Vitamin D 2010 RDA: IOM Lays An Egg

News flash!  The Institute of Medicine (IOM) just released their long awaited (13 years in the making) pronouncement regarding the recommended daily allowance (RDA) of vitamin D and calcium.  Many of us were waiting to see the RDA increased from 400IU daily to 1,000IU daily or even 2,000IU daily.  Maybe the IOM would even increase the upper limit of 10,000IU daily.

Instead, the IOM laid an egg.  That's my opinion (plus that of the Vitamin D Council).  Now, I make no claim as to being a vitamin D expert, although in my prior position as Senior Institute Physician and Executive Director of Physician Education at Cenegenics Medical Institute, I wrote 8 reviews regarding the benefit of vitamin D over the past 3 years.  However, I remember fondly the paraphrase attributed to Newton (who probably pilfered it from Salisbury) about standing on the shoulders of giants.  That's why, rather than re-invent the wheel, I direct you instead to the Vitamin D Council's response.  It's a great summary & rebuttal.

Q&A session at Avvo.com

I live in northern california and my doctor left her practice to work on an air force base. Now I am jammed up to find a Doctor. - Avvo.com

Q&A session at Avvo.com

I'm 16 years old and my boyfriend is 19. We had a bit of an accident and I may be pregnant. - Avvo.com

Q&A session at Avvo.com

Can an elderly person endure dangerous side effects from being medicated daily with multi drugs including 3 anti-depressants? - Avvo.com

Q&A session at Avvo.com

My mom is in her 70's and she is sometimes loses her balance or her hand or arm will just go limp and she drops things. - Avvo.com

Exercise vs Brain (Size & Function)

Exercise.  We spit it out like it's a 4 letter word.  Most of us loathe it.  Yes, there are the dedicated few who actually make use of their gym membership for which they have funds withdrawn painlessly every month.  But for the vast majority of the population, our physical activity consists of walking to the feeding trough to stuff our faces and pointing the remote control to change the TV channel.  Thank goodness for Wii, and now PlayStation Move & XBox 360 Kinect to get some of us off our bottoms.  I'm ranting about this since a recent study demonstrated that walking more was associated with greater brain volume and lower risk of cognitive loss.

The authors followed 299 adults (average 78 years old) who were free of cognitive impairment at baseline.  Brain MRI was performed at baseline & year 9 followed by reassessment of cognitive function at year 13.  All the while, they evaluated the amount of walking performed on a regular basis.  The range of walking varied from none to 300 blocks per week with an average distance of 56 blocks (or 8 blocks per day 7 days per week).  However, the authors concluded that one needed to walk 72 blocks weekly or 10 blocks daily without fail in order to preserve and actually increase brain volume.  This greater amount of gray matter was then associated w/significantly lower risk of cognitive impairment just 4 years later.

Take home point?  Physical activity is protective of brain function as we age which is imperative as our Baby Boomers reach retirement and the age at which risk of dementing illnesses increases dramatically.  But I can hear it now.  How long is a block?  Here in Las Vegas, the major street intersections are a mile apart (granted there are more frequent intersections in between).  But the authors did declare the 72 blocks equivalent to 6-9 miles. 

Now if this study isn't convincing enough to get you off your sofa, a study published in July came to a similar conclusion in women.  Likewise studies from August 2009, September 2008, July 2008, May 2008, and October 2006 all point towards the same conclusion that an increase in physical activity is associated with an increase in cognitive function & lower risk of dementia.  So that you won't later forget that you should have.

FDA Approves Underarm Application of Testosterone

The FDA just announced their approval of Axiron, a 2% topical solution of testosterone that is applied via metered dose pump at 30mg per actuation.  The plan is to apply 1 squirt to each armpit daily (more if necessary), wash hands & get dressed.  Yes, you still need to avoid skin-to-skin contact with your kids & partner.  You should also avoid bathing & swimming for at least 2 hours after application although, hopefully, you already completed the former prior to squirting yourself.  Whether you choose to apply deodorant or antiperspirant is up to you (and your close contacts!) as neither will affect absorption but they recommend applying either one before the testosterone.  And no, you don't have to shave (your pits).  But you might have to wait a while for it to actually hit the market.

In any case, you now have a wide choice of FDA-approved oral & buccal tablets, subcutaneous pellets, transdermal patches, injections, manually applied topical gels/creams, and now, metered dosing to the axilla.  Of these, the only ones I avoid are the oral tablets (due to increase risk of liver irritation) and subcutaneous pellets (difficult to obtain/maintain proper level & requires minor procedure for placement), but that's just me.

Yet Another Q&A session at Avvo.com

I've had a left side pain just above the waist, for several days. It's not a sharp pain, but it is there all of the time. - Avvo.com

Another Q&A session at Avvo.com

Weird pain under shoulder left side, near armpit on back side. - Avvo.com

Q&A from Avvo.com

What is the average testosterone level for a 58 yr. old man? - Avvo.com

Q&A from Avvo.com

How long is too long for hormone therapy for prostate cancer? - Avvo.com

Q&A from Avvo.com

Incontinence in men? - Avvo.com

Q&A from Avvo.com

i cant stop myself from urinating - Avvo.com

HDL vs Chocolate

Just the other day, I reviewed a study looking at the benefit of high cocoa content chocolate on chronic fatigue syndrome.  Yesterday, I reviewed another study looking at the benefit of low carbohydrate caloric restriction on HDL levels.  In the skewed logic of my children, one might then ask whether high cocoa content chocolate might have an impact upon HDL.

In a small, short study published this month (and yes, I do review larger, longer studies, too), the authors randomized 12 participants with well-controlled Type 2 diabetes (average HgbA1c 6.4%) to placebo vs 15g three times daily of 85% cocoa content chocolate for 8 weeks, followed by a 4 week washout period, and then crossed over for a final 8 weeks.  This randomized double blind placebo controlled cross over study allowed each of the subjects to also serve as their own controls.  Parameters were checked at baseline, after the first 8 weeks randomization, after the 4 week washout & after the 8 week cross over.

The first bit of good news?  Despite adding 45g daily of chocolate, the participants did not gain weight, lose glycemic control, or worsen their insulin response.  More importantly, compared to their results from placebo, the consumption of high cocoa content chocolate increased HDL from 1.16mmol/L (45mg/dL) to 1.26mmol/L (49mg/dL) & lowered cholesterol:HDL ratio from 4.4 down to 4.1, both statistically significant findings. In fact, this 10% increase in HDL is equivalent to the results obtained from less tasty pharmacologic assistance.

What's this mean for our patients with T2DM?  Conventional wisdom has always stated that diabetics should avoid candy but this study throws that thought out the window.  High quality, eg 85% cocoa content, chocolate in moderation (15g three times daily) can be a healthy adjunct to their meals.  Given what we know about all the other benefits of this type of chocolate, there's really no reason to avoid it unless you're allergic.  In the meantime, I'll see if I can find a large, long-term study of low carbohydrate caloric restriction vs chronic fatigue syndrome.  But don't hold your breath!

Testosterone vs Heart Failure

Click here for April 19, 2012 update!

I mentioned in an earlier post that I was attending a CME conference last week. One of the lectures covered evidence-based, state of the art care of patients with heart failure. The presenter reminded us that ACE inhibitors, beta blockers & aldosterone antagonists, separately and in combination, have been demonstrated to improve heart failure mortality. He also reviewed evidence that the benefit from beta blockers is not a class effect since there are real differences between the individual drugs. Cardiac resynchronization therapy plus implantable cardioverter-defibrillators has also been demonstrated to improve outcomes.

All told, he pointed out a 77% cumulative risk reduction if all four of these therapies were applied with 27% absolute risk reduction. This translates into treating only 4 persons in order to save 1. Given that heart failure exacerbation is one of the leading causes of (re)hospitalization and that hospital care accounts for the greatest percentage of medical costs, it's clear that we need to be more aggressive in optimally treating our patients with heart failure.

However, he also pointed out that current ACC guidelines do not recommend hormonal therapies other than to replace deficiencies. Based upon the preponderance of new information, I have to disagree. For instance, in a study published just last month, researchers randomized 36 elderly women with stable heart failure (NYHA III without hospitalization in immediate past 3 months with 33% ejection fraction) on maximal medical management to either testosterone transdermal patch (300ug twice weekly) or to placebo and followed them for 6 months.

Those who received testosterone walked further in 6 minutes (standard testing protocol), increased their maximum oxygen consumption (that's a good thing), and strengthened their legs.  If you ask me, that's a touchdown or home run, especially when your average age is 68-69yo.  Even better, no side effects were reported from this dose besides minor allergic dermatitis, common to all patch delivery systems.

Not surprisingly, these findings are consistent with those published last September in which 70 elderly men (average 70yo) with heart failure (NYHA II or III with 32% ejection fraction) responded to intramuscular testosterone for 12 weeks on top of maximal medical management.  They, too, demonstrated improvement in exercise capacity, muscle strength, and even glucose metabolism.  And just as important, the therapy was well tolerated.

In January 2006, 76 men (average 64yo) with heart failure (NYHA II-IV with 32% ejection fraction) were randomized to receive Androderm 5mg daily vs placebo for 12 months.  The authors reported significant improvement in functional capacity as born out by decrease in NYHA classification.  The only issue noted was intolerance to the patch.

Finally, a study in May 2003 demonstrated in 12 men with heart failure that testosterone 60mg via buccal mucosa increased cardiac output immediately.

Now, I'm not suggesting that everyone with heart failure go out and start taking testosterone.  However, I think that the research thus far points to a need for a larger scale study of longer duration to confirm/disprove these consistent results using a very inexpensive drug.  And in the meantime, for those of you waiting for the outcome of said study, perhaps you can discuss the above findings with your cardiologist or primary care provider.

How to Raise Your HDL

Low HDL (usually thought of as <40mg/dL in men & <50mg/dL in women) is the bane of physicians.  Regardless of LDL, the lower your HDL, the greater your risk of heart disease.  However, we don't really have an easy way to increase HDL dramatically. 

As physicians, we recommend strenuous intense exercise but we know how far that's gotten us.  Wine makes a small increase but as we all know, too much of a good thing isn't.  Niacin works but most won't tolerate the flushing & tingling side effects from doses high enough to make an impact.  Fibrates can raise HDL some but requires a prescription.  Of the statins used to lower LDL, only rosuvastatin raises HDL to some extent but doesn't have many outcomes studies yet.  If you're diabetic, pioglitazone raises HDL while rosiglitazone tends to lower HDL.  Recently, at the American Heart Association's annual meeting, researchers announced their findings that Merck's experimental anacetrapib increased HDL substantially in a late phase clinical trial (by inhibiting cholesteryl ester transferase protein (CETP), if you must know).  But it will probably be a while before this wonder drug hits the market, at which point we'll learn about its potential side effects (and financial cost).

So what do we do in the meantime?  In a small, short 4 week study published this month, authors asked 18 men & 25 women (average age 38-39 years old), all overweight or obese, to restrict both their caloric intake (down to 1800kcal/d for men & (1400kcal/d for women) and the resultant fraction of carbohydrates (on average from 55% down to 33% and from 53% down to 30%, respectively), commonly referred to as a "low carb" diet (goal <100g/d).  They were instructed to maintain their current level of physical activity.  In fact, the men were able to drop their average caloric intake down to 1307kcal/d while the women achieved 1243kcal/d.

As a result, men lost 4.7kg on average while women lost 2.4kg, resulting in significant decreases in body mass index.  Furthermore, in the short term, both men & women decreased their waist circumference, body fat percentage, systolic blood pressure, total cholesterol, triglycerides, and insulin.  Most importantly, men increased their HDL from 0.83mmol/L (32mg/dL) to 0.96mmol/L (37mg/dL).  While this increase isn't enough to get these men out of harm's way (generally thought of >60mg/dL), it's certainly a step in the right direction without risk of drug side effects.  Unfortunately, women demonstrated no significant increase in HDL.

It should be noted that this kind of eating wasn't easy to achieve.  The researchers gave food products to minimize noncompliance since it was expensive to stay on this diet.  In fact, only 7 of the 18 men were able to reach their goal of consuming <100g/d of carbohydrates. 

What can we glean from this study?  Well, it supports many other studies that have demonstrated an improvement in HDL by decreasing caloric intake and weight loss.  However, it's not clear whether the increase in HDL was due to the caloric restriction, the decrease in carbohydrate consumption, or the weight loss.  Let's not lose sight of the fact that this was a small, short study.  But given the costs of most new drugs upon hitting the market and the relative lack of side effects (aside from the cost of food), it seems reasonable to recommend again that we eat less (carbs).

Vitamin D vs Depression: Associative or Causative?

So, did you all enjoy Black Friday?  My wife went out last night to run with the bulls, or in this case, her girlfriends, to go shop all the post-Thanksgiving sales.  If you notice an improvement in the local economy, y'all can thank them for doing their part. 

As for me, I've been putting in some late nights/early mornings trying to fix up my website, take care of legal paperwork required to start my practice, and read, read, read.  Thus, I've been spending more time indoors than out.  Less sun exposure leads to lower vitamin D.  And now, lower vitamin D may be associated with risk of depression!

I mention this because in a study published earlier this month, the authors performed a cross-sectional analysis of 7,970 participants of the National Health and Nutrition Examination Survey (NHANES III) with age range 15-39 years old.  Using standardized depression scales, they concluded that those with 25OH vitamin D <50 nmol/L (20ng/mL)  were more likely to be depressed than those with 25OH vitamin D >75nmol/L (30ng/mL). 

Interesting, you say.  But this isn't really a new finding.  A prospective study from May 2008 came to similar conclusions after evaluating a cohort of 1,282 participants 65-95 years old and concluding that a reduction of 14% in vitamin D was associated with an increase risk of depression.  And an earlier cross sectional study of 80 participants from December 2006 came to similar conclusion.

However, just as with the chicken and the egg, it's not always clear whether the relationship is associative in nature or causal.  For instance, vitamin D could be low because patients are too depressed to go outside.  But a smaller study published in July concluded that those euthymic women with lower baseline vitamin D were more likely to become depressed in 3-6 years.  So we have 3 studies demonstrating an association and 1 study raising the question of cause & effect.  To hedge my bets since I'm predominantly indoors these days, I supplement my solar-induced manufacture of vitamin D with appropriate vitamin D directed by regular laboratory analysis of my 25OH vitamin D.

Eat More Protein + Low Glycemic Meals to Maintain Weight Loss

Continuing yesterday's theme (I hope you all had a wonderful Thanksgiving, by the way) of "which is better", there continues to be debate as to whether glycemic index (GI) & load (GL) really matters when it comes to nutrition, and whether high protein or low protein meals are better for you.  In fact, think back to yesterday's big meal.  Did you consume low or high GI foods?  Presumably you had plenty of protein in the form of turkey (turducken, anyone?) and ham.

To address this question, the authors studied 548 participants who had lost 8% body weight (average 11kg) while completing an 800kcal/day diet (extremely low calories!) who were randomized to either control, low protein + low GI, low protein high GI, high protein + low GI, or high protein + high GI for 26 weeks.  Fat content was kept at 25% caloric intake regardless of meal composition.  15 glycemic points were supposed to separate low from high GI while 12% protein calories were supposed to separate those on low vs high protein diets.  The participants were allowed to consume as many calories as they choose as the authors also wanted to determine which diet better satiated the participants.

After completion of the study, the authors discovered that only those on high GI + low protein diet regained some weight (average 1.67kg).  In fact, those assigned to high protein diets regained less weight compared to those randomized to low protein, and those assigned to low GI diets regained less weight compared to those randomized to high GI.  They also reported that more participants assigned to low GI diets completed the study than those randomized to high GI, and likewise for high protein vs low.  What's noteworthy is that these findings were obtained despite only achieving 5 glycemic points & 5% protein calorie separation between the groups.

The editorialists were actually quite warm to these findings, suggesting more reseach but noting the practicality of the low GI + high protein diet for weight maintenance.  As for our patients, I'd suggest Sugar Busters, South Beach, Zone, and the Mediterranean Diet as prime examples.  And for those who aren't interested in reading books, low GI + high protein boils down to what our parents told us.  Eat our veggies & meat.  Just remember to moderate/minimize our consumption of processed grains.

Exercise vs Diabetes: Aerobic, Resistance or Both?

There's always been a great debate regarding the best type of exercise, kind of like white meat versus dark.  Of course, we can all agree that the best exercise is the one that you'll do regularly.  But take it a step further.  Isn't aerobic exercise better for burning fat?  And won't resistance training make you bulky like those bodybuilders?  I'm not going to be able to dispel those myths today but I would like to review a study published yesterday looking at how specific exercise types affect diabetics.

For 9 months, the authors followed 41 controls who did not exercise, 73 participants who performed resistance training only three times weekly, 72 who performed aerobic exercise only, and 76 who combined aerobic exercise with twice weekly resistance training.  Aerobic exercise consisted of 150 minutes/week of moderate intensity at 50-80% maximum oxygen consumption.  The three times weekly resistance training consisted of 2 sets of 4 upper body exercises, 3 sets of 3 leg exercises, and 2 sets each of abdominal crunches & back extensions.  The combination group performed 1 set of each of the above twice weekly.  Each set consisted of 10-12 repetitions with the weight increased once the participant was able to complete 12 repetitions on 2 consecutive sessions.  The total time spent exercising in all three groups was roughly the same.

Let's not forget that these participants (average 56 years old, two-thirds female, average body mass index 34 with 37-38% body fat) were all diabetics with average Hemoglobin A1c 7.7%.  The authors concluded that while the active participants benefited from resistance training alone and from aerobic exercise alone compared to the inactive controls, only combination physical activity was associated with improvement in sugar control compared to controls, enough to decrease cardiovascular & microvascular events.

In reality, these findings shouldn't surprise us.  In fact, a similar size study but of shorter duration demonstrated the same findings 3 years ago.  I've reviewed a number of studies demonstrating the benefit of various exercises and levels of physical activity in disparate populations.  This just adds to the preponderance of evidence that we need to start getting active in one form or another, preferably both.  For today, let's do some resistance exercises before our big meal, after which we can then attempt to walk off the calories. 

And let's all be thankful for the men & women (and their families) who (have) put themselves in harm's way to allow us to sit down with our loved ones to celebrate, worship, and speak without fear of reprisal.  We owe you a debt of gratitude that can never be repaid.

Chocolate vs Chronic Fatigue Syndrome

This just out: chocolate might help alleviate some of the symptoms of chronic fatigue syndrome.  Granted, it's a small study of only 10 subjects but it involved chocolate!  More specifically 15g of chocolate containing 85% cocoa solids three times daily. 

The study was well done in that the participants were randomized to either high cocoa solids chocolate or low cocoa solids chocolate for 8 weeks, given a 2 week washout period, and then received another 8 weeks of the other product.  The authors used standardized measures to objectively determine the level of fatigue and function before, during & after the intervention.  Yet after taking into account issues of calories consumed, glycemic index of the different chocolate products, etc, they concluded that the polyphenols from the high cocoa solids improved the subjects' chronic fatigue score.  Better yet, there was no change in weight, suggesting that increase in physical activity countered the extra calories. 

To be clear, we're not talking about your average chocolate candy bar.  This is the dark stuff for connoisseurs & cognescenti.  So if you're used to a lot of sugar in your chocolate, it might take some getting used to.  I thought it might be difficult to obtain this stuff for personal consumption but a quick search for "85% cocoa chocolate" presented plenty of purchasing options.  For more reasons to include dark chocolate in your daily meals, take a look at some of my older posts from April 2010, October 2008 post #2, October 2008 post #1, & February 2008.

Testing Testosterone

I'm not usually fixated on testosterone but as I mentioned yesterday, some of the confusion in defining hypogonadism is in deciding how low is low.  This is especially problematic when one can obtain widely disparate values from any given sample.  Thus, the Endocrine Society and the Centers for Disease Control & Prevention brought together the various stakeholders earlier this year to develop a plan for standardization.  They published a statement last month outlining their plans to achieve standardization.

For instance, should you choose Quest Diagnostics, your total testosterone is usually assayed via liquid chromatography tandem mass spectrometry (LC/MS/MS), regardless of which test code you choose.  However, free testosterone can be calculated from equilibrium dialysis or based upon constants for binding to sex hormone binding globulin.  Presumably, bio-available testosterone would be calculated based upon binding to sex hormone binding globulin and albumin.  Or vice versa.  But you get the point.  As a clinician (and not a pathologist), I need to be sure that I (or my staff) order the right (same) test each time so that we can compare apples to apples. 

This doesn't even take into account that LabCorp uses immunochemiluminometric assay (ICMA) to measure total testosterone and equilibrium ultrafiltration for free testosterone under one test code while they use LC/MS/MS and direct radioimmunoassay under another.  They even go on to discuss the debate amongst researchers as to the variance in results dependent upon methodology and even population used for reference.

The point of this for you and me is to realize that, at least for now, our patients need to get their testosterone levels checked at the same laboratory facility using the same technique each time for comparability.  Only then can you determine if they are truly hypogonadal and whether your therapeutic regimen is making a difference.

Testosterone vs Mortality

Since I was writing about andropause yesterday, I thought I'd mention a study I stumbled upon (I've got a treasure chest full since I haven't composed anything since the end of July) which ironically was published last month in the UK.  The authors studied 930 men avg 60yo w/CAD who were referred for diagnostic angiography and then followed for ~7yrs. 

When separated into 2 groups dependent upon testosterone (T) levels, those men w/CAD with the lowest T had more than twice the risk of all-cause and vascular mortality compared to those w/CAD & normal T levels.  The only other factors found to impact mortality were left ventricular dysfunction, aspirin use, and beta blocker therapy.

But what constitutes low T?  In this particular study, 20.9% had bio-available T <2.6nmol/L (74.9ng/dL), 16.9% had total T <8.1nmol/L (233ng/dL), and 24% had either.  First, you need to understand that the specific equipment used to measure T will affect the reference range, including the lower limit of normal.  In fact, the reference range for bio-T varies quite dramatically from lab to lab.  However, most facilities use 200-300ng/dL as the lower limit of normal for TT, such that these men most likely would have been considered hypogonadal by most American facilities.  Interestingly, compared to 148 men who were excluded from the study due to normal coronary arteries, those w/CAD had comparable average TT & bio-T. 

It's interesting to note that these mortality findings are consistent w/six others published in the last four years regarding male populations scattered globally, including the VA Puget Sound, Rancho Bernardo, Italy, United Kingdom, Sweden, and National Health and Nutrition Examination Survey (NHANES) III.  Furthermore, this relationship between low T and increased mortality is also found in those men given androgen deprivation therapy to treat their prostate cancers, such that the American Heart Association, American Cancer Society, and American Urological Association published a scientific advisory earlier this year in February detailing their concern.

One final word of caution.  We now know that low T is associated with increased mortality and conversely, normal T is associated with decreased mortality.  However, we haven't yet proven that T supplementation will lower mortality.  So remember, folks, don't try this at home w/o professional supervision!

Andropause - A British Perspective

There's obviously quite a bit of controversy regarding andropause and its existence, much less its definition & treatment.  Consider this recent editorial published in the UK two weeks ago.  On the side of conservative traditional medicine are those who say that andropause is just part of aging.  Leave it alone.  Don't mess w/testosterone b/c it's dangerous.  In other words, male midlife crisis not a real syndrome or condition, unlike menopause.  Others define it only in sexual terms accompanied by absolutely low testosterone levels as demonstrated by your local lab.  Still others are willing to treat base upon symptomatology alone regardless of blood levels.  I'd like to think that I am somewhere in the middleground, willing to treat those w/"C" or "D" levels who are used to "A" or "B" grades.  However, I am also not thrilled with the idea of tutoring someone to an "A+++++" level if you get my drift.  If you have some time, watch my television interview coming up next month.  And let me know your thoughts.

Happy Birthday, Dr. Peter G!

Here's to many more!  A votre sante!

Dihydrotestosterone Prostate Paradox

First, the basics.  Testosterone is converted into dihydrotestosterone (DHT) by 5-alpha-reductase (5AR) enzyme.  Testosterone appears to have some effect on prostate growth & size (but I'm not going to comment upon the strength of this evidence, much less any potential neoplastic effect).  What is the basis for this belief?  Men with benign prostate hypertrophy (BPH) who take 5AR inhibitors (5ARI), currently only available as finasteride & dutasteride here in the US, report an improvement in lower urinary tract symptoms (LUTS) in 6 months accompanied by a 50% decrease in PSA (prostate specific antigen).  So perhaps it's really DHT that causes the prostate to enlarge, since lower levels of DHT are followed soon thereafter by smaller prostates.

However, a study published this week has just thrown this theory out the door.  The authors randomized 114 healthy men >50yo w/o BPH in a double blind fashion to daily transdermal DHT or placebo for 2yrs.  My initial reaction was to ask "Why?" especially given what we know as reviewed above.  On the other hand, the authors hypothesized that exogenous DHT might actually shrink the prostate via its metabolite, 3-beta-androstanediol-5-alpha and by negative feedback on a systemic basis.  Bottomline, it didn't work.  As measured by transrectal ultrasound, the prostate didn't shrink (nor did PSA).  On the other hand, it didn't grow either, at least not due to the addition of DHT (the prostate also grew and PSA increased just from placebo alone, which is what we know happens as we age).  To be sure, those given transdermal DHT saw their DHT levels increase by ten-fold while those randomized to placebo saw no measurable change in DHT.

What else did the authors find out?  The increase DHT was accompanied by a decrease in both testosterone and estradiol.  Most likely this was due to a negative inhibitory effect at the hypothalamic-pituitary axis since both luteinizing hormone and follicle-stimulating hormone plummeted.  Bad news?  Bone mineral density at the lumbar spine (but not the femoral neck) decreased significantly in those given DHT compared to those on placebo.  Hematocrit increased significantly, too, dropping to baseline after cessation.  Good news?  More muscle and less fat in those randomized to DHT versus placebo, despite the fact that DHT is really a pure androgen with minimal anabolic effects.  How much?  Just 1-1.5kg each for a net improvement of 2-3kg. 

So perhaps we don't need to worry so much about elevated DHT levels in our patients receiving testosterone supplementation.  In other words, consider offering a 5ARI only because they're suffering from BPH/LUTS, not just because their DHT is elevated.  It's obviously more complicated than that.  For another perspective, check out the editorial.

Setting Up My Practice

I just finished attending 4 days of continuing medical education in Anaheim and am anxious to get home to my family.  However, Sprint Navigation  (on my phone no less) is showing the usual crush of traffic throughout the LA Basin (isn't technology amazing?) so I've decided to wait it out and contemplate life instead.

More specifically, my thoughts run to how much easier it is to practice medicine than it is to set up a private practice.  As I mentioned earlier today, my practice is going to be non-traditional.  Therefore, I won't need the typical brick and mortar office since most of my interactions will be via phone & email which can be accomplished from any place w/telecommunications service.  But, I will need a room for those times when patients come in for their initial or annual physical examinations.  What to do?  After all, I'd like to keep my overhead as low as possible so that I can pass the savings along to my patients.  The solution is to office share or sublease!  The problem is that all my colleagues who have agreed in principle have different days that their offices are less busy and can accommodate me.  So I would need to see someone in Office A on Mondays & Wednesdays, Office B on Tuesdays and Fridays, and Office C on Thursdays, or something like that.  Therefore, I'm going to see if I can find a more sane solution. 

But I've also been informed that I can't apply for a business license until I come up with a physical address which I also need for incorporating with the state.  And let's not forget setting up with the board of taxation & revenue.  So I'm spinning my wheels for the time being.  Obtaining malpractice insurance was a breeze in comparison. 

And this blog & my website?  It's been accomplished over the last 6 days with the assistance & support of several close friends.  I'll detail the process in a separate post so that you can avoid the headaches & stress ulcers from which I suffered.

Telemedicine, Schmelemedicine

As you know, I'm setting up a small private practice in Las Vegas.  However, I'm breaking trends with tradition by offering to "see" patients outside of my local area.  This will entail the use of phones & email once a formal doctor-patient relationship has been properly established.  But the question of the day is what constitutes a "proper" relationship?  In the good old days, you went to your doctor's office and waited several hours before being seen physically.  With modern technology, you could potentially see your doctor via videoconference, although most states frown against this unless the physician is also licensed in the state in which the patient resides.  Certainly, state & federal regulations currently require at least an initial, if not regular, physical visit.  Because this issue affects me (and you) directly, I am sensitive to any light shed upon the matter, whether on a local or national level, since I don't want to lose my license.  What are your thoughts?

Fructose Sweetened Beverages & Gout

Did you have your daily soda today?  Or perhaps organic juice since it's natural and therefore must be better for you?  Well, it turns out that fructose sweetened beverages can increase a woman's risk for gout, that amazingly disabling arthritic attack.  In a study released online last week, the authors followed 78,906 initially gout-free female participants in the Nurses Health Study for 22 years.  Compared to those who consumed <1 soda per month, those who drank 1 serving per day had a 74% higher risk of developing gout.  Drinking more than 2 servings per day of soda more than doubled one's risk.  Surprisingly (at least to me), 2 servings a day of orange juice also doubled one's risk of developing gout.  Why you ask?  Even though sodas generally are low in purines, fructose can increase uric acid levels .  The silver lining?  Diet soda didn't increase risk (not that I'm recommending it).  One more bit of good news:  the overall risk of developing gout was relatively low, only 778 cases.  Still, why take the risk if you don't have to?  By the way, the men reading this post shouldn't smirk.  A study published 2 years ago demonstrated similar findings.  So what's good for the goose is also good for the gander. Drink water instead.

Starting Up

Welcome to my first post on my new blog.  I haven't written anything since leaving Cenegenics a few months ago but it's time to pick up the pieces and start anew.  So this is my venue to tell you about the latest medical news and research.  It's also one way for you to communicate with me (although if you want more immediate response, it's probably best to email me directly).