It's Q&A time with Anthony Colpo! Brew yourself a strong cup of antioxidant-rich green tea, place your calls on hold, and sit back as Anthony answers your diet and health questions in his famous no-holds-barred, straight-to-the-point fashion!

 

Can Cholesterol Drugs Turn You Into a Musclebound Stud?

Q. Hi Anthony, you're very knowledgeable about cholesterol, statin drugs and weight training, so I figure you're the best person to clear something up for me. I read on a bodybuilding website that statins may increase muscle growth and that [ex-champion bodybuilder] Ronnie Coleman took them. Is this true? This would seem to go against everything we know about these drugs.

A. I've read this too - one article I came across even recommended taking statins for muscle growth based upon some recent research findings. Such a recommendation is wholly premature and potentially dangerous. Before I tell you why, let's take a brief look at the research in question.

A study published in the Journal of Gerontology followed 60-69 year old men and women undertaking a 12-week weight training program. In addition to weight training, they were instructed to take post-workout protein supplements and to record their dietary intake in food logs. The researchers observed that higher self-reported dietary cholesterol intake and serum cholesterol levels were associated with greater lean mass gains[1]. In another study of dieting women with high cholesterol, losses in skeletal muscle mass were associated with decreases in cholesterol absorption[2].

Cholesterol also provides the raw material from which the highly anabolic hormone testosterone is formed. Given that statins lower blood cholesterol, and have been documented to lower testosterone in some users[3], they would thus be expected to be associated with poorer muscle growth in weight training individuals. But surprisingly, in the same study that higher cholesterol levels to be associated with greater muscle growth, statin use was also associated with greater hypertrophy.

So what gives? In a nutshell, researchers speculate that while statins lower cholesterol, their well-known ability to cause muscle breakdown[4] may actually work synergistically with the damage caused during a weight training workout to amplify the subsequent hypertrophy response[5]. Obviously, this effect would only occur in individuals who workout. If you're a sedentary statin user, don't rush out to buy XXL t-shirts and don't expect any audition requests from Chippendales.

And keep in mind that the above observations were not causal findings established from tightly controlled comparisons. To the best of my knowledge, no researcher has yet randomly assigned one group of weight trainees to statins, another group to a placebo, then recorded subsequent muscle gains. The associations reported above are just that: associations. Whether cholesterol and statin drugs do in fact have any direct causal effect on muscle growth at this point of time is unknown.

Another possibility is simply that the statin users in this study had a healthier constitution than the non-statin users (whether they stay that way with continued statin use is another issue entirely). It's well established that in older people, survival is enhanced in those with higher cholesterol levels; low-cholesterol and longevity are not happy bedfellows. There have been numerous observational studies published over the years claiming that statin use was associated with all sorts of health benefits - everything from protection against cancer to slowed progression of multiple sclerosis. However, when these same benefits are pursued in tightly controlled clinical trials (where mean baseline cholesterol levels tend to be similar among the treatment and placebo groups), they never materialize.

 

Why?

 

One very real possibility is simply that older folks with higher cholesterol levels are more likely to be prescribed cholesterol-lowering drugs than those with lower cholesterol levels. Given that higher cholesterol levels are associated with better health and longevity in older folks, this may then give the erroneous impression that statins are "healthy" in observational studies, when it is in fact the users themselves that have better underlying health. When the confounding effect of contrasting cholesterol levels is removed in randomized clinical trials, the alleged health benefits of statins disappear. In the PROSPER trial for example, statin use not only failed to protect against cancer but actually increased its incidence in the elderly participants.

 

The participants in the aforementioned weight training study were aged 60-69, raising the distinct possibility that the statin users were folks with higher cholesterol levels and hence a healthier underlying physiology, one that would respond more favorably to the stimulus of weight training.

As for whether or not any champion bodybuilder uses or used statin drugs for anabolic purposes I can't say. But even if they do/did, that doesn't necessarily constitute evidence that statins boost muscle growth. All niceties and public relations BS aside, anyone who knows anything about professional bodybuilding is aware that simultaneous use of multiple anabolic drugs at high dosages is standard practice. If any anabolic-using bodybuilder also takes statins, what if any effect they have on that user's muscle growth would be virtually impossible to discern. This is a question that can only be answered in the setting of a properly controlled randomized clinical trial.

What I will say is this: if optimal health, performance and longevity are important to you, statins would have to be about the worst possible addition to your hypertrophy regimen. Statins are well documented to cause muscle and tendon disorders[6-10], and the last thing you want when you've got a heavy weight dangling above your head is to hear the delightful sound of connective tissue tearing away from your bones.

Furthermore, it's extremely difficult to get buffed when your muscles are so weak and fatigued you can't muster the energy to get in a good workout. A 2004 study reported on 22 top level professional Austrian athletes who had been prescribed statins for familial hypercholesterolemia and who suffered myopathy as a result. After trying every statin available at the time, only six (20%) were able to eventually find a tolerable statin[11].

A new study, published in the October-November-December 2009 issue of Primary Care Cardiovascular Journal, indicates that statin-induced myopathy is far more common than previously claimed by drug companies and health officials. Researchers analyzed the patient records of one 8,000 patient practice and found only one recorded case of muscle symptoms in a patient taking statins. But after questioning 96 randomly selected statin-using patients from the practice, they identified 19 cases of potential muscle damage[12].

Even if you somehow managed to pile on some extra beef thanks to statins, having a few extra pounds of muscle would be of little benefit if certain key parts of your anatomy failed to giddyup thanks to statin-induced sexual dysfunction[13-15]. And don't get me started about their effects on liver, neural and cognitive function...

Needless to say, even if statins are eventually found to exert anabolic effects under tightly controlled conditions, they are one ergogenic agent I definitely won't be using.

Can You Gain Muscle and Lose Fat at the Same Time?

Q. Anthony, what's your opinion on gaining muscle and losing fat at the same time? Can it be done, or should muscle growth and fat loss be treated as separate goals and pursued at different times?

A. Given the right diet and training, obese people can sometimes build significant amounts of muscle while losing fat. I regularly see and hear from people who, after they start training, become smaller around the waist, but bigger in the chest and shoulders. Sometimes their scale weight shows little change, which often causes them to be discouraged, but they're actually experiencing a best-case scenario - gaining muscle and losing fat at the same time.

However, this effect doesn't last forever, and as you become leaner trying to put on muscle and simultaneously lose fat becomes a lost cause. The best strategy at that point is to focus on distinct fat loss and muscle gain phases. If you happen to be lucky enough to gain some muscle during a cutting phase or drop some fat during a muscle gain phase, that's great, but stay focused on the main goal. Otherwise you're essentially trying to achieve two conflicting goals at the same time. Weight gain comprised of muscle requires a calorie surplus, while weight loss derived primarily from fat requires a calorie deficit.

The advantage with alternating fat loss and muscle gain phases is that, when executed properly, the fat loss phaseS "prime" your body with improved insulin sensitivity, increased activation of glycogen storage enzymes, and accelerated nutrient uptake so that the subsequent muscle gain phases become more effective. And inserting muscle gain phases where you eat a caloric excess gives your body a break from calorie restriction. Dieting continuously, all year round, is not a good thing - for the sake of your thyroid and adrenal glands, not to mention your mental outlook, it's a good idea to take occasional breaks from dieting.

Do Mice Studies Prove Saturated Fat Causes Heart Disease?

Q. Anthony, With a 35 yr old brother w/ 3 stents and a father who has recently had a triple bypass, I read your [The Great Cholesterol Con] book eagerly. While arguing your premise with my cardiologist, he countered with a good point. He said that when they do atherosclerosis research in lab animals such as mice, they feed the animals diets extremely high in saturated fats. The end result is clogged or calcified arteries on which they can conduct experiments. This would seem to go against your premise that saturated fats don't cause heart disease. How would you reconcile this fact with your theory on cholesterol?

A. Hi Andrew, I discuss the numerous problems inherent with animal studies in The Great Cholesterol Con. It might be a good idea to pull it back out and re-read Chapter 4.

As for your cardiologist, here's my suggestion:

1. Show your cardiologist a picture of a mouse, and then a picture of a human. Ask him if he can spot the difference. Seriously.

Humans evolved over millions of years as hunter-gatherer ominivorous creatures that ate saturate-containing animal fats. Mice are primarily herbivorous creatures - it doesn't take a surgeon (unless he's a cardiologist apparently) to figure out force feeding such animals extremely high amounts of animal fats could cause the little critters a spot of bother.

2. Ask him to explain the abundance of evidence showing that saturated fats are not associated with CHD in humans, and the numerous clinical trials that found lowering dietary saturated fat did not reduce CHD mortality in humans. In some studies, mortality was actually increased among those following low-saturate diets. This is all discussed in much detail in Section One of The Great Cholesterol Con. The lack of association between saturated fats and CHD was also discussed in a recent review published under the auspices of the World Health and Food and Agriculture Organizations. You may want to give The Great Cholesterol Con to your cardiologist and tell him to read Chapter 4 also. In fact, he would likely benefit greatly from reading the whole book.

Bottom line: nothing has changed since Ancel Keys published his shamelessly one-sided Six Countries analysis in the 1950s. The lipid hypothesis was a complete crock then, and it still is now.

Are Potatoes OK?

Q. Hi Anthony, phenomenal e-book! I strongly believe that The Fat Loss Bible is the best piece of diet/nutrition related info ever written. It makes it very easy to distinguish the knowledge from the bull**** out there. You did an excellent job putting it all together.

One question if you don't mind...in the Recomended Foods section I noticed that sweet potatoes are highly recomended but could not find anything for regular white poatoes. Would you throw these in the Recommended or Not Recommended category?
 
Thanks for all you do, I truly appreciate it.

A. I get asked about white potatoes a lot. I consider sweet potatoes superior thanks to their lower glycemic index (GI) score, but dietary variety is important to prevent both boredom and the development of food sensitivities. As such, I'm OK with people eating white potatoes (I eat them myself) but with one important caveat. They are a high-GI item, so make sure you mix them with a low-GI vegetable like broccoli, cabbage, cauliflower, Brussels sprouts, etc. This brings down the overall GI of the meal, and helps prevent any unwanted swings in blood glucose levels. I make sure the lower  GI vegetable makes up at least 50% of the mix. This also applies to other high GI foods like white rice or bread.

Be sure to avoid potatoes that have gone green or are sprouting. Do not eat the skins, despite what conventional dietitians (you know, the ones that claim soy milk and whole grain muffins are healthy) may tell you. The skins and the flesh immediately underneath them have the highest concentration of potentially harmful glycosides (these are the compounds that make people sick when they eat raw or green potatoes, or large amounts of potato skins). The reasoning given by dietitians for consumption of potato skins is that they contain fiber, but rest assured there are much better places to get your roughage.

References

1.    Riechman SE, et al. Statins and dietary and serum cholesterol are associated with increased lean mass following resistance training. Journals of Gerontology: Series A, Oct, 2007; 62 (10): 1164-1171.

2.    Santosa S, et al. Cholesterol metabolism and body composition in women: the effects of moderate weight loss. International Journal of Obesity, Jun, 2007; 31 (6): 933-941.

3.    de Graaf L, et al. Is decreased libido associated with the use of HMG-CoA-reductase inhibitors? British Journal of Clinical Pharmacology,

4.    Draeger A, et al. Statin therapy induces ultrastructural damage in skeletal muscle in patients without myalgia. Journal of Pathology, 2006; 210: 94–102.

5.    Riechman SE, et al. Cholesterol and skeletal muscle health. In: A Balanced Omega-6/ Omega-3 Fatty Acid Ratio, Cholesterol and Coronary Heart Disease. Eds: Simopoulos AP, De Meester F. World Review Of Nutrition And Dietetics, Basel, Karger, 2009; 100: 71-79.

6.    Molokhia M, et al. Statin Induced Myopathy and Myalgia: Time Trend Analysis and Comparison of Risk Associated with Statin Class from 1991–2006. PLoS ONE, 2008; 3 (6): e2522.

7.    Tomlinson SS, Mangione KK. Potential adverse effects of statins on muscle. Physical Therapy, 2005; 85: 459–465.

8.    Marie I, Delafenêtre H, Massy N, et al. Tendinous disorders attributed to statins: A study on ninety-six spontaneous reports in the period 1990-2005 and review of the literature. Arthritis Care & Research, 2008; 59: 367-372.

9.    Chazerain P, et al. Four cases of tendinopathy in patients on statin therapy. Joint Bone Spine, 2001 Oct; 68 (5): 430-433.

10.    Pullatt R, et al. Tendon Rupture Associated With Simvastatin/Ezetimibe Therapy. American Journal of Cardiology, 2007; 100 (1): 152-153.

11.    Sinzinger H, O’Grady J. Professional athletes suffering from familial hypercholesterolaemia rarely tolerate statin treatment because of muscular problems. British Journal of Clinical Pharmacology, 2004; 57 (4): 525–528.

12.    Sciberras D, et al. Is general practice the optimal setting for the recognition of statin-induced myotoxicity? Primary Care cardiovascular Journal, Oct-Nov-Dec, 2009; 2: 195-200.
http://www.pccj.eu/pdf/3436/Vol2_Num4_October-November-December_2009_p195-200.pdf?sid=cec4fa03a67dcb01

13.    Azzarito C, Boiardi L, Vergoni W, Zini M, Portioli I. Testicular function in hypercholesterolemic male patients during prolonged simvastatin treatment. Hormone and Metabolic Research, 1996; 28: 193-198.

14.    Dobs AS, Schrott H, Davidson MH, et al. Effects of high-dose simvastatin on adrenal and gonadal steroidogenesis in men with hypercholesterolemia. Metabolism, 2000; 49: 1234-1238.

15.    Farnsworth WH, et al. Testicular function in type II hyperlipoproteinemic patients treated with lovastatin (mevinolin) or neomycin. Journal of Clinical Endocrinology & Metabolism, 1987; 65: 546-549.