SpectraCell Blog

Lipoprotein(a): An Important Risk Factor for Heart Disease

Posted by Nichole Herms on Fri, Feb 16, 2018 @ 03:32 PM

 

Most people assume that standard cholesterol testing offers an adequate assessment of heart disease risk. If you, like many, have never heard of a lipoprotein profile test, you may be surprised to learn that this test assesses an important risk factor called Lipoprotein(a) or Lp(a) (“lipoprotein little a”). Influenced by genetics and strongly linked to heart disease and blood clotting problems, this risk factor unfortunately is NOT part of routine cholesterol tests or standard lipid panels. In fact, lipoprotein(a) is so strongly linked to heart disease, that it is one of the four lipid-related risk factors cited by the National Institutes of Health National Cholesterol Education Program (NCEP) as worthy of monitoring. Unfortunately, Lp(a) has been notoriously difficult to treat pharmacologically, as statins have shown little efficacy in lowering Lp(a) levels.

Why is Lp(a) so harmful?
Evidence suggests that Lp(a) may serve as the link between thrombosis and atherosclerosis. Recent clinical studies have implicated Lp(a) as a risk factor for blood clots whether or not atherosclerosis is present. Because Lp(a) is a small, very dense LDL, it can easily penetrate the arterial lining, become oxidized and build plaque, thus contributing to atherosclerosis independent of its thrombotic potential. 

How is high Lp(a) treated?

In a recent double-blind, placebo-controlled trial, patients with elevated cholesterol and elevated Lp(a) were divided into two groups, each with 29 people: Group 1 received a statin only and Group 2 received the same statin plus 2 grams/day of L-carnitine, a supplement that plays a key role in fatty acid transport within cells. After 12 weeks, the group receiving only a statin showed about a 7% reduction in Lp(a), but the group receiving the L-carnitine in conjunction with the statin demonstrated over 19% reduction in Lp(a) levels. Authors suggest that co-administration of L-carnitine (whose primary function is fatty acid metabolism), may enhance efforts to lower Lp(a) compared to using a statin alone.

Although heredity plays a large role in the levels of Lp(a), treatment with niacin has also been found to lower levels of Lp(a). 

For additional reading refer to the abstract L-Carnitine/Simvastatin Reduces Lipoprotein (a) Levels Compared with Simvastatin Monotherapy: A Randomized Double-Blind Placebo-Controlled Study published in the January 2017 issue of Lipids

Topics: lipoprotein particle profile, Heart Disease, cardiovascular disease, Lipoprotein Particles, Lipoprotein(a), L-carnitine, Lower Lipoprotein(a), High Lipoprotein(a)

Fasting-Mimicking Diet Helps You Eat Your (Own) Heart Out - Reducing Cardiovascular Disease

Posted by Kirstin Keilty, MS, CNS on Fri, Feb 09, 2018 @ 11:00 AM

FMD-1.jpgAs we stroll into heart month (Feb), still the #1 killer of Americans - 20 years after the declaration to reduce heart-related deaths - here we are. Still. Trying like heck to reduce the risk of heart-related (and other co-morbidities) incidences.

According to statistics from the CDC in 2016, 610,000 heart-related deaths occur each year and it is the leading cause of death in both men and women. That is 1 in 4 Americans.

Why are we still here? After all, we know what we can do: exercise more, take our multivitamin, get regular checks-ups at our doctors' office and - oh yeah - eat more healthfully. Many of us are still sticking to our New Year's Resolutions!

Amid our plight to prepare more healthy home-cooked meals with an eye to consuming higher amounts of plant-based foods, with greater amounts of heart-protecting fiber, healthy, lean proteins, less sugar and processed foods, are we able to keep on with these habits - forever?

Some might say a resounding, "YES!", well, others...maybe...not so much. We have the statistics to prove it.

What do we do if we feel like we have "tried it all", and the results don't appear to be paying off?

What if we have test results, like an advanced lipoprotein or cardiometabolic profile that continue to stare us in the face and prove the errors of our ways? It's disheartening when the labors of our actions appear to be largely ignored by our body's metabolism.

Is it time to finally give up? Should New Year's Resolutions focus on some other aspect, other than finally getting healthy?

Perhaps it is time for a different approach…

The practice of fasting has had many surges over the millennia, extending from times of scarcity, to practices of mystics and religious groups and holidays to health-faddists. Some believed it brought spiritual enlightenment, or quick weight loss; while others believed it gave the digestive system a chance to rejuvenate itself, similar to the idea that adequate nightly sleep allows a reset of the nervous system.

It is largely this last assumption which has pioneered continued research into fasting and its multiple health benefits, including heart (but not limited to) health.1-4

I had the good fortune of learning first-hand about the incredible research into fasting this past December while attending the American Academy of Anti-Aging Medicine in Las Vegas. Valter Longo, PhD, who directs the USC Longevity Institute, expertly presented his research on fasting and its connection to a longer, healthier existence.5 Instead of fasting for long periods of time (4 days to a couple of weeks), the same benefits can be achieved through "Time-Restricted Fasting/Re-feeding" (TRF) or "Fasting-Mimicking Diet" (FMD). Below are two links to fascinating presentations featuring Dr. Longo and his work.

BBC Documentary with Longo and Maslow

FoundMyFitness Interview Longo and Rhonda Patrick

Essentially, with TRF and FMD, an individual can positively impact health for prolonged periods of time simply by choosing to consume all of their daily calories in an 8-hour window. If the first caloric consumption (this includes beverages so no cream or sugar in your coffee) of the day starts at 10:00 AM, an individual is done feeding by 6:00 that evening. If 11:00 is start time, 7:00 is finish time, and so forth.

What does FMD do, exactly?

The Fasting-Mimicking Diet creates the time needed to accomplish an "internal housekeeping" on the cellular level known to stimulate a pathway called: autophagy. Whether you choose to say it "Ah-tauf-ah-gee"or "auto-fay-gee" (I've learned both are right), somatic cells auto-phagocytize, literally eat themselves, to sweep out the debris of aberrant (faulty, damaged or maladapted) cells that build up in our cellular metabolism. Additionally, internal organs, like the heart, all shrink to their reset size, which allows for more effective functioning. When we eat too frequently and don't allow the digestive system to rest, clean and rebuild with re-feeding, autophagy processes are disrupted.

How will autophagy improve my heart health, specifically?

As noted earlier, autophagy has profound positive effects on many body systems and functions, as well as cancer prevention and other diseases, but one of the most researched areas in autophagy include cardiovascular disease. Since mitochondria are found in abundance within the cardiac muscle and TRF and FMD precipitate autophagy, another way fasting improves heart health might be through preserving mitochondrial integrity.
6

Dr. Longo's research has also shown that TRF and FMD influences cellular adaptive responses by reducing oxidative damage and inflammation; as well as optimizing energy metabolism and bolstering cellular protection.7

  1. Xie W, Zhou J. Aberrant regulation of autophagy in mammalian diseases. Biol Lett. 2018;14(1).
  2. O'Flanagan CH, Smith LA, McDonell SB, Hursting SD. When less may be more: calorie restriction and response to cancer therapy. BMC Med. 2017;15(1):106.
  3. Choi IY, Piccio L, Childress P, et al. A Diet Mimicking Fasting Promotes Regeneration and Reduces Autoimmunity and Multiple Sclerosis Symptoms. Cell Rep. 2016;15(10):2136-2146.
  4. Brandhorst S, Choi IY, Wei M, et al. A Periodic Diet that Mimics Fasting Promotes Multi-System Regeneration, Enhanced Cognitive Performance, and Healthspan. Cell Metab. 2015;22(1):86-99.
  5. Longo VD, Panda S. Fasting, Circadian Rhythms, and Time-Restricted Feeding in Healthy Lifespan. Cell Metab. 2016;23(6):1048-1059.
  6. Traba J, Sack MN. The role of caloric load and mitochondrial homeostasis in the regulation of the NLRP3 inflammasome. Cell Mol Life Sci. 2017;74(10):1777-1791.
  7. Longo VD, Mattson MP. Fasting: molecular mechanisms and clinical applications. Cell Metab. 2014;19(2):181-192.

Topics: Cardiovascular Health, Heart Disease, Heart Health, Fasting-Mimicking Diet, FMD, FMD Helps Reduce Cardiovascular Disease, Autophagy, Cellular Metabolism

Clearing Up the Cholesterol Confusion

Posted by SpectraCell Laboratories, Inc. on Thu, Feb 01, 2018 @ 01:52 PM

heart apple.jpgConsider this startling statistic: 50% of people who have heart attacks have "normal" cholesterol.  Stated differently, half of all heart attack victims could have a routine cholesterol test done on the very day they have a heart attack and their cholesterol (by routine testing standards) would be "normal" range. So, why do so many practitioners use a diagnostic test that is only 50% accurate?  The reason is simple:  it’s the test with which they are familiar and have been using for decades.  Knowing your HDL and LDL - the "good" and "bad" cholesterol is only the beginning.  SpectraCell’s LPP (Lipoprotein Particle Profile) test goes much, much further.
 
Here is the basic scenario of heart disease:  When our blood vessels are "scratched," or injured, plaque builds up in our arteries to repair the injury, sort of like a scab on the inside of  the blood vessel, causing reduced blood flow. Since plaque buildup is our bodies' response to injury of the blood vessels, reducing the injury to our arteries is key.  
 
That's where cholesterol comes in. Cholesterol is actually a response to vascular injury - not the cause of it. Cholesterol is really not the culprit. Lipoproteins are. Lipoproteins are what "scratch" or "burrow" into our arteries causing injury.  They are actually tiny balls in our blood that carry the cholesterol, our vascular scapegoat. Lipoproteins are what do the damage, not the cholesterol inside them. Cholesterol is really just along for the ride. Lipoproteins, at least the dangerous ones, are the real villain.
 
There are different sizes of lipoproteins. In general, bigger is better.  Here's why: Larger, fluffier LDL particles cannot lodge into your arteries (which is an injury to the artery) as easily as the smaller LDL particles can. Less injury to the artery means less plaque formation and clearer, more pliable blood vessels - a good thing. So it is imperative to understand what kind of LDL (low density lipoproteins) you have floating around in your blood. There are some that are extraordinarily dangerous and some that are completely benign.
 
For example, RLP (also called remnant lipoprotein) has been cited by the government as a very high risk factor for heart disease. But statins, which lower LDL, will do nothing to help your RLP, which are best lowered by high dose omega 3 fatty acids. So, if you don't know what kind of lipoproteins you have, you're shooting in the dark in terms of what treatments you should take. You can see why measuring just plain old cholesterol is certainly not enough. That is why 50% of the people who have fatal heart attacks have "normal" cholesterol - they are not getting the right cholesterol/ lipoprotein test done.
 
Here's the best part:  SpectraCell's LPP® test costs about the same as an outdated cholesterol test and it is also often covered by insurance. Why wouldn't you want an LPP® done?

Topics: Cholesterol, Heart Disease, Heart Attack, Heart Health, Lipoprotein Particles, LDL and HDL, HDL, Standard Cholesterol Testing, Lower LDL, Plaque Formation