Cardiovasular Disease Protocol

Inflammation plays a central role in the process of atherosclerosis, in which fatty deposits clog … Measuring CRP alone won’t tell your doctor your risk of heart disease. Below you will find my protocol for normalizing and preventing cardiovascular disease. The following are Cardiovascular Tests to recommend to patients. They can order these at a discount from Direct Labs on my website. Or you can order them for the patient. It would be good for you to create an account with Direct Labs and use my name so that you get the same prices for your patients.

  • Creactive protein
  • Fibrinogen
  • Homocysteine
  • Cholesterol test
  • Lipoprotein (a)
  • Natriuretic peptides

We are going to explore both the necessary testing, new advancements for treatment and my protocol. The possiblecauses of CVD are numerous. From Epigenetic, genetics, dietary, lifestyle, lack of exercise and just your belief systems and identities. This is so much research in this area, going back more than a decade, I am listing most of it in the references below. This is just one Study From Archives of Internal Medicine (1999) Elevated fasting total homocysteine (tHcy)levels were recently shown to confer an independent risk for all-cause and cardiovascular disease (CVD) mortality among selected Norwegian patients with confirmed coronary heart disease. We examined whether elevated fasting plasma tHcy levels were predictive of all-cause and CVD mortality in a large, population-based sample of elderly US women and men.

Cardiovascular & Homocysteine Protocol

Dr. Dale’s Formulas & Protocol You will not find a more effective protocol for cardiovascular disease and prevention. For quickest results, without detox side effects, this protocol has beenused in critical situations, decreasing plaque, lowering a lifetime of high LDL TriG & T.Cholest within three months: Actually saving people’s lives. It is up to you to test for dosages and keep up with changing them every two to four weeks. You cannot fix CVD with one formulas of any product. It needs to be a comprehensive program as this disease can be fatal. This protocol should be followed for three months. Test for Dosages…

  • Hepatic Glutathione Pathway formula. (HGP) This product has natural Folate and all that is necessary to lower homocysteine and normalize C Reactive Protein and regulate the methylation pathway.
  • Mind, Body, Meridian #3 (Heart) (homeopathy)
  • Cholest: with meals: Handles Low HDL, High LDL, and Blood Pressure.
  • Niacinamide: Depression, High BP, Homocysteine, Circulation, etc.
  • Slow Cleanse: instruction included: Detoxify inflammation causing pathogens
  • BioFilm Detox: Eliminates BioFilm hiding pathogens.
  • Nano Ionic Multiple with Silica (liquid)
  • Nano Ionic Magnesium (liquid)
  • Optimal Multi Pro: Homocysteine management
  • Raw Nattokinase: Handles Inflammation and Fibrinogen

If there is an infection add the following to the protocol above.

  • Test for Bowel Nosode and BioTox Nosode.
  • Add Ocean Med’s: 2. 2x daily and
  • Nano Ionic Immune

If there is arterial plaque, chelation is recommended. I recommend rectal suppositories and possibly IV Chelation. Detoxamin has worked very well for my patients. I don’t recommend oral chelation for everyone because it is difficult to absorb and digest.

Purchase at Store:

  • DHA, EPA (purified) High potency
  • Ubiquinol without stearates or excipients.
  • Vitamin C, (Camu-Camu)
  • Organic, Nearly Vegan & Gluten Free Diet: Abundance of fresh raw veggies or lightly steamed, eliminate dairy and other inflammatory foods like junk, fried, sugar, red meat. Smaller portions of whole grains, gluten free.
  • Cardiovascular and stretching Exercise regularly

CReactive Protein (CRP) Testing

It’s all about reducing inflammation! THIS TEST IS AN INFLAMMATION MARKER!

If there is a known active or chronic infection, virus or bacteria then add Ocean Med’s and Nano Ionic Immune to the above protocol.

CRP is reflects inflammation. We also need to relate inflammation to Depression (Neurotransmitters, Methylation). The Above protocol will address all of this.

Interesting Study on Epigenetic and inflammatory marker profiles associated with depression in a community-based epidemiologic sample.

C-reactive protein (CRP) is a protein found in the blood, the levels of which rise in response to inflammation (i.e. C-reactive protein is an acute-phase protein). Its physiological role is to bind to phosphocholine expressed on the surface of dead or dying cells (and some types of bacteria) in order to activate the complement system via the C1Q complex.[1]

CRP is synthesized by the liver[2] in response to factors released by fat cells (adipocytes).[3] It is a member of the pentraxin family of proteins.[2] It is not related to C-peptide or protein

The CRP gene is located on the first chromosome (1q21-q23). CRP is a 224-residue protein[5]with a monomer molar mass of 25106 Da. The protein is an annular pentameric disc in shape and a member of the small pentraxins family.

CRP is a member of the class of acute-phase reactants, as its levels rise dramatically during inflammatory processes occurring in the body. This increment is due to a rise in the plasma concentration of IL-6, which is produced predominantly by macrophages[2] as well as adipocytes.[3] CRP binds to phosphocholine on microbes. It is thought to assist in complement binding to foreign and damaged cells and enhances phagocytosis by macrophages (opsonin mediated phagocytosis), which express a receptor for CRP. It is also believed to play another important role in innate immunity, as an early defense system against infections. CRP rises up to 50,000-fold in acute inflammation, such as infection. It rises above normal limits within 6 hours, and peaks at 48 hours. Its halflife is constant, and therefore its level is mainly determined by the rate of production (and hence the severity of the precipitating cause). Serum amyloid A is a related acute-phase marker that responds rapidly in similar circumstances.[2]

Apart from liver failure, there are few known factors that interfere with CRP production.[2]

Various analytical methods are available for CRP determination, such as ELISA, immunoturbidimetry, rapid immunodiffusion, and visual agglutination.

Normal concentration in healthy human serum is usually lower than 10 mg/L, slightly increasing with aging. Higher levels are found in late pregnant women, mild inflammation and viral infections (10–40 mg/L), active inflammation, bacterial infection (40–200 mg/L), severe bacterial infections and burns (>200 mg/L).[6]

Cardiology diagnostic test

Arterial damage results from white blood cell invasion and inflammation within the wall. CRP is a general marker for inflammation and infection, so it can be used as a very rough proxy for heart disease risk. Since many things can cause elevated CRP, this is not a very specific prognosticindicator.[7] Nevertheless, a level above 2.4 mg/l has been associated with a doubled risk of a coronary event compared to levels below 1 mg/l;[2] however, the study group in this case consisted of patients who had been diagnosed with unstable angina pectoris; whether elevated CRP has any predictive value of acute coronary events in the general population of all age ranges remains unclear.

Recent research suggests that patients with elevated basal levels of CRP are at an increased risk of diabetes,[8][9] hypertension and cardiovascular disease. A study of over 700 nurses showed that those in the highest quartile of trans fat consumption had blood levels of CRP that were 73%higher than those in the lowest quartile.[10] Although one group of researchers indicated that CRP may be only a moderate risk factor for cardiovascular disease,[11] this study (known as the Reykjavik Study) was found to have some problems for this type of analysis related to thecharacteristics of the population studied, and there was an extremely long follow-up time, which may have attenuated the association between CRP and future outcomes.[12] Others have shown that CRP can exacerbate ischemic necrosis in a complement-dependent fashion and that CRPinhibition can be a safe and effective therapy for myocardial and cerebral infarcts; so far, this has been demonstrated in animal models only.[1

Fibrinogen Test

See protocol for lowering Fibrinogen below. Fibrinogen is a protein in your blood that helps blood clot. But too much fibrinogen can cause a clot to form in an artery, leading to a heart attackor stroke. Having too much fibrinogen may also mean that you have atherosclerosis. It may also worsen existing injury to artery walls. Your doctor may check your fibrinogen level if you have an increased risk of heart disease. Smoking, inactivity, drinking too much alcohol and taking supplemental estrogen — whether from birth control pills or hormone therapy — may increase your fibrinogen level. A normal fibrinogen level is considered to be between 200 and 400 mg/L.Optimal reference ranges is to the lower end of this spectrum.

Homocysteine Test

Homocysteine is a substance your body uses to make protein and to build and maintain tissue. But too much homocysteine may increase your risk of stroke, certain types of heart disease, and disease of the blood vessels of the arms, legs and feet (peripheral artery disease).

Cholesterol Tests

A cholesterol test, also called a lipid panel or lipid profile, measures the fats (lipids) in your blood. The measurements can indicate your risk of having a heart attack or other heart disease. The test typically includes measurements of:

  • Total cholesterol. This is a sum of your blood’s cholesterol content. A high level can put you at increased risk of heart disease.
  • Low-density lipoprotein (LDL) cholesterol. This is sometimes called the “bad” cholesterol. Too much of it in your blood causes the accumulation of fatty deposits (plaques) in your arteries (atherosclerosis), which reduces blood flow. These plaques sometimes rupture and lead to major heart and vascular problems.
  • High-density lipoprotein (HDL) cholesterol. This is sometimes called the “good” cholesterol because it helps carry away LDL cholesterol, keeping arteries open and your blood flowing more freely.
  • Triglycerides. High triglyceride levels usually mean you regularly eat more calories than you burn. High levels increase your risk of heart disease.


^ Thompson, D; Pepys, MB; Wood, SP (February 1999). “The physiological structure of human C-reactive protein and its complex with phosphocholine”. Structure 7 (2): 169–77. doi:10.1016/S0969-2126(99)80023-9. PMID 10368284. · ^ a b c d e f g h Pepys, MB; Hirschfield, GM (June 2003). “C-reactive protein: a critical update” (PDF). J Clin Invest 111 (12): 1805–12. doi:10.1172/JCI18921. PMC 161431. PMID 12813013. · ^ a b Lau, DC; Dhillon, B; Yan, H; Szmitko, PE; Verma, S (May 2005). “Adipokines: molecular links between obesity and atheroslcerosis”. Am J Physiol Heart Circ Physiol 288 (5): H2031– 41. doi:10.1152/ajpheart.01058.2004. PMID 15653761. · ^ Tillett, WS; Francis, T (1930). “Serological reactions in pneumonia with a nonprotein somatic fraction of pneumococcus” (PDF). J Exp Med 52 (4): 561–85.doi:10.1084/jem.52.4.561. PMC 2131884. PMID 19869788. · ^ NCBI Entrez Protein #CAA39671 · ^ Clyne, Brian; Jonathan S. Olshaker (1999). “The C-reactive protein”. Journal of Emergency Medicine 17 (6): 1019–25. doi:10.1016/S0736-4679(99)00135-3. ISSN 0736-4679. PMID 10595891. Retrieved 2009-09-24. · ^ Lloyd-Jones DM, Liu K, Tian L, Greenland P (June 2006). “Narrative review: assessment ofC-reactive protein in risk prediction for cardiovascular disease”. Ann Intern Med 145 (1): 35– 42. PMID 16818927. · ^ Pradhan AD; Manson, JE; Rifai, N; Buring, JE; Ridker, PM (2001). “C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus”. JAMA 286 (3): 327–34. doi:10.1001/jama.286.3.327. PMID 11466099. · ^ Dehghan A; Kardys, I; de Maat, MP; Uitterlinden, AG; Sijbrands, EJ; Bootsma, AH; Stijnen, T; Hofman, A et al. (March 2007). “Genetic variation, C-reactive protein levels, and incidence of diabetes”. Diabetes 56 (3): 872–8. doi:10.2337/db06-0922. PMID 17327459. · ^ Lopez-Garcia, E; Schulze, MB; Meigs, JB; Manson, JE; Rifai, N; Stampfer, MJ; Willett, WC; Hu, FB (March 2005). “Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction”. J Nutr 135 (3): 562–6. PMID 15735094. · ^ John Danesh; Wheeler, JG; Hirschfield, GM; Eda, S; Eiriksdottir, G; Rumley, A; Lowe, GD; Pepys, MB et al. (2004). “C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease”. N Engl J Med 350 (14): 1387–97.doi:10.1056/NEJMoa032804. PMID 15070788. · ^ Koenig, Wolfgang (2006). “C-reactive protein – a critical cardiovascular risk marker”. · ^ Pepys MB, Hirschfield GM, Tennent GA, Gallimore JR, Kahan MC, Bellotti V, Hawkins PN, Myers RM, Smith MD, Polara A, Cobb AJ, Ley SV, Aquilina JA, Robinson CV, Sharif I, Gray GA,Sabin CA, Jenvey MC, Kolstoe SE, Thompson D, Wood SP (2006). “Targeting C-reactive protein for the treatment of cardiovascular disease”. Nature 440 (7088): 1217–21. doi:10.1038/nature04672. PMID 16642000. · ^ Ridker PM, Danielson E, et al. (November 2008). “Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein”. N Engl J Med 359 (21): 2195–207. doi:10.1056/NEJMoa0807646. PMID 18997196. · ^ “C-reactive protein concentration and the vascular benefits of statin therapy: an analysis of 20 536 patients in the Heart Protection Study”. Lancet. Retrieved 28 January 2011. · ^ Zacho J, Tybjærg-Hansen A, Jensen JS, Grande P, Sillesen H, Nordestgaard BG (October 2008). “Genetically elevated C-reactive protein and ischemic vascular disease” (PDF). N Engl J Med 359 (18): 1897–908. doi:10.1056/NEJMoa0707402. PMID 18971492. · ^ St-Onge, MP; Zhang, S; Darnell, B; Allison, DB (April 2009). “Baseline serum C-reactive protein is associated with lipid responses to low-fat and high-polyunsaturated fat diets”. J Nutr 139 (4): 680–3. doi:10.3945/jn.108.098251. PMC 2666362. PMID 19297430. · ^ Erlinger TP, Platz EA, Rifai N, Helzlsouer KJ (February 2004). “C-reactive protein and the risk of incident colorectal cancer”. Journal of the American Medical Association 291 (5): 585– 90. doi:10.1001/jama.291.5.585. PMID 14762037. · ^ Baron JA, et al. (2003). “A randomized trial of aspirin to prevent colorectal adenomas”. NEngl J Med 348 (10): 891–9. doi:10.1056/NEJMoa021735. PMID 12621133.