If you have Heart Disease, and your Doctor doesn't teat for this, he is clueless about this problem. I just read an example of a Doctor who DOES test and missed this problem.
Unique Strategies for Lipoprotein(a) Reduction
TYP
Lipoprotein(a), or Lp(a), can be among the most frustrating causes of coronary atherosclerotic plaque. Sometimes treatment of this genetic pattern can be simple and straightforward. Other times it can test even the most patient and persistent. Lp(a) is by no means a rare pattern. Of everyone with a heart scan score above zero, 1 in 5 (20%) will have it.
There is fairly broad consensus that increasing Lp(a) does, indeed, increase risk for heart attack and stroke. A review (meta-analysis) of 27 studies examining the effects of increased Lp(a) concluded that persons in the highest third of Lp(a) levels in the population carry a 70% increased risk for heart disease (Danesh J et al 2000). In the Track Your Plaque experience, increased levels of Lp(a) are a significant risk for increasing heart scan scores. Lp(a) is also unique in that it amplifies the dangers of other patterns, such as LDL cholesterol, low HDL, small LDL, and increased C-reactive protein (a measure of inflammation). In the 1100-participant Italian Longitudinal Study on Aging, for instance, the combination of Lp(a) =20 mg/dl and LDL=140 mg/dl increased heart attack risk by a factor of 2.75; the combination of Lp(a) =20 mg/dl and type II diabetes increased risk by a factor 6.65 (Solfrizzi V et al 2002). A 1997 University of Utah study of 170 participants, all of whom had established coronary disease, determined that having a total/HDL ratio >5.8 along with two or more non-lipid risk factors such as smoking, hypertension, diabetes, smoking, or high homocysteine, escalated risk an amazing 122-fold (Hopkins PN et al 1997).
Niacin is the mainstay of Lp(a) treatment, followed by testosterone in men, estrogen in women. Sometimes, spectacular results are obtained with just niacin. In others, adding testosterone or estrogen may be required. In others, both treatments fail to yield the effects we desire, or there are reasons that prevent full use of either treatment.
For this reason, here we survey the possibilities for treatment of Lp(a). We have tried some of these unique therapies, others we have not. (We do specify which.) We cannot pretend to have all the answers to the Lp(a) dilemma. It is, undoubtedly, a sometimes frustrating genetic pattern that tests everyone's resourcefulness and patience. Hopefully, this report will not just suggest some potential therapies for readers, but also trigger interest in exploring new treatments.
A quick Lp(a) review
Lp(a) is really an LDL cholesterol particle bound to an additional protein called apoprotein(a) (apo(a)). LDL cholesterol particles, just like VLDL and IDL, each contain one apoprotein B molecule (apo B). The apo(a) particle binds to the LDL particle via apo B, and they do so through two linked sulfur molecules, the so-called "disulfide linkage."
The apo(a) component of Lp(a) varies tremendously in size from one individual to the next. Studies are in wide agreement that, the smaller the apo(a), the more powerfully it contributes to coronary plaque. Thus far, 34–45 different sub-types of Lp(a) based on variable apo(a) size have been identified.
To add even further to the complexity of Lp(a), the size of the LDL particle can vary, also. It means that people with small LDL particles also have small LDL in Lp(a); people with big LDL particles have big LDL in Lp(a). Some early data, in addition to the Track Your Plaque experience, suggest that small apo(a) in combination with small LDL particles may be the most atherosclerosis-causing of all.
For additional basic discussion of Lp(a), please also see these Special Reports on the Track Your Plaque website:
Lipoprotein(a): What it is, why it's important, and why you need to know if you've got it!
Lipoprotein(a) Checklist
Measuring Lp(a)
Lp(a) can be measured by most clinical laboratories. It therefore does not necessitate the special arrangements often necessary to obtain other lipoprotein testing (i.e., NMR, Berkeley, VAP).
However, the test is not standardized and may vary tremendously from lab to lab. This can cause great confusion if you use more than one laboratory for your blood work. It's therefore important to stick to the same laboratory every time you have Lp(a) checked to eliminate this source of confusion.
Ideally, the laboratory you or your doctor chooses measures Lp(a) in nmol/L, which is a measure of Lp(a) particle number and is less influenced by the variable size of Lp(a) particles. If your measure is in mg/dl or mg/L—measures of weight—then it may be affected by particle size and may not accurately reflect your true risk. But even a weight measure is better than nothing if you don't have a choice. In future, as laboratories adopt standardized means of measurement, we will likely be able to routinely measure both quantity of particles in nmol/l and Lp(a) particle size (or apo(a) particle size).
What's a desirable value for Lp(a)? As with LDL cholesterol, this is the toughest question of all. However, some guidelines: If measured in nmol/l, then 75 nmol/l or less is desirable. In mg/dl, 30 mg/dl or less is desirable. (However, because of the lack of standardization, "normal" values in your laboratory may vary, depending on the means of measurement; discuss with your doctor. Also, to convert mg/L to mg/L, divide the mg/L value by 10. A very crude conversion of mg/dl to nmol/L can be obtained by multiplying by 2.5; however, this is only an approximation, since it ignores the fact that Lp(a) particles vary in size and weight.)
One important issue to keep in mind when discussing treatment of Lp(a) is that the magnitude of reduction in Lp(a) is highly dependent on the starting level: the higher the starting level, the greater the percentage reduction in Lp(a) achieved with various treatments; the lower the starting Lp(a), the smaller the percentage reduction. This holds true with virtually all treatments for high Lp(a).
Another issue will emerge as you peruse these treatments: They are frustratingly variable in effect from one person to another, one study to another. Treatment X will work great in one study, not at all in another. This variation plagues all Lp(a) experiences due to its genetic variability from one group of people to another, one race to another, and the varied methods of measurement. Nonetheless, we will try and distill some wisdom out of this hodgepodge.
The standard Track Your Plaque approach to Lp(a)
Niacin is our number one choice for treatment of Lp(a) (Carlson LA et al 1989). At present, it is the most effective direct treatment. Higher doses of niacin may be required than for other abnormalities like low HDL or small LDL. The niacin preparations we favor are prescription Niaspan® (Kos Pharmaceuticals) or over-the-counter Slo-Niacin® (Upsher-Smith). Both are better tolerated than over-the-counter "immediate-release" niacin, which tends to cause intolerable hot flushing. Both Niaspan® and Slo-Niacin® are very safe, with little risk of liver toxicity if taken properly (once per day). Both preparations should be taken with the supervision of your physician.
We begin with 500 mg niacin per day, increasing by 500 mg every 4 weeks until the desired dose is achieved. A common dose is 2000 mg per day, with occasional people requiring 3000 mg, rarely higher. We urge everyone to be patient before checking Lp(a) on niacin, as the effect can require many months before it shows a reduction. We usually wait 6 months after achieving a stable dose before rechecking. (This is another potential explanation for the lukewarm results sometimes obtained in clinical trials in which shorter timelines were used.)
Second choice in Lp(a) treatment are hormonal preparations, estrogen and testosterone. In females, estrogen preparations reduce Lp(a) around 25%. Estrogen, of course, has other considerations that need to be fully discussed with your doctor. Estrogen's Lp(a)-reducing effect has been confirmed in a number of trials, including the large, 3-year Postmenopausal Estrogen/Progestin Interventions (PEPI) study of 350 women aged 45 to 65 years (Espeland MA et al 1998). It may be important to remind your doctor or gynecologist that, despite the drawbacks of estrogen treatment, the Heart and Estrogen/progestin Replacement Study (HERS) trial, while demonstrating no reduction in heart attack risk in a broad population of women, showed a 20% reduction in heart attack in the 1400 women with Lp(a) (Shlipak MG et al 2000). Whenever possible, we advocate use of "bio-identical," i.e., human, preparations, rather than the non-human preparations commonly used like Premarin®, (even though it was the horse, non-human preparation Premarin® used in the WHI and other trials).
Testosterone can be very helpful for men and reduces Lp(a) by 25–59% (Zmuda JM et al 1996; Marcovina SM et al 1996). Most men enjoy the effects of testosterone (increased physical stamina, strength, improved mood, and occasionally improved libido). We use testosterone cream with great success. Both estrogen and testosterone treatment need to be conducted with the help of your physician.
The statin cholesterol drugs do not appear to exert significant effects on reduction of Lp(a); some studies have shown modest reductions with atorvastatin (Lipitor®); others have demonstrated increases in Lp(a) by as much as 30% (Randall OS et al 2004). Persons with heterozygous familial hypercholesterolemia, an inherited condition that permits high LDL cholesterol values of 300 mg/dl and higher, may represent a group that does achieve modest reductions of Lp(a) with statin drugs, with Lp(a) reductions of 20% with treatment (van Wissen S et al 2003). In the Track Your Plaque experience, statin agents do not exert significant nor consistent effects on Lp(a).
Despite the lack of direct Lp(a)-reducing effect by statin agents, some have argued that statin drugs provide indirect benefit. An analysis of the FATS Study showed that participants taking lovastatin who experienced greater reductions in LDL cholesterol experienced less events than those who did showed only minimal LDL reductions on the drug ((Maher VM et al 1995). (Despite the weakness of the statistical analysis that led to this observation and the lack of confirmation, this single analysis has gotten more than its due in the medical literature, likely due to the intense marketing by drug manufacturers.)
Aspirin, a mainstay for reduction of cardiovascular events, has been shown to reduce Lp(a) levels by 18–46% using doses of 81–150 mg per day (Ranga GS et al 2007; Akaike M et al 2002.) However, in our experience this does not seem to hold up in real life practice, with minimal to no reductions in Lp(a). The explanation for the discrepancy is not clear.
After this, treatment of Lp(a) becomes even sketchier. Here is where we now turn to some unusual, little-known treatments to be aware of and perhaps consider. The potential treatments are listed in order of usefulness, starting with most useful. You will note that the world of Lp(a) is filled with observations in small numbers of people and results that are sometimes confusing and contradictory. Keep in mind, also, that results in treatment for Lp(a) are notoriously variable: what works for one will not work for another, and vice versa. Nonetheless, we will try to distill some wisdom from the existing knowledge base.
Unique strategies that may be potentially helpful
Omega-3 fatty acids
Eating plentiful quantities of fish (omega-3 fatty acids representing the presumed active constituent) reduces Lp(a).
This observation gained credibility with the insightful and carefully-conducted Lugalawa Study of 1300 Bantu fishermen in Tanzania, Africa. The Lugalawa study compared the Lp(a) levels of Bantu fishermen, who eat up to a pound of (freshwater) fish per day, providing an omega-3 intake of 3000 to 5000 mg per day (combined EPA + DHA), with another Bantu group who were strictly vegetarian and did not eat+ fish. The fish-eating Bantus showed 47.8% lower Lp(a) compared to the vegetarian farming population (Marcovina SM et al 1999). Interestingly, the fishermen also showed far less expression of the most dangerous small apo(a) variety of Lp(a), even though both populations were capable of expressing both small and large apo(a).
The Lugalawa observation was confirmed by a small German study using very high doses of omega-3 fatty acids of 8500 mg of EPA + DHA (as fish oil capsules) reduced Lp(a) by up to 24% after only four weeks of treatment, compared to a group taking canola oil capsules (Herrmann W et al 1995).
A small study suggested that Lp(a) reductions may be somewhat more marked in those with higher triglyceride levels (Beil FU et al 1991).
One observation made in the Lugalawa study, as well as other studies, is that treatment with omega-3 fatty acids may require a year or more for full Lp(a)-reducing effect to be come evident, though the reasons for this are not clear.
Dietary strategies
Low-carbohydrate diets may reduce Lp(a) modestly. A carefully conducted University of Connecticut study in 29 overweight men showed that a diet of 13% carbohydrate, 60% fat (no controlled proportions of saturated, polyunsaturated, etc.), 27% protein, without restriction in calories resulted in an average of 11% reduction in Lp(a). Interestingly, the average weight loss was 16.5 lbs over the three month period (Wood RJ et al, 2006).
On the other hand, fat restriction (low-fat, high-carbohydrate diet) raises Lp(a), as demonstrated by another study in 37 healthy women in which Lp(a) increased 7–9% by reducing total fat intake from 36% of calories to 31%, achieved by reducing saturated fat (Silaste M et al 2004). Another study in 140 men showed a similar effect (Shin MJ et al 2007).
With regards to fat composition of the diet, omega-3 fatty acids from fish oil capsules and eating fish (see above) have the potential for both reducing Lp(a) levels, as well as suppressing production of the most undesirable small apo(a) portion of the Lp(a) molecule. Saturated fats also reduce Lp(a). Saturated fat effects show great variation among different individuals, ranging from 5% to 30% lower Lp(a) with diet unrestricted in saturated fat. Interestingly, the stearic acid component of saturated fats stands out as the factor that raises Lp(a), unlike other saturated fatty acids palmitic, lauric, and myristic fatty acids, which do not (Müller H et al 2003; Sanders TAB et al 1997). Stearic acid is especially plentiful in the saturated fat from chocolate (43% of total fat) and red meats (14%). (There are no studies specifically examining the effects of dark chocolate or cocoa on Lp(a).) Nonetheless, the net effect of saturated fat is Lp(a) reduction. Trans fatty acids (hydrogenated fats) raise Lp(a), generally around 5%, though some people show much greater increases (Clevidence BA et al 1997; Mensink RP et al 1992). Although monounsaturated fats (e.g, canola, olive) may be desirable from an insulin-sensitizing standpoint, they may also raise Lp(a) by 10–12% (Vessby B et al 2002). From a fat composition viewpoint, a diet rich in omega-3 fatty acids and saturated fats, and low in hydrogenated trans-fats and perhaps monounsaturates, is therefore most beneficial for Lp(a) reduction.
Weight loss may result in modest reduction of Lp(a) in obese or overweight people. In one small French experience in 62 overweight people, participants with Lp(a) >20 mg/dl experienced 17.6% reduction in Lp(a) with weight loss of approximately 15 lbs over 6 weeks, achieved through calorie restriction (Kiortsis DN et al 2001).
Soy proteins, while exerting a modest LDL-reducing effect, may also increase Lp(a) 15-20%, while the dairy protein, casein, may reduce Lp(a) (Nilausen K 1999; Teede HJ et al 2001). However, these observations have not been consistent; one small study in females suggested no Lp(a) effect (Merz-Demlow BE et al 2000), another larger study in 130 participants receiving 30 grams soy protein also showed no effect (Tonstad S et al 2002).
Alcohol
Alcohol, i.e., ethanol provided by alcoholic beverages, reduces Lp(a) in a dose-dependent manner: the more you drink, the more Lp(a) is reduced, up to 57% reduction, an observation confirmed in a number of studies (Fontana P et al 1999; Välimeli M et al 1991; Marth E et al). Unlike the apo(a)-size effects of omega-3 fatty acids, alcohol did not exert any beneficial effect on apo(a) profile, despite the reduction in Lp(a), according to one very well-conducted study (Fontana P et al 1999). Conversely, withdrawal of alcohol from chronic users triggers a rebound of Lp(a), an effect also confirmed in several studies (Huang CM et al 1992).
Although deeply-pigmented red wines are suspected to provide benefits over and above their alcohol content (presumably due to flavonoid content), no such specific relationship with Lp(a) has been identified.
Of course, there are other effects of alcohol to consider, including beneficial rises in HDL at low quantities (up to two servings a day), but increasingly adverse effects, including increased triglycerides and blood pressure (more than four drinks per day), with greater amounts.
DHEA
DHEA has been shown to reduce Lp(a) by 15–18% in one study involving females in the peri- and post-menopausal period taking 50 mg per day (Barnhart KT et al 1999). Unfortunately, this relationship has not been well-explored in males. We have used DHEA supplementation in men with modest success when DHEA blood levels are low.
Flaxseed and almonds
Ground flaxseed (2 tbsp/day) and raw almonds (1/4 cup/day) achieves Lp(a) reductions of approximately 7% (Jenkins DJ et al 2002). Both foods not only reduce Lp(a), but also reduce LDL and may partly counteract the small LDL particle size tendency through their blood sugar-reducing effect.
Coenzyme Q10
In one Italian study, the nutritional supplement, coenzyme Q10 (CoQ10), reduced Lp(a) 12% at a dose of 150 mg per day) (Cicero AFG et al 2005). Remember that oil-based gelcaps only should be used, never encapsulated powders or tablets.
L-carnitine
The amino acid supplement, L-carnitine, 2000–4000 mg per day (1000 mg twice a day), has been shown to reduce Lp(a) 7–8%, and occasionally will reduce it up to 20%, with 77% of participants in one study showing a Lp(a) reduction (Sirtori CR 2000). Several publications have suggested that there is, indeed, a Lp(a)-reducing effect, but all the studies originate from the same research group. Unfortunately, we have not reproduced l-carnitine's Lp(a)-reducing effect in our Track Your Plaque experience; whether the preparations have been faulty, or there is simply no significant effect on populations outside of the Italian participants in these studies is presently unclear.
N-acetylcysteine
N-acetylcysteine, NAC, is classified as a pharmaceutical agent used for treatment of acetaminophen poisoning (intravenous administration) and for clearance of thick airway secretions (inhalational administration, usually for cystic fibrosis and other lung diseases). It is commonly used orally in hospital settings to block the toxic effects of x-ray (angiographic) dyes on kidneys, for which it has shown moderate efficacy.
Several small studies have suggested that NAC at doses of 1200 to 4000 mg per day taken orally may reduce Lp(a). In one small case study of just two people, Lp(a) reductions of up to 70% were seen (Gavish D 1991). In this small but well-characterized experience, NAC was felt to reduce Lp(a) by interfering with assembly of the apo(a) and apo B molecules. Importantly, no increase in the blood level of apo(a) was seen, a concern since increased free and unassembled apo(a) might, by itself, represent another source of plaque and blood clotting activation. Another small experience in 19 subjects showed much smaller reductions of up to 7% with NAC doses of up to 2400 mg per day (Kroon AA et al 1991.) However, another small experience involving 11 subjects showed no effect (Wiklund O et al 1996).
NAC may therefore represent a potential treatment for Lp(a), though clearly larger experiences over a longer period are needed. Unfortunately, the long-term safety of NAC has not been well-studied. A recent publication in mice suggests that a condition called pulmonary hypertension may develop with doses higher than that used in humans; whether this is applicable to the human dose is uncertain (Palmer LA et al 2007).
Homocysteine reduction
Several studies have recently called into question whether reduction of homocysteine with high doses of B vitamins results in reduction in heart attack and other cardiovascular events. However, the well-established fact remains that homocysteine is a powerful predictor of cardiovascular events. (In other words, it is not clear whether homocysteine exerts a causal effect on atherosclerosis, or is just a phenomenon that parallels it.) Homocysteine is an especially effective predictor of events when elevated levels occur in combination with other risk factors.
Several studies have suggested that increased Lp(a) in the presence of increased homocysteine carries heightened risk. The University of Utah study cited above (Hopkins PN et al 1997) found that the combination of Lp(a) =40 mg/dl with increased homocysteine levels increased risk of cardiovascular events 31-fold. A 1999 Cleveland Clinic study of 1150 men and women showed that a Lp(a) level =30 mg/dl and homocysteine =17 µmol/L increased risk for heart disease 12-fold in men <60 years old, 6-fold <65 years; approximately 3-fold in women <65 years old (Foody JM et al 2000).
Emerging data suggest that, in the presence of increased homocysteine levels, the structure of the apo(a) of Lp(a) is modified. This modification increases adhesion of Lp(a) to plaque (fibrin) up to 20-fold (Harpel PC et al 1992; Sotirou SN et al 2006). Another interesting observation from a French group suggests that, while the small apo(a) form of Lp(a) poses increased risk by itself, the presence of elevated homocysteine causes even the large, ordinarily less harmful large apo(a) form of Lp(a) to be more adherent to plaque (fibrin) (Nardulli M et al 2005).
Thus, the plaque-forming potential of Lp(a) appears to be increased when homocysteine levels are increased. Unfortunately, of the several recent trials examining homocysteine reduction with B vitamins, none examined whether there was an effect in a subset with increased Lp(a). It is therefore unknown whether B vitamins, or other means of homocysteine reduction, exert additional benefits when Lp(a) is increased. However, this will be a fascinating area for future investigation. In the meantime, reduction of homocysteine to desirable levels is still worth strong consideration when Lp(a) levels are high. (See Homocysteine: An update)
Fibrates
There are presently two fibrate drugs in the U.S.: fenofibrate (Tricor®) and gemfibrozil (Lopid®). However, there are surprisingly little data in this area.
One interesting experience with gemfibrozil showed that, while 18 participants taking 600 mg of the drug showed an average Lp(a) reduction of 17% in those with "normal" triglycerides (152 mg/dl) but little or no change when triglycerides were high (364 mg/dl), individual responses differed dramatically (Jones PH et al 1996). Among the entire group, Lp(a) response on treatment ranged from a reduction of 26% to an increase of 184.6%. The reasons for the wildly disparate responses are not clear. A small experience suggests that fenofibrate reduces Lp(a) modestly (Farnier M et al 1994). However, results with both fibrates have been inconsistent with little or no effect demonstrated in another experience (Insua A et al 2002).
All in all, there are little data with the fibrate class of drugs. In the Track Your Plaque experience, some people who prove resistant to niacin may show significant reductions of Lp(a) in the neighborhood of 30% with fenofibrate, 148–200 mg per day.
Thyroid hormone
It's been known for many years that people with underactive thyroid glands ("hypothyroidism") display higher LDL cholesterol, higher triglycerides, and lower HDL. They also usually show higher Lp(a) levels. It's also widely accepted that correction of hypothyroidism returns these phenomenon back to their previous levels.
What is not clear is whether treatment of marginally underactive thyroid glands, so-called "subclinical hypothyroidism," also reduces Lp(a). This degree of thyroid underactivity may or may not even yield symptoms of low thyroid hormone. To complicate matters, there are two thyroid hormones: the more popularly prescribed T4, or thyroxine, and the less prescribed T3, or triiodothyroxine.
Treatment with T4 alone exerts a small, though inconsistent, effect on reducing Lp(a) (Milionis HJ et al 2003; Martinez-Triguero ML et al 1998). Several older studies dating back to the 1960s have documented a Lp(a)-reducing effect of T3 replacement when T3 blood levels have been low. One small clinical trial, for instance, documented Lp(a) reductions of 29–50% with T3 replacement after surgical thyroid gland removal (Dullaart RP et al 1995).
Low T3 levels may be an issue for people who either have under-active thyroid glands (hypothyroidism). T3 levels can also be low when standard thyroid replacement treatment, which is usually only T4, or thyroxine, without T3, is being prescribed. In this case, there may be value in specifically assessing T3 levels to ensure levels within the normal (high-normal?) range.
Diabetes treatments
People with type I and II diabetes or metabolic syndrome have higher levels of Lp(a), but improved control of blood sugar does not appear to exert any Lp(a) reduction (Kikuchi T et al 1994; Perez A et al 1998).
However, some drugs used to treat type II diabetes may exert some Lp(a)-reducing effects: metformin (Glucophage®), up to 42% reduction (Velazquez EM et al 1997; pioglitazone (Actos®), 20% reduction with a dose of 4 mg per day (Derosa G et al 2006). However, this observation has not been made consistently with some studies showing a modest increase of 10% in Lp(a) on pioglitazone (Perez A et al 2004).
Gingko biloba
Gingko biloba, a nutritional supplement that may provide benefits in memory, showed a 23% reduction in Lp(a) in a preliminary German trial at a dose of 120 mg per day (Siegel G et al 2007).
Unique strategies that are probably not helpful
This is a list of agents that can reduce Lp(a) but are not helpful, since they post unacceptable side-effects or simply don't work.
Anabolic steroids—These are the synthetic hormones used by bodybuilders and occasionally in treatment of conditions like endometriosis. The fact that steroids like stanozolol and nandrolone can reduce Lp(a) by 80% raises some important questions on how and why this enormous effects develops (Hartgens F et al 2004). Unfortunately, the startling effect of anabolic steroids has not yielded any insights into alternative treatments that might exert similar Lp(a)-reducing effects yet lack the toxicity of these agents, such as kidney failure, liver cancer, etc.
Vitamin C—Dr. Mathias Rath has been a vocal proponent of vitamin C supplementation at high doses to treat Lp(a). This is based on speculation and preliminary observations that suggest that vitamin C (ascorbate) deficiency permits infiltration of Lp(a) particles into the artery wall, and that vitamin C also may block the binding of the Lp(a) to fibrin. In one small experience of 11 participants, Lp(a) was reduced 27% by vitamin C, 9000 mg, over 14 weeks (Rath M 1992). However, the weight of evidence in humans does not support an effect of vitamin C at lower doses of 1000 mg per day (Jenner Jl et al 2000) and 4500 mg per day (Bostom AG et al 1995). In the Track Your Plaque experience, lower doses have not exerted a substantial effect, and nor have higher doses.
Exercise—Contrary to conversations in the media that have suggested that vigorous exercise like marathon running can increase risk of heart disease, exercise, regardless of whether modest, moderate, or vigorous, seems to exert no effect on Lp(a) levels (Durstine JL et al 2001; Drowatzky KL et al 2001). That's not to say that exercise has no benefits in a person with Lp(a); it just means that exercise does not specifically reduce Lp(a) itself.
Neomycin—Neomycin is an antibiotic, still used for topical application, that, when taken orally, can reduce Lp(a) by 24%. However, neomycin has fallen into disuse because of an intolerable side-effect of deafness and kidney toxicity (Gurakar A 1985).
Policosanol—Despite the glowing results initially published by a research group from Havana, the purported LDL-reducing, HDL-increasing results have not been successfully reproduced for this sugar cane derivative. Nonetheless, the same Cuban researchers have made unsubstantiated claims that policosanol also reduces Lp(a) and this claim has trickled into many media reports. However, the meager data that do exist on policosanol's effect on Lp(a) have not demonstrated any effect (Reiner Z et al 2005), nor have we witnessed any Lp(a)-reducing benefit with our use.
A practical approach to Lp(a)
It is nearly always worth beginning with the treatments most well-studied for reduction of Lp(a):
* Niacin—Doses may be higher than that for other conditions, up to 2000–4000 mg or more per day (only under physician supervision).
* Testosterone for men; estrogens for women.
* DHEA
* LDL reduction—with statin drugs or otherwise
* A diet rich in fish and omega-3 fatty acids, perhaps unrestricted in saturated fats (from good sources like organic or farm-raised red meats, eggs, cheese; not cured meats like bacon and sausage, or fried foods whose structure has been altered by high-temperature oxidation).
* Raw almonds, ground flaxseed
* Alcoholic beverages, preferably deeply-pigmented red wines
* Aspirin
After this basic starting list, that's when we begin to turn to the less well-tried strategies. The treatments most likely to yield useful effects include:
* High-dose fish oil
* Fibrate drugs—especially fenofibrate (Tricor®)
* If diabetic, treatment with metformin (Glucophage® and/or pioglitazone (Actos®)
Although more investigation is needed, we are advocates of reducing homocysteine levels when Lp(a) levels are high, since these two molecules have the potential for adverse interaction that heightens plaque-growing risk. Since the treatment is relatively benign and inexpensive (B vitamin supplementation), it is a small price to pay for added peace of mind.
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