What You Should Know About Cancer

When cancer spreads to other areas in the body it is called metastasis and can be the deadliest.  But remember, the original cancer cells are growing in an anaerobic (without oxygen) environment. In order to spread, a cancer cell must first detach from the primary cancer and move through the wall of a blood vessel to get into the bloodstream.

These mobile cancer cells are called circulating tumor cells (CTC’s) or cancer stem cells and look a little like speculated burrs not unlike the burrs you may find on you pant legs after a walk through the meadow, only microscopic.

When CTC’s enter the bloodstream, the circulating blood sweeps them along until they stick somewhere, usually in another opportunistic position that enables it to lodge and multiply.

This can be a complicated journey but as long as the host (the person) has done little to strengthen their immune system’s ability to defend against secondary attacks like this, it is common. Most CTC’s do not survive this journey and there is a simple, yet profound nutritional approach that can help assure they do not. Besides everything the patient should be doing to strengthen their immune response, oxygenate their tissue, alkalize their body, and feed their cells good nutrition, every cancer patient MUST be taking one simple nutrient to help prevent metastasis – Modified Citrus Pectin (MCP).

MCP isn’t even an expensive product and does a wonderful job grabbing these little CTC’s in their claws to escort them out of the body.  Like any approach to cancer, MCP is just one addition to the arsenal that every cancer patient should consider, but like always – correct the cause!

Again, to help prevent metastasis, take 1-3 scoops of MCP per day along with everything you are doing to up-regulate your immune system to help kill these cells.

Here’s another recent article I wrote for my “Doctor’s Only” newsletter:

 

Chronic Biotoxin Load a Precursor for Cancer and… 

Several recent studies confirm that patients with chronic biotoxins are more susceptible to cancer (1)(2). Certain gram-negative bacteria have the ability to alter intracellular communication pathways that disrupts normal function (3). H. pylori, a chronic biotoxin most notably associated with gastric ulcers, gastric, duodenal, and esophageal cancers have been shown to initially increase gastric epithelial apoptosis through a specific pathway (called the TRAIL apoptotic system) increasing stomach cell premature death leading to symptoms associated with ulcers. Later in its progressive cycle it blocks other apoptotic pathways leading to an inability of normal, programmed cell death as well as a disruption of cellular replication phase, hence, cancer.

Another example is Chlamydophila pneumonia, a common etiological agent of respiratory tract infections that can linger for decades as a sub-clinical pathogen linked to lung cancer, arthritis, Alzheimer’s disease, multiple sclerosis, sarcoidosis and erythema nodosum (4).

During chronic, systemic Helicobacter pylori infection, bone marrow-derived-mesenchymal stem cells (BMD-MSCs) have been found to migrate to distant tissue sites causing various carcinomas (5)(6).  Other reports on Propionibacterium acnes (P. acnes, a gram-positive skin infection) suggest that this bacterium is also prevalent in the prostate, is associated with acute and chronic prostatic inflammation, and might have a role in prostate carcinogenesis (7).

Clinically, we saw a 4-year old female previously diagnosed with Ollier disease and left with no hope and a dismal future. Ollier disease is a grossly deforming bone disorder where multiple enchondromas form in epiphyseal plates and intraosseously near growth plate cartilage.

We concluded, after testing, that there existed a biotoxin source to her disease that sparked a TH2 dominant autoimmune attack on the epiphyseal growth plates. Modern medicine may scream ‘foul’ based on the fact that their named disease was first classified as a genetic variant therefore the “once written into a textbook, never shalt thou alter” rule applies (as often is the case), but I really don’t give a hoot!

A quick search of recent studies may support my theory of causation in this case. Schipani and Provot  (7) discovered the relationship between parathyroid-hormone-related peptide (PTHrP), parathyroid hormone (PTH), and the PTH/PTHrP receptor in endochondral bone development in such proliferative diseases. These proteins act as a switch that regulates bone growth and cellular differentiation of chondrocytes, as well as their replacement by bone cells.

Disruption of this mechanism, in this case by a parasitic infiltration, ‘flips the switch’ and creates problems.

In future newsletters, I’ll follow up with this and a plethora of other case studies to help convince you to at least consider biotoxin sources for chronic disorders, but for now…

What you need to consider:

  1. Do not disregard the possibility of chronic infection as a causative agent in your patient’s health picture regardless of revealed negative testing.
  2. Testing for chronic, subclinical infections is inaccurate at best. The doctor would do better to make an informed (through symptomatology) decision if they don’t have access to someone who can test with other measures such as AK. No one reading this remembers, but there existed a time that doctors actually made decisions based on years of experience and wisdom gleaned more from pouring over case studies and consulting with elder peers as opposed to dependency on MRIs and Labs.

Get your hard-copy of Stop Fighting Cancer & Start Treating the Cause to learn more about how to treat cancer with alternative medicine, and for even more in-depth education and help, check out Dr. Conners’ Stop Fighting Cancer COURSE. 

References:

  1. Achenbach CH et al. HIV viremia and incidence of non-Hodgkin lymphoma in patients successfully treated with antiretroviral therapy. Clin Infect Dis 2014 Feb 12;
  2. Indian J Med Paediatr Oncol. 2013 Oct;34(4):323-6. doi: 10.4103/0971-5851.125259. Human immunodeficiency virus Infection in a patient of chronic myelogenous leukemia. Tuljapurkar VB, Phatak UA.
  3. Clin Me. 2002 Mar-Apr;2(2):147-52. Helicobacter pylori: 20 years on. Marshall B
  4. Adv Clin Exp Med. 2014 January-February;23(1):123-126. Infections Caused by Chlamydophila pneumoniae.
  5. Adv Biomed Res. 2014 Jan 9;3:19. doi: 10.4103/2277-9175.124650. Effect of Helicobacter pylori infection on stromal-derived factor-1/CXCR4 axis in bone marrow-derived mesenchymal stem cells.
  6. World J Gastroenterol. 2014 Feb 14;20(6):1485-1492. Helicobacter pylori-related chronic gastritis as a risk factor for colonic neoplasms.
  7. PLoS One. 2014 Feb 28;9(2):e90324. doi: 10.1371/journal.pone.0090324. Intracellular Propionibacterium acnes Infection in Glandular Epithelium and Stromal Macrophages of the Prostate with or without Cancer.
  8. Birth Defects Res C Embryo Today. 2003 Nov;69(4):352-62. PTHrP, PTH, and the PTH/PTHrP receptor in endochondral bone development. Schipani E, Provot S.