increase T levels in the body, one must attempt to not only increase total T. More importantly, one must attempt to increase bioavailable T. If you increase total T, but you increase SHBG to a larger extent, they you will actually have less bioavailable T for muscle building purposes!

A great example of this is the use of both thyroid drugs and tamoxifen (Nolvadex). Both may increase total T levels in the body, but both also increase SHBG to a large extent. Although you may get a bit of a T surge with each (hurray!), the increase in SHBG may bind up any extra, and actually decrease your bioavailable T (boo!).

Well, now that the class is up to speed with our physiology and endocrinology (will someone please wake up Mr. Luoma! � he's always falling asleep during my physiology lectures), we can dive, full force, into how lifestyle factors including things like diet, training, recreational drugs, over the counter medications, altitude, and how psychological mood states influence T levels. There's an abundance of Testosterone literature out there and some of it is applicable for us while some is not, but to a science geek like me who both likes facts and likes being big and lean, it's all interesting nevertheless.

Oh wait, I almost forgot! Before we go on, I promised a test didn't I? Settle down! Although there are no actual grades on this test, I hope that you take away a few fundamental things from this article. If you can answer these questions, you're ready to take on next week's article in which I'll review a number of environmental and lifestyle factors that can influence your levels of free T, total T, and bioavailable T.

Rest easy, next week's article ties in all that you learned this week and makes some recommendations about how to up the T levels. And next week there won't be a test!

Question #1 � True or False

John Berardi is the most intelligent man on the face of the earth.

(I thought I'd start off with an easy one � And the answer of course is "True")

Question #2 � Short Answer

What are the three main organs/glands that regulate T production and what are the big three hormones they release?

Question #3 � True or False

Testosterone is synthesized directly from cholesterol.

Question #4 � Short answer

What are the cells that actually produce T and where are they located?

Question #5 � Short answer

All the Testosterone in the body, bound and unbound is referred to as what?

Question #6 � Short answer

All the Testosterone that is not bound to SHBG is referred to as what?

Question #7 � Short answer

All the Testosterone not bound to any blood protein is known as what?

Question #8 � True or False

If you are interested in the anabolic effects of Testosterone, the optimal situation is to increase total T levels and decrease SHBG?


John M Berardi is a former national level competitive bodybuilder and an exercise biochemist at the University of Western Ontario. He can be reached for consultation at JMBMUSCLE@hotmail.com.

Testosterone, Environment, and Lifestyle

After last week's physiology and endocrine primer, I thought you might need a break, a chance to let the smoking gray matter cool down. All that science is heavy. As a result of your week off, I hope you're ready to move on to this week's topic. This week we delve into the factors that affect T and what you can do about your own T levels.


A Testosterone Summer

Summer time is just about gone, and in addition to there having been lots of extra daylight and vacation time, there seems to have been lots of extra Testosterone floating around. This may just be a personal observation but in the summer, men and women seem more likely to want to meet, and as my 10th grade musical hero, Tone Loc, would say� do the wild thing.

Ever wonder why? Sure it may have something to do with the fact that there's less thread and more tanned flesh readily visible. But it may be something else as well.

In a study examining the effects of season on total Testosterone levels, men with average T levels of 666 ng/dl (normal levels are between 300-1000 ng/dl) were studied during the months of April, July, October, January, and April again.(21) It appears that T levels increase about 12% during July and 15% during October and return to April levels throughout the rest of the winter. So remember, summer and early fall may be the time to start a growth phase since T will be the highest. In addition, the winter might be a nice time to cycle prohormones or other Testosterone boosters in an effort to keep the T up to summer highs.

One side note. No one knows why T levels fluctuate this way, but researchers speculate that T levels may be regulated by light-dark cycles. If this is true, then perhaps exposing yourself to extra sunlight throughout the winter months may keep T levels up. Who knows, a little extra winter tanning might even help to keep the T up, but that's just speculation. Give it a try. If your T doesn't go up, then at least you'll have a nice tan.

Training With A Capital T

There's nothing new about the fact that acute exercise increases T levels. It's been shown that in men, T levels rise both during exercise and up to about 15 minutes after exercise. But not all exercise increases T levels. Certain workloads and intensities produce no increase at all. Exercise at a certain threshold, however, leads to T increases that are proportional to the amount of muscle mass involved in the workout, the amount of total work (sets X reps), and the intensity.

With respect to weight training, a powerlifting-type workout consisting of 3 sets of 5 reps with 3 minutes rest between sets and a bodybuilding-type workout consisting of 3 sets of 10 reps with 1 minute rest between sets were compared. It appears that total T levels were increased for 15 minutes following exercise and that the bodybuilding workout (67% increase) is superior to the powerlifting workout (32% increase) for increasing total T levels.(14)

What about an activity like running? In a study done comparing elite distance runners with sedentary men, it was interesting to note that at rest, the sedentary men had 54% more total and free T floating around in their blood than the runners. It seems to be the case that most volume-training athletes have lower levels of T. The volume threshold seems to be at about 8 hours of exercise per week. In this study, the runners did, however, have larger free T increases in response to the running. Here's a table of the results:


(BTW, this graph got messed up...sorry.)
Running Intensity
and Duration

Sedentary
Runners

Elite Runners


80% HR max
for 120 minutes

47% Increase

76% Increase


80% HR max
for 20 minutes

31% Increase

62% Increase


50% HR max
for 120 minutes

Nothing

Nothing


50% HR max
for 20 minutes

Nothing

Nothing




From these results, it appears that intense running (80% of max HR) can lead to increases in free T similar to the increases seen with resistance training.(6) If your goal is to increase your Testosterone, though, I wouldn't necessarily recommend very intense continuous running or a very high volume of exercise (greater than 8 hours per week).

Doing so would probably ensure that any increased T as a result of a single exercise session would probably be canceled out by lower resting levels of T. If you still insist on volume training, supplementing with over-the-counter androgens might help normalize T levels during intense periods of training.

Unfortunately and paradoxically, although T levels are increased directly after a training bout, some research has shown that they might then take a nosedive into subnormal levels for 1-3 days after the exercise session.

This means that although your squat day might jack your T levels up for a little while, ultimately those T levels are destined to come back down and end up lower than you started with. They might also stay low for a day or two before coming back to normal.

With that said, my advice would be to stop training altogether. Well, no, but I thought that might get your attention. Actually, inserting rest days between intense exercise bouts might be a better solution to allow T to come back to normal before hammering out another intense workout. Of course, you could always rely on OTC androgens, but since intense exercise might always promote this effect and you don't want to stay on androgens year round, perhaps program manipulation might be the best option.


Mood, Sex, and T

Most people think that stress and depression are psychological phenomenon that have minimal impact on the body. Wrong! Mood states and stressors have major effects on physical systems, especially the endocrine system.

In a bad mood? Stress and depression tend to cause the release of a hormone called corticotropin-releasing hormone (CRH) from our friend, the hypothalamus. This hormone ultimately leads to increases in the release of cortisol, the nasty catabolic adrenal hormone that munches up hard-earned muscle tissue with extreme prejudice.

Increases in CRH and cortisol as a result of both physical and psychological stress, including depression, anxiety, injury, fever, disease, etc. lead to decreased T levels.(25) To highlight the importance of this, one marker of overtraining and a catabolic state is the Testosterone-cortisol ratio. The higher the ratio, the more anabolism. The lower the ratio, well, let's not discuss that.

Many studies have been conducted to examine the relationship between stress, mood, cortisol, and Testosterone. Studies in humans and animals show that both acute and chronic stress lower total Testosterone levels. Here's the evidence:

� Psychiatric inpatients with major depression tend to have higher cortisol and 40% lower T than control subjects with no depression.(19)

� Healthy male internal medicine residents have higher stress and cortisol levels than controls and as a result, have 80% lower T levels.(20)

� Chronic headache sufferers have 50% lower T vs. controls.(7)

� In male endurance athletes T decreases by 17% as cortisol increases post exercise.(13)

� In monkeys forced to remain seated in a chair for 30 minutes, cortisol goes up and T levels decrease.(22)

� Police officers who were threatened with the loss of their jobs had lower T and higher cortisol than after the job stress had subsided.(11)

So relax and take things easy. Life delivers some pretty hefty blows but the less stress, anxiety and depression you feel as a result of it, the lower your cortisol will stay, the more muscle you will retain, and the higher your T will soar.(18)

Perhaps during stressful times in your life, your training intensity should be moderated. Don't plan a growth cycle when you know your mental and emotional circumstances will prevent your best gains. Or if you do want to blast through personal crises, perhaps supplementing with T boosters might be the answer.

Enough about negative moods. What about when you feel good? I don't know about you, but when my favorite hockey team stomps the hell out of a rival I feel pretty good. Actually I feel better than pretty good, I feel obnoxiously, tauntingly good. Why? Perhaps victory, either personal or vicarious, can increase T. Here's the evidence:

� Spectators of a basketball event and a soccer event whose favorite teams won benefited from increased T while those rooting for the losing teams had decreased total T.(1)

� Male college students who won $5 on a task controlled entirely by chance had increased levels of total T when compared to baseline, while those who lost $5 had lower levels of total T.(16)

� Collegiate competitive tennis players show increases in T after winning a match while those who lose do not.(2)

And what about when you feel horny, baby? Well intercourse, masturbation, and viewing erotic stimuli may all cause rises in your� T. Actually, LH is better correlated with sexual arousal than T, but if LH pulses occur during arousal, then T is soon to follow.(17) Take a look at the following findings, but I'll leave you alone to come up with your own conclusions.

� Measured over the course of several weeks, men's T levels went up on 11 nights in which they had sex while the T levels went down during 11 sexless nights.(5)

� Increases in LH are seen during sexual arousal while watching erotic movies.

� Increases in LH and T are seen during sexual activity including masturbation.

And finally, what about those horny rats? This study will have frightening implications if it's released to the females of the world. Think about it!

� Rats release LH and total T by being exposed to a sexually responsive female. In one particular study, the rats were conditioned, Pavlov style, by presenting a sexually receptive female along with a strong background odor.(9) In the future, the odor alone was enough to cause a similar increase in LH and T as when the sexy rat was present.

T and Drugs

As a former willing participant in the bodybuilding subculture, I know quite a bit about what makes bodybuilders tick as well as many of the oddities of the lifestyle. One observation I've made over the years is that bodybuilders really like to take pills.

Regardless of whether they're prescription drugs, OTC drugs and supplements, or even good old Fred, Barney and Wilma in sugary vitamin form, bodybuilders will down handfuls at a time as a ritual of worship to the muscle gods. And I'll be the first one to admit that in my day, I had a thing for Betty Rubble. I used to eat mouthfuls of the tiny vixen while making poor Barney watch.

Although Flintstones vitamins probably do not impact T, many recreational, prescription, and OTC drugs do. Lets start with everyone's favorite drug, alcohol. In my opinion, alcohol is the single best legal Testosterone suppressor known to mankind. And you don't need a biochemistry experiment to realize that. Just look at the physique of any alcoholic for the evidence. And not only do chronic alcoholics suffer from low T as a result of sippin' a cold one. Numerous studies have shown that even one night on the town can cause T levels to plummet.

In one particular study, men consumed the equivalent of giving 200 ml of alcohol to a 176-lb man. While intoxicated, T levels were 25% lower on average than before consumption. In addition, the time course of T decrease correlated exactly with blood alcohol so when blood alcohol was the highest, blood T was the lowest.(17) With even lower doses, T levels remained suppressed for 10-16 hours, even after blood alcohol returned to normal.(23,24)

As a side note, one question I'm often asked by men concerns why they get so aroused when drinking. Well gents, in addition to the decrease of inhibitions, the body is fighting to maintain Testosterone homeostasis. As a result, high amounts of LH are released in order to bring T levels back to normal. As mentioned earlier, LH is correlated more with arousal than T, so that's why you get horny, you dogs. The problem, though, is that high LH secretion is ineffective at increasing T during an alcoholic stupor. Alcohol, you see, prevents T production at the Leydig cell level and not at the pituitary level. So you're arousal is up, but T stays down.

You don't drink? Well here is just a list of other drugs that decrease T levels in one way or another3,4,25)

1) Aspirin

2) Marijuana

3) Codeine

4) Opioids like Morphine, Methadone, and Heroin

You'll notice that a few of these drugs are used for pain. These drugs act on the central nervous system to produce analgesia, a desired effect for guys who pound their muscles day in and day out in the gym. Before you load up on the painkillers though, consider that one group of researchers actually uses T depletion in the blood as an assay for narcotic effectiveness.(3)

What this means is that the better a drug is at producing analgesia, the more it will reduce Testosterone levels. It's believed that these drugs act on the pituitary to block LH secretion and ultimately, T production.(25)

Two other drugs I'd like to mention are Nolvadex and thyroid hormone. Some authors have speculated that both drugs can increase T levels. I'm not convinced. In men who are severely hypothyroid, thyroid medication can increase total T levels.(10) But the doses needed are high. If you're dumb enough to try huge doses of thyroid hormone to try to increase your total T, the catabolic effects of that amount of thyroid would negate any anabolic effects of the increased T.

Both Nolvadex and thyroid drugs also increase SHBG.(10) Remember that the goal in increasing Testosterone levels is to increase bioavailable T � not just total T. If SHBG goes up as total T goes up, then the bioavailable Testosterone may stay the same, or worse yet, decrease. Don't get the wrong idea, though. Optimizing thyroid function through supplements produces a different effect than taking thyroid drugs. Either way, this course of action should help you lose body fat, but I don't think it will increase T levels one bit.

In summary, for maximum T, be cautious of how you use alcohol, marijuana, and painkillers. If you're going to assault your boys with alcohol, perhaps a few shots of diol would be an appropriate chaser. If painkillers have a shelf of their own in your medicine cabinet, perhaps an LH booster like Tribulus would be of benefit to your testis.

T Diet

The effects of diet on Testosterone are very unclear, as the research tends to contradict itself over and over again regarding what impact protein, carbs, and fats have on T levels.

In reviewing the literature, I'm convinced of one thing, though. Diets higher in protein, cholesterol, and saturated fat � as well as total fat content � tend to maintain higher T levels. I know, I know, these recommendations fly right in the face of what is deemed "healthy," but I just report what I know.

One particular study showed that decreasing dietary fat from 40% to 25% while at the same time decreasing saturated fat and increasing polyunsaturated fats led to decreased total Testosterone levels (18%) and free Testosterone levels (15%). Upon resuming their normal diet, Testosterone levels increased back to normal.(12)

One problem with the study was that subjects ate about 500 fewer calories on the lower fat diet, so it's hard to say that fat levels and not the caloric restriction led to the decrease in T. From this and other research, though, it's obvious that eating an adequate amount of fat and cholesterol is necessary to maintain T levels.

Of course, I wouldn't recommend eating large amounts of saturated fats and cholesterol, but what I do recommend for maximizing T levels during a growth phase is eating a diet of about 30% fat with some saturates and unsaturates, as well as cholesterol.

I can hear the nutty dietitians going crazy now, squawking about heart disease, etc., but if you're training hard, the cardio protective effects of the training will far out weigh any negatives of moderate amounts of saturated fat and cholesterol in the diet.

As far as protein intake, there's some correlational research to suggest that those who consume more protein have higher T levels.(15) I have a feeling, however, that perhaps the reason for this is that those who eat more protein also typically eat more animal products higher in fat and cholesterol.

Since higher T levels are the goal, severe food restriction or undernutrition is a terrible idea. Negative energy balance (i.e., the precontest diet) is associated with very large decreases in T.

In a really Testosterone-ish study, army rangers going through summer training in climates like the forest, the desert, the mountains, and the swamplands were given only 1000 to 2000 calories per day while their bodies had requirements of about 5000 (sounds like how I used to diet for shows).

As a result of the extreme training and undernutrition, these soldiers had T levels that, as the authors stated, "approached castrate levels".( SHBG increased as well. We're talking about 350% decreases in T levels with 67% increases in SHBG. Fortunately, SHBG and T levels returned to normal within 7 days of re-feeding. Identical results have been seen with T decreases after 48 hours of fasting.

This is a frightening illustration of the endocrine crash that can happen when bodybuilders go into huge caloric deficits during pre-contest preparation. All the more reason to stagger and fluctuate caloric intake while attempting to stimulate T production with supplements during dieting. This way, you won't end up with the endocrine profile of a castrated man.


Long Live Testosterone

Although T levels will fluctuate throughout the day, the week, and the year, there are predictable times during which T will be high (summer, winning streaks, higher fat eating periods, or when you're gettin' some). And there are times when it will be low (winter, losing streaks, stress and depression, low fat diets, drug and alcohol binges, or "dry spells").

During these times we can plan our training around our hormonal changes or we can take aggressive supplemental and dietary action to maximize our T potential. Knowing how each factor affects T can help plan your supplemental strategies. Make your T all that it can be!

As a result of the surge in Testosterone's popularity, perhaps another question will be added to the age-old inquiries, "How much can you bench?" and "Let me see your muscle!" Perhaps in the not too distant future, muscleheads will be measuring their manliness by a new yardstick and asking each other "What's your free and total T?"


References

1)Bernhardt, PC et al., Physiol Behav 65 (1): 59-62, 1998.

2)Booth, A et al., Horm Behav 23 (40): 556-571, 1989.

3)Cicero, TJ. J Pharm Exp Thera 202 (3): 670-675, 1977.

4)Conte, D et al., Am J Physiol (Endocrinol Metab, 40) 277: E1032-E1037, 1999.

5)Dabbs, JM et al., Physiol Behav 52 (1): 195-197, 1992.

6)Duclos, M et al., Eur J Appl Physiol 73 (5): 427-433, 1996.

7)Facchinetti, F et al., Cephalalgia 6 (1): 29-34, 1986.

8)Friedl, KE et al., J Appl Physiol 88: 1820-1830, 2000.

9)Graham, JM et al., Science 210 (4473): 1039-1041, 1980.

10)Greenspan, FS et al., Basic and Clinical Endocrinology. Appleton and Lange, 1997.

11)Grossi, G et al., Integr Physiol Behav Sci 34 (1): 30-42, 1999.

12)Hamalainen, E et al., J Steroid Biochem 20 (1): 459-464, 1984.

13)Hoogeveen, AR et al., Int J Sports Med 17 (6): 423-428, 1996.

14)Kraemer, WJ et al., Int J Sports Med 12 (2): 228-235, 1991.

15)Longscope, C et al., J Clin Endocrinol Met 85 (1): 293-296, 2000.

16)McCaul, KD et al., Hormonal Behav 26 (4): 486-504, 1992.

17)Mendelson, JH et al., J Pharmacol Exp Ther 202 (3): 676-682, 1977.

18)Rosmond, R et al., J Endocrinol Invest 22 (4): 279-278, 1999.

19)Schweiger, U et al., Psychosom Med 61 (3): 292-296, 1999.

20)Singer, F et al., Steroids 57 (2): 86-89, 1992

21)Smals, AG, J Clin Endocrinol Metab 42 (5): 979-982, 1976.

22)Torii, R et al., Jikken Dobutsu 42 (1): 67-73, 1993.

23)Valemaki, M et al., Alcohol Clin Exp 14: 928-931, 1990.

24)Valemaki, M et al, Alcoholism 1: 89-93, 1984.

25)Vermeulen A, Environmental Health Perspectives Supplements 101 (supplement 2): 91-100, 1998.

Good article Bro!

Nicely done.