Jump to content

Leaderboard


Popular Content

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

  1. 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!
  2. 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.
  3. 7 points
    Burton

    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.
  4. 7 points
    anoopbal

    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. ☺️
  5. 7 points
    SeanM

    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
  6. 6 points
    Niflheim

    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.
  7. 6 points
    Sanction

    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
  8. 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.
  9. 6 points
    STENDEC

    IcyHot

    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.
  10. 6 points
    STENDEC

    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.
  11. 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.
  12. 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.
  13. 6 points
    Construct

    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.
  14. 5 points
    This is sort of interesting and shows that while running appears to reduce all-cause and CV mortality, there appears to be very little dose response...compared to not running, a very little bit of running and a fairly slow pace appears to be just about as good (possibly better) as a lot of fast running. Journal of the American College of Cardiology Volume 64, Issue 5, August 2014 Leisure-Time Running Reduces All-Cause and Cardiovascular Mortality Risk Duck-chul Lee, Russell R. Pate, Carl J. Lavie, Xuemei Sui, Timothy S. Church and Steven N. Blair Background Although running is a popular leisure-time physical activity, little is known about the long-term effects of running on mortality. The dose-response relations between running, as well as the change in running behaviors over time, and mortality remain uncertain. Objectives We examined the associations of running with all-cause and cardiovascular mortality risks in 55,137 adults, 18 to 100 years of age (mean age 44 years). Methods Running was assessed on a medical history questionnaire by leisure-time activity. Results During a mean follow-up of 15 years, 3,413 all-cause and 1,217 cardiovascular deaths occurred. Approximately 24% of adults participated in running in this population. Compared with nonrunners, runners had 30% and 45% lower adjusted risks of all-cause and cardiovascular mortality, respectively, with a 3-year life expectancy benefit. In dose-response analyses, the mortality benefits in runners were similar across quintiles of running time, distance, frequency, amount, and speed, compared with nonrunners. Weekly running even <51 min, <6 miles, 1 to 2 times, <506 metabolic equivalent-minutes, or <6 miles/h was sufficient to reduce risk of mortality, compared with not running. In the analyses of change in running behaviors and mortality, persistent runners had the most significant benefits, with 29% and 50% lower risks of all-cause and cardiovascular mortality, respectively, compared with never-runners. Conclusions Running, even 5 to 10 min/day and at slow speeds <6 miles/h, is associated with markedly reduced risks of death from all causes and cardiovascular disease. This study may motivate healthy but sedentary individuals to begin and continue running for substantial and attainable mortality benefits. FFT
  15. 5 points
    Sanction

    Sanction lifted

    Having been haRASsed by my evil twin about my sarcopenic sedentariness over the last year, I dropped by the local community pool/gym to check out at drop-in class on "Body Sculpt" "Tone your muscles and shape your body in this strength and cardio class" Present: 5 women of a certain age Activity: Poses of a rather elementary nature Conclusion: why not Objection: mere observation is inadequate Rebuttal: none
  16. 5 points
    Emperor G_D

    Liftin' weights and other shit

    I don't feel that fulfilling your duty as their employee, and taking their required training for their job while awaiting a possible other job constitutes a bridge-burning. If you decided to take the training because 'fuck them' and you run up the minibar and porno bills and then promptly post your hand-written-while-drunk-on-the-minibar resignation for all of your co-workers to see on the internal email system message list, then it's a reputation issue. If you take the training because you don't know when the other company will-or ever-hire you, and you just happen to get hired a few weeks after, and you politely resign and thank them for everything, then your reputation shouldn't be too bad off. We all have to do what we have to do to survive. You need to find yourself a way to survive without this job...unless you can't find other employment. You also need to be a good employee in the event that you stay longer than you intend.
  17. 5 points
    Burton

    Liftin' weights and other shit

    I mentioned it in the chat box but I’m gonna get engaged. at some point in the nearish future. I refuse to go into debt for a ring so I’ve gotta save for a bit. Good thing is that there’s a stone that her mom has been saving for her for her whole life so I only have to buy the ring. since you are all men of great taste, I submit this to you all for your consideration: https://www.verragio.com/Verragio-Engagement-Rings/Parisian-Engagement-Rings/PARISIAN-124P/1005 I’m gonna have it all white gold with black diamonds as the accent stones to the side of the main stone. I know I’ve bitched to you all about shit before but the truth is that I’m prone to being overly emotional (as you’ve probably been able to figure out over the years) and at the end of the day, I like my life with her and I can’t imagine it being different nor do I really want to. also, I’ve had enough. I’m gonna work out every day this week in some capacity. Tired of being a fat slob, I’d like to be a slightly less fat slob. I’ll update later when that happens.
  18. 5 points
    Ras

    Tomahawk HUGE update with a log

    Bit of an aside: because 'lazy' and ''unmotivated' seem to have a moral component and are tied to the very vague concept of willpower, I wonder how much of it is actually allostatic stress and overreaching that we are blaming on a perceived character flaw. I am not saying don't reach deep and push, I'm just not sure how helpful the guilt narrative is for long-term perseverance as it tends to be a) cognitively taxing and b) deepening avoidance patterns. I find it useful to dig beyond the surface to look at why I am avoiding anything, whether it be training or something else. Lazy and unmotivated are symptoms. Back to Tom's log: from your first sentence, it sounds like you may be close to the DMZ of overtraining for some reason (stress, nutrition, sleep, etc.).
  19. 5 points
    mwarren

    Resurrection of Blu

    Okay so I had an interview for an insurance company today and fucking nailed it so well that he wants to meet again tomorrow and make me an offer. However, I'm going to ask for a like time to consider other options. I really would like to meet with Pfizer before I make any decisions.
  20. 5 points
    STENDEC

    One (New) Direction

    Shoulders OHP to 175x3, Front/Lateral DB Raises, Inch Press, Heavy DB Shrugs I'm pretty sure that OHP was a PR...and before you ask @mwarren they were strict from below the chin to full lockout with no leg drive although I was leaning back some and looking at the ceiling.
  21. 5 points
    Ras

    Muscle Memory Revisited

    This could probably be posted in a variety of places, but: "These and other data argue against the current interpretation of the myonuclear domain hypothesis and suggest that once a nucleus has been acquired by a muscle fiber it persists." https://www.frontiersin.org/articles/10.3389/fphys.2018.01887/full?utm_source=FWEB&utm_medium=NBLOG&utm_campaign=ECO_FPHYS_muscle-memory
  22. 5 points
    Burton

    Liftin' weights and other shit

    It's a decent opportunity. It's with Smucker's as an analytical chemist in their coffee R&D group. As of right now it's a contract job for 6 months but the reason why it's open in the first place is that the previous person had moved into another position within the company so it's not just a position they're filling to cope with a sudden surge in work, it's likely a job that will be replaced at some point, likely after this contract. The work is GC-MS work for the first 3 months, which is the weakest of my chromatography skills so I'll be happy to get some more work in that area. It's rare for anyone in small moleucle analysis to be well rounded in both LC and GC. Plus I have IC, ICP (magnets, right?), AA and FTIR/NIR experience so that puts me in a spot that not a lot of people can claim. Anyway, after 3 months, one of the other people goes on maternity leave so then it will become a mix of GC-MS, LC and LC-MS/MS work. Basically, that gives me 3 months to show that I know all of the shit they do and would be a good addition to their team. It's definitely a job I can do and one I think I can do well at. So I'm thinking if I get in there, do a good job, show that I know my shit, they'll maybe offer me a full-time position going forward. It's certainly not a guarantee but my recruiter seems to think it's a job they're obviously gonna fill but might not be able to secure funding right now due to whatever idiosyncrasy may exist in their corporation re: budgets, hiring freezes, etc. When I was at Scotts, R&D could literally only ever hire anyone in the first 8 months of the fiscal year. After May of every year, that shit was shut down until October for some reason no one could ever explain to me. If I can get hired on as a full-time employee, they're a great place to work, rated generally in the top 50 in the country, the campus/facilities are beautiful and I'll be getting back all the benefits I lost from Scotts: On site fitness center, catered lunches, time off for charity work, great insurance, good 401k match, etc. If I can't get on full time, it's 6 months of steady income, and even a 10% pay bump over my last job, which was 10% above my previous job. So in the end, I'll be making ~18% more money than I was 12 months ago. I'm gonna worry about all that later down the line/what if stuff later. I'll just go there, bust my ass and do as well as I'm able. Hopefully, it turns out to be more. If not, it's 6 months of good experience broadening my instrumentation skills and more importantly, my data analysis capabilities. Finally, it's me getting back in the workforce in a good position, which has been priority #1 for me, for obvious reasons. Only downside is that it's about a 90 min drive. But luckily it's in the outskirts of Cleveland so I can find a house/room share for at worst, 500 bucks a month. I'll take that during the weeks, come home on the weekends, hang with the girlfriend, go back Sunday night. If it ends up being permanent, she can work remotely from home and go into the office once or twice a week for necessary meetings and such so she won't have to find a new job. So that gives us the option to relocate. Probably try to find something in the middle between here and there but there's a lot of decent places to live there, just gonna miss Columbus if I'm being honest. There's just so much cool shit to do here. That place is very much rural but with a ton of shit in a 30-45 minute radius. I don't like the hassle of the drive to go do things but such is life I guess.
  23. 5 points
    Something Anonymous

    Super Poopers

    Yea I have. It was in 2013 when this happened and FMT’s at that time were considered experimental medicine. I had to sign a bunch of release waivers and the GI doc basically told me he had no idea if this would help or hurt her but case reports had shown some promise. The donor had to be from someone who did not live with her but was related so her sister took a big crap in a Tupperware container, and they blended it up and pushed it through her ng tube. It was the craziest thing in the world man. She was hooked to 3 or 4 powerful abx for weeks and tube full of shit ended up saving her life. The last time we saw her GI doc last year he told us it was now a common treatment for sepsis related C.Diff infections in the ICU at that hospital.
  24. 5 points
    Ras

    Occult Blooded Occlusion Grimoire

    I am pretty sold on it from the literature for rehab and recovery and really couldn't give much of a shit about hypertrophy. My original interest came from using a cuff for tendonitis while training and noticing much more rapid recovery. Nuckols wrote the best synopsis on mechanisms that I have read to date: https://www.strongerbyscience.com/blood-flow-restriction-the-holy-grail-for-accessory-work/
  25. 5 points
    Kimbo

    Kimbo's PR Log

    I've been off of Lexapro entirely for a few weeks now, and honestly, I feel amazing. I was getting progressively more and more fatigued on the shit, plus I felt unmotivated and sad. I think it works well for some people, and it did work well for me at first, but eventually it wasn't worth it for me to continue taking it. No issues with anxiety since I've come off, either. My left knee has been feeling great, but I recently hurt my right knee. It doesn't feel as bad as my left did, so I think I'll recover from it sooner. And despite the injury, my muscle snatch numbers have continued to climb. I have a competition coming up next month. I'll post results here after.
  26. 5 points
  27. 5 points
    Kimbo

    Kimbo's PR Log

    Mostly posting this so you guys can look at my gut poking out of my shirt. But my knee is on the mend, too.
  28. 5 points
  29. 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.
  30. 5 points
    STENDEC

    Pass The Salt

    It comes from the connection between salt and hypertension in salt-sensitive individuals...just like a lot of nutritional advice, it got completely dumbed down and turned into universal advice despite a small mountain of data showing that it wasn't good advice. I think there is also a little American Puritanesque self-denial in this, like a lot of "health" advice....salt makes things taste good therefore, it is probably somewhat evil...purify yourself with the self-flagellation of bland food....
  31. 5 points
    Emperor G_D

    Mr.Kite is doing 5/3/1

    Needs MOAR tits.
  32. 5 points
    STENDEC

    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
  33. 5 points
    STENDEC

    Vindication for saturated fats!

    Saturated Fat Does Not Clog the Arteries Coronary Heart Disease Is a Chronic Inflammatory Condition, the Risk of Which Can Be Effectively Reduced From Healthy Lifestyle Interventions Aseem Malhotra; Rita F Redberg; Pascal Meier Br J Sports Med. 2017;51(15):1111-1112. Coronary artery disease pathogenesis and treatment urgently requires a paradigm shift. Despite popular belief among doctors and the public, the conceptual model of dietary saturated fat clogging a pipe is just plain wrong. A landmark systematic review and meta-analysis of observational studies showed no association between saturated fat consumption and (1) all-cause mortality, (2) coronary heart disease (CHD), (3) CHD mortality, (4) ischaemic stroke or (5) type 2 diabetes in healthy adults.[1] Similarly in the secondary prevention of CHD there is no benefit from reduced fat, including saturated fat, on myocardial infarction, cardiovascular or all-cause mortality.[2] It is instructive to note that in an angiographic study of postmenopausal women with CHD, greater intake of saturated fat was associated with less progression of atherosclerosis whereas carbohydrate and polyunsaturated fat intake were associated with greater progression.[3] Preventing the Development of Atherosclerosis is Important But It is Atherothrombosis That is the Real Killer The inflammatory processes that contribute to cholesterol deposition within the artery wall and subsequent plaque formation (atherosclerosis), more closely resembles a 'pimple' (Figure 1). Most cardiac events occur at sites with <70% coronary artery obstruction and these do not generate ischaemia on stress testing.[4] When plaques rupture (analogous to a pimple bursting), coronary thrombosis and myocardial infarction can occur within minutes. The limitation of the current plumbing approach ('unclogging a pipe') to the management of coronary disease is revealed by a series of randomised controlled trials (RCTs) which prove that stenting significantly obstructive stable lesions fail to prevent myocardial infarction or to reduce mortality.[5] Dietary Rcts With Outcome Benefit in Primary and Secondary Prevention In comparison with advice to follow a 'low fat' diet (37% fat), an energy-unrestricted Mediterranean diet (41% fat) supplemented with at least four tablespoons of extra virgin olive oil or a handful of nuts (PREDIMED) achieved a significant 30% (number needed to treat (NNT)=61) reduction in cardiovascular events in over 7500 high-risk patients. Furthermore, the Lyon Heart study showed that adopting a Mediterranean diet in secondary prevention improved hard outcomes for both recurrent myocardial infarction (NNT=18) and all-cause mortality (NNT=30), despite there being no significant difference in plasma low-density lipoprotein (LDL) cholesterol between the two groups. It is the alpha linoleic acid, polyphenols and omega-3 fatty acids present in nuts, extra virgin olive oil, vegetables and oily fish that rapidly attenuate inflammation and coronary thrombosis.[6] Both control diets in these studies were relatively healthy, which make it highly likely that even larger benefits would be observed if the Mediterranean diets discussed above were compared with a typical western diet. LDL Cholesterol Risk has Been Exaggerated Decades of emphasis on the primacy of lowering plasma cholesterol, as if this was an end in itself and driving a market of 'proven to lower cholesterol' and 'low-fat' foods and medications, has been misguided. Selective reporting may partly explain this misconception. Reanalysis of unpublished data from the Sydney Diet Heart Study and the Minnesota coronary experiment reveal replacing saturated fat with linoleic acid containing vegetable oils increased mortality risk despite significant reductions in LDL and total cholesterol (TC).[7] A high TC to high-density lipoprotein (HDL) ratio is the best predictor of cardiovascular risk (hence this calculation, not LDL, is used in recognised cardiovascular risk calculators such as that from Framingham). A high TC to HDL ratio is also a surrogate marker for insulin resistance (ie, chronically elevated serum insulin at the root of heart disease, type 2 diabetes and obesity). And in those over 60 years, a recent systematic review concluded that LDL cholesterol is not associated with cardiovascular disease and is inversely associated with all-cause mortality.[8] A high TC to HDL ratio drops rapidly with dietary changes such as replacing refined carbohydrates with healthy high fat foods. A Simple Way to Combat Insulin Resistance (Chronically High Levels of Serum Insulin) and Inflammation Compared with physically inactive individuals, those who walk briskly at or above 150 min/week can increase life expectancy by 3.4–4.5 years independent of body weight.[9] Regular brisk walking may also be more effective than running in preventing coronary disease. And just 30 min of moderate activity a day more than three times/week significantly improves insulin sensitivity and helps reverse insulin resistance (ie, lowers the chronically elevated levels of insulin that are associated with obesity) within months in sedentary middle-aged adults. This occurs independent of weight loss and suggests even a little activity goes a long way. Another risk factor for CHD is environmental stress. Childhood trauma can lead to an average decrease in life expectancy of 20 years. Chronic stress increases glucocorticoid receptor resistance, which results in failure to down regulate the inflammatory response. Combining a complete lifestyle approach of a healthful diet, regular movement and stress reduction will improve quality of life, reduce cardiovascular and all-cause mortality.[10] It is time to shift the public health message in the prevention and treatment of coronary artery disease away from measuring serum lipids and reducing dietary saturated fat. Coronary artery disease is a chronic inflammatory disease and it can be reduced effectively by walking 22 min a day and eating real food. There is no business model or market to help spread this simple yet powerful intervention. 1. de Souza RJ, Mente A, Maroleanu A, et al. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ 2015;351:h3978. 2. Schwingshackl L, Hoffmann G. Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression. BMJ Open 2014;4:e004487. 3. Mozaffarian D, Rimm EB, Herrington DM. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. Am J Clin Nutr 2004;80:1175–84. 4. Rothberg MB. Coronary artery disease as clogged pipes: a misconceptual model. Circ Cardiovasc Qual Outcomes 2013;6:129–32. 5. Malhotra A. The whole truth about coronary stents: the elephant in the room. JAMA Intern Med 2014;174:1367–8. 6. Chakrabarti S, Freedman JE. Review: nutriceuticals as antithrombotic agents. Cardiovasc Ther 2010;28:227–35. 7. Ramsden CE, Zamora D, Majchrzak-Hong S, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota coronary experiment (1968–73). BMJ 2016;353:i1246. 8. Ravnskov U, Diamond DM, Hama R, et al. Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Open 2016;6:e010401. 9. Moore SC, Patel AV, Matthews CE, et al. Leisure time physical activity of moderate to vigorous intensity and mortality: a large pooled cohort analysis. PLoS Med 2012;9:e1001335. 10. Blackburn EH, Epel ES. Too toxic to ignore. Nature 2012;490:169–71. Comments
  34. 5 points
    STENDEC

    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.
  35. 5 points
    Sanction

    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.
  36. 5 points
    For those who want the Cliff's Notes version of the above study:
  37. 5 points
    Quick update. I've been in therapy for months. I feel like kicking myself for not doing this sooner. Basically at the root, I've been suppressing this shit forever so its going to take a lot of time and dedication to become more mindful. I meditate everyday. I use http://self-compassion.org/category/exercises/ and the app called insight timer. I got taken off that Zoloft quickly. I fired that Doctor and found a new one. She is trying Prozac, its only been a week and I think the nervous sides are just kicking in. I guess we'll see. I'm not feeling any better really but I am more aware of the changes I need to make. That job sucks, they did sell and are outsourcing everything to India. Its hard to "get right" under such stress. I might lose my job. I'm not sure if I care or not...
  38. 5 points
    Sanction

    Liftin' weights and other shit

    Many leaders owe some of their successes to psychopathic tendencies. If it weren't for personality disorders we would still be swinging from trees.
  39. 5 points
    STENDEC

    Renaissance Diet Auto Templates

    lol...I meant to go back and flesh this out but got doing something else. This is a high protein, relatively low fat, low carb diet. My concern about this sort of diet for you JJ is that it is highly regimented and requires a lot of preplanning and prep work and I worry that doesn't really lend itself to your lifestyle ATM...it's also very low on the sort of "comfort foods" you seem drawn to. I'll go back to my suggestion that straight up Atkins is probably the best diet for you because it requires almost no planning or prepping, is easy to follow in that you know what is in and what is out, it's not calorie limited and will allow you to consume lots of fat which helps with the satiety of the diet and keeps you from straying off the reservation. It's also fairly adaptable to eating out. You can get a big slab of meat at just about any fast food place and so long as you don't eat the bun or the fries, you're generally okay on Atkins.
  40. 5 points
    STENDEC

    A Cure For Alzheimer's?

    Liraglutide is a GLP-1 agonist drug used to treat T2DM. In mice, at least, it's got another use that may prove to be far more exciting if it also works this way in humans... J Neurosci. 2011 Apr 27;31(17):6587-94. doi: 10.1523/JNEUROSCI.0529-11.2011. The diabetes drug liraglutide prevents degenerative processes in a mouse model of Alzheimer's disease. McClean PL1, Parthsarathy V, Faivre E, Hölscher C. Author information Abstract Type 2 diabetes is a risk factor for Alzheimer's disease, most likely linked to an impairment of insulin signaling in the brain. The incretin hormone glucagon-like peptide-1 (GLP-1) facilitates insulin signaling, and novel long-lasting GLP-1 analogs, such as liraglutide, are on the market as diabetes therapeutics. GLP-1 has been shown to have neuroprotective properties in vitro and in vivo. Here we tested the effects of peripherally injected liraglutide in an Alzheimer mouse model, APP(swe)/PS1(ΔE9) (APP/PS1). Liraglutide was shown to cross the blood-brain barrier in an acute study. Liraglutide was injected for 8 weeks at 25 nmol/kg body weight i.p. once daily in 7-month-old APP/PS1 and wild-type littermate controls. In APP/PS1 mice, liraglutide prevented memory impairments in object recognition and water maze tasks, and prevented synapse loss and deterioration of synaptic plasticity in the hippocampus, commonly observed in this model. Overall β-amyloid plaque count in the cortex and dense-core plaque numbers were reduced by 40-50%, while levels of soluble amyloid oligomers were reduced by 25%. The inflammation response as measured by activated microglia numbers was halved in liraglutide-treated APP/PS1 mice. Numbers of young neurons in the dentate gyrus were increased in APP/PS1 mice with treatment. Liraglutide treatment had little effect on littermate control mice, whose behavior was comparable to wild-type saline controls; however, synaptic plasticity was enhanced in the drug group. Our results show that liraglutide prevents key neurodegenerative developments found in Alzheimer's disease, suggesting that GLP-1 analogs represent a novel treatment strategy for Alzheimer's disease. PMID: 21525299 http://www.jneurosci.org/content/31/17/6587.long Neuropharmacology. 2014 Jan;76 Pt A:57-67. doi: 10.1016/j.neuropharm.2013.08.005. Epub 2013 Aug 21. Liraglutide can reverse memory impairment, synaptic loss and reduce plaque load in aged APP/PS1 mice, a model of Alzheimer's disease. McClean PL1, Hölscher C. Author information Abstract Type 2 diabetes is a risk factor in the development of Alzheimer's disease (AD). It has been shown that insulin signalling is desensitised in the brains of AD patients. The incretin hormone Glucagon-like peptide-1 (GLP-1) facilitates insulin signalling, and long-lasting analogues such as liraglutide (Victoza(®)) are on the market as type 2 diabetes treatments. We have previously shown that liraglutide improved cognitive function, reduced amyloid plaque deposition, inflammation, overall APP and oligomer levels and enhanced LTP when injected peripherally for two months in 7 month old APPswe/PS1ΔE9 (APP/PS1) mice. This showed that liraglutide has preventive effects at the early stage of AD development. The current study investigated whether Liraglutide would have restorative effects in late-stage Alzheimer's disease in mice. Accordingly, 14-month-old APP/PS1 and littermate control mice were injected with Liraglutide (25 nmol/kg bw) ip. for 2 months. Spatial memory was improved by Liraglutide-treatment in APP/PS1 mice compared with APP/PS1 saline-treated mice. Overall plaque load was reduced by 33%, and inflammation reduced by 30%, while neuronal progenitor cell count in the dentate gyrus was increased by 50%. LTP was significantly enhanced in APP/PS1 liraglutide-treated mice compared with APP/PS1 saline mice, corroborated with increased synapse numbers in hippocampus and cortex. Total brain APP and beta-amyloid oligomer levels were reduced in Liraglutide-treated APP/PS1 mice while IDE levels were increased. These results demonstrate that Liraglutide not only has preventive properties, but also can reverse some of the key pathological hallmarks of AD. Liraglutide is now being tested in clinical trials in AD patients. This article is part of the Special Issue entitled 'The Synaptic Basis of Neurodegenerative Disorders'. Copyright © 2013 Elsevier Ltd. All rights reserved. PMID: 23973293
  41. 5 points
    This is pretty cool. http://www.academia.edu/4830630/A_pocket-sized_metabolic_analyzer_for_assessment_of_resting_energy_expenditure A pocket-sized metabolic analyzer for assessment of resting energy expenditure. Clin Nutr. 2014 Apr;33(2):341-7 Authors: Zhao D, Xian X, Terrera M, Krishnan R, Miller D, Bridgeman D, Tao K, Zhang L, Tsow F, Forzani ES, Tao N Abstract BACKGROUND & AIMS: The assessment of metabolic parameters related to energy expenditure has a proven value for weight management; however these measurements remain too difficult and costly for monitoring individuals at home. The objective of this study is to evaluate the accuracy of a new pocket-sized metabolic analyzer device for assessing energy expenditure at rest (REE) and during sedentary activities (EE). The new device performs indirect calorimetry by measuring an individual's oxygen consumption (VO2) and carbon dioxide production (VCO2) rates, which allows the determination of resting- and sedentary activity-related energy expenditure. METHODS: VO2 and VCO2 values of 17 volunteer adult subjects were measured during resting and sedentary activities in order to compare the metabolic analyzer with the Douglas bag method. The Douglas bag method is considered the Gold Standard method for indirect calorimetry. Metabolic parameters of VO2, VCO2, and energy expenditure were compared using linear regression analysis, paired t-tests, and Bland-Altman plots. RESULTS: Linear regression analysis of measured VO2 and VCO2 values, as well as calculated energy expenditure assessed with the new analyzer and Douglas bag method, had the following linear regression parameters (linear regression slope LRS0, and R-squared coefficient, r(2)) with p = 0: LRS0 (SD) = 1.00 (0.01), r(2) = 0.9933 for VO2; LRS0 (SD) = 1.00 (0.01), r(2) = 0.9929 for VCO2; and LRS0 (SD) = 1.00 (0.01), r(2) = 0.9942 for energy expenditure. In addition, results from paired t-tests did not show statistical significant difference between the methods with a significance level of α = 0.05 for VO2, VCO2, REE, and EE. Furthermore, the Bland-Altman plot for REE showed good agreement between methods with 100% of the results within ±2SD, which was equivalent to ≤10% error. CONCLUSION: The findings demonstrate that the new pocket-sized metabolic analyzer device is accurate for determining VO2, VCO2, and energy expenditure. PMID: 23827182 [PubMed - indexed for MEDLINE]
  42. 5 points
    STENDEC

    Nerve Block for PTSD

    Interesting stuff. This is one of the first truly effective medical therapies for PTSD. Science Daily 11 October 2014 A single application of a common anesthetic procedure could be the answer to alleviating anxiety, depression and psychological pain in those suffering from chronic, extreme post-traumatic stress disorder (PTSD). In a study presented at the ANESTHESIOLOGYâ„¢ 2014 annual meeting, researchers followed 12 patients with PTSD who had undergone a simple anesthetic procedure called a stellate ganglion block (SGB). This common procedure involves injecting a small amount of local anesthesia into the base of the neck. SGB is traditionally used to treat a variety of conditions, from pain syndromes to sleep disorders. "While it doesn't cure the problem, we found that SGB appears to be a fast-acting and effective long-term treatment for chronic, extreme PTSD in veterans," said Michael T. Alkire, M.D., staff anesthesiologist at the Long Beach VA Healthcare System in California. "These improvements far outlasted what we would expect from SGB, which is usually used as a temporary nerve block and typically lasts three to five hours." In the study, the patients each were given one SGB and followed closely with structured interviews and other psychological tests for six months after treatment. The positive effects of the SGB were evident often within minutes and resulted in significant improvement of scores for the Clinician Administered PTSD Score, or CAPS, the test used to measure the severity of PTSD. Symptoms improved over time, and after one month, CAPS scores registered normal to mild PTSD levels for most of the patients. Positive effects were still seen at three months, but began fading and were generally gone by six months. Overall, 75 percent of the participants reported significant improvement of their PTSD symptoms after the SGB. Data from the study further suggested that SGB might also be an effective initial treatment for depression and anxiety disorders. "Further work is needed to identify which patients might respond best to this treatment as well as understand the mechanisms involved that produce such a rapid, dramatic and long-term change in psychological health for some patients," said Dr. Alkire, who also is a professor of anesthesiology at the University of California-Irvine. http://www.sciencedaily.com/releases/2014/10/141011172042.htm
  43. 5 points
    Sanction

    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.
  44. 5 points
    There may be some benefit from ALCAR. Lipoic acid may be synergistic with ALCAR for mitochondrial function, but it's likely to cause stomach upset. Valproate and/or lithium may have some neuroprotective benefits over the long term. I haven't kept up on research of these for a few years though. As we know the brain can be highly plastic, but it is not always so. Her motivation is important to the success of any cognitive exercise, so try to notice which cognitive activities are intrinsically motivating for her. If you can afford neurofeedback then have her do that. Which city are you in? Then there is the psycho-social side of things. You need to take care of yourself in the same way that airlines advise parents to put the oxygen mask on themselves first, and then on the child. You are her lifeline, so make sure you are getting the equivalent of oxygen in your life. "Caregiver fatigue" is a real phenomenon, and it is quite common, so find a way to look after yourself. In many cities there are brain-injury recovery groups. If they are run well, they give a social space to meet others without being ashamed of whatever disability exists. Like this forum, they can give peer support and learning about practical things so that you have more information about what to do.
  45. 4 points
    Growth Factor

    GF's "CS Goes Pubic" Log

    Sorry folks, but this news was all related to me 2nd hand by my mom. As it turns out, after receiving my 2nd registered letter about the situation the owner tried to retrieve my stuff from sellers. They were only able to get back my stuff from one person. The thing is, it appears that while this may be only like 10% of my things (it was more than "4-5 boxes"), it's all the valuable or sentimental items. It's my rock and mineral collection, my fossils, my action figure collection, notebooks from college, my insects, some of my artwork, and even my piano!
  46. 4 points
    https://www.nature.com/articles/s41598-019-44097-3?utm_source=share&utm_medium=ios_app Now obviously this has a huge correlation component as those in poor health won’t be outdoors as much in the first place. However, you can’t spend 2 hours outside without getting at least a little bit of sunlight, exercise, and mental stimulation. from new scenery.
  47. 4 points
    Try a Clickbait Title And You Won't Believe the 5 Things You're Doing Wrong That Will Make You Laugh! Formulate a 3 part structure. Examples: Fats, carbs, protein Past, present, future Problem 1, Problem 2, Solution An idea, the opposite idea, novel combination (thesis antithesis synthesis) Cell, Body, Society Chemistry, Physiology, Psychology Heroes, Villains, You
  48. 4 points
    Weekly doses of glucocorticoid steroids, such as prednisone, help speed recovery in muscle injuries, reports a new Northwestern Medicine study. The weekly steroids also repaired muscles damaged by muscular dystrophy. The studies were conducted in mice, with broad implications for humans. One of the major problems of using steroids such as prednisone is they cause muscle wasting and weakness when taken long term. This is a significant problem for people who take steroids for many chronic conditions, and can often result in patients having to stop steroid treatments. But the new study in mice showed weekly doses — rather than daily ones — promote muscle repair. “We don’t have human data yet, but these findings strongly suggest some alternative ways of giving a very commonly used drug in a manner that doesn’t harm, but in fact helps muscle,” said lead investigator Dr. Elizabeth McNally, the Elizabeth J. Ward Professor of Genetic Medicine at Northwestern University Feinberg School of Medicine and a Northwestern Medicine physician. https://knowridge.com/2017/05/weekly-steroids-can-strengthen-and-repair-muscles/
  49. 4 points
    Emperor G_D

    Manly log

    Polypharmacy++ When you really don't want to know what worked, do it all at once!
  50. 4 points
    Growth Factor

    520 Days of Isolation

    In the west, you get to sign up for experiments. In Russia, experiments sign up for you.
×
×
  • Create New...