http://fightaging.org/archives/2009/05/exercise-reactive-oxygen-species-and-antioxidants.php

Mitochondrial reaction to ROS ("free radicals") is part of how we gain increased work capacity through exercise.

Some guy recently showed a 30% increase in mouse lifespan with some mitochondrial-ROS-protective drug (which you can't obtain yet).  This would probably come at the cost of decreased adaptation to exercise.

Most antioxidants do a terrible job of protecting the mitochondria but somehow prevent the ROS generated in exercise from triggering the exercise benefit - worst of all possible outcomes.  This may explain why a recent study of antioxidants in humans found them to be harmful (esp. Vit E, but also others) to overall lifespan.

There are several antioxidants which protect mitochondria, all of which are avaliable as supplements:

1. CoQ10

http://dx.doi.org/10.1016/j.expneurol.2005.07.012

2. Chlorophyllin

http://dx.doi.org/10.1016/S0300-483X(00)00278-X

3. Carnitine and Lipoic Acid

http://pmid.us/16802113

4. Quercetin 

http://www.wellnessresources.com/studies/entry/quercetin_protects_mitochondria

None of which extend life notably in healthy mice. e.g. see this null result for CoQ10:

http://pmid.us/16443163

So there's nothing really great available.  Resveratrol, which is among other things an antioxidant, has some weak evidence of providing a net longevity benefit:

In the only positive human trial, extremely high doses (3–5 g) of resveratrol in a proprietary formulation have been necessary to significantly lower blood sugar.^[2] Despite mainstream press alleging resveratrol's anti-aging effects,^[3] there is little present scientific basis for the application of these claims to mammals

Red grapes have the most resveratrol; blueberries have 1/10th the amount (blueberries have some other compound, thought to be brain-protective)

Autophagy removes cell components - including ROS-damaged proteins and organelles - by engulfing and digesting them, producing wastes and recycled nutrients. ... Upregulating autophagy [has] extraordinarily wide-ranging benefits. Interventions that extend healthy lifespan in animal models include calorie restriction, resveratrol, spermidine, and rapamycin, and in each operates, at least in part, through autophagy. Upregulating autophagy has positive effects in models of several specific neurodegenerative diseases, too ... antioxidants inhibit basal autophagy and block the induction of autophagy by calorie restriction and other means. Because this effect inhibits the central mechanism of cell repair, it helps explain why dietary antioxidants have failed to deliver their expected benefits to health and longevity." I would have said it has more to do with failing to target mitochondria, given the benefits demonstrated by mitochondrially targeted antioxidants. As Drexler notes, however, there's research to back up the antioxidant-autophagy link, which may have some relation to earlier research showing antioxidant supplementation to interfere with the processes of hormesis, and thus block beneficial effects of mild stress such as exercise. 

Autophagy is good (if you want to live long).  Antioxidants also generally interfere with that.

Rapamycin is immunosuppresive and so not of practical interest (unless you want to live in a bubble).

Spermadine (exact mechanism unknown) increases autophagy in cultured cells, and lifespan in yeast, nematodes, and flies.

This sign could use a "the" and another "l":

Criticisms of the recent Gabbert et al AD36<->obesity paper:

(found via http://scienceblogs.com/erv/2010/09/we_are_exposed_to_more_viruses_1.php ):

(also, another study of mostly-fit and all-exercising army adults finds no link between AD36 and obesity)

The data indicated that for the AD36 Negative group, the ages were 8-11 yrs (18%), 12-15 yrs (65%), and 15-18 yrs (17%). For the AD36 Positive group, the ages were 8-11 yrs (5%), 12-15 yrs (32%), and 15-18 yrs (63%). This is as we surmised above: more older kids are in the AD36 group. The weight average for the AD36 Negative group was 69 kg (+/- 24 kg SD); for the AD36 Positive group is was 93 kg (+/- 24 kg SD).

Thus, one sure finding is that older kids are heavier: in fact, they were about 24 kg heavier, which translated to about 50 lbs. It is at least good to see that the press release got this figure correct.

Another finding is that older kids are more likely to have been previously infected by AD36, also as we surmised (in two years, you have have plenty of colds).

There is no modeling of the expected distribution of biometric properties of the two populations (AD36-negative and -positive) given the other statistics (age,sex,race) reported. This is extremely surprising to me.

However, it's not just that older kids (adults, really) weigh more - the size-relative metrics BMI, and waist/height ratio were also higher in the AD36 antibody group. But still, those should be adjusted for age as well; their distribution (and mean) will surely change with age, and definitely will change for the worse with age in the destined-to-be-obese (it takes time to blossom into full adult obesity). The fact that no such adjustment was made means that the study contributes almost no additional evidence, but this could be corrected with a proper analysis. And, supposing the raw data is available, this can happen.

The two populations also have a significant sex difference: the AD36-negative group is 58% male, and the AD36-positive is only 47%. However, it looks like adult men and women have similar recommended BMI and waist/height ratios (actually, women are recommended to have slightly lower) - I don't know what the actual averages are. Racially, there's a 13% shift from "non-hispanic white" to "hispanic" in the AD36-positive population. While I don't know how different those groups are re: AD36-positivity or BMI etc., this should be considered as well. The age mismatch is definitely the most severe problem.

The "discussion" section lists much other work which seems to provide better evidence of a AD36-obesity link (I assume the authors are leaving out any negative results that don't support their views). For example:

[In] a small substudy of adult twins with discordant AD36-specific antibody status, 13 Twins with antibodies to AD36 were noted to have higher BMI values and greater proportions of body fat then their respective antibody-negative twins.

(evidence of correlation, not causality - would be quite strong evidence if the number of twins and BMI/body fat mismatch were large enough)

infection of nonhuman primates, rodents, and chickens with AD36 increased total body fat independent of energy intake

(causality in animal models, although i would hope for exposure rather than infection as the trigger - perhaps p(infection|exposure) is high enough that it doesn't matter)

adipose-derived stem/stromal cells ... infected with AD36 showed increased differentiation and higher levels of lipid accumulation than noninfected control cells

(causal, but in vitro: doesn't guarantee net fattening in the context of a human body)

 

from http://en.wikipedia.org/wiki/Aids#Prevention

Estimated per act risk for acquisition
of HIV by exposure route (US only) ^[80] Exposure Route Estimated infections
per 10,000 exposures
to an infected source Blood Transfusion 9,000^[81] Childbirth (to child) 2,500^[61] Needle-sharing injection drug use 67^[82] Percutaneous needle stick 30^[83] Receptive anal intercourse^* 50^[84][85] Insertive anal intercourse^* 6.5^[84][85] Receptive penile-vaginal intercourse^* 10^[84][85][86] Insertive penile-vaginal intercourse^* 5^[84][85] Receptive oral intercourse^*§ 1^[85] Insertive oral intercourse^*§ 0.5^{[85] *} assuming no condom use
^§ source refers to oral intercourse
performed on a man

So the reason to use a condom is to prevent insemination, and the spread of the much more prevalent and virulent STDs like chlamydia and gonorrhea.  I guess HIV is scarier because it's less curable, and often leads to AIDS, which is usually fatal.

In Study 1, the scent of women near peak levels of fertility heightened the men’s implicit accessibility to sexual concepts. Study 2 demonstrated that, among men who reported being particularly sensitive to odors, scent cues of fertility triggered heightened perceptions of women’s sexual arousal. Study 3 revealed that in a face-to-face interaction, cues of fertility increased men’s tendency to make risky decisions and to behaviorally mimic a female partner. …

Whereas women may have been selected to suppress cues of ovulation in order to sustain men’s commitment, men have been selected to identify fertility cues in order to enhance a short-term mating endeavor’s probability of reproductive success. … It is unlikely that all indicators of fertility could be suppressed, because some detectable shifts in hormones are needed to facilitate ovulation. Consequently, men must rely on fairly subtle cues (e.g., changes in scent and skin tone) associated with those hormonal shifts to help them respond adaptively to women’s changing levels of fertility.

A 

book review 

in the latest Quarterly Review of Biology:

The Evolutionary Biology of Human Female Sexuality. [2008] … Thornhill and Gangestad argue that [human] women possess two distinct evolved sexualities. One is the “extended sexuality” that women engage in when conception is impossible; the other they call “estrous” sexuality. The former functions to elicit “material benefits” from males, the latter to acquire “good genes” for offspring, and in keeping with these distinct functions, candidate male partners are evaluated on distinct criteria in the two contexts.

Cheating happens.  Men are more likely to push for it with a fertile woman, and woman are more likely to desire it when fertile.

In their article, to be published in a forthcoming

Psychological Science, Cuddy and coauthors Dana R. Carney and Andy J. Yap of Columbia University detail the results of an experiment in which forty-two male and female participants were randomly assigned to a high- or low-power pose group. No one was told what the study was about; instead, each participant believed it was related to the placement of ECG electrodes above and below his or her heart.

Subjects in the high-power group were manipulated into two expansive poses for one minute each: first, the classic feet on desk, hands behind head; then, standing and leaning on one's hands over a desk. Those in the low-power group were posed for the time period in two restrictive poses: sitting in a chair with arms held close and hands folded, and standing with arms and legs crossed tightly. Saliva samples taken before and after the posing measured testosterone and cortisol levels. To evaluate risk tolerance, participants were given $2 and told they could roll a die for even odds of winning $4. Finally, participants were asked to indicate how "powerful" and "in charge" they felt on a scale from one to four.

Controlling for subjects' baseline levels of both hormones, Cuddy and her coauthors found that high-power poses decreased cortisol by about 25 percent and increased testosterone by about 19 percent for both men and women. In contrast, low-power poses increased cortisol about 17 percent and decreased testosterone about 10 percent.

Not surprisingly, high-power posers of both sexes also reported greater feelings of being powerful and in charge. In addition, those in the high-power group were more likely to take the risk of gambling their $2; 86 percent rolled the die in the high-power group as opposed to 60 percent of the low-power posers.

Previous research established that situational role changes can cause shifts in hormone levels. In primate groups, for example, after an alpha male dies the testosterone levels of the animal replacing him go up. The hormonal shifts measured in this experiment show that such changes can be influenced independent of role, situation, or any consciously focused thoughts about power. The physical poses are enough.

Does being told to take such poses explain the effect? Does taking the poses voluntarily in solitude preserve the effect? Or is it only taking the pose in an environment where you're watched by others?