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Showing content with the highest reputation since 03/20/2014 in all areas

  1. 8 points
    Wow, this topic is a lot to digest. That list of supplements you're consuming is unreal. Past a certain point, I can't believe all of those individual supplements are a net positive for you all the time. Some of those supplements are weak stimulants as well, with different half-lives that will guarantee you're lightly withdrawing from different compounds all day long and experiencing some long-term changes in response to those compounds. At this point, it would be helpful if you could ditch literally all of the non-prescribed supplements and let your body wash out for at least a couple weeks. The purpose of this is to re-learn what your baseline actually feels like. It's entirely likely that at least some of the lethargy and flatness you're feeling is a result of the giant supplement cocktail you're taking. Next, like Sanction said, you really need to get on top of your addictive tendencies and genuinely understand what the medications are for in the long-term. If you find yourself constantly escalating your Adderall dose as a way out, that's your top problem to solve. Adderall has short-term effects when you first start taking a new dose, which give way to long-term effects once your brain adjusts. If you're constantly escalating the dose each time your brain adjusts, that means you're chasing the short-term effects. As you well know, those effects are not sustainable, just as escalating dose patterns are not sustainable. If you're going to stick with the Adderall, you must strictly adhere to a dosing schedule with purely therapeutic value. You will find that this does work long-term for ADHD symptoms, but it won't provide motivation, euphoria, and excessive energy in the long-term. This is perfectly normal and entirely expected, and should not be taken as damage to your dopaminergic system. That's just normal acclimation to the drug. It's not possible to derive long-term euphoria and motivation from it. If you can't take it without escalating your dose, you need to taper off and be done with it, because it's not doing you any favors. Something Anonymous' suggestion to switch to Modafinil is worth considering. Don't be fooled: Modafinil still has abuse potential, though it does appear to be less prone to abuse by addictive individuals. It's actually used in recovering Methamphetamine and other stimulant addicts for exactly what you're describing. Finally: You've got a lot going on with your supplement laundry list, Lexapro, Lamictal, Vyvanse, Adderall, Testosterone. It's extremely likely that even some combination of those medications and one of your 30? 40? supplements is inducing some amount of the anhedonia and fatigue that you've convinced yourself is damage to your dopamine system. Give some minimal time to withdraw, like 2-4 weeks, you should really be close to your original pre-Adderall baseline state. That's my advice: Instead of looking for more substances to add to the list, start cutting back, and cut back significantly. Less is more here. Find baseline, understand your baseline, and know what you're really working with. Throwing more drugs and supplements at the problem isn't likely to move things in the right direction, but it certainly could add one more problem to the pile.
  2. 8 points
    Clin Nutr. 2015 Feb 7. pii: S0261-5614(15)00040-0. doi: 10.1016/j.clnu.2015.01.018. [Epub ahead of print] Muscle strength gains during resistance exercise training are attenuated with soy compared with dairy or usual protein intake in older adults: A randomized controlled trial. Thomson RL1, Brinkworth GD2, Noakes M2, Buckley JD3. Author information Abstract BACKGROUND & AIMS: Maintenance of muscle mass and strength into older age is critical to maintain health. The aim was to determine whether increased dairy or soy protein intake combined with resistance training enhanced strength gains in older adults. METHODS: 179 healthy older adults (age 61.5 ± 7.4 yrs, BMI 27.6 ± 3.6 kg/m2) performed resistance training three times per week for 12 weeks and were randomized to one of three eucaloric dietary treatments which delivered >20 g of protein at each main meal or immediately after resistance training: high dairy protein (HP-D, >1.2 g of protein/kg body weight/d; ∼27 g/d dairy protein); high soy protein (HP-S, >1.2 g of protein/kg body weight/d; ∼27 g/d soy protein); usual protein intake (UP, <1.2 g of protein/kg body weight/d). Muscle strength, body composition, physical function and quality of life were assessed at baseline and 12 weeks. Treatments effects were analyzed using two-way ANOVA. RESULTS: 83 participants completed the intervention per protocol (HP-D = 34, HP-S = 26, UP = 23). Protein intake was higher in HP-D and HP-S compared with UP (HP-D 1.41 ± 0.14 g/kg/d, HP-S 1.42 ± 0.61 g/kg/d, UP 1.10 ± 0.10 g/kg/d; P < 0.001 treatment effect). Strength increased less in HP-S compared with HP-D and UP (HP-D 92.1 ± 40.8%, HP-S 63.0 ± 23.8%,UP 92.3 ± 35.4%; P = 0.002 treatment effect). Lean mass, physical function and mental health scores increased and fat mass decreased (P ≤ 0.006), with no treatment effect (P > 0.06). CONCLUSIONS: Increased soy protein intake attenuated gains in muscle strength during resistance training in older adults compared with increased intake of dairy protein or usual protein intake. Clinical Trial Registration: ACTRN12612000177853 www.anzctr.org.au. Copyright © 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved. KEYWORDS: Dairy; Older adults; Protein; Resistance training; Soy; Strength PMID: 25702958 [PubMed - as supplied by publisher]
  3. 8 points

    More Proof Gym Rats are Gay

    Depending on the intensity of your anaerobic training, your preference for riskiness may be anything from vanilla frottage in an NBC suit through to public demonstrations of aggressive blood play and gratuitous non-consensual fecal transfer in the Liberia / Guinea region. If you do tabatas too, you can add tattooing the word Allah onto the forehead of the recipient of your carnal affections in the previous case. J
  4. 7 points
    Growth Factor

    GF's "CS Goes Pubic" Log

    By the way, I think I shared the news a few years ago that my mom was diagnosed with stage 4 melanoma. As of yesterday, she is officially (cancer) disease free! Long live nivolumab/pembrolizumab!
  5. 7 points
    Growth Factor

    GF's "CS Goes Pubic" Log

    I want to share this story without having you guys read too much into this or interpret it the wrong way. I just had one of the most fun moments of the past 12 years of my life. I got to the gym late because of my PT today, which was actually very hard and again very humbling with banded monster walks that kicked my ass. Anyways, I'm feeling super gassed a little past midway through my workout, and after finishing dips I decide I just need a break and would walk home and finish up dumbbell arm work at my apt gym. I noticed a storm was brewing outside earlier, and as I approach the doors I see torrential rains slamming hard. You can hear this stuff it's so loud. I decided it'd be fun to walk in the rain since I couldnt remember the last time I did something like this (maybe mud-sliding or tackle football in college?). I take all my precious belongings, and I take my shirt off, I shove them into my slinger, and I start back. Well. This rain is coming down fucking hard. 100% this felt like getting hosed down by a fire engine hose. If this hasn't happened to you before, it's pretty brutal. I start running. The winds start picking up hard. As I'm running by this newly constructed apt complex with fencing and canvas covering the fence, the wind blows this WHOLE fence down on me. With the canvas, it's like it's added resistance (think like a parachute). I basically have to hold the fence up from crushing me, walk, pick the other side of the fence up while letting the side I just walked past down, until I clear it all. My path is completely constrained by construction median that's making a temporary sidewalk right on a heavily trafficked street. I take shelter in a nearby parking deck just to catch something resembling a breath after that absolutely intense core workout. I start back up, and I get to a large intersection with a red light for pedestrians, and I start getting hit with waves of water from passing cars. It's actually hilarious. After I get the walk and continue jogging, I'm now ankle deep in puddles of water. At some point, the sewage was overflowing and was shooting water up in the air right under me when I went over a manhole. I finally get back to my apartment, and I somehow decide to attempt to continue the rest of my workout which was DB hammer curls and extensions. I pick up the 60s and I felt like I just performed a max effort deadlift. It's time to call it. I honestly can't remember the last time I had a moment of this intense, pure joy like running through this storm.Even the the rain hurting me as it came down and that fence challenge added to the experience. I'd run it again 10/10. Gonna think about ordering a pizza after that one.
  6. 7 points

    Liftin' weights and other shit

    Went to my first day at my fancy new job today. Seems like it'll be cool. You know, if you're into that stupid science bullshit. Gonna be learning a bit of shit by shadowing in the Columbus area this week and then in house training for 2 weeks after that followed by another 4-8 weeks of shadowing. Then I get to be released into the world to fuck shit up on my own. If I ever come near any of your towns, we should hang out (no homo). Or some homo. Really, however much homo you need to make it work for you is fine.
  7. 7 points

    Liftin' weights and other shit

    Got called by Mettler today and offered the position for the traveling service engineer. They're gonna get the paperwork together to give me an official offer and such but it's mine. I should probably get that next week and hopefully, I'll be starting within 2-3 weeks. I feel like I can breathe again. First time in fucking months, damn near a year.
  8. 7 points

    fasted or not ?

    None of the studies which measured actual FAT LOSS showed any benefits with fasted cardio compared to fed cardio. Acute studies that showed increased fat oxidation and lipolysis didn't pan out in chronic studies. The article above is looking at an acute study looking at surrogate outcomes, but still giving strong lifestyle recommendations which is misleading and untrue. So based on the current research, food after or before cardio is a personal choice. ☺️
  9. 7 points

    It's The Carbs, Stupid.

    Yes...I mean I was still losing when drinking vodka and diet coke, but I think got about an 8-10 lb boost once I put that shit down. I started at 270 (crazy, didn't even know I weighed that much), and am now down to 206/207. I'm going to try and get under 200, like 190-195, then go to phase II, and hit the weights again. Once in awhile, I eat one of my kids nuggets, or go off by a little bit (very little bit), but because I've been doing it for so long, it still keeps me in ketosis, just small...then 2 or so days later, I'm right back in moderate/large. I'll be honest, I haven't been hitting the intervals as much, but plan to this week more....but had I been, I would have been under 200 already. Another thing I noticed....my ankles were swollen, and I had those spots all over them. Seriously, it got pretty bad looking for a bit there. Since losing all of this weight, and stopped drinking, not only do my ankles look alot smaller and normal, but my skin has cleared up for the most part. 91 days no alcohol, and honestly don't miss it at this point.
  10. 7 points

    Xfit vacations.... wtf?

    Guys, I'm hosting a Powerlifting Vacation package. It will be held at my house. Cost will be $500/day. That price may seem steep but trust me...it is FULLY inclusive. The days activities will be as follows: -Wake up and eat leftover dinner -Fold my laundry for me so my wife gets off my back -You can walk my dog -Your personal chef will make shitty skillet hamburgers on potato bread because I forgot to buy buns -Go to the gym and squat for about an hour straight -I'll drive you to Lã McDönald's for a fabulous, calorie dense, postworkout meal (you must limit your meal to $10 in order for it to be included in the price package) -We'll go back and take a group epsom salt bath - FYI, Gas for my truck will be at your expense My paypal is ready
  11. 7 points


    The times, they are a'changing...
  12. 6 points
    Emperor G_D

    Old Powerlifters don't just die...

    Day 2 I made day 2! Woot. OK: Deadlift 135x10 185x10 225x8 245x8 265x8 275x8 Hamstring curls 35x10 45x10 50x8 DB Bench Wondering if this will treat my disk issues a bit better than flat, arched benching 65x10 70x10 75x10 80x10 Machine chest shit No clue what name, or angle it is, but it was inclined and I hated the fuck out of it. 90x10 180x5 200x5 140x8 90x7 Seated row Interesting machine with an actual rowing motion (like on a skell). The arms come back, and then out as you approach your chest. I liked it. 130x10 90x10 95x8 100x8 Triceps hell new machine; new weight scale. lol 57.5lbsx20x2 (overhand) 42.5x20, 47.5x20 (underhand) Biceps curls on the same machine 57.5x10x3S My glute med is a bit tweaky. Hopefully it relaxes in the next hour. My Uncle had a 2-artery heart attack this week. The widowmaker was 100% blocked, and there is another one that is 70% blocked. He drove himself to the hospital in his RV, since he was out in the woods. He received his first stent within the first hour of having his heart attack, and it looks like there was no muscle tissue damage, or at least very minor damage. They won't apply the second stent for a while, since I guess it's not fully blocked? My wife heads off to work a new job on top of her other 2 jobs, so after some time, I'm guessing the money stress will lessen a little bit. I'm IFing, since I have to do something to trim some weight. My uncle is a "large" guy, but his weight at admission time was 231...
  13. 6 points

    Logging Yggdrasil

    Thanks for the feedback guys, I appreciate it. And I'm really bad with following up. Apparently my deload continues. Lacking an actual workout to log, I'll share one of my delusions, or if you want to be charitable, superstitions. You know how there are men on this globe that leave the impression that all woman, world wide, got together and conspired that these men should never get laid, much less procreate? For many years now I've had the suspicion that in my case, the opposite has taken place. That all women got together and for whatever reason decided that I always should have a willing companion. Maybe it's to ward of a great evil. Maybe if I would have stayed a kissless virgin I would have had too much time on my hands to go down one rabbit hole or another. I've seen it happen. While I was out with one girl or another my childhood best friend spent his time "researching" the truth about the second world war and, well, got lost. God only knows what might have happened to me, I was quite the ambitious youth. Though my friend hooked up with a cam girl in his twenties and mellowed out.. Somewhat. I mean, it's my guilty pleasure to read online forums like askmen or relationship advice on reddit, or if I'm feeling adventurous, various incel and proto incel boards. I've also talked with many men about quotidian life, some handsome, some not, most average - and my experience has generally been different. I read and hear stories about men being all but invisible to women, always having to make a first move, still living of the memory of a compliment they got years ago, the memory salient because of it's rareness. And here I am, having had nothing but luck in the dating area, with very little work on my part. I generally showed up, some girl ended up showing an interest, and depending on my interest we slept together or dated. I guess what Louis ck said about tall skinny dudes is true. Can't really be my looks, I'd rate myself rather average. I've been told that while I don't give off a confident vibe, it's more of a I don't care and I want to be here vibe. Maybe if you're naive enough that looks like confidence. In any case, I'm sticking to the hypothesis that women secretly meet up and that my sexual wellbeing is on the agenda, on the account of "We don't need another Breivik, someone better take one for the team". That reminds me of one of the strangest, sweetest and somewhat humiliating sexual experiences I had. I was out with my friends, drinking vigorously, when we met acquaintances of a friend of mine. Among them a girl I knew in passing and was smitten with. I'm not very clear on the entire evening, but I ended up making out with the girl and taking her home. Now I know tastes differ, but I generally enjoy some post coital talk and aftercare, so the next morning, after subtly making sure she was into that, I made breakfast instead of graciously giving her the option of silently evacuating, and had a talk. During that I learned that I had slept with one of the sweetest, most giving and sexually liberal girls I've met so far, who wasn't all that into me. Her reasoning? I looked kinda lost and sad to her, was evidently into her and horny, and she wanted to provide me with some good time and nice memories. Thanks, I guess. I didn't take it negatively then, but sometimes I wonder. Mostly it's an amusing anecdote.
  14. 6 points
    Ex Dubio


    I was recently asked to post an update to this thread, with a particular focus on what treatments eventually worked for bruxism. While I wouldn't say my jaw clenching is completely gone, it's been vastly improved for the past several years to the point that it doesn't have a negative effect on day-to-day quality of life. Here's a run-down of the treatments that I credit for ultimately resolving my fairly severe case of bruxism: Permanently stopped SSRI. Permanently stopped amphetamine. Cut back almost completely on caffeine. Did a 3-month course of the muscle relaxant cyclobenzaprine. Got a strong, custom-fit nighttime mouthguard. Did a 6-month course of bruxism-specific physical therapy at a top university dental hospital. Daily mindfulness meditation. My impression is that (1), (2), and (3) were critical, and may have been sufficient by themselves, though (4) and (6) had a significant impact in controlling muscle pain when symptoms were at their peak. I'm not sure (5) made a difference on the root etiology, but it's pretty critical for preserving dental health. (7) is more of a late addition, but has proven useful for reducing re-emergence of bruxism symptoms during stressful periods. Interestingly, whatever caused my case of bruxism seems to have involved permanent changes to my brain neurochemistry. To this day, stimulants, SSRIs, and even large cups of coffee can consistently and robustly induce re-emergence of jaw clenching and associated symptoms. Thankfully, the meditation noted in (7) has been remarkably beneficial for focus and attention, so the absence of stimulants does not seem to have adversely affected my productivity. One final observation is that none of these treatments except (4) -- which is the treatment I have the most reservations about recommending -- involve additional pharmacology. I don't think this is a coincidence; every supplement- or drug-based treatment that helped with bruxism either eventually stopped helping (and in some cases started hurting) or had such prohibitive side effects that it wasn't feasible to take for an extended period of time.
  15. 6 points

    Logging Yggdrasil

    Some basics. I have no idea what my weight is as I don't own a scale, but my waist circumference is 33 inches, I think that's quite okay at 6'4. I do a casual form of intermittent fasting, mostly because I neither like breakfast nor snacking and am often too lazy to buy and/or prepare food. So it's 2 meals a day, sometimes 1 a day if I work the early shift. Mostly low(ish) carb foods, vegetables, cheese, meat, milk. No desserts, including Sachertorte, which is a highly overrated commodity. I plan on getting back in the gym soon. One of these days. Next week probably. Two weeks max. Surely before spring starts.
  16. 6 points
    Just switch to cowgirl.
  17. 6 points
    https://doi.org/10.3389/fphar.2016.00359 Δ9-THC Intoxication by Cannabidiol-Enriched Cannabis Extract in Two Children with RefractoryEpilepsy: Full Remission after Switching to Purified Cannabidiol. Crippa JA1, Crippa AC2, Hallak JE1, Martín-Santos R3, Zuardi AW1. Author information Abstract Animal studies and preliminary clinical trials have shown that cannabidiol (CBD)-enriched extracts may have beneficial effects for childrenwith treatment-resistant epilepsy. However, these compounds are not yet registered as medicines by regulatory agencies. We describe the cases of two children with treatment-resistant epilepsy (Case A with left frontal dysplasia and Case B with Dravet Syndrome) with initial symptom improvement after the introduction of CBD extracts followed by seizure worsening after a short time. The children presented typical signs of intoxication by Δ9-THC (inappropriate laughter, ataxia, reduced attention, and eye redness) after using a CBD-enriched extract. The extract was replaced by the same dose of purified CBD with no Δ9-THC in both cases, which led to improvement in intoxication signs and seizure remission. These cases support pre-clinical and preliminary clinical evidence suggesting that CBD may be effective for some patients with epilepsy. Moreover, the cases highlight the need for randomized clinical trials using high-quality and reliable substances to ascertain the safety and efficacy of cannabinoids as medicines. So, it appears in this study that the trace THC present in CBD-enriched extract was enough to offset the beneficial effects of CBD on treatment-resistant epilepsy in these two children. By swapping this enriched extract to a purified extract, the researchers were able to restore the potent effects of CBD on controlling these two children's condition. What's not clear, and this may be detailed in the paper itself that I have yet to read, is what is this "enriched extract" and what is the purified CBD. I ask this because, at least with the THC cannabinoids, it is known that the terpenes in flowers also have their own effects that change the way you experience the cannabinoids you consume. If the extract from either the "enriched extract" or the purified CBD was processed in such a way that it did not remove the terpenes then this could also be a confounding factor. Nonetheless, it's interesting that the THC present in the enriched extracts was both enough to get them high and enough to offset the relevant medicinal effects of CBD.
  18. 6 points

    Sanction lifted

    Watching two middle-aged masters of lifting in the gym today, here's the method I observed: - sit at a machine for a while, then do a warm up set - when partner arrives discuss pro golfing watched on tv during the weekend - discuss cancellation of Big Bang theory - Johnny Depp has gone broke -- theorize as to his character and drug habits - one partner does a warm-up set - Real estate. Really there is no topic more fertile at the gym than real estate. Except for... - cars, especially about the time 10 years ago when you had to fix both your Challenger and your Porsche at the same fricken time - do a final warm up set - It is not allowed that both partners should do a set at the same time, and anything that would cause audible breathing would interfere with conversation, so don't
  19. 6 points

    Sanction lifted

    Chart looks good. At this rate, you'll be lifting 100 mystery units in no time.
  20. 6 points
    Something Anonymous

    Eat shit!

    In early 2014 my wife became massively septic with C. Diff to the point that she went into multi-system organ failure and was comatose for two month. Every antibiotic available was tried to no avail. They were even flushing the small bowel directly with antibiotics via an ostomy port and the infection would not relent. After all all of that I was presented with two options: a surgical resection of the small bowell leaving my wife with short bowell syndrome and unable to digest anything other than liquid food for the rest of her life, or a fecal transplant. Obviously I opted for the transplant and I had to sign several waivers and then find a donor (I was not allowed to donate since we shared a living space). Her sister and mother were selected as donors. After whipping up their poo into a milkshake they administered the poo through her feeding tube. In a little over 12 hours her fever went from 105 to 101 and the seizures began to subside. 48 hours later they administered a second transplant and within 24 hours her fever was gone and by the end of the week she had come out of her coma. It was unreal how effective and rapid it worked.
  21. 6 points

    Oral ATP

    Appears to work when consumed acutely pre-workout. In this study, a single 400mg dose increased total volume by almost 1000kg... J Strength Cond Res. 2017 Oct 16. doi: 10.1519/JSC.0000000000002198. [Epub ahead of print] A Single Dose Of Oral Atp Supplementation Improves Performance And Physiological Response During Lower Body Resistance Exercise In Recreational Resistance Trained Males. Freitas MC1, Cholewa JM, Gerosa-Neto J, Gonçalves DC, Caperuto EC, Lira FS, Rossi FE. The aim of this study was to investigate the acute effect of ATP supplementation on performance and physiological responses during resistance exercise in recreationally resistance trained males. Eleven men (age= 27.5±5.5 yrs, weight= 83.4±9.8 kg, height= 182±0.04 cm) completed two randomized, double-blind trials: ATP supplement condition (ATP=400mg) or a placebo condition. Thirty minutes after supplement consumption, subjects performed four sets of half-squats until momentary muscular failure at 80% of the 1RM with two minutes of recovery between sets. The total number of repetitions, blood pressure, heart rate, blood lactate, and oxygen consumption were evaluated. The total weight lifted were higher for the ATP condition compared to placebo (Placebo= 3995.7±1137.8, ATP= 4967.4±1497.9 Kg; p= 0.005). Heart rate was higher at set-4 for ATP compared to placebo (p<0.001) and oxygen consumption during exercise was greater for ATP (p=0.021). There were no differences between conditions for lactate and blood pressure. In summary, a single oral dose of ATP supplementation improved lower body resistance training performance and energy expenditure in recreational resistance trained males. PMID: 29045315
  22. 6 points
    The talk went really well! The group was small, so it lent itself to lots of questions, discussion and personal stories. Win! I have a gym in Toronto I'm affiliated with, and I'm hoping they're keen to have me come in to give a chat. I'll likely break the seminar up into 2 or 3 parts, and give them over a series of days; short and sweet.
  23. 6 points


    I am not quite sure where to put this but I need to sing the praises of this stuff. It's not too methol-ly but it works really well for sore muscles/tendons/ligaments. I am still getting some post-exercise pain in my pec/anterior delt where I suffered the tear back in November and this stuff works beautifully to relieve it. I find it works better than unmetholated lidocaine cream at the same strength.
  24. 6 points

    LBM/Strength Changes with AIs in Men

    I once made the statement that despite many studies that had documented the increase in T levels in men as a result of aromatase inhibitor use, nobody had ever documented favorable changes in LBM or strength as a result of these improved testosterone levels. I now must retract that statement: Andrology. 2016 Jan;4(1):33-40. doi: 10.1111/andr.12126. Epub 2015 Nov 20. Effects of aromatase inhibition vs. testosterone in older men with low testosterone: randomized-controlled trial. Dias JP1, Melvin D1, Simonsick EM2, Carlson O1, Shardell MD2, Ferrucci L2, Chia CW2, Basaria S3, Egan JM1. Abstract Aging in men is associated with loss of bone mass, impaired physical function and altered body composition. The objective of this proof-of-concept randomized, double-blind, placebo-controlled, parallel-group, single-center trial was to determine the relative effects of testosterone (T) and estradiol (E(2)) on bone mineral density, body composition, and physical performance in older men. The primary outcome was lumbar spine bone mineral density (BMD), and secondary outcomes were body composition, muscle strength, gait speed, and sex hormone concentrations. Forty three men (age range, 65-82 years; mean age 71 years) with low total T levels <350 ng/dL were randomized to one of three groups: 5 g transdermal testosterone gel (TT) (N = 16), anastrozole (AI) 1 mg (N = 14) or placebo daily (N = 13) for 12 months. Outcomes were assessed at baseline, 3, 6, and 12 months. Both TT and AI increased serum TT levels (>500 ng/dL, p < 0.05) compared to baseline; T values remained stable throughout the duration of the trial. At 12 months, TT improved the primary outcome of lumbar spine BMD (p < 0.01).Both interventions improved knee strength at 12 months compared to baseline (p < 0.05) while lean body mass significantly increased only in the AI group at 6 and 12 months (1.49 ± 0.38 kg, p < 0.01; 1.24 ± 0.39 kg, p < 0.05, respectively) compared to baseline. Interestingly, TT improved fast gait speed at 3 and 12 months (p < 0.01, p < 0.05, respectively). In summary, this proof-of-concept study confirms that aromatization of T is required for maintaining BMD in older men with low-T levels. The trial also uncovered the novel finding that aromatization of T is required for improvement in fast gait speed, an observation that needs to be verified in future studies. © 2015 American Society of Andrology and European Academy of Andrology. PMID: 26588809 http://onlinelibrary.wiley.com/doi/10.1111/andr.12126/epdf In elderly men with low baseline T, anastrozole increases T levels and improves both LBM and muscle strength. However, it did not improve functional strength (gait speed) or bone density.
  25. 6 points

    vaginal weightlifting

    I like the comment:
  26. 6 points
    Maybe somebody already posted this in the last month when I had the Ebola (okay, it was a cold, but it was a manly manflu kind of thing). I've heard that visualization like this works, but it sounded like brodreaming at the time. But here's a new study from Ohio University: There were 3 groups: - Control (n=15) - Immobilized wrist (n=15), nothing else - Immobilized wrist with 4 weeks of visualization (n=14) Here were the instructions to the third group: I'm pretty sure this was in a non-sexual situation. They didn't specify that in the press release. Anyway, the mere act of imagining the exercise had an effect. http://www.the-aps.org/mm/hp/Audiences/Public-Press/2014/30.html
  27. 6 points

    Manly log

    Did 181....was 181.2 on the nose. Lifts... 455 squat 300 bench 455 deadlift Im tired.
  28. 6 points
    I quite like wada - browsing their deliberations and concerns has given me some great ideas and new leads. J
  29. 6 points
    Emperor G_D

    More Proof Gym Rats are Gay

    Belonging to this forum says a lot about a person's sexuality. Just sayin.
  30. 6 points


  31. 6 points
    Growth Factor

    Protein give you Diabeetus

    Fucking nice. My second bet was right, and it gets better. High protein diets are 20% protein, high carb compared to <20% protein, higher carb. Further, all (1-6 month) short-term intervention studies cited showed an improvement/reduction or no significant effect on insulin resistance. There were some longitudinal studies cited, but all but 2 were observational. The two intervention studies had contradictory results.
  32. 6 points
    Solid read: "Seize every opportunity along the way, for how sad it would be if the road you chose became the road not taken. As Editor-in-Chief of our extraordinarily special publication, The Journal of Sexual Medicine (JSM), I am honoring freelance writer Robert Brault and taking that road. I am proudly writing this editorial to publicly discuss what I believe to be a highly impactful article that is considered by many to be ill-conceived and filled with conclusions that simply do not make sense. I feel it is important to discuss and challenge this now. It is my duty and responsibility to speak out here. My motivation is the well-being of and management opportunities for all of our patients. Being silent is not an option. Knowledge is power. Let me share an anecdote showing the true clinical impact of published data. A long-time patient of mine, now 59 years old, contacted me. His erectile dysfunction had been successfully treated, in part by oral PDE5 inhibitors, and his hypogonadal symptoms of fatigue, low energy, depressive symptoms, low sexual drive, variable erectile function, and general malaise had been successfully managed by daily administration of transdermal testosterone therapy. Recent follow-up blood tests of total and free testosterone had returned results in the middle tertile of the normal range. He also had occasional angina secondary to underlying coronary artery disease that had been treated, in part, by multiple drug-eluting stents in the right and left coronary arteries. He contacted me with urgency in his voice because his cardiologist wanted him to immediately stop the testosterone treatment based on data from a new article in The Journal of the American Medical Association (JAMA) claiming testosterone was dangerous in men with coronary artery disease [1]. His wife became extremely distressed that he was taking the testosterone. I told him that the information published was contrary to previous evidence on the use of testosterone treatment in men with hypogonadism and promised to speak with his cardiologist. Despite my short conversation with his busy cardiologist, the patient made the decision to stop his testosterone treatment. As of this editorial, he still remains off testosterone treatment, with many of the hypogonadal symptoms returning, especially low energy, fatigue, and general malaise. The same day, a 55-year-old ophthalmologist patient of mine with low sexual drive and hypogonadism called me to tell me he would no longer take testosterone treatment because of a recent publication on the negative effects of testosterone that was “all over the media†[2]. He too remains off testosterone treatment. Four other patients on testosterone either called or sent e-mails expressing concerns over their testosterone therapy. That same afternoon I arrived at the monthly Sexual Medicine Rounds at Alvarado Hospital, and before I even started to lecture, a colleague in the audience raised his hand to ask for my take on the new JAMA article and my thoughts concerning the safety of testosterone therapy. By day's end I was too was reading in multiple media outlets about this new JAMA article [3] espousing what I thought to be unusual data: that testosterone was associated with a higher risk of death, heart attack, and stroke. Author Gertrude Stein wrote, “Everybody gets so much information all day long that they lose their common sense.†Given the daily barrage of information, often coming through media sound bites, it is our responsibility to make sense of new data that may affect our patients—especially as in this case the data from the JAMA article simply did not make sense to me and many of my colleagues. The new JAMA data differ greatly from what has been published for years in the JSM and other journals. Knowledge is power. There are numerous epidemiologic studies in the JSM and in other journals showing correlation between low testosterone levels and sexual dysfunctions such as low libido and decreased erectile function. There are multiple epidemiologic studies showing correlations between low testosterone levels and multiple metabolic diseases, such as cardiovascular disease, diabetes mellitus, hypertension, hypercholesterolemia, obesity, and metabolic syndrome. There are also prospective studies showing that treatments with biologically available testosterone may improve diabetes mellitus, hypertension, hypercholesterolemia, and metabolic syndrome. Furthermore, the risks realized in those patients in prospective placebo-controlled studies did not include early death, myocardial infarction, or stroke [4–27]. There is no question that we need large, multi-institutional, long-term, placebo-controlled, prospective safety and efficacy data on testosterone treatment in hypogonadal men, especially with regard to morbidity and mortality concerns. But was the recent JAMA article [1] such a prospective investigation? I needed to know more than the sound bite. I needed to understand how the article in question came to such very different conclusions about the risks of testosterone treatment. When I finally had the opportunity to read “Association of Testosterone Therapy with Mortality, Myocardial Infarction, and Stroke in Men with Low Testosterone Levels†[1] later that day, I was struck by several disconcerting observations concerning the study design. I reread the article five times that evening, as it is actually a very complicated study, with approximately 50 different variables studied. First, the study by Vigen and colleagues was a very statistically oriented study, not a classic double-blind, placebo-controlled, prospective study of the type from which clinical conclusions are traditionally fashioned. This was a retrospective, observational study of men who had had significant health concerns—that is, they had undergone a coronary angiography procedure. I was then struck by the treatment testosterone level. This value was only 332 ng/dL, and that did not seem to be very therapeutic, being far below what most of us consider a good target value post-treatment. Other methodological issues with the study were also noted. Subjects were not randomized to testosterone treatment vs. no testosterone treatment. The most frequent testosterone treatment prescribed was the testosterone patch, and in my clinical experience, there is poor compliance with this delivery system because of allergic reactions to the patch adhesive. In addition, the conclusions of this team of authors seemed unrealistic, as they were based on testosterone use even though 17% of treatment patients filled their prescriptions for testosterone only once. That level of minimal treatment exposure to testosterone is simply insufficient to make conclusions concerning serious health risks. Further, there was no evidence that patients assigned to testosterone treatment were actually compliant with their testosterone, as none of these patients were contacted. And why were follow-up testosterone levels measured in only 60% of treated men? There were no follow-up testosterone measurements over time. Another interesting negative aspect of this study was that the median starting time of testosterone treatment after the coronary angiogram was approximately 1.5 years later. The mean time after the start of testosterone treatment was actually less than a year. This time period is insufficient for one to be able to draw conclusions about the definitive risk or benefit of testosterone therapy. The current consensus definition of the diagnosis of hypogonadism is a combination of (i) low testosterone blood levels and (ii) concurrent clinical symptoms of androgen deficiency. In the JAMA publication, the diagnosis of hypogonadism was based solely on blood levels of testosterone as determined by assays that, incidentally, were not performed in a central laboratory but in a variety of laboratories. The article in question is not simply a poorly conceived and poorly designed study. The data do not reflect current data from prospective studies. While new studies with new data will always be valued, that value will be based on the quality of the research. As a clinician, I felt compelled to write about this highly clinically impactful article (as measured by the intense media exposure) because of patient fear resulting in withdrawal from therapy. If you are interested in investigating further, please read the accompanying invited commentary, “Death by Testosterone? We Think Not!†More than 20 recognized international experts in testosterone treatment for use in hypogonadal patients have signed this document. Knowledge is power. Now, when patients and health-care providers ask me about the benefits and dangers of testosterone treatment based on the newly published article, I provide them with multiple other publications of prospective and placebo-controlled research and let them draw their own conclusions. Knowledge is power. With this editorial and the accompanying commentary, The Journal of Sexual Medicine has taken an important stand in the field of sexual medicine. For the record, a PubMed search of articles published in 2013 with the keyword “testosterone†returned 5 articles in JAMA and 46 in your JSM. The JSM represents the field. The JSM represents the experts in testosterone and sexual medicine. While we are all awaiting carefully designed, long-term, multi-institutional, placebo-controlled, prospective safety and efficacy data on testosterone treatment in men with hypogonadism, we will not remain silent concerning the clinical implications of an article that simply does not make sense and that interferes with sexual medicine patients' treatment confidence. Knowledge is power. Please read your JSM to gain the knowledge. Cite your journal regularly. Review for it and write for it. We can all make a difference. In the end, our patients who are bothered by sexual health concerns rely upon our knowledge of good clinical data to help make important and meaningful sexual medicine management choices." _____ Taken from: http://dx.doi.org/10.1111/jsm.12466
  33. 6 points

    Tell me about cortisol.

    Manipulating cortisol in a sustainable manner isn't anywhere near as easy as the supplement makers would like you to believe. There are quite a few threads in the neuroscience subforum on HPA axis regulation and cortisol-related issues. All of them have a lot more questions than answers. Cortisol plays a role in a long list of systems in the body. As such, for an otherwise healthy person you can't make any blanket statements about how raising or lowering cortisol levels is "good" or "bad". In fact, at the extreme ranges high and low cortisol are actually serious medical conditions (See Cushing's disease and Addison's disease). Manipulating cortisol levels isn't easy, either. If you supplement with an glucocorticoid like prednisone or by capping hydrocortisone cream, for example, you will feel "better" in the short term due to the acute effects. But cortisol production is regulated relatively closely by the HPA axis, so your internal cortisol production will quickly decline as those control loops adjust to correct for the elevated levels. Once you discontinue the exogenous glucocorticoid, you'll be in bad shape until your internal production recovers. This is why prednisone is usually only prescribed for short periods of time and with generous tapering periods to avoid sudden changes. But even if you could continually dose with a corticosteroid with a full replacement dose, it still wouldn't be as ideal as your body's own production. Cortisol levels are dynamically elevated in response to various stresses and other short-term needs. There's no way you'd ever be able to approximate that tight regulation with exogenous dosing. Depression is frequently associated with abnormal cortisol levels. Melancholic depression is strongly correlated with elevated cortisol levels, while atypical depression and seasonal affective disorder are associated with below-normal cortisol levels. That alone is enough to make any suggestion of raising or lowering cortisol levels sound like a really bad idea.
  34. 5 points
    dr. frankenstein

    Diet 2019

    . i like to think on grams per kilo ( X LBM weight) macros are (carb-pro-fat) get lean 1-2-1 1-3-1 growth (lean) 2-2-2 3-2-2 .
  35. 5 points

    fasted or not ?

    Hope the OMG is in a good way Remember, I try to stand where science stands. And that is the physiology of pain so that is not going to change. I think it's taught now in most of the PT school curriculums. I wrote a second article about pain in 2014. I am not sure if I posted it here. And based on the recent studies I have seen, the results have not been very successful. It is like weight loss, I feel. We know the physiology, but we just can't get people to lose and keep it off. The same with pain. But I don't read as much about pain as I used to. I just follow a few of the pain guys. So I finished my Phd from Univ of Miami. I did a post doctorate for a couple of years. Now an exercise science faculty at a university. Now all discussions are on facebook. But I find facebook to be very bad for discussions - and people cannot express their views openly. Hope everyone is doing good here.
  36. 5 points

    Rapid Fat Loss

    Obese mice lose a third of their fat using a natural protein October 29, 2018 Science News To the great surprise of cancer researchers, a protein they investigated for its possible role in cancer turned out to be a powerful regulator of metabolism. The Georgetown University-led study found that forced expression of this protein in a laboratory strain of obese mice showed a remarkable reduction of their fat mass despite a genetic predisposition to eat all the time. The study, published in Scientific Reports, suggests that the protein FGFBP3 (BP3 for short) might offer novel therapy to reverse disorders associated with metabolic syndrome, such as type 2 diabetes and fatty liver disease. Because BP3 is a natural protein and not an artificial drug, clinical trials of recombinant human BP3 could begin after a final round of preclinical studies, investigators say. "We found that eight BP3 treatments over 18 days was enough to reduce the fat in obese mice by over a third," says the study's senior investigator, Anton Wellstein, MD, PhD, a professor of oncology and pharmacology at Georgetown Lombardi Comprehensive Cancer Center. The treatments also reduced a number of obesity-related disorders in the mice, such as hyperglycemia -- excess blood sugar that is often linked to diabetes -- and eliminated the fat in their once fatty livers. Clinical as well as microscopic examination of the mice showed no side effects, researchers say. Obesity, which affects more than 650 million people worldwide, is the major driver for metabolic syndromes, which includes disorders such as insulin resistance, glucose intolerance, hypertension and elevated lipids in the blood. BP3 belongs to the family of fibroblast growth factor (FGF) binding proteins (BP). FGFs are found in organisms ranging from worms to humans and are involved in a wide range of biological processes, such as regulating cell growth, wound healing and response to injury. Some FGFs act like hormones. BP1, 2, and 3 are "chaperone" proteins that latch on to FGF proteins and enhance their activities in the body. Wellstein has long researched the BP1 gene because its production is elevated in a range of cancers, suggesting that growth of some cancers is linked to the excess delivery of FGFs. Only recently has Wellstein turned his attention, and that of his lab and colleagues, to BP3 to understand its role. The researchers found that this chaperone binds to three FGF proteins (19, 21, and 23) that are involved in the control of metabolism. FGF19 and FGF 21 signaling regulates the storage and use of carbohydrates (sugars) and lipids (fats). FGF23 controls phosphate metabolism. "We found that BP3 exerts a striking contribution to metabolic control," Wellstein says. "When you have more BP3 chaperone available, FGF19 and FGF21 effect is increased through the increase of their signaling. That makes BP3 a strong driver of carbohydrate and lipid metabolism. It's like having a lot more taxis available in New York City to pick up all the people who need a ride." "With metabolism revved up, sugar in the blood, and fat processed in the liver are used for energy and is not stored," Wellstein says. "And warehouses of fat are tapped as well. For example, the job of FGF21 is to control break down of fat, whether it is stored or just eaten." While the study results are exciting, additional research is required before BP3 protein can be investigated as a human therapy for metabolic syndromes, he says. Journal Reference: Elena Tassi, Khalid A. Garman, Marcel O. Schmidt, Xiaoting Ma, Khaled W. Kabbara, Aykut Uren, York Tomita, Regina Goetz, Moosa Mohammadi, Christopher S. Wilcox, Anna T. Riegel, Mattias Carlstrom, Anton Wellstein. Fibroblast Growth Factor Binding Protein 3 (FGFBP3) impacts carbohydrate and lipid metabolism. Scientific Reports, 2018; 8 (1) DOI: 10.1038/s41598-018-34238-5
  37. 5 points
  38. 5 points
    Emperor G_D

    Pass The Salt

    The worst part about the 'salt is evil' approach to dietary advice is that even when you restrict salt in hypertensive adults, there's not much advantage to overall bp. Better to teach them to increase Ca/Mg/K or take a cal-mag-K supplement, take some vitamin D, and go for a walk than to flagellate themselves with bland-ass food. Just like the anti-fat generation, the anti-Na stuff just hinders people's health and well-being. Same with the over-hydration preachers, the damned statin-pushers, etc.
  39. 5 points

    The Metformin Project

    I've become convinced that metformin has some real potential as a metabolic optimizer that may be able to counteract some of the negative changes that appear to be associated with normal aging. So with the help of my friends in the South Pacific, I've decided to embark on an experiment using 1g of sustained release metformin daily to see what sort of changes I can detect in myself...my hope is for some fat loss and general shift in fat distribution to a more youthful pattern. As drugs go, metformin generally appears quite safe and without many side effects. The most commonly reported issue is nausea which appears to usually go away after a couple of days. The only serious side effect is lactic acidosis but this appears to really only be a concern in people with compromised kidney function. I am on day two of my trial. I noticed exactly no digestive issues at all. Today I went to the gym and did some HIIT followed by some beach muscle lifts...from my reading, I expected a small negative impact on my cardio performance but was happy to experience just the opposite. My 30 min HIIT workout felt remarkably easy and my lifts were also not impacted. One of the things metformin is known to do is shift energy substrate during exercise from glucose to FFA, sort of like a ketogenic diet mimetic and I may simply be fat enough that this shift just gave me a ready source of energy to power my workout... Anyway, I plan to get a complete set of labs in the next two weeks and I'll report anything of interest as I go along.
  40. 5 points

    Whiter, Brighter, Better Teeth

    Also, there are some new active remineralizing toothpastes available. These introduce what is essentially a biocompatible ceramic into the tooth enamel making it harder and less susceptible to damage, less hospitable to plaque formation and reducing gingivities. They also reduce hot/cold sensitivity by sealing off the dentin tubules and can even reverse nascent cavities. GSK's write up on Novamin None of this technology is available directly to US customers of course who are being protected against new medical advances by the ever-vigilant FDA...but Amazon sells Novamin-containing toothpastes from Canada and the UK. J Clin Periodontol. 2006 Feb;33(2):86-91. Anti-gingivitis effect of a dentifrice containing bioactive glass (NovaMin) particulate. Tai BJ1, Bian Z, Jiang H, Greenspan DC, Zhong J, Clark AE, Du MQ. BACKGROUND: The objective of this pilot clinical trial was to evaluate the anti-gingivitis and anti-plaque effects of a dentifrice containing bioactive glass (NovaMin) compared with a placebo control dentifrice in a 6 weeks clinical study. METHODS: The study design was a randomized, double-blinded, controlled clinical trial. One hundred volunteers took part in the study and were matched for plaque index (PLI), gingival bleeding index (GBI), age and gender. The protocol was reviewed and approved by the Ethical Committee of the University. The subjects received a supragingival prophylaxis to remove all plaque, calculus and extrinsic stain. Following the baseline examination, subjects were instructed to brush with their assigned dentifrice and toothbrush. The PLI and GBI were determined for the baseline and 6 weeks. The data were analysed using a repeated-measures anova conducted on the two dependent measures to compare the effect between the test and control group. RESULTS: Ninety-five subjects finished the study. The results showed that the PLI (baseline=1.54, 6 weeks=1.29) and GBI (baseline=1.14, 6 weeks=0.47) were significantly reduced, respectively, over the 6 weeks period in the test group (p<0.001 for each measure). There was a 58.8% reduction in gingival bleeding and a 16.4% reduction in plaque growth. There was no difference of the PLI (baseline=1.60, 6 weeks=1.57) and GBI (baseline=1.18, 6-week=1.02) over the 6 week period in the control group. CONCLUSION: This study demonstrated that a dentifrice containing NovaMin significantly improves oral health as measured by a reduction in gingival bleeding and reduction in supragingival plaque compared with a negative dentifrice over the 6 weeks study period. PMID: 16441730 J Contemp Dent Pract. 2016 Aug 1;17(8):645-9. Remineralizing Effect of Topical NovaMin and Nano-hydroxyapatite on caries-like Lesions in Primary teeth. Haghgoo R1, Ahmadvand M1, Moshaverinia S2. INTRODUCTION: NovaMin is a synthetic mineral compound composed of calcium, sodium, phosphorus, and silica. It releases crystalline hydroxyl-carbonate apatite (HCA), which structurally resembles the minerals naturally found in the teeth. Nano-hydroxyapatite (NHA) is a biocompatible compound with high affinity for tooth enamel. NHA particles morphologically resemble dental enamel apatite crystals. Considering the efficacy of remineralizing agents and the importance of conservative preventive measures, this study aimed to compare the remineralizing effects of NovaMin and NHA on caries-like lesions in primary teeth. MATERIALS AND METHODS: This in vitro experimental study was conducted on 30 sound human primary anterior teeth with no cracks or fractures. The surface microhardness (SMH) of each tooth was measured at baseline using a Vickers microhardness tester. The teeth were then subjected to remineralization/ demineralization cycles, and artificial caries lesions were created in them. The SMH of each tooth was measured again and the teeth were then randomly treated with toothpastes containing NovaMin or 10% NHA powder for 2 minutes daily for a period of 5 days. The SMH of each was again measured afterward. Data were statistically analyzed using independent t-tests and Mann-Whitney U tests. RESULTS: The mean SMH was found to be higher in the teeth treated with NovaMin toothpaste (422.67 kgf/mm(2)) than in the teeth treated with NHA (384.2 kgf/mm(2)); However, this difference was not statistically significant. CONCLUSION: Both NHA and NovaMin were effective for remineralization of caries-like lesions of primary teeth and no significant difference was detected in their efficacy. PMID: 27659081
  41. 5 points

    The Death of a Theory

    The science of serum lipids has been largely dumbed down to "good" (HDL) and "bad" (LDL) cholesterol and the idea that if we just had more of the former and less of the latter, we would be healthier...this makes perfect sense and is also completely wrong...CVD and CV mortality are largely unrelated to serum cholesterol levels and drugs that give us more "good" and/or less "bad" do not consistently lead to less CVD or CV mortality...emphasis mine Cholesterol Paradox: A Correlate Does Not a Surrogate Make Robert DuBroff Evid Based Med. 2017;22(1):15-19. Nobel laureates Brown and Goldstein published an editorial in 1996 predicting that "Exploitation of recent breakthroughs … may well end coronary disease as a major public health problem early in the next century." They based their optimism largely on 'proof of the cholesterol hypothesis' which posits that lowering serum cholesterol reduces the risk of coronary heart disease (CHD). Paradoxically, CHD is now pandemic. Some may argue that this pandemic is secondary to the global explosion of obesity and diabetes, but it is equally plausible that the cholesterol hypothesis is incorrect. The results of the recently presented ACCELERATE trial may hold the key to understanding this paradox. The cholesterol hypothesis has been debated for years, but in light of recent clinical trial results, a reappraisal of the evidence is warranted. Cholesterol is an ostensibly ideal surrogate target: it is present in atherosclerotic plaque; cholesterol is an established risk factor for CHD; Mendelian randomisation studies suggest benefit from lifelong reduced cholesterol levels and cholesterol-lowering drug trials have reduced the risk of cardiovascular (CV) events. Consequently, it seemed impossible that the gold standard of modern medical research—a large, double-blind, randomised controlled trial (RCT)—could undermine, rather than confirm, this theory. Yet the ACCELERATE trial reported that evacetrapib, a novel cholesteryl ester transfer protein inhibitor, reduced low-density lipoprotein (LDL) cholesterol by 37%, raised high-density lipoprotein (HDL) cholesterol by 130%, but produced no discernible reduction in CV events or mortality in high-risk patients. I believe the ACCELERATE trial adds to the chorus that cholesterol is not a valid surrogate end point. Rudolf Virchow first described the microscopy of the atherosclerotic plaque, but Nikolay Anichkov is credited with elucidating the central role of cholesterol in atherosclerosis. Ironically, cholesterol is also essential for life as a key component of cell membranes, steroid hormones and bile acids. The Framingham Heart Study further clarified the role of cholesterol as a major risk factor for CHD. Ideally, a risk factor should help us distinguish those individuals who will develop a disease from those who will not. Figure 1 illustrates this concept and the original Framingham cholesterol data. The cholesterol levels of Framingham participants who did and did not develop CHD are remarkably similar except when the cholesterol level was extremely low (<150 mg/dL) or extremely high (>380 mg/dL). For the vast majority of patients, cholesterol levels do not help us differentiate those who will and will not develop CHD. Figure 1. Comparison of ideal risk factor with Framingham Heart Study cholesterol distribution in patients who developed coronary heart disease (CHD) and those that did not develop coronary heart disease (NON-CHD).3 Cholesterol values are mg/dL. Reprinted with permission of the publisher. Mendelian randomisation studies are often cited in support of the cholesterol hypothesis. Conceptually, individuals born with genetically low LDL cholesterol should be protected from CHD since their cholesterol levels are reduced throughout life. Yet the report of PCSK9 sequence variations associated with low LDL cholesterol illustrates many of the shortcomings of this model. This study reported that 2.6% of 3363 black patients in the Atherosclerosis Risk in Communities study had nonsense mutations in PCSK9 associated with a 28% reduction in LDL cholesterol. The authors calculated an 88% reduction in the risk of CHD by statistically comparing one fatal myocardial infarction in the PCSK9 group with 319 composite CHD events in the control group (unspecified, but defined as "definite or probable myocardial infarction, a silent myocardial infarction detected by electrocardiographic interval changes consistent with an intercurrent ischemic event, death due to CHD, or a coronary-revascularization procedure"). Such a comparison may not be valid and by ascribing equal importance to different events such as a CHD death and ischaemic electrocardiogram (EKG) changes the perceived benefit can easily be exaggerated.[5] Moreover, adjudicating CHD events based on death certificates and soft end points such as EKG changes limits the validity of the primary end point. Notably, this study reported no mortality or stroke benefit. These PCSK9 sequence variations were also associated with a statistically significant lower incidence of hypertension, which raises the question of whether LDL cholesterol lowering alone explains the reduction in CHD events. Medication and statin usage that might potentially impact CHD events were not reported. Ultimately, we must ask ourselves if this study proves the cholesterol hypothesis and should it be extrapolated to support the initiation of lipid lowering therapy in our adult patients? I believe Mendelian randomisation studies are hypothesis generating, not hypothesis proving. Many experts cite numerous RCTs of statins in support of the cholesterol hypothesis, but we should not ignore the dozens of cholesterol-lowering trials that do not. There have been 44 published cholesterol-lowering RCTs that reported no mortality benefit. Most reported no reduction in CV events, and several reported substantial harm (CDP, HERS, Minnesota Coronary Experiment, Sydney Diet Heart Study, WHI, WHO). This lack of benefit was seen even with profound reductions in LDL cholesterol (50% in the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) trial). Although several studies were not specifically designed to assess mortality, the reported lack of mortality benefit should not be disregarded. While some experts have dismissed or criticised these negative trials, the totality of evidence simply cannot be ignored. Even when researchers demonstrate a statin mortality benefit, the findings are underwhelming. A recent analysis concluded that statins would only postpone death by a median of 3.1 and 4.2 days for primary and secondary prevention, respectively. Some researchers also point to meta-analyses as proof of the cholesterol hypothesis. Meta-analysis can provide an efficient mechanism of pooling similar, smaller studies and generating robust statistical results. But not all biostatisticians concur, and some refer to meta-analysis as 'statistical alchemy for the twenty-first century'. Moreover, the results of meta-analyses pertaining to cholesterol lowering are inconsistent. For example, the Cholesterol Treatment Trialists' meta-analysis of 27 statin trials in people at low risk of vascular disease concluded that there was substantial benefit, but a subsequent meta-analysis of the same 27 statin trials concluded there was no mortality benefit. Similarly, a meta-analysis of 11 statin trials in high-risk primary prevention found no mortality benefit and no correlation between the degree of LDL lowering and mortality rates. Cochrane meta-analyses of cholesterol lowering in peripheral arterial disease of the lower extremities and statin use in acute coronary syndromes also reported no benefit. Notably, the results of meta-analyses are often discordant with the results of subsequent large RCTs. Finally, consider that the cholesterol hypothesis may have inadvertently contributed to the very disease we seek to prevent. The cholesterol hypothesis risks oversimplifying the complex interaction of cholesterol, diet and coronary disease, leading many statin users to overeat with consequent obesity. Nearly 50 years ago, three Harvard researchers were paid thousands of dollars by the sugar industry to write a review in the New England Journal of Medicine emphasising the importance of fat and cholesterol in CHD while minimising the importance of sugar. Hence, the food industry developed and continues to promote low-cholesterol foods that are nonetheless high in sugar and refined carbohydrates. These dietary changes have likely contributed to the current epidemic of obesity and diabetes that can lead to CV disease. "A correlate does not a surrogate make," and by definition, treatment of a valid surrogate end point should result in a consistent clinical benefit. The empirical record is now clear that lowering cholesterol through diet or with eight different classes of drugs does not significantly prolong life or consistently prevent CHD. Yet experts continue to proclaim the success of cholesterol lowering. Fifty-four years ago, Thomas Kuhn described this reluctance to acknowledge anomalies in a theory. Dr Kuhn wrote that a paradigm shift would only occur when the evidence contradicting a theory is overwhelming. Therefore, we must accept the empirical record even though it contradicts our long-held beliefs. Other researchers believe this reluctance can be explained by the tendency to "see what you want to see," and ignore what you do not. For example, a recent editorial in the New England Journal of Medicine proclaimed, "Proof That Lower Is Better—LDL Cholesterol and IMPROVE-IT." IMPROVE-IT, a RCT of ezetimibe added to simvastatin in patients with a recent acute coronary syndrome, reported a 24% reduction in LDL cholesterol, but an absolute risk reduction in combined CV events of only 2% after 6 years. Furthermore, the results barely achieved statistical significance (HR 0.936, 95% CI 0.89 to 0.99) and there was no mortality benefit. The conclusions of this study must also be viewed cautiously since 42% of patients discontinued their study medications. The editorial further asserts that "IMPROVE-IT is a landmark study in that it is the first clinical trial to show a benefit of adding a nonstatin lipid-modifying agent to statin therapy." Conspicuous by its absence is any mention of ENHANCE, another RCT of ezetimibe that reported no benefit when added to statin therapy in familial hypercholesterolaemic patients, or AIM-HIGH and HPS2-THRIVE, two RCTs that reported no benefit of niacin when added to statin therapy in patients with CV disease. The debate over the cholesterol hypothesis has continued because the results of cholesterol lowering interventions are inconsistent and contradictory. Nevertheless, clinical guidelines continue to emphasise the critical importance of cholesterol lowering to prevent CHD. Unfortunately, I believe this one-dimensional approach may have impeded the advancement of science and our search for other preventive strategies. The ACCELERATE trial may well herald our tipping point and a sea change in our approach to CHD prevention.
  42. 5 points

    Tomahawk High Intensity Training Log

    You are, however, older than me and that's really old...
  43. 5 points

    Tomahawk High Intensity Training Log

    Don't get involved with a recently divorced person for at least 6 months, preferably a year, after the divorce. They go through a crazy time in which it is impossible for them to start a real relationship. Their ego and rationality are at a very low point, no matter how well behaved they appear to be. If you do get involved early, just be aware that you'll be the rebound guy for about 3 months before she moves on to someone else.
  44. 5 points

    A New Log: Into Darkness

    Chest/Tris Flat Bench to 365x1 (just barely), Incline DB Press, Standing Cable Flyes/Rope Pullovers, Pec Deck/Machine Tris, Machine Flat Press/Machine Incline Press, Hack Squat I don't really do legs, ever, so I am going to try and toss in some hack squats at least a couple of days per week so my lower half doesn't waste away completely...
  45. 5 points
    She looks like she has had some practice with this sort of thing...
  46. 5 points


    So I'm at just about 30 lbs lost. It's my fault that I haven't had the chance to evercise as much cause of work. I still do, but if I did more, I'd weigh less. Still, it's a big accomplishment, and about another 15-20 lbs, I'm gonna slowly move to phase 2, add a few good carbs in, and start weight training again. One thing I've learned about this diet. You gotta respect it. Even the 2 times I've cheated (barely), it almost throws me out of ketosis. But my pants and jeans are mad loose, and my face is slimmer, making me look younger and people are noticing. Shit def works.
  47. 5 points

    Some tips on finding FT's....

    Many of the FT's that I have posted throughout the years, that other members couldn't find were straight from google search. Copy & paste the study title into google, then click [image] search. It's often the easiest way. For example, here's one I recently found.... And here's the full text - which is not readily available via google or google scholar: http://www.fasebj.org/content/18/13/1499.full Additionally [on occasions], you can try editing the url's that have 'abstract' in the title to 'full', and it's as simple as that. Try it: http://www.fasebj.org/content/18/13/1499.abstract
  48. 5 points
    This study has plenty of potential pitfalls (strong placebo response, small sample size, potentially large number of scored variables) but the idea that Curcumin could be useful in the treatment of atypical depression is not without merit. Kudos to the study founders for differentiating between depression subtypes, although with such a small sample size I'm not sure if that aspect can really be considered significant. The study used 500mg twice daily, but I'd be interested in seeing the full text to determine if there were any additional bioavailability confounders in play such as piperine or any of the supposedly more effective delivery mechanisms. I'll need to see if I can find some more concrete numbers for Curcumin's purported MAOI activities.
  49. 5 points

    725lb Raw Bench Attempt

    He benches 725lbs like I bench 725lbs...maybe he was going for the Xfit bench record...he got that lift!
  50. 5 points

    Reading Books != Reading a Screen

    I suspect that books allow the brain to link spatial navigation with memory for storylines. Memory cognitions were used by ancient Greeks (method of loci) and modern memory masters. Primarily, these cognitions consist of imaginary walking adventures or linked visualizations, and they give impressive results. The process involves more than just memory though -- it's a system of imagination that binds disparate elements into a coherent whole in the mind. This coherent whole feels like a story rather than a collection of unrelated events. The electronic screen literally and figuratively flattens the material. Consequently, a person is less able to use the profound navigational search cognitions that humans developed in a million years of hunting and story-telling culture. The physical book format allows a person to see book marks, thickness, and other cues that help build up memory formation, recall, anticipation and self-awareness (meta-cognition) about the reading process. This allows for more sophisticated navigation cognitions (probably the same processes used in allocentric/egocentric navigation in space) that help bind the material read into a coherent narrative in the mind. The flat panel of an e-reader shows only one or two pages. It hides most other cues of position relative to the beginning and end of the book, and it offers only weak visual analogies to the physical reality of a book. It gives weaker memory cues about previously read material. It is less convenient to backtrack to any other location since the screens present page navigation in a very linear way, at least as compared to printed paper in the hand. Cognition is far more subtle and complex than most people know.
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