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zarfas wrote:And no matter how far or how fast you run, your risk of premature death could drop by 40 percent by taking up the activity.
Long-term physical exercise and lipoprotein(a) levels in a previously sedentary male and female population.
Abstract
We investigated the effect of long-term physical exercise on serum lipoprotein(a) levels. 21 sedentary men and 15 sedentary women were trained three to four times a week with increasing intensity during 9 months. After 24 weeks all subjects ran a 15 km race and after 36 weeks a half marathon run (21 km). Blood samples were drawn before the training programme, 5 days before both races and 5 days after the half marathon run. Median (interquartile range) pre-training values in the male group were 32 (11-63) mg/L and in the female group 65 (23-199) mg/L. After 24 weeks of training, serum lipoprotein(a) concentrations had risen significantly in both male and female groups. Moreover, after 36 weeks of training, in preparation for the half marathon competition, median serum lipoprotein(a) rose almost twofold in both groups and was still elevated 5 days later. This study demonstrates that an exercise programme which includes running of increasing distances significantly increases serum lipoprotein(a) concentration.
Lipoprotein Checklist: Lipoprotein(a)
Lipoprotein(a)
Lipoprotein (a), or Lp (a) (read “L–P little a”) is a powerful and underappreciated cause of heart disease. Up to 20% of people with heart disease will have increased Lp(a). It can trigger heart attacks early in life, as early as 40s or 50s. Lp (a) also magnifies dangers of other abnormalities.
Several studies have shown that LDL cholesterol assumes greater importance when Lp(a) is present. In the Track Your Plaque approach, we aim for an LDL of 60 mg/dl or an LDL particle number (NMR) of 600–700 nmol/l or apoprotein B of 50–60 mg/dl. LDL values in these ranges seem to provide greater protection than conventional targets (e.g., LDL 100 mg/dl).
Small LDL particles hugely magnify risk when Lp(a) is present. We therefore aim to eliminate small LDL particles in order to effectively treat this pattern. A useful goal is to reduce small LDL to <10% of total LDL. Another interesting aspect of the small LDL question is that LDL particle size and Lp(a) particle size seem to be connected to each other. In other words, when small LDL is present, Lp(a) is also small and may pose greater risk. This may provide another reason to eliminate small LDL, since eliminating small LDL may make Lp(a) less harmful.
Treatment of Lp(a) therefore requires attention to other abnormalities, as well, particularly LDL cholesterol and small LDL.
Lipoprotein(a) is reduced by:
- Niacin is the most effective direct treatment for Lp(a). However, higher doses 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. However, immediate-release niacin is otherwise safe but should not be taken more frequently than twice a day. All three preparations are very safe, with little risk of liver toxicity if taken properly. Total daily niacin doses of >500 mg should be taken with the supervision of a physician.
- Estrogen in females may lower Lp(a) around 25%, though estrogen, of course, has other considerations that need to be fully discussed with your doctor. Testosterone can be helpful for men and reduces Lp(a) by 25%. We use testosterone cream with great success. (A common dose for men >50 years old is 50 mg twice per day of a topical cream; dosing is best based on blood levels and must be prescribed). For any hormonal preparation, we advise bio-identical human preparations, i.e, preparations that are identical to the human form, not Premarin® or other non-human forms.
- L-carnitine can be a useful nutritional supplement; 2000–4000 mg per day (e.g., 1000 mg twice a day) can reduce Lp(a) 7–8%, and occasionally will reduce it up to 20%. The only drawback is cost; it can be pretty pricey. L-carnitine is not powerful enough to be used as sole treatment, however. It’s better as an adjunct with either niacin and/or hormones.
- Ground flaxseed (2–3 Tbsp/day) exerts a modest effect of no more than 7% Lp(a) reduction, but it’s healthy effects on reducing LDL and perhaps small LDL make it a useful adjunct. Use it as a hot cereal or added to yogurt or other foods. The seeds must be ground (e.g., purchased ground or ground in your coffee grinder).
- Almonds—Preferably raw or dry roasted (with no added ingredients like hydrogenated oils), ¼–1/2 cup/day, are our favorite, as they not only reduce Lp(a) but also reduce LDL and partly counteract the small LDL particle abnormality.
- Vitamin C—1000–3000 mg/day, with reported reductions of approximately 7%.
Track Your Plaque target: If measured in nmol/l, <75 nmol/l is desirable. In mg/dl, <30 mg/dl 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.)
Copyright 2006, Track Your Plaque.
Treatments for Lp(a) include (in order of my current preference):
1) High-dose fish oil--We currently use 6000 mg EPA + DHA per day
2) Niacin
3) DHEA
4) Thyroid normalization--especially T3
Hormonal strategies beyond DHEA can exert a small Lp(a)-reducing effect: testosterone for men, estrogens (human, no horse!) for women.
In other words, there is no high-ticket pharmaceutical treatment for Lp(a). All the treatments are either nutritional, like high-dose fish oil, or low-cost generic drugs, like liothyronine (T3) or Armour thyroid.
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pamojja wrote:Only a meager 11% improvement all these years.
zarfas wrote:Im not following the "graph", but have you gotton estradiol 20-30pg/ml?
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guitarplayer007 wrote:So Vitamin C therapy doesn't help reduce Lpa?
pamojja wrote:No heard attack or stroke. 'Just' a 80% blockage..
Old infarction in the left cerebellum hemisphere mediobasal belonging to the current region of the cerebellar artery posterior inferior (6/40-44) from ap up to 3 cm, tranversal up to 1 <cm and craniokaudal scarcely 2cm size in each largest diameter. Otherwise, the structure and signal behavior of the brain are regular. Regular diffusion ratios. Symmetrical, medium, normal wide supra- and infratentorial ventricular system. The external CSF spaces are normal. Virchow-Rubin's rooms in the typical places. Discretely diverging axes of the bulbi oculorum with closed eyelids. Otherwise the orbits and their contents are regular. Individual delicate mucosal swellings in several ethmoidal cells on the left more pronounced than on the right, and extremely faint on the left forehead. The remaining nasal sinuses and temporal bones on both sides are properly signalless.
zarfas wrote:are you on aromastate inhibitors, TRT, or just gained/lost fat?
pamojja wrote: - except some occasional vision disturbances between 1992-2006 (for some 20 minutes flickering like the visual snow of an off-line TV at the focus, followed by paresthesia mostly in tongue and parts of the face) -
Johnwen wrote:Pamojja;
Sounds more like a Aura from a migraine to me!
Next time you get it pop a Tylenol or aspirin and see if it goes away in about 10min.
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