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marylin monroe
Showing posts with label menopause. Show all posts
Showing posts with label menopause. Show all posts

Pomegranate for Statin Users, Magnesium for Cancer-Free Colons, Cialis for Diabetic & Healthy Women and Protein Supplementation for 0.81kg More Muscle & 13.5kg More Strength Gains Than Placebo (Data From Meta-Analysis)

As the data in the graphs at the bottom shows, only vigorous physical activity (right), yet not moderate (middle), let alone light physical activity (left) will help kids to stave off the bad visceral body fat, which increases their waist line from year to year. The photo in the background was by the way taken in 1989 on Orchard Beach, in the Bronx. If I remember correctly that's 6 years before the release of Nintendo's first "Game Boy". And yeah, I got one and it really doubled if not tripled my sedentary time!
7 minutes! That's the SuppVersity figure of the week and a number that should actually ring a bell with everyone of you who is following my advice and pays a daily visit to the SuppVersity Facebook Wall. "Seven minutes" that's what scientists from the University of Alberta and their Canadian colleagues believe would be the amount of "vigorous physical activities" our kids should get (Hay. 2012). I am not sure, if those scientists are still youths, but assuming they are not, I wonder if they cannot remember the amount of "vigorous activity" (which was back in the day simply called "play") they themselves or at least their parents or grand parents got, in the days when you still had to physically kick a ball, if you wanted to play soccer with your friends.

I mean, it's already bad enough that today's kids spend 70% of their time with sedentary activity, only 23% with light activity (like walking from the sofa to freezer ;-), 7% with modest and only 0.6% with vigorous physical activity, wouldn't it be wise then, to rather shoot for the stars and work towards a much higher amount of vigorous activity? After all, even Hay's own study shows that only vigorous activity was associated with a reduced waist circumference and lower markers of metabolic disease (see illustration on the right).

Even if the kids don't make it to the moon, but over to the neighbor's basketball hoop or a public playground that would be a major improvement over the 'exhausting' walks from the Playstation to the fridge and back, wouldn't it?
  • Pomegranate the better statin? Adding pomegranate phytosterol (β-sitosterol) and polyphenolic antioxidant (punicalagin) to a statin and reduce adipose tissue ROS production by a whopping 73%!  In their most recent paper Mira Rosenblat, Nina Volkova, Michael Aviram report that the administration of Simvastatin (15 μg/ml) to macrophages in the petri dish did only only "modestly decreased macrophage reactive oxygen species (ROS)" (Rosenblat. 2012), the presence of punicalagin (15 or 30 μM) almost 'extinguished the fire' cutting back inflammation dose-dependently by another 61% or 79%.

    As a regular here at the SuppVersity yo will still be aware that Pomegranate does also contain a potent plant version of CLA, called CLnA, no? Well then go back and read the full article!
    Intriguingly, β-sitosterol alone showed had minor pro-oxidant activity, when it was administered to the J774A.1 macrophages cell line the researchers from The Lipid Research Laboratory in Haifa (Israel) were analyzing,
    "the combination of simvastatin, β-sitosterol and punicalagin, clearly demonstrated a remarkable 73% reduction in ROS production."
    So what's the use of the statin, then? After all the scientists also found (but rather not mention in their abstract) that the combination of β-sitosterol and punicalagin actually suppressed macrophage cholesterol synthesis as effectively as low dose Simvastin or high dose Pravastatin (Click here to read about pomegranate in the SuppVersity news)
  • Organo-Magnesium stops colon cancer in its tracks by inhibiting inflammation, and the findings a group of researchers from the Gifu University Graduate School report in a soon-to-be published paper are not surprising. After all many epidemiological studies studies like Folsom & Hong (2006), for example, have already shown that there is a -23% reduced risk of developing colon cancer for 55-65 year-old Swedish women in the highest vs. lowers quantile of magnesium intake. Earlier this year Wark et al. conducted a randomized trial and meta-analysis of the hitherto published studies and found:
    "Our findings support the hypothesis that higher intakes of dietary magnesium are associated with lower risk of colorectal tumors. The consumption of magnesium-rich foods may be a new avenue to explore further in the search for cancer-prevention strategies." (Wark. 2012)
    Tabs or capsules? A 2010 study has the answer to the question which form of supplemental minerals is the best for you. Roswitha Siener and her colleagues from the University of Bonn in Germany found that magnesium oxide from effervescent tablets is better absorbed than from capsules and you can be pretty sure that similar results will be found for other forms of magnesium. My advice would yet be: Save the money and just go for plain magnesium citrate powder.
    The meta analysis yielded 13% lower risk of colorectal adenomas and 12% lower risk of colorectal cancer for every additional 100mg of magnesium per day. This does yet not mean that by eating pounds of magnesium you could render yourself 'cancer proof', but it is good evidence to make sure to get at least the into the 380-500mg range. And if you want to supplement, you really won't need the organ-magnesium Kuno et al. produced by mixing magnesium oxide (0.22 g), citric acid (0.55 g), malic acid (0.55 g), and glycine (0.22 g) - unless you can't tolerate it, cheap magnesium citrate will do just as well.
  • Taldalafil for insulin resistant and healthy post-menopausal women?! (Murdolo. 2012) A group of European scientists have found that the administration of 10mg of Taldalfil (the notorious PDE-5 inhibitor in Cialis) to both diabetic and healthy controls led to
    • an increase in permeability surface area product for glucose , and
    • skeletal muscle interstitial lactate levels r
    The forearm glucose uptake, as well as the arterial lactate levels showed differential responses, while there was a trend for increased glucose uptake in the healthy controls, the latter was absent in the diabetic group. The profound decrease in arterial lactate levels in the diabetic patients, on the other hand, was not present in the healthy controls, whose lactate levels had already been in the normal range (see figure 1).

    Figure 1: Effects of 10mg of Taldalafil on arterial and intramuscular lactate concentration (Murdolo. 2012). The increase in intramuscular glucose oxidation (evidenced by the lactate that is generated during this process) could even be of interest to healthy women (and men?).
    Based on these findings, Guiseppe Murdolo and his colleagues argue that the results would suggest that acute Tadalafil administration can increase the capillary recruitment and nonoxidative glucose metabolism, without having consistent effects on forearm blood flow and regional lipolytic rate. However...
    "[...] notwithstanding the lack of measurable changes on forearm glucose uptake, the microvascular response to tadalafil emerged as an independent predictor of muscle glucose disposal in both T2D patients and insulin-sensitive controls."
    Well, and if those effects don't reach statistical significance, maybe 'others' will. After all a 2003 study by Caruso et al. suggests that Taldalafil can also increase "the frequency of sexual fantasies and of sexual intercourse, and enjoyment" (Caruso. 2003) in a group of  53 pre-menopausal women (age 22–28) years affected by arousal disorders. Maybe we should simply put Taldalfil into the drinking... ah, I am just kidding ;-)
  • Finally! Scientists determine 'exactly'*rofl* how much more muscle you can gain with supplemental protein (Cermak. 2012). I hope I do not have to point you towards the irony in the headline of this On Short Notice item. If this ain't your first visit to the SuppVersity you should by now be aware that calculations like add 1g of protein per day and gain x-amounts of lean muscle mass per month, year or whatever timespan are nonsensical and will provide, if anything, a very general orientation.

    That said, it is still interesting to see the actual results Naomi M Cermak et al.'s quantitative meta-analysis of 22 studies, of which 77% were conducted with untrained individuals (64% with young trainees) produced. Most studies, which had a duration of 6-24 weeks (median: 12 weeks), used 3-5 x whole body workouts / splits coupled with milk (mostly whey) protein supplementation in amounts that ranged from 10g to 106g - keep that in mind when you think about how 'exact' the following figures can actually be:
    • Size-wise and even more so strength-wise Arnold could still benefit from a protein shake after a workout. When it comes to the increases in type I and type II fiber CSA, his age could however put a spoke in his wheel.
      Fat free and fat mass - Compared with the placebo, protein supplementation significantly augmented the gain in FFM during prolonged resistance-type exercise training (weighted mean difference: 0.69 kg). A subgroup analysis for age showed that protein supplementation was beneficial for both the young and the old trainees, but that the total effect size in terms of fat free mass gains were ~1.7x higher in the young subject (+0.81 kg) than in the older ones (+0.48 kg;) subjects.

      What I find particularly surprising is that the subgroup analysis also revealed that training status had no significant and what's more, if anything a beneficial effect on the effect sizes in the young untrained (+0.75 kg) and trained subjects (+0.98 kg), respectively.

      As far as fat loss is concerned the scientists did not record any statistical significant differences compared to placebo and that despite the fact that the placebo in most of the 22 studies was a sugary carbohydrate drink.
    • Muscle fiber cross sectional area - As the gains in lean mass already suggest, the cross sectional area (CSA) of the muscle fibers increased: By ~ 212µm² in the type I fibers and 291µm² in type II fibers. Unfortunately, both the increases in type I and type II fibers were statistically significant only in the young trainees.
    • 1-RM Strength - The performance for the one-rep maximum (1RM) on the leg press improved across the board (+13.5kg more than in placebo) and that did work almost equally well for younger (+14.4kg) and older trainees (+13.1kg).
    I will leave it up do you what you want to do with this data and whether you think that studies like this are actually useful for the individual practitioner who does not - contrary to way too many dietitians - have to be convinced of the benefits of protein supplementation on top of the low 0.8g per body weight the dietary guidelines recommend.
That's it another saturdaily installment of On Short Notice and in case you feel that you could use some more educative news, tomorrow is another day ;-)

References:

  • Caruso S, Intelisano G, Lupo L, Agnello C. Premenopausal women affected by sexual arousal disorder treated with sildenafil: a double-blind, cross-over, placebo-controlled study. BJOG. 2001 Jun;108(6):623-8.
  • Cermak NM, Res PT, de Groot LC, Saris WH, van Loon LJ. Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: a meta-analysis. Am J Clin Nutr. 2012 Nov 7.
  • Folsom AR, Hong CP. Magnesium intake and reduced risk of colon cancer in a prospective study of women. Am J Epidemiol. 2006 Feb 1;163(3):232-5.
  • Hay J, Maximova K, Durksen A, Carson V, Rinaldi RL, Torrance B, Ball GD, Majumdar SR, Plotnikoff RC, Veugelers P, Boulé NG, Wozny P, McCargar L, Downs S, Lewanczuk R, McGavock J. Physical Activity Intensity and Cardiometabolic Risk in Youth. Arch Pediatr Adolesc Med. 2012 Sep 10:1-8. doi: 10.1001/archpediatrics.2012.1028.
  • Kuno T, Hatano Y, Tomita H, Hara A, Hirose Y, Hirata A, Mori H, Terasaki M, Masuda S, Tanaka T. Organo-Magnesium Suppresses Inflammation-Associated Colon Carcinogenesis in Male Crj: CD-1 Mice. Carcinogenesis. 2012 Nov 3.
  • Murdolo G, Sjöstrand M, Strindberg L, Lönnroth P, Jansson PA. The Selective Phosphodiesterase-5 Inhibitor Tadalafil Induces Microvascular and Metabolic Effects in Type 2 Diabetic Postmenopausal Females. J Clin Endocrinol Metab. 2012 Nov 1.
  • Rosenblat M, Volkova N, Aviram M. Pomegranate phytosterol (β-sitosterol) and polyphenolic antioxidant (punicalagin) addition to statin, significantly protected against macrophage foam cells formation. Atherosclerosis. Available online 31 October 2012.
  • Siener R, Jahnen A, Hesse A. Bioavailability of magnesium from different pharmaceutical formulations. Urol Res. 2011 Apr;39(2):123-7.
  • Wark PA, Lau R, Norat T, Kampman E. Magnesium intake and colorectal tumor risk: a case-control study and meta-analysis. Am J Clin Nutr. 2012 Sep;96(3):622-31. doi: 10.3945/ajcn.111.030924. Epub 2012 Aug 1.

Measuring Overtraining; Phosphatidic Acid to Potentiate the mTOR Effects of Leucine? Plus: Built-in Serm in Menopausal HRT Blocks Breast Cancer, Creatine Bumps Up Performance Not Body Weight, Estrogen Timing & Brain NDMA Toxicity

Weight-supported sports such as cycling precipitate overtraining
"20%", that's the SuppVersity figure of the week. It tailors directly to the first item in today's installment of On Short Notice and denotes the amount of professional athletes who exhibit symptoms of overtraining syndrome at any given time in their career.
"The prevalence varies by sport and is thought to be highest in endurance sports requiring high volume intense training, such as swimming, triathlon, road cycling, rowing and, to a lesser extent, distance running."  (MacKinnon. 2000)
What all those sports (except for distance running) have in common are long training hours on 6 days per week for several months without appreciable time off. Notably, the chances of overtraining also increase, when the equipment supports your body mass. With weight-bearing activities, such as distance running, on the other hand, the risk of musculoskeletal injury limits training volume and therefore reduces the chance of "running" (literally) into overtraining.

Overall, there is however no group of athletes that is immune to training too long, too hard and without appropriate recovery times. And yes, this goes for power sports, such as weight lifting and judo, as well (cf. Callister. 1990, Fry. 1994)!

Identifying overtraining by psychomotoric evaluation  

When you come to think of it, it does actually stand to reason: Static and dynamic tasks for finger, hand, and arm movements, as they are assessed during a  series of tests to assess motor performance are a way better yardstick to determine the stress (over-)load on the central nervous system (CNS), than simply looking at "how much ya bench". Why? The nasty, creepy and easy to overlook form of overtraining happens largely in your head and your nerves, it's not muscular. Your skeletal muscle can be fully rested, while your central nervous system is at the verge of collapsing.

What does the motor-skill test measure? (1) steadiness (one or both hands) - assesses hand unrest, tremor; (2) inserting long pins (one or both hands) - assesses rate of arm and hand movements, precision of arm-hand movements, manual and digital dexterity; (3) tapping (one or both hands) - assesses wrist-finger speed
Usually the latter goes hand in hand with other not exactly exercise related stress symptoms such as nervousness, and the inability to cope with the imposed stress and piling-up difficulties. Therefore Paul et al. required that all the one-hundred 18-25y athletes (M=65, F=35; university to international level) from various athletic backgrounds, i.e.
  • hockey (14%), volleyball (14%), basketball (13%), handball (12%), football (6%), cricket (2%),
  • cycling (13%),  running (11%), kabaddi (8%),  swimming  (5%),  gymnastics (1%), and sprinting (1%)
to fill out a "classic" Training Stress Scale (TSS) questionnaire as well. The TSS is a 19-item scale to check the symptoms of acute overtraining which includes a subset of questions designed to assess  the ability of bouncing back mentally after setbacks and mistakes (REB).
Figure 1: Motor performance (steadiness error duration; inserting long pins task duration; tap hits) in 100 athletes grouped into low (LS), medium (MSG), and high (HSG) groups according to their scores on the TSS test (calculated based on Paul. 2012)
As you can see in figure 1 the results of the motor performance test did not just correlate with the data from the stress test questionnaire, they also depict a very good picture of the state of the nervous system, with highly significant difference between the highly stressed and almost certainly overtrained athletes (green) and their lightly stressed peers (figure 1, blue; stress data was assessed by the aformentioned TSS test).

Professional athletes rarely end up  like Christian Bale in the Machinist but as I discussed at length in a previous post, overtraining was one of the two pillars of the crazy regimen the actor used to starve himself into a state that hardly allowed him to perform in front of the camera.
Aside from the high correlation and the confirmation of the hypothesis that psychomotoric tests could prove a valid tool to access the training status of athletes and ambitious gymrats, the investigation yielded the following main results:
  • The athletes with lowest training stress symptoms showed the highest reboundability (resilience) from their mistakes. 
  • Increased intensity of training stress symptoms indicates attention deficit leading to poor psychomotor performance.
  • Along with physical training, psychological training has to be considered as one of the eminent aspects of overall development of an athlete.
In order to maximize athletic performance, it is therefore more or less obligatory to "carefully and timely diagnose for any signs and symptoms for physical and psychological distress" (Paul. 2012). Needless to say that the combination of the TSS and psychomotor performance test offers a way to do just that - to monitor, control and optimize the training routine.

Phosphatidic acid a novel 'mTOR potentiator' for superior gains?

I somehow forget this one in the last installment of On Short Notice, but before the first supplements are going to hit the market (two of the authors have already filed a patent back in 2011 that hasbeen  published in June 2012; see De Ferra. 2012), I thought I'd briefly discuss the results of a recently published study on the potential ergogenic and muscle building effects of phosphatidic acid (PA) by Hoffman et al. (Hoffman. 2012).

The study that was published online in the Journal of the International Society of Sports Nutrition evaluated the effects of an 8-week resistance training on 16 resistance-trained men who had been randomly assigned to consume either 750 mg of PA or a placebo.
Figure 2: Effect of 8 weeks of strength training + post-wporkout amino acid supplementation with and without  750mg phosphatidic acid  per day (left) and ratio of beneficial, trivial and negative effects of supplementation on the respective outcome parameters (Hoffman. 2012)
As the data in figure 2 goes to show you, the supplementation regimen had beneficial effects almost all of the (except for the pennation angle, btw. where greater the angles of pennation, means translates to a smaller amount of effective force transmitted to the tendon), however not a single statistical significant difference was observed. And while the scientists assessment that the overwhelmingly beneficial effect of PA supplementation on lean mass gains is "very likely beneficial", this does not change that the 750mg of PA did not add to allegedly highly beneficial effects of the workout regimen.

Figure 3: Training protocol and amino acid content (in g/100g) of the post-workout supplement (identical in both groups).
Since all particpants had taken part in identical 4-day per week, split routine resistance training programs for 8-weeks (70% of their 1-repetition maximum (1-RM) for all exercises;  90-s rest period was required between each set, for all exercises; for the exercises check out figure 3) and were advised to consume a standardized post-workout protein formula (containing 36-g amino acid and collagen protein blend) mixed in a 500 ml commercial sports drink within 30 minutes post-exercise, the supplemental confounding factors were pretty tightly controlled. If anything but the consumption of the PA supplement would have been responsible for the inter-group differences this would therefore have to be related to
  • the non-supervised training sessions at the subjects respective local gyms (training logs regardless of whether they are evaluated by "certified personnel", or not, can obviously be faked), and
  • the absence of a prescribed nutritional regimen (the participants kept 3-day food-logs and were advised to stay on their habitual diet; no significant differences in total intake ~3,200kcal/day; according to Hoffman et al. likewise not statistical significant, but wrt to the the changes in body composition maybe noteworthy, were the -17% lower carb and +18.2% higher protein intake in the active = PA arm of the study)
Both the missing supervision, as well as the absence of a fixed nutritional protocol would however pertain to both groups and are thus likely to average out. Plus, they actually make the study more realistic. After all, you are interested in what happens if the average strength trainee (in this case young men with a mean age of ~23years, at least 1 year of training experience and a BMI of 27.7kg/m²) and not to 10 identical clones, don't you?

"So this stuff is not useful, right?"

Figure 4: Exogenous phosphatidic acid is metabolized to lysophosphatidic acid (LPA) in the body and LPA has been shown to work synergistically w/ leucine to increase mTORC1 activity (in vitro data from Winter. 2010).
Despite the "likely" and "very likely beneficial" effects on lower body power and lean body mass, of which only the latter could maybe have reached statistical significance with a larger number of participants (with only 20 subjects, i.e. 10 per group differences need to be more pronounced to reach statistical significance). It should be quite obvious that PA is probably not the next creatine.

Maybe the increased mTORC1 expression Winter et al. have observed upon co-incubation of leucine with LPA are not pronounced enough (figure 4). Or simply not necessary with enough leucine and insulin in the blood stream. After all, the Winter study also showed that basically identical effects were observed when the cells were incubated with leucine + insulin, instead of LPA + insulin (data not shown in figure 4).

So even if oral PA acts just like in-vitro LPA synergistically with leucine to activate the mTOR pathway (Fang. 2001; Winter. 2010; figure 4), the real world benefits in the study at hand are probably about as significant as the hypothetical 500g increase in net protein retention I discussed in he protein timing news earlier this week. Whether this may change with higher and/or more frequent doses in future studies remains to be seen, though. It does at least not appear to be impossible...

Additional news

  • 'Built-in SERM' could help making post-menopausal estrogen replacement breast cancer proof At least this is what the results of a recent rodent trial that was conducted by researchers from the Division of Endocrinology at the Department of Medicine of the University of Virginia Health System in Charlottesville would suggest. Even in the absence of a progestin, which does have some ameliorative effects on the pro-carcinogenic effects of estrogen, the addition of the tissue-specific selective estrogen receptor modulator bazedoxifene (BZA) to the allegedly questionable, yet still widely prescribed conjugated equine estrogen (CEE) blocked the CEE- and, in a second control study, even the more potent E2-stimulated ductal and terminal end bud growth of mammary gland and the corresponding estrogen-responsive gene expression (Song. 2012). 
  • Just like any athlete, man or woman who is interested in increasing his / her athletic performance, German Olympic lifter Julia Rohde could benefit from taking regular creatine monohydrate without necessarily running the risk of having to compete in a higher weight class (img sportzentrum-flora.de)
    5g creatine monohydrate (CM) per day helps soccer players to improve their game - or, more precisely, the time they needed to complete a standardized sprint running and dribbling test. And while you will probably not be surprised that CM supplementation did not affect the accuracy of their shots, you may very well be surprised that it did neither induce greater weight gain or any other changes in body composition (Mohebbi. 2012).

    The latter may also be interesting for athletes competing in sports where increased muscle mass can become an issue. After all, the results Mohebbi et al. present in the latest issue of the Middle-East Journal of Scientific Research would suggest that unless your training is geared towards increased muscle gain (which is obviously shouldn't be if that would be an issue for you) regular creatine, i.e. not the sugar laden 'cell-volumizers', can help you increase your performance in the absence of the (again, only for certain people) disadvantageous weight gain.
  • Whether estrogen will save your brain cells or actually exacerbate the damaging effect of NMDA exposure depends on timing I guess you will all have heard of the protective effects of estrogen against N-methyl-d-aspartate (NMDA) toxicity. Now, a group of researchers from the University of Catania and the University of Rome Sapienza,both obviously in Italy, found that only pretreatment with estrogen will provide these beneficial effects, while the co-incubation or subsequent administration of estrogen will only potentiate the NMDA-induced cell death (Spampinato. 2012)
Have a nice weekend, everyone! As far as the On Short Notice items go, that's it for today. If you want more, just check out the SuppVersity Facebook Wall. I must forewarn you, though, since I am pretty busy this weekend, I am not sure if there will be another installment of the Athlete's Triad Series, tomorrow. If that's not the case, you will however get a regular news item, so don't worry you won't get bored ;-)

References:
  • Callister R, Callister RG, Fleck SJ, Dudley GA. Physiological and performance responses to overtraining in elite judo athletes. Med. Sci. Sports Exerc. 1990; 22: 816–24.
  • Fang Y, Vilella-Bach M, Bachmann R, Flanigan A, Chen J: Phosphatidic acid-mediated mitogenic activation of mTOR signaling. Science 2001, 294:1942–1945.  
  • De Ferra L, Heuer M, Hagerman S, Purpura S, Jäger R. Method for increasing muscle mass and strength. Filed November 23, 2011. US 2012/0141448 A1. Published on June 7, 2012.
  • Fry AC, Kraemer WJ, van Borselen F et al. Performance decrements with high-intensity resistance exercise overtraining. Med. Sci. Sports Exerc. 1994; 26: 1165–73. 
  • MacKinnon LT. Special feature for the Olympics: effects of exercise on the immune system: overtraining effects on immunity and performance in athletes. Immunol Cell Biol. 2000 Oct;78(5):502-9.
  • Mohebbi H, Rahnama N, Moghadassi M, Ranjbar K. Effect of Creatine Supplementation on Sprint and Skill Performance in Young Soccer Players. Middle-East Journal of Scientific Research. 2012; 12 (3): 397-401.
  • Paul M, Khenna N, Sandhu JS. Psychomotor analysis of athletes under overtraining stresss. Serb J Sports Sci. 2012;6(3): 95-10.
  • Song Y, Santen RJ, Wang JP, Yue W. Effects of the Conjugated Equine Estrogen/ Bazedoxifene Tissue-Selective Estrogen Complex (TSEC) on Mammary Gland and Breast Cancer in Mice. Endocrinology. 2012 Oct 15.
  • Spampinato SF, Merlo S, Molinaro G, Battaglia G, Bruno V, Nicoletti F, Sortino MA. Dual Effect of 17β-Estradiol on NMDA-Induced Neuronal Death: Involvement of Metabotropic Glutamate Receptor 1. Endocrinology. 2012 Oct 17.
  • Winter JN, Fox TE, Kester M, Jefferson LS, Kimball SR: Phosphatidic acid mediates activation of mTORC1 through the ERK signaling pathway. Am J Physiol Cell Physiol 2010, 299:C335–C344.

With >50% Increased Risk to Develop New-Onset Diabetes, Statins are "Starter Drugs" for Post-Menopausal Women. Plus: Younger, Leaner & Asian Women at Greatest Risk

Image 1: A statin here, some metformin to keep the collateral at bay, add an ACE inhibitor and some anti-coagulant drugs and you have a delicious cocktail of highly profitable pharmaceuticals...
Do you remember how creatine has gotten a bad rep within the mass media, a few years ago? Initially touted as an over-the-counter "steroid" by a clueless journalist, the did not, as you would have expected backpedal, or at least forget about the whole thing, when some experts raised their hands and said: "Wait a minute! Creatine is a naturally occuring amino acid with thousands of studies backing its efficacy...", no, they just turned it around and said: "Look, this is how it goes: First creatine, then androstenedione, next real gear! This stuff is a starter drug which will make our youth go astray!" ... Today, or I should say, on January 9, 2012, a study on another, yet in the eyes of the press obviously way less "starter drug" has been published - the title: "Statin Use and Risk of Diabetes Mellitus in Postmenopausal Women in the Women’s Health Initiative"

Keep an eye on your mommy, she might be doing drugs!

As a diligent student of the SuppVersity and thoughtful observer of the blogosphere, I probably won't have to tell you that taking a stating, although they could be life-saving for a infinitesimal percentage of the population, is not as good an idea as the luckily in this part of the world forbidden TV commercials will make. At least for women, the "preventive" use that is so highly advertised by the statin producing pharmaceutical industry, is associated with a 61% increase to develop new-onset diabetes (48% if in addition to age, race and ethnicity, education, cigarette smoking, BMI, physical activity, alcohol intake, energy intake, familiy history of diabetes, and hormone therapy were also considered as confounding factors in the calculation of the hazard ratio), in the 120,173 women without pre-existing cardiovascular disease in the enormous cohort of the Women's Health Initiative study.
Figure 1:  Risk of developing diabetes by statin use among women with and without medical history of cardiovascular disease at baseline; unadjusted, age-and race/ethnicity and multivariate (age, race/ethnicity, education, cigarette smoking, body mass index, physical activity, alcohol intake, energy intake, family history of DM, and hormone therapy use) adjusted hazard ratios (data adapted from Culver. 2011)
When all confounding factors (see brackets above) are considered the "additional" risk decreases (BMI, physical activity and hormone therapy are probably the culprits, here) and the inter-group difference vanishes, so that this leaves us with a ~50% increased risk to develop type II diabetes in a cohort of 153,840 women, whose mean age was 63.17 years - now, if one discarded that the data in column 2 of figure 1 is already age-adjusted you could well argue, that at this age, it is "just normal" to develop some blood sugar issues.
Figure 2: Association between new-onset diabetes risk and statin use at baseline within different age, race/ethnicity, and BMI subgroups of the 153,840 participants; data shown as unadjusted and multivariate (age, race/ethnicity, education, cigarette smoking, body mass index, physical activity, alcohol intake, energy intake, family history of DM, and hormone therapy use - age, race and BMI were obviously excluded in the respective subgroup analysis) adjusted hazard ratios (data adapted from Culver. 2011)
Aside from the fact that this is an absolutely idiotic, yet often uttered statement (I hear that esp. from people who are already "at that age" and unwilling to do something about their (pre-)diabetic state, by the way), the data in figure 2 shows quite clearly that the "younger" ladies are at particular risk to develop diabetes. Even after the aforementioned adjustments for BMI, physical activity and co. were made the hazard ratio (a measure of the increased risk, with 1.0 = normal and e.g. 1.5 = 50% increased risk) of developing new-onset diabetes was slightly higher (+3%). It would thusly be interesting to see the hazard ratios for pre-menopausal women, or even teens and twens, an increasing number of whom is put on a "live-saving" statin - at the latest, when their cholesterol levels surpass the repeatedly lowered "cut-off" limit of currently 240mg/dl (NHLBI. 2012).

If your mama takes statins is a "light-weight" (for her age) and from Asia or the pacific islands, you better get her some Metformin - she probably is going to need it soon...

If you further scrutinize the data in figure 2, it become pretty obvious that the group(s) with the highest risk to develop new-onset diabetes upon being treated with statins are
  • women from Asia or the Pacific Islands, with an increased risk of +112% (unadjusted) and +78% (adjusted for the aforementioned variables except from ethnicity, obviously), and
     
  • women with a BMI of <25 kg/m², with an increased risk of +240% (unadjusted) and +89% (adjusted for the aforementioned variables except from BMI, obviously)
Whether this would mean that light-weight Asians / Pacific Islanders who are put on statin therapy would be even more likely to develop new-onset diabetes, would admittedly need further elucidation.
Figure 3: Association between new-onest diabetes risk and statin use at baseline in 153,840 participants; data shown as unadjusted, adjusted for age / race /ethnicity and multivariate (details see figure 1) adjusted hazard ratios (data adapted from Culver. 2011)
It is however, at least in my mind, not unlikely - in particular if they are / are going to be on the statin for an extended period of time (cf. figure 3). Against that background it is quite comforting to know that most statin dealers... ah, pardon pharma companies, also have one, many even a whole host of diabetes drugs for doctors to chose from, when - after a few months of treatment - their formerly only "hypercholesterolemic" female patients have developed full-blown diabetes!

So, let's just hope that the sons and grandsons of these women did not resort to creatine or other dangerous "steroids" from their local GNCs by then! I mean, otherwise it would be likely that they were going on a "roid rage" against their mommy's and granny's doctors, when they see the muscles and brains of their insulin-dependent loved ones wither under the influence of their cholesterol lowering medication.