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Cardiometabolic Health

Cholesterol, Blood Fats and Sugars, and Vascular Tone

Understanding cardiovascular disease (CVD) risk factors and lipid profiles is an essential first step towards long-term cardiovascular health! Serum cholesterol totals, lipid and lipoprotein measurements, glucose levels, and other blood labs are an important part of an effective, science-based Patient Plan for CVD Management.

What Every Patient Should Understand

Atherosclerotic Cardiovascular Disease (ASCVD): A Lifestyle Epidemic

ASCVD (or Atherosclerosis) is characterized by a progressive narrowing of the arteries and is the primary cause of coronary heart disease (CHD), stroke, and other vascular diseases in developed nations. ASCVD is a lifestyle disease resulting predominantly from a western Standard American Diet (SAD) of processed foods that lack essential nutrients and include high amounts of sugar, sodium, unhealthy fats, and other inflammatory food-like substances and chemicals. Other modifiable risk factors include: cigarette smoking, excess caloric intake, body weight and composition, physical inactivity, and chronic stress.

Atherogenesis: “The Bad Cholesterol” (LDL-C)

A complex series of pathological processes leads to the accumulation of fatty plaque (within the arterial intima) that characterizes ASCVD. However, atherosclerosis pathology virtually always requires the presence of 2 essential factors: (1) elevated serum cholesterol and (2) chronic subclinical inflammation.

Lipoproteins are the particles that transport cholesterol and triglycerides throughout the body to meet cellular needs and support metabolic activity. As the primary predictive indicator of cardiovascular disease (CVD), most guidelines recognize low-density lipoprotein cholesterol (LDL-C) as the major atherogenic lipoprotein, and thus the primary target for ASCVD prevention. (1, 2)

Notably, LDL-C accounts for more than 75% of atherogenic lipoproteins; increases in LDL-C alone can lead to ASCVD, even in the absence of smoking, low HDL-C, and other risk factors! (1) Although additional measures of non-HDL-C & LDL particle numbers and/or ApoB-100 may be considered, LDL-C remains the essential risk indicator due to its feasibility in clinical practice and robust data supporting its usefulness as a predictor of ASCVD. (1, 2) As such, the goal of ASCVD treatment protocols should focus on reducing chronic subclinical inflammation and normalizing lipoprotein profiles, especially LDL-C.

NEW: Recent findings show Lipoprotein particle size/density (LDL-P) and numbers are stronger predictor of cardiovascular event, compared to cholesterol totals alone (LDL-C).
>> Learn more about LDL Particles and lipid profiles here.

Nitric Oxide: Supporting Vascular Tone

Nitric Oxide (NO) is a signaling molecule with far-reaching biological significance. NO plays an essential role in cardiovascular health by increasing vasodilation of blood vessels, maintaining blood fluidity, and regulating inflammation and immune activity – all of which can have a profound impact on blood pressure control. Supporting optimal levels of bioavailable nitric oxide, combined with a healthy lipid profile and decreased inflammation, can significantly reduce the likelihood of major cardiovascular complications and disease risk.

 

Adressing Arterial Plaque, Cholesterol ASCVD

The Prothrombotic State:
An increased likelihood of Arterial Plaque Rupture

Atherosclerosis (ASCVD) is essentially an inflammatory disease triggered by cholesterol-rich lipoproteins and other noxious factors that exacerbate the inflammatory response. However, in the absence of excessive inflammation, a gradual accumulation of plaque (and the arterial narrowing that follows) is rarely cause for concern until much later in disease progression. Rather, of immediate concern and danger is the prothrombotic state – an increased tendency of arterial plaque rupture that can lead to complete occlusion of blood flow, as experienced in catastrophic cardiovascular (heart attack) or cerebrovascular (stroke) events.

In most adults, clinically relevant plaques (atheromas) are present, but stabilized by fibrous tissue composed of collagens, elastin, and various types of proteoglycans that form a protective cap. Lipid associated inflammation introduces tissue degrading effects, which destabilize an atheroma (protective cap) and cause the central core of extracellular lipids and debris to leak into the artery – often causing complete arterial blockage and death. (7)

Stabilizing a prothrombotic atheroma by reducing endothelial inflammation and promoting tissue integrity (and repair) is crucial for minimizing the risk for acute cardiovascular events.

 

Cholesterol Complete:
The Cornerstone of Nutraceutical Lipid Management*

Cholesterol Complete is a specialized formula designed to help manage overall serum cholesterol levels, promote an optimum balance between LDL and HDL cholesterol and enhance healthy homocysteine metabolism — all major factors in cardiovascular disease.*

  • A unique blend of Red Yeast Rice Extract, Guggulipid and Policosanols to promote healthy blood lipid levels.*
  • Provides vital methyl donors; Folic Acid, Vitamin B-6, B-12 and Trimethylglycine.*
  • Formula delivers clinically significant results for most patients with just four tablets daily.*

Increasing HDL levels by just 10% can reduce risk of heart attack by 40%. Lowering triglycerides can also reduce risk for heart disease. Monitor lab biomarkers and utilize Cholesterol Complete to help lower “bad cholesterol”, and increase “good cholesterol”.

 

The Role of Nitric Oxide:
Endothelial Dysfunction & Hypertension

Atherosclerosis (ASCVD) is essentially an inflammatory disease triggered by cholesterol-rich lipoproteins and other noxious factors that exacerbate the inflammatory response. However, in the absence of excessive inflammation, a gradual accumulation of plaque (and the arterial narrowing that follows) is rarely cause for concern until much later in disease progression. Rather, of immediate concern and danger is the prothrombotic state – an increased tendency of arterial plaque rupture that can lead to complete occlusion of blood flow, as experienced in catastrophic cardiovascular (heart attack) or cerebrovascular (stroke) events.

In most adults, clinically relevant plaques (atheromas) are present, but stabilized by fibrous tissue composed of collagens, elastin, and various types of proteoglycans that form a protective cap. Lipid associated inflammation introduces tissue degrading effects, which destabilize an atheroma (protective cap) and cause the central core of extracellular lipids and debris to leak into the artery – often causing complete arterial blockage and death. (7)

Nutritional interventions involving hypertension should serve to increase NO bioavailability, while also neutralizing inflammatory and reactive molecules with antioxidant support.

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References:

  1. J Clin Lipid. 2014; 8(1): 29-60.
  2. J Am Coll Cardiol; 2008; 51(15): 1512-1524.
  3. Cardiovasc Drugs Ther, 2005(19): 403-414.
  4. Med Sci Monit. 2014; 20: 2183–2188.
  5. J Clin Hypertens (Greenwich). 2012;14:121–132.
  6. PLoS One. 2014; 9(6): e98611.
  7. Cardiovas Research. 1999; 41(2): 334-344.
  8. Eur J Heart Fail. 2008 Dec; 10(12):1255-63.
  9. Am J Physiol Endocrinol Metab. 2008;295(6):E1390-400.
  10. Angiology. 2001;52 Suppl 2:S69-73.
  11. J Med Food. 2008 Dec; 11(4):610-4.