By Decker Weiss, NMD, FASA – Specialty: Cardiology
Company Affiliation: Clinical Advisory Board Member for NeuroScience, Inc.
The song, “(You Gotta) Fight for Your Right (To Party!)” from the Beastie Boys, has been named one of the Rock and Roll Hall of Fame’s 500 Songs that Shaped Rock and Roll.1 The 2015 medical equivalent to this seminal hit may be biochemical inflammatory individuality. Heart disease (an inflammatory disease) is still the number one killer of women and men,2 and in 2015 an estimated 1,658,370 new cases of cancer (an inflammatory disease) will be diagnosed in the United States and 589,430 people will die from the disease.3 While we have made positive strides in that we are surviving both heart disease and cancer diseases at a higher rate,2,3 as a population we are sick, and our ability to positively predict and/or prevent these inflammatory diseases is poor.

A New Option, the Individuality Revolution

Biochemical inflammatory individuality is a technology, which is now upon us. In simpler terms, let’s call it a person’s inflammatory fingerprint. At this point, it consists of three things:

  1. Individual genetic methylation and mitochondrial single-nucleotide polymorphisms (SNPs)
  2. Neurotransmitters to look at inflammation, oxidation, and sympathetic tone
  3. Cytokines

Let’s look at an example of how to use our new tool with a simple case. A 50 year-old male with a strong family history of heart disease comes into the office. He is overweight and has hypertension and hyperlipidemia. Two options: (1) control BP and support him with diet, exercise, supplements and medications that are really “good ideas”, (2) run tests to find his inflammatory fingerprint.
In the case of this patient, it was found that he is a poor methylator in both genetic SNP (C667T, rs1801133) and epigenetics with a homocysteine at 18.4 Additionally, a low norepinephrine,5 low IL-10, high TNF-α,6 low serotonin7 and high taurine8 indicate acute and chronic inflammation on a very specific level. All of these factors have been linked to both endothelial dysfunction and myocardial infarction either directly or through a risk factor such as depression.9-13
So with the patient’s individual inflammatory fingerprint in hand, we can consider improving methylation support and including additional supplementation with 5-HTP and tyrosine (to support serotonin and norepinephrine respectively). We can also monitor specific biomarkers (taurine, TNF-α, and to IL-10 in the case) to gauge success or failure of therapy. In our fight for the right for individual treatment, this can be looked at as a victory.
In predicting the future, we just need to look at what has happened in the past. In the 1900s, we largely died from infectious disease, but now in the present, we are passing from inflammatory diseases like cancer, depression and heart disease. We have decreased mortality, but allowed morbidity to flourish. An individual approach to inflammation, from joint pain to cancer may be what is needed to not only save lives, but also protect quality of life. Consider joining the individual biochemical inflammatory fingerprint movement and fighting for your patient’s right to be healthy and happy.


  1. Rock and Roll Hall of Fame and Museum. “Experience The Music: One Hit Wonders and The Songs that Shaped Rock and Roll”. Retrieved March 25, 2014.
  2. Circulation: Special Report Increasing Burden of Cardiovascular Disease Current Knowledge an Future Directions for Research on Risk Factors Charles H. Hennekens, CH. Presented as the Lewis A. Conner Memorial Lecture at the 69th Scientific Sessions of the American Heart Association, New Orleans, La, 1996 Nov. 10.
  3. NCI: reported on the website:, as of 2015 Nov. 3.
  4. Previmedica. Understanding MTHFR genetic mutation Posted on 01/19/2015.  DiLuglio, BE. Posted as of 2015 Nov. 3:
  5. Schlachetzki, JCM. et al.: Function of norepinephrine in neuroinflammation and chronic neurodegenerative diseases: as posted 2015 Nov. 3.
  6. Avdiushko R, et al. J Leukoc Biol. 2001 Oct;70(4):624-32.
  7. Bischoff SC, et al., Am J Physiol Gastrointest Liver Physiol. 2008;296:685-695.
  8. Marcinkiewicz J and Kontny E. Amino Acids. 2014 Jan;46(1):7-20.
  9. Dees C, et al. JEM, 2011:208(5):961-972.
  10. Neuropsychiatr Dis Treat. 2011;7(Suppl 1): 9–13.
    1. Biological Psychiatry. 1999 Feb. 15;45(4):458–463.
    2. Heeschen, C., et al. Serum Level of the Antiinflammatory Cytokine Interleukin-10 Is an Important Prognostic Determinant in Patients with Acute Coronary Syndromes. for the CAPTURE Study Investigators
    3. Ferrari R. Pharmacol Res. 1999 Aug;40(2):97-105. 

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.