I suppose every man reaches a point in his life where he realizes his own mortality, a point where he decides to care about being healthy and living a long life. Well, until recently, I wasn’t concerned very much with what risky behavior I engaged in, but a turn of events allowed me to realize that perhaps I’m not invincible.
Of course, I’ve always known this, but younger people rarely stop and think how something will affect them ten years down the road, or even fifteen minutes down the road for that matter. My point is that we should all care about being healthy in at least some aspects. Now, I’m not saying you have to watch every last thing that you eat and stay inside of a bubble the rest of your life. However, I do want to share with you some ways to improve your cholesterol profile.
Yeah, yeah, I know it sounds somewhat boring, but the fact is if your cholesterol levels are unfavorable, it could be deleterious to your health. The worse your cholesterol profile is, the more likely you are to suffer from cardiovascular disease. Of the 2.2 million people that die each year in the US, cardiovascular diseases account for the most victims, more than 48% of all deaths! Now how are you supposed to chase women when you’re dead?
As such, it’s very important to keep tabs of your cholesterol profile. This includes total cholesterol, LDL-Cholesterol, HDL-Cholesterol and your Total to HDL-Ratio. These all have importance. Your total cholesterol should be below 200 mg/dl. Anything in between 200 and 240 is considered borderline. Over 240 is considered to be high risk.
Your HDL and LDL fractions are important, too. In fact, the government recently decided that it’s very important to have your fractions checked as well as your total cholesterol since your total cholesterol doesn’t always tell the entire story.
Just to let you know, LDL or Low Density Lipoprotein-Cholesterol is the “bad” kind which can collect and deposit in arterial walls. An LDL cholesterol level of 160 is considered high risk and anything below 130 is considered to be ideal. Obviously, anything in between is considered borderline high risk.
HDL-Cholesterol is the “good” kind as it transports cholesterol from peripheral areas to the liver. Think of it as a scavenger, or if you prefer a more Testosteronish example, think of HDL-C as a massive bastard that bounces loud mouth jerks out of the club. Your HDL-C should be at least 35 or higher. Sixty and higher is ideal and anything below 35 is considered a risk factor.
Finally, your Total to HDL-ratio is simply the amount of total cholesterol divided by your HDL levels. So if your total cholesterol is 200 and your HDL is 50, your HDL-ratio is 4. Men should have a ratio below 4.5 and women should be below 4. The ideal ratio is below 3.5.
Triglyceride levels can also be a risk factor, as well as a few other things like homocysteine levels, oxidative stress, and plain ol’ everyday stress.(1,2) However, the cholesterol profile seems to be the best determinant of your chances for a heart attack.
Let’s move on to what you can do to improve your profile. While there are a ton of things you can do to potentially improve your lipid profile, I’m just going to list the easiest and most promising here. Here we go!
I know I may seem like I’m being a square, but if you want to have an optimal lipid profile, regardless of age, you shouldn’t smoke. Not a problem for most of us, but there are those in the iron game who still do. A dumbbell in one hand and a Newport in the other – it just doesn’t make sense to me.
Anyhow, smoking has been shown to negatively affect your blood cholesterol by increasing LDL and decreasing HDL significantly. It also raises triglyceride levels. So don’t smoke! (3)
While we’re on the subject, I should bring up alcohol. Now before you freak out and try to justify your bottle of wine by telling me alcohol can increase HDL, just hear me out. As I’ll show you later, having a normal to high-normal endogenous Testosterone level can improve your HDL and LDL levels. However, alcohol can lower endogenous T levels.
So, how can we get the benefits of drinking while avoiding the lowering of Testosterone and useless calories? Well, proanthocyanidins, the main polyphenols found in red wine, are likely one of the main reasons why red wine works so well to improve blood cholesterol concentrations. So what’s a better alternative? Grape juice! This was found to be more effective than red wine in one study. If you don’t want grape juice, you could also buy some grape seed extract standardized for a high concentration of proanthocyanidins.(4,5)
Now before you remark with, “No shit, Sherlock,” listen to me for a second. Yes, of course you wouldn’t be reading this if you didn’t at least lift weights. The purpose of this section is simply to inform you of what specific type of exercise will improve your cholesterol profile the most.
With that said, it appears that weight training doesn’t have much of an effect on your cholesterol profile. However, aerobic training has been shown to increase HDL levels significantly. Aerobic exercise can also potentiate the effects of lipid-lowering drugs, which we’ll discuss later.(6,7,8)
The take home message here is, if you’re interested in improving your cholesterol profile, incorporate at least twenty minutes of aerobic exercise a few times per week.
I’m sure most bodybuilders get enough fiber in their diet via vegetables, oatmeal and some fruit. However, if you’re one of those guys who doesn’t get much fiber, you should consider adding some. Around 25 to 35 grams per day would be a good figure to shoot for, but at least try for 15.
Adding a good amount of fiber to your diet will allow you to lower your LDL levels. This is likely due to the fiber preventing the cholesterol from being absorbed through the intestine.(9,10)
Sure, we used to joke about sterols because of their supposed ability to increase muscle mass. They didn’t work for that purpose because, well, we ain’t plants! Hmm, reminds me of something else, can’t quite remember though… Ah yes, bug juice (ecdysterones)! Okay, okay, I’ll leave that hot topic alone.
Anyhow, these plant sterols can actually have some positive effect on LDL levels. They can reduce intestinal cholesterol absorption, like fiber, and their usage has resulted in a 10 to 15% reduction of LDL. So, it appears plant sterols aren’t so useless after all. They can also be used to further improve cholesterol profiles when added to cholesterol-lowering drugs. (11)
This B-complex vitamin has been used for some time to improve cholesterol levels. It’s been shown to reduce LDL levels significantly while simultaneously increasing HDL to a very good degree.(12,13) As a side note, it may cause some hepatotoxicity. However, it takes rather large dosages before you start to see adverse effects.
Dosages commonly used are 100 milligrams given three times daily. This is gradually increased to around one gram three times daily with a maximum dose of six grams per day. However, if you’re going to use some, just stick to 100 mg per day and gradually work up to 300 mg per day and assess what, if any, side effects you experience. If you don’t experience any, you may slowly increase your dosage.
Ah yes, my personal favorite! Now, before you break out the Sostenon or T-400, hear me out. Endogenous Testosterone levels in the mid to high-normal range can have a very beneficial effect on your cholesterol profile. Keeping or raising your endogenous levels to the mid to high-normal range can result in a decrease in LDL and an increase in HDL levels. Now remember, as you age, your endogenous Testosterone levels start to gradually decrease, leading to decreased HDL and increased triglycerides.
What does this mean? Well, using something like Tribex-500 or clomiphene citrate to increase your endogenous Testosterone levels could possibly increase HDL and lower LDL levels. Very cool. Also, clomiphene itself can have some beneficial effects which will be discussed later. (14-17)
Now, as bodybuilders, we strive to have low body fat percentages. However, there are those who continue on their 52 week per year “bulking phase”. So, for those guys, it’s important that they at least make an attempt to reduce body fat. A reduction of body fat may increase HDL and lower LDL levels, therefore leaving you with a better cholesterol profile.
Now, obviously, some of these things go hand-in-hand. For instance, you’ll likely be performing cardio and consuming fiber if you’re trying to reduce body fat. Still, the point needs to be made that not only does a low body fat percentage make you look better, it improves your cholesterol profile and subsequently, could extend your life. (18,19)
Now let’s take a closer look at dietary fats and their affects on cholesterol.
Saturated Fats – If you ask me, these are the real bad guys. Saturated fat can suppress LDL receptor activity on the liver, thus leading to a higher blood level of LDL. It’s also thought that trans-fatty acids or hydrogenated fat increases LDL levels as well. (20,21)
Monounsaturated Fats – This type of fat can increase levels of HDL, the good kind of cholesterol. Some sources are high oleic acid safflower oil, olive oil, and pistachios. (22,23,24)
Omega-3s – These fats can reduce the risk of cardiovascular disease by a significant amount. This is accomplished by a decrease in LDL levels. (25,26) Flax seed oil is one of the most common sources of omega 3s used by bodybuilders.
Omega-6s – These fats can also increase HDL levels, but it’s likely that you already get plenty of them in your current diet. Safflower and sunflower oil contain high amounts of omega 6 fatty acids. (22)
Let’s move onto another favorite area, drugs!
Beta-2 agonists, like clenbuterol, albuterol, or even ephedrine (although it’s not specific) can all increase HDL levels, and that’s good. (27,28)
An alpha 2 antagonist like yohimbine may increase HDL while also decreasing LDL to a modest extent.(28) Now, I do want to add a note of caution (or common sense rather). If your cholesterol levels are absurdly high and you have a history of heart disease in your family and you haven’t taken beta agonists or alpha antagonists before, you should hold off. At least start at very low dosages and work your way up after looking for any side effects.
In other words, if you’re in terrible shape, don’t start popping ephedrine thinking it’ll get your cholesterol profile back to normal. It’ll help, but I wouldn’t want to have a heart attack as a result. Most people, however, will do fine.
Anti-Estrogens (clomiphene citrate and tamoxifen citrate)
As I mentioned earlier, clomiphene use can give you the advantage of increasing endogenous Testosterone levels which could improve your lipid profile. However, as an added benefit, clomiphene and tamoxifen themselves can reduce LDL levels. This is accomplished because of their estrogen-like effects on the cardiovascular system. (29,30)
No, I’m not giving you the green light to go slam some Loeffler D-bol tabs! Instead, this next section is about how to possibly improve or prevent to some degree, the negative changes in blood cholesterol during anabolic steroid use. Just as a side note, you can use the methods listed previously in this article to improve your cholesterol profile after an androgen cycle.
I know you guys have either heard of or experienced the dreaded “zero HDL” cholesterol count. Doctors are told in school that it’s likely the person is using anabolic steroids when this occurs. I figure it’s more likely that it’s the 300-pound bastard in the waiting room gnawing on a chair leg that’s more likley a user, but I digress. Anyway, this next part will help you to prevent that decline in HDL and rise in LDL.
According to the research I’ve looked at, it appears as though the two key determinants of how your cholesterol levels will be affected are whether the anabolic steroid is A) alpha alkylated and B) whether it can aromatize. It seems alpha alkylation plays a bigger role, however. In one study, that alpha-alkylated steroid stanozolol (6 mg/day) reduced HDL by 33% and caused a 29% increase in LDL. I should note that this was found in eleven healthy male weightlifters.
Testosterone on the other hand, at 200 mg per week, only decreased HDL by 9% while LDL actually decreased by 16%. (31) On average, alpha alkylated androgens were shown to decrease HDL by 50% while 17 beta-esterfied androgens caused anywhere from 0% to 16% reduction. (32) This is thought to occur because of estrogen’s beneficial effects on the cardiovascular system once it’s formed via the aromatization of Testosterone. (33) Furthermore, drugs such as oxandrolone, which are 17-AA and non-aromatizing, have also been shown to have detrimental effects on blood lipids. (34)
Another benefit of Testosterone usage was seen in a study where normal men were given 150 mg, 300 mg, and 600 mg of Testosterone cypionate for two weeks each. While they did find a 21% reduction in HDL after the 300 mg injection, HDL levels remained unchanged thereafter, even after the two 600 mg injections. They also found no change in LDL levels. Interesting. (35)
Another study compared Testosterone cypionate and nandrolone decanoate. While Testosterone reduced HDL, it didn’t affect the Total-HDL ratio. Nandrolone, on the other hand, increased the Total-HDL ratio. (36) With this in mind, the safest anabolic steroids to use in terms of cholesterol profiles would be Testosterone and, to a lesser extent, nandrolone and boldenone. Methenolone and trenbolone wouldn’t be as bad either.
The worst would be the steroids that are both 17-AA and non-aromatizing. So, steroids like stanozolol, oxandrolone, and oxymetholone would all fit in this category. Methandrostenolone may be slightly better. Just remember the key determinant is whether or not it is 17-AA.
This class of drugs includes atorvastatin (Lipitor), fluvastatin (Baycol) Simvastatin (Zocor) as well as a few others. Basically, these drugs work by inhibiting the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase, or HMG-CoA. This enzyme is responsible for the synthesis of cholesterol; therefore, inhibition of this enzyme can and will lower cholesterol concentrations. This then causes an increase in LDL receptors on the liver and stimulates LDL catabolism. This is a good thing. (37,38)
Statins may also effect blood vessel walls, blood flow, and constituents of blood. (39,40) They are powerful agents and in fact are the most effective agents currently available in terms of reducing LDL cholesterol. They can also increase HDL cholesterol as well as decrease triglyceride levels.
So, which is the best statin out of all of these? Well, it appears as though atorvastatin, also know as Lipitor, is the most potent. It causes a greater reduction in LDL than other statins at equal or higher dosages. (41) It’s just as effective as all the other statins at raising HDL and reducing triglyceride levels and has been shown to be slightly more effective in some studies. (42) The dosages commonly used are 10 to 80 mg daily. However, if it’s being used along with something like niacin, the dosages may be reduced.
I should also add a note of caution here. Adding niacin to HMG-CoA reductase inhibitors, such as atorvastatin, can increase the risk for myopathy. In other words, you may experience muscular pain, tenderness and/or weakness. Also, being as some of you may have used some 17-AA anabolic steroids (which can have some liver toxicity) you should definitely have a liver function test. If liver transamines rise to a level higher than three times the upper limit of normal, you should immediately stop taking the drug. It’s not worth the risk.
Now, this isn’t to say you are going to experience hepatotoxicity, but keep in mind that the risk is there. Also, this would mean that it wouldn’t be a good idea to use both 17-AA steroids and statins concurrently. So no, don’t think you can keep your blood lipids in check while taking 17-AA steroids by simply taking statins. You’ll probably end up with severe liver damage.
Another drug that can have some potent effects on LDL, HDL, and triglycerides are fibrates or more specifically, clofibrate. In case this seems familiar, I mentioned it in my Taming of Insulin article. Dosages used are one to two grams per day in divided dosages. Clofibrate has even been shown in one study to lower triglycerides and increase HDL to a greater extent than atorvastatin. (43) Another benefit is that it hasn’t been associated with hepatotoxicity.
A Word about Dietary Cholesterol
Now as I’ve explained, the real culprit for the increase in cholesterol levels is saturated fat as well as hydrogenated fats. However, there are still people out there worrying about how much cholesterol they consume. Look, dietary cholesterol has been shown to have little or no effect on total and LDL cholesterol! (44,45)
Now, if you’re eating hundreds of grams of saturated fat per day and consequently reducing the amount of LDL receptors on the liver, and then on top of that you consume huge amounts of cholesterol, then and only then will you see an increase in LDL. The reason being is that you have no place for this extra cholesterol to bind. So don’t buy into the bullshit talk of dietary cholesterol raising your blood cholesterol in a direct fashion. This just doesn’t happen.
So, to sum it up, try the following dosages and monitor your results accordingly. Try this for at least a month or two before assessing your progress:
• 25-35 grams fiber per day
• 100-300 mg niacin per day
• 6 grams(minimum) fish oil per day for Omega 3’s and try to take in 30-50 grams of monounsaturated fats. (Most food labels will let you know just how much is in each serving. There is really no need to supplement with omega 6’s.)
• 2-3 grams of sterols per day
I can’t really give any specific dosages for the polyphenols, but I’d recommend either consuming a few glasses of grape juice per day or simply following the label directions for the grape seed extract product. You may want to double the recommended dosage however, just to be safe.
If, however, these “natural” remedies don’t do the job and get your blood back up to snuff, then you should consider using the various drugs outlined. As for their dosages, simply use what is considered to be the normal dosages. So, for example, if you’re going to consider using ephedrine, use 20 mg 3 times per day. Or, use yohimbine at around 5-15 mg per day. As far as clomiphene or tamoxifen, 50 mg per day should suffice for the first and 20 mg. a day should suffice for the latter. And finally, 10-80 mg per day is the “norm” for atorvastatin.
Hopefully, I’ll have saved a few lives after this article is published. Perhaps some of you will try some of these things out and keep an eye on your cholesterol profile. True, we only have one life to live, and therefore you should have fun during the short time that you occupy space on this planet. If having fun to you means eating poorly here and there and using anabolic steroids, fine.
However, there’s no reason not to take an intelligent and responsible approach by simply taking some preventative measures in order to keep your blood “good” while you have fun.
1. Cullen P. “Evidence that triglycerides are an independent coronary heart disease risk factor.” Am J Cardiol 2000 Nov 1;86(9):943-9
2. Harjai KJ. “Potential new cardiovascular risk factors: left ventricular hypertrophy, homocysteine, lipoprotein(a), triglycerides, oxidative stress, and fibrinogen.” Ann Intern Med 1999 Sep 7;131(5):376-86
3. Sinha AK, et al. “Effect of cigarette smoking on lipid profile in the young.” J Assoc Physicians India 1995 Mar;43(3):185-8
4. Vinson JA, et al. “Red wine, dealcoholized red wine, and especially grape juice, inhibit atherosclerosis in a hamster model.” Atherosclerosis 2001 May;156(1):67-72
5. Yamakoshi J, et al. “Proanthocyanidin-rich extract from grape seeds attenuates the development of aortic atherosclerosis in cholesterol-fed rabbits.” Atherosclerosis 1999 Jan;142(1):139-49
6. Bounds, et al. “Diet and short term plasma lipoprotein-lipid changes after exercise in trained men.” Int J Sport Nutr Exerc Metab 2000 Jun;10(2):114-27
7. Warber J, Bazzarre T. “A comparison between running and weight lifting on fasting plasma lipids of a well-conditioned hypercholesterolemic male.” Int J Sport Nutr 1991 Sep;1(3):265-78
8. Wittke R. “Effect of fluvastatin in combination with moderate endurance training on parameters of lipid metabolism.” Sports Med 1999 May;27(5):329-35
9. Spiller GA, et al. “Guar gum and plasma cholesterol. Effect of guar gum and an oat fiber source on plasma lipoproteins and cholesterol in hypercholesterolemic adults.” Arterioscler Thromb 1991 Sep-Oct;11(5):1204-8
10. Neal GW, Balm TK. “Synergistic effects of psyllium in the dietary treatment of hypercholesterolemia.” South Med J 1990 Oct;83(10):1131-7
11. Plat J, Mensink RP. “Effects of plant sterols and stanols on lipid metabolism and cardiovascular risk.” Nutr Metab Cardiovasc Dis 2001 Feb;11(1):31-40
12. Figge HL, et al. “Nicotinic acid: A review of its clinical use in the treatment of lipid disorders.” Pharmacotherapy 1988;8(5):287-294
13. AMA Department of Drugs: AMA Drug Evaluations, 6th ed. American Medical Association, Chicago, IL, 1986.
14. Zhao S, et al. “Plasma levels of lipids, lipoproteins and apolipoproteins affected by endogenous testosterone.” Hunan Yi Ke Da Xue Xue Bao 1998;23(3):299-301
15. Shapiro J, et al. “Testosterone and other anabolic steroids as cardiovascular drugs.” Am J Ther 1999 May;6(3):167-74
16. Zmuda JM, et al. “Longitudinal relation between endogenous testosterone and cardiovascular disease risk factors in middle-aged men. A 13-year follow-up of former Multiple Risk Factor Intervention Trial participants.” Am J Epidemiol 1997 Oct 15;146(8):609-17
17. Barret-Connor EL. “Testosterone and risk factors for cardiovascular disease in men.” Diabete Metab 1995 Jun;21(3):156-61
18. Too D, et al. “Effect of a precompetition bodybuilding diet and training regimen on body composition and blood chemistry.” J Sports Med Phys Fitness 1998 Sep;38(3):245-52
19. Poirier P, et al. “Role of body fat loss in the exercise-induced improvement of the plasma lipid profile in non-insulin-dependent diabetes mellitus.” Metabolism 1996 Nov;45(11):1383-7
20. Nicolosi RJ. “Dietary fat saturation effects on low-density-lipoprotein concentrations and metabolism in various animal models.” Am J Clin Nutr 1997 May;65(5 Suppl):16178-16278
21. Lichtenstein AH, et al. “Impact of hydrogenated fat on high density lipoprotein subfractions and metabolism.” J Lipid Res 2001 Apr;42(4):597-604
22. Sanders K, et al. “The effect of dietary fat level and quality on plasma lipoprotein lipids and plasma fatty acids in normocholesterolemic subjects.” Lipids 1994 Feb;29(2):129-38
23. Mensink RP, Katan MB. “Effect of monounsaturated fatty acids versus complex carbohydrates on high-density lipoproteins in healthy men and women.” Lancet 1987 Jan 17;1(8525):122-5
24. Thomsen C, et al. “Differential effects of saturated and monounsaturated fatty acids on postprandial lipemia and incretin responses in healthy subjects.” Am J Clin Nutr 1999 Jun;69(6):1135-43
25. Hu FB, et al. “Types of dietary fat and risk of coronary heart disease: A critical review.” J Am Coll Nutr 2001 Feb;20(1):5-19
26. Tripodi A, et al. “Effect of fish oil and coconut oil diet on the LDL receptor activity of rat liver plasma membranes.” Biochim Biophys Acta 1991 Jun 3;1083(3):298-304
27. Floren CH, et al. “Bambuterol raises high-density lipoprotein levels in patients with hyperlipidaemia.” J Intern Med 1997 Aug;242(2):167-71
28. Hunninghake DB. “The effects of cardioselective vasodilating beta-blockers on lipids.” Am Heart J 1991 Mar;121(3 Pt 2):1029-32
29. Pasqualini JR, et al. “Pharmacodynamic and biological effects of anti-estrogens in different models.”
30. Love RR, et al. “Effects of tamoxifen on cardiovascular risk factors in postmenopausal women.” Ann Intern Med 1991; 115:860-864
31. Thompson PD, et al. “Contrasting effects of testosterone and stanozolol on serum lipoprotein levels.” JAMA 1989 Feb 24;261(8):1165-8
32. Glazer G, Suchman AL. “Lack of demonstrated effect of nandrolone on serum lipids.” Metabolism 1994 Feb;43(2):204-10
33. Zmuda JM, et al. “The effect of testosterone aromatization on high-density lipoprotein cholesterol level and postheparin lipolytic activity.” Metabolism 1993 Apr;42(4):446-50
34. Lovejoy JC, et al. “Oral anabolic steroid treatment, but not parenteral androgen treatment, decreases abdominal fat in obese, older men.” Int J Obes Relat Metab Disord 1995 Sep;19(9):614-24
35. Kouri EM, et al. “Changes in lipoprotein-lipid levels in normal men following administration of increasing doses of testosterone cypionate.” Clin J Sport Med 1996 Jul;6(3):152-7
36. Crist DM, et al. “Lipemic and lipoproteinemic effects of natural and synthetic androgens in humans.” Clin Exp Pharmacol Physiol 1986 Jul;13(7):513-8
37. Hardman JG, et al. Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 9th ed. McGraw-Hill, New York, NY, 1996.
38. Gibson DM, et al. “Effect of age and gender on pharmacokinetics of atorvastatin in humans.” J Clin Pharmacol 1996;36:242-246
39. Smilde TJ, et al. “The effect of cholesterol lowering on carotid and femoral artery wall stiffness and thickness in patients with familial hypercholesterolaemia.” Eur J Cin Invest 2000;30:473-480
40. Vaughan CJ, et al. “Statins do more than just lower cholesterol.” Lancet 1996;348:1079-1082
41. Folkers K, et al. “Lovastatin decreases coenzyme Q levels in humans.” Proc Natl Acad Sci USA 1990;87:8931-8934
42. Davidson M, et al. “Comparison of one-year efficacy and safety of atorvastatin versus lovastatin in primary hypercholesterolemia.” Am J Cardiol 1997;79:1475-1481
43. Bairaktari ET, et al. “Comparison of the efficacy of atorvastatin and micronized fenofibrate in the treatment of mixed hyperlipidemia.” J Cardiovasc Risk 1999;6:113-116
44. Reaven GM, et al. “Insulin resistance, dietary cholesterol, and cholesterol concentration in postmenopausal women.” Metabolism 2001 May;50(5):594-7
45. Bowman MP, et al. “Effect of dietary fat and cholesterol on plasma lipids and lipoprotein fractions in normolipidemic men.” J Nutr 1988 May;118(5):555-60