Men must drink with male friends twice a week to stay healthy, study finds

Well, I'm deficient.  I usually get this with female friends instead. Can't find the actual research. So you male stroke survivors need to be out drinking with your buddies twice a week. What is your doctor doing to accomplish that?    

Men must drink with male friends twice a week to stay healthy, study finds

January generally marks the month of New Year’s Resolutions – many times including the vow to swear off alcohol.
But, hold on. Don’t move too quickly.
A new study conducted by the University of Oxford has discovered that for men, going out for a few pints isn’t just fun, it’s downright essential.
In fact, according to this report, men should go out twice a week by necessity to stay healthy.
The study, conducted by Robin Dunbar, a psychologist, and director of Oxford University’s social and evolutionary neuroscience research group, determined that men must physically meet with four friends, two times a week, in order to reap the full benefits of male friendship.
Benefits of strong male friendships include a stronger immune system, the release of endorphins, an overall decrease in anxiety levels, and (apparently) even higher levels of generosity.
Dunbar goes so far as to recommend guys “do stuff” while they socialize, and that going bar crawling for a night reinforces a sense of teamwork and camaraderie.
“Bonds can be formed through a range of activities from team sports to male banter — or simply having a pint with your pals on a Friday night,” Dunbar states.
According to the same study, most men get far less male bonding time than what they require. One in three men in the United Kingdom can’t find the time to meet with friends once a week, and 40% of men are only able to make a “guys’ night” a weekly affair.
Dunbar suggests that despite spending 20% of their day interacting through other means, men need to meet face to face to keep their friendships strong, and meeting for a few pints is the perfect way to achieve this.
So there you have it.
An apparent free pass for the men twice a week, and an opportunity to for the ladies to have a couple nights off from the old man!
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Male Scent May Compromise Biomedical Research

Another problem in rodents to watch out for. Goes along with rodent inflammation is not the same as human inflammation.

Male Scent May Compromise Biomedical Research 

Testosterone increases neurotoxicity of glutamate in vitro and ischemia-reperfusion injury in an animal model

When will someone from that Great stroke association analyze all this about testosterone and create a stroke protocol? Do you really think every neurologist is up to studying this and coming to the same conclusion?
http://jap.physiology.org/content/92/1/195.short

Abstract

Increasing evidence has demonstrated striking sex differences in the outcome of neurological injury. Whereas estrogens contribute to these differences by attenuating neurotoxicity and ischemia-reperfusion injury, the effects of testosterone are unclear. The present study was undertaken to determine the effects of testosterone on neuronal injury in both a cell-culture model and a rodent ischemia-reperfusion model. Glutamate-induced HT-22 cell-death model was used to evaluate the effects of testosterone on cell survival. Testosterone was shown to significantly increase the toxicity of glutamate at a 10 μM concentration, whereas 17β-estradiol significantly attenuated the toxicity at the same concentration. In a rodent stroke model, ischemia-reperfusion injury was induced by temporal middle cerebral artery occlusion (MCAO) for 1 h and reperfusion for 24 h. To avoid the stress-related testosterone reduction, male rats were castrated and testosterone was replaced by testosterone pellet implantation. Testosterone pellets were removed at 1, 2, 4, or 6 h before MCAO to determine the duration of acute testosterone depletion effects on infarct volume. Ischemic lesion volume was significantly decreased from 239.6 ± 25.9 mm³ in control to 122.5 ± 28.6 mm³ when testosterone pellets were removed at 6 h before MCAO. Reduction of lesion volume was associated with amelioration of the hyperemia during reperfusion. Our in vitro and in vivo studies suggest that sex differences in response to brain injury are partly due to the consequence of damaging effects of testosterone.

Estrogen-Mediated Neuroprotection After Experimental Stroke in Male Rats

If we don't know about testosterone then how about estrogen?  Your doctor should know  how to use this in your stroke protocol. Its only 14 years old so if your doctor hasn't figured out how to incorporate this into your protocol then you need to find an up-to-date doctor. We really need a Great stroke association, this luck of the draw in hoping your doctor is up-to-date is stupid. But don't listen to me, your medical gods are omnipotent.
http://stroke.ahajournals.org/content/29/8/1666.short

Abstract

Background and Purpose—We have previously shown that 17β-estradiol reduces infarction volume in female rats. The present study determined whether single injection or chronic implantation of estrogen confers neuroprotection in male animals with middle cerebral artery occlusion (MCAO) and whether there is an interaction with endogenous testosterone.

Methods—Male Wistar rats were treated with 2 hours of reversible MCAO. In protocol 1, acute versus chronic estrogen administration was examined in groups receiving the following: Premarin (USP) 1 mg/kg IV, immediately before MCAO (Acute, n=13, plasma estradiol=171±51 pg/mL); 7 days of 25 μg (E25, n=10, 10±3 pg/mL) or 100 μg 17β-estradiol (E100, n=12, 69±20 pg/mL) by subcutaneous implant; or saline (SAL, n=21, 3±1 pg/mL). Laser-Doppler flowmetry was used to monitor the ipsilateral parietal cortex throughout the ischemic period and early reperfusion. At 22 hours of reperfusion, infarction volume was determined by 0 2,3,5-triphenyltetrazolium chloride staining and image analysis. In protocol 2, rats were castrated to deplete endogenous testosterone and then treated with estradiol implants: castration only (CAST, n=13, estradiol=5±2 pg/mL), sham-operated (SHAM, n=10, 4±2 pg/mL), estradiol implant 25 μg (CAST+E25, n=16, 7±2 pg/mL) or 100 μg (CAST+E100, n=14, 77±14 pg/mL).

Results—Cortical infarct volumes were reduced in all estrogen-treated groups: Acute (21±4% of ipsilateral cortex), E25 (12±5%), and E100 (12±3%) relative to SAL (38±5%). Caudate infarction was similarly decreased: Acute (39±7% of ipsilateral striatum), E25 (25±7%), and E100 (34±6%) relative to SAL (63±4%). Castration did not alter ischemic outcome; cortical and caudate infarction (percentage of respective ipsilateral regions) were 37±5% and 59±5% in CAST and 39±7% and 57±5% in SHAM, respectively. Estrogen replacement reduced infarction volume in castrated animals in cortex (19±4% in CAST+E25 and 12±4% in CAST+E100) and in caudate (42±6% in CAST+25 and 20±7% in CAST+100). Laser-Doppler flowmetry results during ischemia and reperfusion was not different among groups.

Conclusions—Both acute and chronic 17β-estradiol treatments protect male brain in experimental stroke. Testosterone availability does not alter estradiol-mediated tissue salvage after MCAO.

Could androgens maintain specific domains of mental health in aging men by preserving hippocampal neurogenesis?

 Hell, I'm aging and I want to know the answer. Ask your doctor if you have low-T.
http://scholar.google.com/scholar_url?hl=en&q=http://www.nrronline.org/nrren/ch/nrr-2012-pdf/28k/2227-2239.pdf&sa=X&scisig=AAGBfm0r33jqJ-f7n0w86tRLvT9F7irwpA&oi=scholaralrt
Florey Neurosciences Institute, Melbourne Brain Centre, the University of Melbourne, Parkville, Victoria 3010, Australia
Abstract
Interest surrounds the role of sex-hormones in regulating brain function outside of reproductive behaviour. Declining androgen production in aging males has been associated with cognitive impairment, depression and increased risk of developing Alzheimer's disease. Indication for testosterone replacement therapy is based on biochemically determined low circulating testosterone combined with manifest symptoms. However, which aspects of age-related cognitive decline are attributable to low circulating testosterone remain ambiguous. Studies examining cognition in aging men receiving testosterone replacement therapy have yielded equivocal results. The exact role of testosterone in maintaining cognitive function and the underlying neural mechanisms are largely unknown, though it would appear to be domain specific. Clarity in this area will provide clinical direction toward addressing an increasing healthcare burden of mental health decline coincident with increasing longevity. The premise that androgens contribute to maintaining aspects of mental health in aging men by preserving hippocampal neurogenesis will be used as a forum in this review to discuss current knowledge and the need for further studies to better define testosterone replacement strategies for aging male health.