Men Are Not Always Thinking About Sex. Study Says: There Are At Least 4 "Good" Reasons They Don't - Stress Is #1! Plus: A Proven De-Stress Protocol to Restore Your Libido

If either of these individuals remind you of yourself, you should reduce his stress levels.

Recent research suggest: The good old saying that "Men always think about sex!" is essentially untrue (The "!" indicates that I used the feminist version of this common "wisdom").

If we put faith in the results of a recent European study from the Department of Clinical Psychology at the Instituto Universitário in Lisbon, Portugal, the Department of Psychology at the University of Tromsø in Tromsø, Norway, and the Sexology Unit at the Faculty of Humanities and Social Sciences, University of Zagreb, Croatia, stress is the common denominator that distracts men from their original duty to do what has to be done for the survival of the human race ;-)

Homo coitum quaerens aut evitarens?

It may sound surprising, but unlike sexual function, the sexual desire of the male members of the human race has not been examined as extensively as the one of their female counterparts. When you think about the initially quoted "wisdom", it is actually not that surprising.  Men are are after all believed to be always looking for the next "catch".

The problem cannot be that prevalent, can it? Yes it can! According to recent data from the The National Health and Social Life Survey (NHSLS), the average American's prevalence of “lacking desire for sex” ranged from 14% (for those 18–29 years old) to 17% (for those 50–59 years old). In spite of the fact that the exact figures are debatable, the currently available literature supports the notion that 15-20% of the US men 'don't think about sex at all'. If we take a look at international data the figures don't look better: Depending on the geographic region 13% to 28% of the ~14,000 men aged 40–80 years from 29 countries in the Global Study of Sexual Attitudes and Behaviours said that their sexual desire had been low for at least 2 months Laumann. 2005).

After focusing more or less exclusively on functional aspects of male sexuality for decades, research does now start to draw and embrace a more versatile image of male and general human sexuality. According to studies by Hyde and Janssen, the black-and-white gender differences which is also at the heard of the saying "men think about sex all day" is in fact non-existent. On the contrary, gender theorists have recently suggested that greater diversity exists within gender than between gender (Hyde. 2005+2007; Janssen. 2008).

Sexual disinterest is stressful!

Faced with the surprisingly high rates of sexual disinterest in men, scientists like Mccarthy et al. have already identified several major relationship problems as potential culprits. In view of what you've learned already, it should be obvious that these problems are not necessarily related to the 'classic' mismatch in sexual interests between a hyperactive male and an (under-)active female partner. On the contrary, the data in Figure 1 makes it plain obvious that for men in their thirties, it would not be unlikely that they are disinterested and their wives or girlfriends dissatisfied.

It goes without saying that problems like these and the mismatch between the perceived and the expected level of sexual desire are stressing - very stressing, according to the data Ana Carvalheira's, Bente Træen's and Aleksandar Štulhofer gathered in inteviews with heterosexual men from Portugal, Croatia, and Norway (Carcalheira. 2013):

Figure 1:Lack of desire and professional stress, two sides of the same coin? Data based on Carcalheira (2013)

In the worst case scenario a man will get caught in a vicious circle of professional stress ⇆ lack of sexual desire ⇆ private stress that is hard to break. Against that background it's only logical that the essence of the recommendations in the bottom line of this article is to get rid of the stress that's keeping you from thinking about sex.

"Stress ⇆ Sexual Disinterest" - it's that easy!

A 2013 study by Talbott et al. suggests that Tongkat Ali, a traditional testosterone and libido booster works mainly be reducing stress levels (learn more)

If you don't believe in the deeper truth of this 'equation', I suggest you go back to an article I wrote earlier this year (see Beyond Testosterone: 200mg/day of Tongkat Ali (Eurycoma Longifolia) for Stress Management & Improved Mood!?" | read more). It deals with a traditional "testosterone booster" and its effects on stressed individuals... you will see: Stress is not only a libido-, it's also a testosterone -killer (no surprise, right?).

It is thus not really surprising that the data from the Carcalheira study tells us that men who feel distressed about their own lack of libido were 2.5x more likely to suffer from anxiety right before sex  and/or have trouble maintaining an erection.

To be stressed or not to be stressed - that's the question!

Just as the cliche would have it, the highly reserved Norwegians were 3x more likely than the red-blooded self-proclaimed Latin lovers from Portugal to suffer from a lack of sexual desire. With a 50% higher risk of losing interest in the other sex, the participants from Croatia end up somewhere in between the 'Latin lovers' and the 'prudish Vikings'.

Table 1: Sociodemographic characteristics, individual variables, and relationship-related characteristics as correlates of a distressing lack of sexual interest among healthy heterosexual men who are not using antidepressants (Carcalheira. 2013)

Aside from their origin there were other sociodemographic characteristics, individual variables, and relationship-related characteristics which were found to be associated with the an increased risk of suffering from a lack of sexual desire. As the data in Table 1 goes to show you, having children, even young ones, was, contrary to what you may have expected, not among these characteristics. In contrast to the self-confidence on erectile function, of course.

What's I personally find quite telling is the high rate of a distressing lack of sexual desire in long-term (5years +) relationships and as a consequence of an indifferent attitude towards the attractiveness of the sexual partner. Interestingly, finding your wife or girlfriend "neither attractive, nor unattractive" is an even greater turn down than thinking of her as a "very unattractive" (see Table 1).

"And that's all stress?"

No, that's not all stress... In the previous paragraph we have already learned about a libido killer that cannot be traced back to stress: The lack of 'adventure', 'novelty' or whatever you may call it - a phenomenon which is probably also the reason that people start looking at their partner as "neither attractive nor unattractive" is another important contributor to sexual disinterested in men. One out of 22 if you will - 22 items on the scientists list of potential causes of a reduced sexual interest:

Table 2: Self-assessed causes of a reduced sexual interest during the past 6 months among heterosexual Portuguese, Croatian, and Norwegian men in percent (Carvalheira. 2013)

I know, not all of them appear logical. Why would masturbating too often be associated with a reduced interest in sex? ⇦ That does not sound right - right? Something similar can be said for the Croatian porn fans (22.5%). In the end, though, it does not change the overall picture: It is stress that's gnawing at our sexual desire, guys.

The Dimou protocol: Diaphragmatic breathing is performed by taking deep diaphragmatic inspirations followed by slow prolonged expirations.  In the second phase of PMR relaxation, patients were guided through successive contractions and relaxations of different large muscle groups in a down-top orientation. The process was complemented by guided imagery involving mental exercises, designed to allow the mind to influence the health and well-being of the body (GI is used with standard medical treatment in people with cancer and other diseases, such as fibromyalgia, as it can help to reduce stress, depression and manage pain). In each step, the patients were encouraged to focus on the difference between tension and relaxation, thus gradually sharpening the perception of the relaxation response.

What So what can be done? By now the question "what can be done" should - at least on the surface level - already have a rhetorical character. It's obvious that you have to de-stress. The only question is: How do you do that? Luckily (for us), P.A. Dimou et al. have just successfully tested an anti-stress program that consisted of progressive muscular relaxation (PMR), diaphragmatic breathing and guided imagery and was topped off with a handful of tips to achieve better time management. The program was designed to optimize sexual health in young men and it worked! It worked like a charm: Over the course of the 8-week stress management program practicing the PMR + diaphragmatic breathing + guided imagery regime twice a day effectively reduced the number of men who were totally or somehow dissatisfied with their sex life decreased from 9 to 4 (-55%; cf. Dimou. 2013). Aside from the intended benefits in sexual satisfaction, the young 60 young men in the active arm of the Dimou study also lost weight (-3% BMI), felt less overall less stressed (-23%; social stress subscale -11%) and achieved +6% higher scores in the general health evaluation.

PMR and guided imagery does not sound like you? Well, I guess simply limiting your mobile phone, email, Facebook and SMS use, making room for the occasional time out with a cup of tea during the working hours, a rigorous 7h+ sleeping regimen and letting go of the 'more is more principle' will work wonders even in the absence of 'meditative' interventions....ah, and don't forget: Don't stress about de-stressing that would ruin all your efforts to find inner peace ;-)

Reference:

• Carvalheira A, Træen B, Štulhofer A. Correlates of Men’s Sexual Interest: A Cross-Cultural Study. J Sex Med. 2013 [accepted manuscript]
• Dimou PA, Bacopoulou F, Darviri C, Chrousos GP. Stress management and sexual health of young adults: a pilot randomised controlled trial. Andrologia2013,xx, 1–10 [accepted manuscript]
• Hyde JS. The gender similarities hypothesis. Am Psychol 2005;60:581–92.
• Hyde JS. New directions in the study of gender similarities and differences. Curr Dir Psychol Sci 2007;16:259–63.
• Janssen E, McBride K, Yarber W, Hill B, Butler S. Factors that influence sexual arousal in men: A focus group study. Arch Sex Behav 2008;37:252–65.
• Laumann EO, Nicolosi A, Glasser DB, Paik A, Gingell C, Moreira E, Wang T; GSSAB Investigators’ Group. Sexual problems among women and men aged 40–80 y: Prevalence and correlates identified in the Global Study of Sexual Attitudes and Behaviors. Int J Impot Res 2005;17:39–57
• Mccarthy B, McDonald D. Sex therapy failures: A crucial, yet ignored, issue. J Sex Marital Ther 2009;35:320–9.

T-Gel with or Without an Aromatase Inhibitor? If You Are Healthy & Lean and Want to Stay This Way, There is Only One Answer: T-Gel Without Aromatase Inhibitor!

Don't let her talk you into participating in studies that risk your manliness ;-)

Would you be willing to participate in a study, where you could end up without testosterone? No? Well me neither... strangely Joel S. Finkelstein et al. were able to find 198 healthy men between 20 and 50 years who were stupid enough to participate in an experiment, where they were randomized to placebo, or testosterone gel (1.25, 2.5, 5, or 10g per day) while being on gosererelin acetate, which did suppress their natural testosterone production.

With additional 202 subjects receiving an identical "treatment", but in this case alongside a whoppy dose of the aromatase inhibitor anastrazol as a bonus, the study design leaves us with plenty of groups and tons of subjects. To "determine the relative degree of testosterone deficiency, estradiol defi­ciency, or both at which undesirable changes in body composition, strength, and sexual function begin to occur." (Finkelstein 2013)

Yep, that is the study you don't not want to be part of, but....

I bet you will still be interested in the results. Am I right? Ok, let's see then. In men receiving goserelin acetate (kills the natural testosterone production) and 0 g (pla­cebo), 1.25 g, 2.5 g, 5 g, or 10 g of testosterone gel daily (cohort 1), the mean testosterone levels were

• 0g testosterone: 44±13 ng per deciliter, 
• 1.25g testosterone: 191±78 ng per deci­liter
• 2.5g testosterone: 337±173 ng per deciliter, 
• 5g testosterone 470±201 ng per, and
• 10g testosterone 805±355 ng per deciliter

With 1.4 pg per milliliter, 7.9±2.9 pg per mil­liliter, 11.9±5.7 pg per milliliter, 18.2±10.2 pg per milliliter, and 33.3±15.3 pg per milliliter the estrogen levels of all participants were all well within the normal range (<55pg/ml).

Update: As Dr. Crisler (www.allthingsmale.com) just told me the accuracy of the information about estrogen may be questionable, because the essay the scientists used is not reliable in adult men. Instead, he suggest you use a "sensitive" essay like LabCorp (#500108), which uses the "cutting edge" LC/MS technology, Mayo Clinic's "Enhanced Estradiol" (#81816) or LabCorp's "Sensitive Estradiol (#140244), which is less expensive and thus probably a good choice for those without insurance. Dr. Crisler also pointed out that the wide variations you see in T-levels are actually a "very good thing, since this more closely mimics the serum profile of young healthy men". I do not deny that, but I still thought that it was wise to point out that the difference between 805ng/dl and 924ng/dl is absolutely non-significant when you have a range of ±521ng/dl.

Now the latter was obviously true for the guys on the aromatase inhibitor as well, with 1-2pg/ml their levels were however pathologically low and considering the high standard deviations, their T-levels were not that much higher:

Figure 1: Testosterone (ng/dl) and estrogen (pg/ml x10) in healthy men on 0, 1.25, 2.5, 5 and 10g (T0-T10) of testosterone gel with and without an additional aromatase inhibitor (Finkelstein. 2013)

"In men who also received anastrozole (cohort 2), the corresponding mean testosterone levels were 41±13 ng per deciliter, 231±171 ng per deciliter, 367±248 ng per deciliter, 485±240 ng per deci­liter, and 924±521 ng per deciliter and the corresponding mean estradiol levels were 1.0±0.4 pg per milliliter, 1.2±0.4 pg per milliliter, 2.0±2.3 pg per milliliter, 2.1±1.9 pg per millili­ter, and 2.8±1.8 pg per milliliter." (Finkelstein 2003)

[*please note the high (up to 50%!) standard deviations which tell you that the response to transdermal testosterone may vary profoundly from one men to another]

If you take a closer look at the data in Figure 1 and keep in mind that I had to multiply the estrogen levels by x10 in order to fit them into the same graph, it becomes all the more evident that the men in the non-AI group all had normal (<55pg/ml) estrogen levels. Their peers in the anastrazole group, on the other hand, had basically no estrogen at all and correspondingly high testosterone to estrogen ratios. In the worst case (yep, that is something bad!), namely 10g of t-gel + A,I the latter was as high as 335, which is almost 12x higher than in the 2.5g testosterone group without anastrazole (cohort 1).

No T, but tons of body fat

Apropos, cohort 1, in this group of men those who received the anti-androgen goserelin alongside a low(ish) doses of T-gel, i.e. either 0 g, 1.25 g, or 2.5 g of testosterone, daily, had significantly higher body fat levels and those in the 0 and 1.25g of T-gel significantly lower levels of lean mass compared to their peers in the 5g T-gel per day group.

Just a reminder: The testosterone level of the guys in the 5g group was only 470ng/dl and thus still rock bottom - the age adjusted normal levels for men are after all (I highlighted the group, where most of the subjects were in):

• 

  Effects of high and low testosterone on body composition (learn more)

  14-15 yr: 33-585 ng/dL
• 16-17 yr: 185-886 ng/dL
• 18-39 yr: 400-1080 ng/dL
• 40-59 yr: 350-890 ng/dL
• > 60 yr: 350-720 ng/dL

Those on the highest dose of T-gel (10g) ended up at the top (remember the standard deviations) of the normal range for testosterone and right in the happy medium for estrogen (normal range is 14-55pg/ml). These guys  experienced a significant decrease in body fat and increases in tigh muscle area and leg press strength.

Interestingly, both the decrease and increase in body in response to high and low testosterone levels occurred almost exclusively in the "benign" subcutaneous adipose tissue. The intra-abdominal­ fat area, on the other hand did not change significantly in any group. If we follow the standard interpretation of the health effects of the different body fat stores, the conclusion would thus be that low T is not so much of a problem, after all it's all "healthy fat" that you will gain... to bad that too much of that "healthy fat" will make you just as insulin resistance as the visceral fat - it just takes longer for the negative effects to occur.

Now what did the AI do?

Suggested read explaining why the annihilation of E2 has negative effects on your body comp: "Estrogen, Friend or Foe of Muscle Hypertrophy? Plus: Are You 'SERMing' Away Your Satellite Cells?" | more

I know, the most intriguing question has not been answered yet: What was the role of anastrazole in all this? And how did the subjects in cohort 2 fare compared to their "high" (remember even the 10g guys had normal estrogen levels) estrogen counterparts. Well,...

"In cohort 2, the percentage of body fat increased in all groups when the aromatization of testosterone to estradiol was inhibited. The magni­tudes of these increases were similar with doses of 0 g, 1.25 g, 2.5 g, and 5 g of testosterone daily, a finding that suggests a predominantly estro­genic effect" (Finkelstein. 2013)

Yep, I deliberately quoted this, because I know that you've been brain-washed to believe the opposite would happen. The big bad estrogen is what keeps you lean... good that you have been taking natural AIs for years, right? Well, no obviously not. Probably rather the reason that you still don't have the cover-model look you are aspiring.

---

Did you know that (a) the endogenous production of estrogens has significant protective effects on your heard cardiovascular health (Sudhir. 1999) and that (b) aromatase is neuroprotective and low levels of it have been associated with the occurance + progression of neurological diseases such as dementia, Alzheimer's and Parkinsons as well as an inability to recover from mechanic (trauma) or chemical (intlammation) damage to the brain (Azcoitia. 2001)? No? Well, let's hope that this is because you've never heard it and not because you've been abusing AIs for the past decade ;-)

So, to use an AI or not - is that even a question? A direct comparison of all the data from cohort 1 (no aromatase inhibitor) and cohort 2 (using anastrazole), informs us that

"The cohort–testosterone dose interaction was significant for the percentage of body fat (P = 0.001), intraabdominal­fat area (P = 0.021), subcutaneous ­fat area (P = 0.029), sexual desire (P = 0.045), and erectile function (P = 0.032)" (Finkelstein. 2013)

Or, to put it another way: The study shows us that estradiol exerts an inde­pendent effect on body fat, sexual desire and erectile function. So you better don't ignore the real world implications you are about to suffer, when you put too much faith in hearsay instead of looking at your actual blood levels:

"In the groups that received testosterone, inhibi­tion of estrogen synthesis (cohort 2), as com­pared with intact estrogen synthesis (cohort 1), was associated with significant increases in the percentage of body fat (P<0.001), subcutaneous­ fat area (P<0.001), and intraabdominal­fat area (P = 0.002) and with significant decreases in sexual desire (P<0.001) and erectile function (P = 0.022)" (Finkelstein. 2013)

Yes, you heard the scientists right. Suppressing your estrogen levels is going to make you fat, rob you of your sexual desire and render you unable to perform the deed.

At the same time it had no beneficial effect on the increases in lean body mass or strength or any other positive outcome the subjects got from using T-gel. On the contrary, the low estrogen levels on in the 10g T-gel group did actually blunt reduce the lean mass gains and the fat loss the men in cohort 1 (no anastrozole) experienced, when they used 10g of T-gel per day was effectively reversed by the AI.

Figure 2: Fat gain, lower lean mass gain, less sexual desire & lower sexual function (not shown) and the list goes on... there really is nothing remotely beneficial about low estrogen (figures from Finkelstein. 2013).

It should thus be absolutely obvious that the only reason you should use an aromatase inhibitor with your testosterone replacement therapy is blood work that indicates that you have serious issues with over-aromatization. In many cases those can be reduced if not solved by (a) reducing inflammation and (b) getting rid of your belly.

To deliberately annihilate your estrogen levels, on the other hand, is simply stupid - irrespective of whether you are on TRT or not and even if you don't care about the negative long-term effects on your brain and heart health.

References:

• Azcoitia I, Sierra A, Veiga S, Honda S, Harada N, Garcia-Segura LM. Brain aromatase is neuroprotective. J Neurobiol. 2001 Jun 15;47(4):318-29.
• Sudhir K, Komesaroff PA. Clinical review 110: Cardiovascular actions of estrogens in men. J Clin Endocrinol Metab. 1999 Oct;84(10):3411-5. Review.

Gingko Biloba, Your Dopaminergic Brain Viagra. Plant Extract Stimulates Sexual Arousal via the Paraventricular Nucleus and the Mesolimbic System.

Image 1: Gingko biloba
trees are one of a kind, with
no close living relatives
(image Schwabe Pharm.)

I bet you got one of those Viagra spam mails, today, as well, didn't you? Well, although I assume you would not need the small blue pills, anyway, you may be interest to read that researchers from the People's Republic of China may have found a viable Viagra alternative in a longstanding (pun intended ;-) ingredient of Traditional Chinese (and meanwhile also Western) Medicine: Gingko biloba.

In order to elucidate the underlying mechanisms of previously (Yeh. 2010) observed beneficial effects of Ginkgo biloba extract on noncontact erections in male rats, Yeh et al. (Yeh. 2011) recorded both copulation, as well as non-contact erections in a group of 20 male Long-Evans (telling name, isn't it?) rats, which had been randomly assigned to a treatment (50mg/kg body weight Gingko biloba extract [EGb 761 from Schwabe Pharmaceuticals], human equivalent 8mg/kg ~ 640mg for an 80kg man) or a control group. 14 days after initiation of treatment, there was "a significant increase in the number of NCEs [non contact erections]" in the 10 rats of the treatment group. Furthermore,

[...] the expression of catecholaminergic neurons in the PVN [paraventricular nucleus] and the VTA [ventral tegmental area] was seen [to be significantly increased ...] and tissue levels of dopamine and 3,4-dihydroxyphenylacetic acid in the NAc [nucleus accubens] were also markedly increased in the EGb 761-treated animals. However, the norepinephrine tissue levels in the PVN and the NAc in the EGb 761-treated group were not significantly different from those in the controls.

In other words, the increased number of catecholaminergic neurons did not, as one might have expected, increase the total amount of the stress-related neurotransmitter /hormone norepinephrine. In agreement with previous work by Mas et al., 1990; Pfaus et al., 1990; Pleim et al., 1990;Wenkstern et al., 1993; Tsai et al., 2006, it's dopaminergenic effects in the nuccleus accubens (dopamine levels in the increased by 66%), on the other hand, had profound effects on their sexual behavior (cf. figure 1).

Figure 1: Effect of Gingko biloba extract @ 50mg/kg on non-contact erection frequency in male Long-Evans rats before and after 14 day treatment (data adapted from Yeh. 2011)

In view of the effect, that the scientist do not want to "exclude that EGb 761 treatment may also influence dopaminergic activity in other brain areas", these results may be of interest even to those among you, who do not have any trouble "getting it up".

Note: The mechanism by which Gingko biloba increases sexual desire is different from the one of PDE-5 inhibitors such as avanafil, lodenafil, mirodenafil, sildenafil citrate, tadalafil and all the other "-afils". While the systemic effect on nitric oxide induced vasolidation of Viagra and Co. will help with erection quality and quantity, Gingko biloba probably won't help if blood flow restriction in your most valuable part is an issue. The different mechanisms of action, on the other hand, would suggest the two would make an interesting stack. And in fact back in 2010 Kim et al. found that "GBE [Gingko biloba extract] could increase the relaxant potency of mirodenafil even at a minimally effective dose" (Kim. 2010).

With dopamine playing an important role in behavior and cognition, voluntary movement, motivation, punishment and reward, inhibition of prolactin production (juicers did you read that?), sleep, mood, attention, working memory, and learning, the implications of this finding reach beyond sexual function alone. Even in the etiology of the dubious central fatique syndrome, every second visitor of one of the major internet health bulletin boards claims to experience, these days, may involve dopamine or rather a lack thereof (Caldizán Uzón. 2008). That being said, the group of patients who benefit from one of the readily available over-the-counter Gingko biloba supplements may soon expand from best agers, who are concerned about cognitive decline to (pre-)andropausal men who want to regain their interest in the fairer sex and, eventually, everyone who feels he/she would benefit from some additional dopaminergic drive.

The "20 / 30 Principle" Sheds 15% Body Fat in 6 Months, Boosts Testosterone & Sexual Performance in Overweight Men. Plus: Six Signs You're Doing Too Much, Already.

One out of four men with newly diagnosed erectile dysfunction is under 40 (more)

You will probably remember the post about the increasing prevalence of erectile dysfunction in young(er) men on Facebook, the other day (learn more)!? As of now, one out of four patients who are newly diagnosed with erectile dysfunction are 40 years or younger. That's an alarming trend that certainly cannot be reversed by the use of adulterated OTC libido boosters with high amounts of pharmacological PDE-5 inhibitors that are not listed on the label (read more on the SuppVersity Facebook Wall and listen live to today's installment of the Science Round Up starting at 12PM EST!). With  30-40% of the overweight men not being able to achieve an erection of maintain it long enough to engage in sexual intercourse, it stands out of question that the root cause for the exploding numbers of impotent young men is diabesity.

Against that background it is only logical that Joan Khoo and his colleagues from the Department of Endocrinology at the Changi General Hospital, the Departments of Sports Medicine and Rehabilitative Services at the Changi General Hospital assumed that diet and exercise should be more than an alternative to drug interventions. The latter has in fact been established in numerous previous studies, already. In obese Australian men who lost an average of 10% of baseline weight from caloric restriction alone using meal replacements or a low-fat diet and in men after 2 years of weight loss using Mediterranean diet and exercise, for example, the test scores in the International Index of Erectile Function 5-item (IIEF-5) improved by ~20% (Khoo 2011; Esposito. 2004).

Exercise works, but how much exercise does it take?

What has been missing up to know is yet a study that would establish the amount of exercise that's necessary to boost the existing benefits of energy restriction. And guess what!? That's exactly what Khoo et al. set out to do - conduct a trial that would compare the effects of 24 weeks of ...

• low volume medium intensity exercise training (<150 minutes/week) and
• (relatively) high volume medium intensity exercise (>200m/w) training

on the body weight, waist circumference (WC), body composition, International Index of Erectile
Function 5-item (IIEF-5), International Prostate Symptom Scale (IPSS) (for LUTS), and 36-item Short Form Survey version 2 Instrument (SF-36) (for QoL) scores, plasma testosterone, sex-hormone binding globulin, glucose, insulin and lipids, and endothelial function (by Reactive Hyperaemia Index [RHI] using finger plethysmography) of 90 abdominally obese Asian men (BMI >27.5 kg/m²; WC>90 cm; mean age 43.6y), who ha not moved an inch all day long in the past years (average amount of "exercise" ~80 minutes/week).

Freedom of choice: Exercise when and where you want

The aerobic only *sigh* exercise program could be performed on whatever equipment / sportive activity the subject like - stationary cycling, treadmill, elliptical crosstraining, brisk walking, jogging, cycling, and swimming, all were eligible for 90–150 minutes/week - the subjects were free to chose and pick, but they had to record type and exercise duration and make sure that they would hit their target heart rates of 55–70% of their individual maximal heart rate (HR_max=220-age) on whatever they did.

Figure 1: Absolute (body composition) and relative changes (lipids, sex hormones & erectile function); after 6 months on the diet + low vs. high volume exercise regiment;LUTS = lower urinary tract symptoms; IIEF-5 = International Index of Erectile Function 5-item questionnaire; IPSS = International Prostate Symptom Scale; SF-36 PCS and MCS = 36-item Short Form Survey version 2 Instrument Physical Component Summary and Mental Component Summary scores (Khoo. 2013)

In combination with the obligatory reduction in energy intake (-400kcal/day; ~15-20% of their baseline intake) both groups made significant progress. In comparison to the -4.7kg of body fat the guys in the "high volume" group (I use the quationmarks to emphasize that I would not consider ~30min of exercise/day exorbitantly high, considering the fact that the this was cycling, walking or swimming at a relatively moderate intensity) lost in the course of the 6-months intervention, the -1.1kg of total fat mass the guys in the low volume group dropped do yet look pretty pathetic.


"Doing more" for total & free testostosterone!?

What are signs that you are already doing too much ?

• constant fatigue that does not disappear, when you take a day off and get enough sleep (too much volume)
• inability to fall asleep (too much high intensity work)
• inability to sleep through (too much volume)
• getting up to pee every 1-2h (too much volume, too few carbs vs. too much protein)
• the 4am wake-up call = inability to sleep through (see above, fasting in the evening)
• no fat loss despite caloric deficit (eating too little + high training volume)
• losing muscle, not fat (too much volume, too much medium intensity cardio)
• low sex hormones / drive, low thyroid function, high rT3 (too much volume, too much protein, too little fat & carbs, not eating enough)

If you want more insights, you can find them in the Athletes Triad Series.

If we take a look at a couple of other parameters the scientists evaluated, you will notice a clear dose-response relationship. Much contrary to the participants in the Rosenklide study, I wrote about in 2012, which had a much higher training volume and intensity, doing more did - within this narrow relatively low volume moderate intensity regimen - did thus really yield superior results. Even more, the dose-response relationship is almost linear: 2x more exercise, 2x more weight loss, 2x more fat loss, 2x greater reduction in insulin, 2x greater reduction in blood glucose.

For testosterone (>2x more) and free testosterone (almost 5x more), the benefits were even more pronounced and the difference between the ratio of fat and lean mass lost 6.7 for the high vs. 5.5 for the low volume group are certainly not to be scoffed at, either.

Still, we just have to go back to the counterproductive effects Rosenkilde et al. observed in their study (go back and learn more), to see that the 30 minutes of exercise per day are probably not the end of the flagpole, but a very happy medium beyond which previously untrained individuals, and experienced trainees who work out at a correspondingly higher intensity level, could hit a wall and spiral down into the abyss of chronic overtraining - especially when exercise habits like that are combined with a diet that does not only induce an energy deficit of 20% but does at the same time make it particularly hard for the body to use the energy it gets... yep, I am talking about the notorious high protein, low carb, low fat diets the scaremongerism on both sides of the low-carb vs. low-fat divide have made so popular (learn more).

---

Bottom line: Diabesity, erectile dysfunction and hypogonadism? The solution to this triad is there! It's not complicated, but it requires commitment, it requires discipline and it will cut your daily screen time by 30 min... if you or your overweight friends don't feel that this is worth it, let them waste their money and risk their health by jumping from one "quick fix" solution and diet (e-)book to the other. If not, write the numbers "20/30 x 6" on a DinA4 sheet and pin that to your or your friends' fridge to remind yourself or them that it takes a caloric reduction of 20% + 30min of moderate intensity exercise and the stubbornness to adhere to that protocol for 6 months day in day out (I guess 90% compliance would even be enough) to take a huge step on your way towards normalizing your body composition, glucose and lipid metabolism and endocrine and erectile function... and on a last note: I bet this works for overweight women with PCOs, as well.

References:

• Esposito K, Giugliano F, Di Palo C, Giugliano G, Marfella R, D’Andrea F, D’Armiento M, Giugliano D. Effect of lifestyle changes on erectile dysfunction in obese men: A randomized controlled trial. JAMA 2004;291:2978–84.
• Khoo J, Piantadosi C, Duncan R, Worthley SG, Jenkins A, Noakes M, Worthley MI, Lange K, Wittert GA. Comparing effects of a low-energy diet and a high-protein low-fat diet on sexual and endothelial function, urinary tract symptoms, and inflammation in obese diabetic men. J Sex Med 2011;8:2868– 75.

Glycogen-Depleted Athletes may Benefit from 0.3g/kg BCAA Supplementation: Improved Endurance & Lipid Oxidation

If you have ever read up on the general recommendations concerning "cardio on an empty stomach" you will most likely have encountered the advice to supplement with branched-chained amino acids (BCAA) before or in the course of the workout. I have always considered this to be a solid advice, up to now, I had yet not seen a study underpinning the common sense reasoning behind the suggestion.

Now, Gualano et al. (Gualano. 2011) published a study that investigated the effect of BCAA supplementation on exercise performance and energy metabolism in glycogen-depleted athletes (let's assume by now that an athlete following a low carb diet is in fact glycogen-depleted when he wakes up). In a double-blind placebo controlled fashion the scientists provided their subjects with either 0.3g/kg BCAA or placebo for 3 days...

On the second day, subjects were submitted to an exercise-induced glycogen depletion protocol. They then performed an exhaustive exercise test on the third day, after which time to exhaustion, respiratory exchange ratio (RER), plasma glucose, free fatty acids (FFA), blood ketones and lactate were determined. BCAA supplementation promoted a greater resistance to fatigue when compared to the placebo (+17.2%). Moreover, subjects supplemented with BCAA showed reduced RER and higher plasma glucose levels during the exhaustive exercise test.

For all of you who are now asking themselves, what validates the claim of increased fatty acid oxidation, its the reduced respiratory exchange ratio. Although its arguable how reliable a measure the ratio between O2 in and CO2 out is in terms of fatty acid metabolism, these results support the hypothesis and real world observation that BCAA-supplemented cardio on an empty stomach reliably promotes fat loss.