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blood-test

What Common Blood Tests Can Detect Early Signs of Cancer

While there is no simple blood test for predicting who will get cancer, there is a lot of information to be gleaned from basic blood work that, taken together, reveals much about an individual’s predispositions for many forms of cancer. By monitoring selected biomarkers routinely measured in primary care, you can learn a lot about physiological patterns that promote carcinogenesis, proliferation, progression, and recurrence long before tumor markers emerge or there are radiological or pathological findings indicating cancer.

The art of assessment lies in part in recognizing the patterns. By learning how to read the multiple biochemical signals that emerge from a pro-carcinogenic “tumor microenvironment,” you can begin to practice real prevention, and give your patients the opportunity for significant improvements in both health-span and lifespan.

The tests included in this article here are ones you are routinely ordering in the integrative and functional medicine setting. While they are not to be misconstrued as diagnostic tests for cancer, they can indicate that a patient is at increased risk, and that further assessment and action is required to identify potential malignancy.

In people who’ve had cancer, these common tests are often prognostic for disease progression and recurrence.

It is vital that primary care practitioners do a better job of recognizing the early signs of recurrence among cancer survivors. According to the American Cancer Society’s 2016-2017 Survivorship Facts and Figures, the population of cancer survivors will increase to 20.3 million by January 1, 2026.

After conventional oncology treatment is finished, these patients typically return to their primary care physicians. They are highly motivated, ripe for change, and in search of clinicians who can support their efforts to restore health and prevent recurrence.

The tests described below will help you fill that role.

Complete Blood Count

One of the most common biomarkers of overall health is the Complete Blood Cell panel, which can be used to monitor hematologic abnormalities caused by solid tumors, hematologic malignancies, as well as the side-effects of the therapies used to treat them.

The following findings are not definitive diagnostic signals, but taken together, they suggest that someone is at greatly increased risk:

  • Elevated White Blood Cells > 11.0 109/L
  • Elevated Platelets > 350 109/L
  • Low Hemoglobin <10.0 g/dL
  • High Neutrophil to Lymphocyte Ratio (NLR)

The latter finding—a high NLR—is especially important.

Neutrophils promote cancer progression, proliferation, and metastasis by increasing vascular endothelial growth factor (VEGF), Hepatocyte growth factors, inflammatory cytokines IL-6, IL-8, matrix metalloproteinases (MMP), and elastase. Neutrophils and macrophages secrete tumor growth promoting factors and contribute to a proliferative tumor microenvironment.

Therefore a high neutrophil count is suggestive of a neoplastic process somewhere in the body.

According to a 2014 metanalysis of 57 studies, an NLR greater than 4.0 was associated with a hazard ratio for overall survival (OS) of 1.81 (95% CI = 1.67 to 1.97; P < .001), an effect observed in all disease subgroups, sites, and stages and that predicts increased risk of mortality (Templeton AJ, et al. JNCI. 2014:106(6).)

Simply put, an NLR over 4 predicts tumor progression and poor overall survival. This is a readily available and inexpensive biomarker with a lot of prognostic value.

Hyperglycemia

A fasting glucose in the range of 100-126 mg/dl is suggestive of cancer risk.

Glucose may have a direct role in cancer development. Tumor cells have increased numbers of receptors for insulin, insulin-like growth factor, and GLUT4. Thus, they transport more glucose into themselves, and this promotes growth and proliferation. It is the main reason for using a low-glycemic, modified ketogenic diet in patients with cancer.

Proliferating tumor cells have up- regulated glucose transporters. Elevated serum glucose is linked to increased risk and progression of many solid cancers, including breast cancer (Haseen SD, et al. Asian Pac J Cancer Prev, 2015:  16, 675-8).

High glucose levels also result in a state of chronic inflammation, which leads to an increase of cytokines, such as interleukin 6 (IL-6), tissue necrosis factor alpha (TNF-α) and vascular endothelial growth factor (VEGF). All of these promote cancer progression, proliferation, and metastasis (Crawley DJ, et al. BMC Cancer, 14(1), 985).

Given the high prevalence of diabetes, metabolic syndrome, and insulin resistance in the US, this is an important indicator to watch.

Serum glucose is a modifiable risk factor. Diet and lifestyle changes that reduce and regulate glucose will also help to reduce risk and progression of cancer.

High Insulin & Low SHBG 

Prolonged hyperinsulinemia leads to reduced hepatic production of sex hormone binding globulin (SHBG). This, in turn, increases risk of steroid hormone driven cancers. Low SHBG results in increased amounts of unbound estrogens and androgens that drive carcinogenesis in breast, endometrial, prostate lung, colorectal and pancreatic tissues.

Free unbound estrogen also exerts immunosuppressive effects in the tumor microenvironment, and has a profound impact on anti-tumor immunity and tumor-promoting inflammation that is completely independent from its direct activity on tumor cells (Svoronos N, et al. Cancer Discovery, 2017: 7(1), 72-85).

Low Serum Albumin

Serum albumin levels have prognostic significance in cancer, and can be used to better define baseline risk in cancer patients. It is generally useful in assessing the nutritional status, disease severity, disease progression, and prognosis.

In a multivariate analysis of 29 studies, Gupta and Lis found, “higher serum albumin levels to be associated with better survival.” (Gupta D, Lis CG. Nutrition Journal, 2010: 9(1), 69).

In the early stages of cancer, there is slight or no hypoalbuminemia. But as the disease progresses, malnutrition and inflammation suppress albumin synthesis, and albumin levels drop significantly.

Albumin levels under 3.5 g/dL are often seen in patients with sarcopenia and cachexia. Malnutrition is a predictor of reduced survival. It is also associated with deteriorating quality of life, decreased response to treatment, increased risk of chemotherapy-induced toxicity, and a reduction in cancer survival.

On the high side, albumin concentrations above 37.5 g/L are predictive of both chemotoxicity and of survival (Srdic D, et al. Supportive Care in Cancer, 2016: 24(11), 4495-4502).

It is also important to look at the Albumin-to-Globulin Ratio.

A ratio of less than 1.66 is a risk factor for cancer incidence and mortality, both short- and long term, in generally healthy screened adults. In people who’ve already developed some form of cancer, a low albumin-to-globulin ratio predicts low overall survival (Suh B, et al. Ann Ocol (2014): 25(11), 2260-2266).

Elevated Ferritin

Ferritin, a strong negative survival predictor, has been associated with the pathological processes of inflammation and infection. High ferritin is suggestive of inflammation, immunosuppression, tumor angiogenesis, and proliferation.

Elevated serum ferritin—indicated by levels over 200 ng/ml in men, and over 150 ng/ml in women–have been seen in people with breast cancer, pancreatic cancer, non-small cell lung cancer, hepatocellular carcinoma, leukemia, colorectal cancer and lymphoma.

High ferritin levels are significantly associated with reduced survival time and increased mortality in cancer patients (Lee S, et al. J Cancer, 2016: 7(8), 957-964)

25-OH Vitamin D Deficiency

Vitamin D has a multi-functional impact on the tumor microenvironment. Increased levels of Vitamin D are associated with reduced occurrence and reduced mortality of different types of cancer, including skin, prostate, breast, colon, ovary, kidney, and bladder.

Vitamin D is involved in a very wide range of physiological processes relevant to cancer development, including: Regulation of Gene Transcription; Growth Arrest; Apoptosis; Cellular Differentiation; DNA Repair; Antioxidant Protection; Immune Modulation; Regulation of Pro-Inflammatory Cytokines; and Control of Angiogenesis & Metastasis.

Low or suboptimal levels of 25-OH Vitamin D are associated not only with increased risk of various forms of cancer, but also with poor prognosis, and more aggressive disease (McDonnell SL, et al. PloS One, 2016: 11(4), e0152441).

This is particularly true in breast cancer. In one study, vitamin D-deficient women with breast cancer typically had more aggressive molecular phenotypes and worse prognostic indicators than those with adequate vitamin D (Williams JD, et al. Endocrinology, 2016: 157(4), 1341-1347).

The Vitamin D Council suggests repletion to 40 to 80 ng/mL, with a target of 50 ng/ml, for optimal health on multiple fronts, including colorectal cancer prevention (Bischoff-Ferrari HA, et al. Am J Clin Nutr, 2006: 84(1), 18-28).

Supplementation to reach mean serum concentrations of 72 nmol/L showed a beneficial effect  against cancer development (Lappe JM, et al. Am J Clin Nutr. 2007: 85(6), 1586-1591).

When assessing patients in the context of cancer risk, the following guidelines are useful:

25 –hydroxy- Vitamin D (ng/ml)

Deficient                                                        < 50

Optimal                                                           50-70

Optimal for Cancer & CVD                70-99

Excess                                                            >100

Elevated Lactic Acid Dehydrogenase

Lactate dehydrogenase (LDH) is an enzyme that catalyzes the reduction of pyruvate to lactate.

Aberrant metabolism and inefficient fuel production is a characteristic of tumor cells, which are dominated by aerobic glycolysis, increased lactate production, and a higher uptake of glucose (the Warburg effect).

Elevated LDH may be a marker of these aberrant metabolic processes in cancer cells.

The normal range for LDH is thought to be 100-333 u/L, with levels greater than 245 u/L considered to be in the upper quartile of normal. Above that 245 u/L mark, it is suggestive of early carcinogenesis, tumor cell proliferation, tumor progression, and poor prognosis.

It is often highly elevated in aggressive forms of cancer and hematological malignancies including: melanoma, lymphoma, acute leukemia, seminoma germ cell, pancreatic, gastric, lung, renal cell, nasopharyngeal, esophageal, cervical, and prostate cancers (Wulaningsih W, et al. Br J Cancer. 2015:113(9). Zhang J, et al. Sci Rep. 2015:5, 9800).

Elevated C-Reactive Protein

C-Reactive Protein (CRP) is a well-established inflammatory marker. It is also a biomarker of cancer survival.

CRP is elevated in patients with solid tumors, and high levels predict poor prognosis, blunted treatment response, as well as tumor recurrence.

As part of the systemic inflammatory response to a tumor, the body releases pro-inflammatory cytokines and growth factors. Interleukin-6, produced by the tumor or surrounding cells, stimulates liver production of acute-phase reaction proteins that increase C-reactive protein (CRP) and fibrinogen.

Elevated CRP correlates with disease stage and increased cancer mortality (Shrotriya S, et al. PloS One. 2015: 10(12), e0143080). Individuals with a high baseline CRP (>3 mg/L) have an 80% greater risk of early death compared with those with low CRP levels (<1 mg/L).  

Patients with invasive breast cancer and CRP levels>3 mg/L at diagnosis have a 1.7 fold increased risk of death compared to those with CRP levels<1 mg/L at diagnosis (Allin KH, et al. Breast Cancer Res. 2011: 13(3), R55).

Converging Signals

No one of the aforementioned test parameters is, in and of itself, an indicator that someone has cancer. But by looking at standard blood test results in a new way, you can start to recognize the patterns of high risk and active cancer physiology. This is crucial to early identification and early intervention.

Clinicians who are aware of the converging signs can meaningfully shift the microenvironment from one that promotes cancer to one that is not supportive of carcinogenesis, proliferation, or progression. In the same way, we can provide meaningful support for the rising tide of underserved cancer survivors and at-risk patients in need of not only a disease plan, but also a health plan.

Prostate-Cancer-Control

Boron and Prostate Cancer Control

Aside from non-melanoma skin cancer, prostate cancer is the most common cancer among men in the United States. It is also one of the leading causes of cancer death among men of all races and Hispanic origin populations.(1)

Dietary Boron intake is inversely correlated with prostate cancer incidence. (5)

Prostate risk is  52% lower in men whose diets contain at least 1.8mg boron daily. Prostate cancer risk reduction is correlated with boron intake.  Recommended optimal daily dose of elemental boron is 3 mg/day for health maintenance.

Mechanisms of Action

Boron-containing compounds interfere with the physiology and reproduction of cancer cells through diverse mechanisms, including inhibition of serine proteases, NAD-dehydrogenases, mRNA splicing and cell division, receptor binding mimicry, and induction of apoptosis. (2) 

normal-prostate

In several studies Barranco et al (7, 8, 9, 10) demonstrate that increased boron intake is associated with lower levels of Prostate Specific Antigen (a biomarker for prostatitis and prostate cancer) as well as modulation of serum estradiol leading to increased expression of ER-beta receptors and decrease of ER-alpha receptors on tumor cells decreasing proliferation and growth signaling.  Furthermore boron supplementation increased regulation of cell cycle arrest, increased apoptosis, decreased cell adhesion, migration and metastatic progression. 

Boron decreases cancer associated inflammatory factors including hs CRP, TNFa, Interleukin-6 all of which are elevated in the tumor microenvironment.   “Elevated hs-CRP is associated with an increased risk for breast cancer, obesity and metabolic syndrome (MetS) in children, atherosclerosis, unstable angina, insulin resistance, type 2 diabetes, nonalcoholic fatty liver disease (NAFLD), metastatic prostate cancer, lung cancer, adult depression, depression in childhood and psychosis in young adult life, coronary heart disease, and stroke." (2)

In  murine study Insulin Like Growth Factor was significantly reduced in the prostate tumor cells in boron dosed animals. The IGF-1 signaling pathway promotes cancer progression and its down regulation is associated with lower risk of prostate cancer. (6)

“Increased intracellular concentration of borate activates borate transporters and leads to growth inhibition and increased apoptosis. “ (2) (3) (11)

Boron may act as a Histone De-acetylase Inhibitor (HDI).  HDI’s act as therapeutic agents for cancer due to their impact on gene expression on growth arrest signaling, cell differentiation and apoptosis in cancer cells. (2)

Boronic Acid has been shown to inhibit hypoxia inducible factor (HIF) which is a physiological stimulus for tumor induced angiogenesis.  Inhibition of HIF leads to inhibition of Vascular Endothelial Growth Factor (VEGF) and the production of capillary blood supply to tumor cells. Angiogenesis leads to exponential tumor growth and to metastatic progression of solid tumors. (11)

Plant foods rich in boron include Avocados, dried apricots, dried prunes, raisins, red kidney beans, lentils, almonds, hazelnuts, brazil nuts, pistachios, cashews and walnuts.

In summary, dietary and supplemental oral boron intake should be optimized to create a tumor microenvironment and cancer terrain that decreases risk of prostate carcinogenesis,proliferation and disease progression through angiogenesis and metastasis. 

 

Selected References

1. American Cancer Society Statistics https://cancerstatisticscenter.cancer.org/

2. Scorei RI, Popa R Jr. Boron-containing compounds as preventive and chemotherapeutic agents for cancer. Anticancer Agents Med Chem. 2010 May;10(4):346-51. doi: 10.2174/187152010791162289. PMID: 19912103.

3. Romulus Ion Scorei and Radu Popa, Sugar-Borate Esters –Potential Chemical Agents in Prostate Cancer Chemoprevention  DOI: 10.2174/18715206113139990124 Volume 13, Issue 6, 2013 Page: [901 - 909]

4. Kiliccioglu I, Konac E, Varol N, Gurocak S, Yucel Bilen C. Apoptotic effects of proteasome and histone deacetylase inhibitors in prostate cancer cell lines. Genet Mol Res. 2014 May 9;13(2):3721-31. doi: 10.4238/2014.May.9.17. PMID: 24854658.

5. Cui Y, Winton MI, Zhang ZF, et al. Dietary boron intake and prostate cancer risk. Oncol Rep. 2004;11(4):887-892.

6. Pizzorno, L.  Review: Nothing boring about boron. Integrative Medicine Vol. 14, No. 4 August 2015

7. Barranco WT, Hudak PF, Eckhert CD. Evaluation of ecological and in vitro

effects of boron on prostate cancer risk (United States). Cancer Causes Control. 2007;18(1):71-77.

8. Barranco WT, Eckhert CD. Boric acid inhibits human prostate cancer cell proliferation. Cancer Lett. 2004;216(1):21-29.

9. Barranco WT, Eckhert CD. Cellular changes in boric acid-treated DU-145 prostate cancer cells. Br J Cancer. 2006;94(6):884-890.

10. Barranco WT, Kim DH, Stella SL Jr, Eckhert CD. Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. Cell Biol Toxicol. 2009;25(4):309-320.

11. Shimizu K, Maruyama M, Yasui Y, Minegishi H, Ban HS, Nakamura H. Boron-containing phenoxyacetanilide derivatives as hypoxia-inducible factor (HIF)-1alpha inhibitors. Bioorg Med Chem Lett. 2010;20(4):1453-1456.

OutSmart-Cancer-Immuno-Therapy

Modulating Extreme Adverse Effects of Immunotherapy Treatments

Today, more and more patients are avoiding toxic chemotherapy in favor of targeted cancer therapies.  Among the many new therapies available are a class of immunotherapy drugs that take the brakes off of the immune system and mobilize T cells against tumor cells.

Because tumor cells have the capacity to disable T cells, this therapy addresses the huge problem of immune resistance in many cancers.  Drugs in the class of PD1 and PDL1 inhibitors were some of the first to be developed.  These drugs bind to PD1 or PDL1 receptors on the tumor surface and unleash the fury of the immune system upon the tumors by removing the inhibitory function of these ligands.

Nature has designed the immune system with both a gas pedal and a brake.  The PD1 and PDL1 inhibitors are the brakes.  Take off the brakes and the immune system is activated.

The best of outcomes with these treatments may result in complete tumor eradication, a truly miraculous outcome for some patients.  I have a patient who came to me with Stage 4 Endometrial Cancer with Lung Metastases some years ago.  After reduction of some of her tumor burden with surgery and rather brutal chemotherapy, her very forward-thinking Gynecologic Oncologist included a course of Keytruda (Pembrolizumab), which was a new immunotherapy treatment at the time. 

The historical prognosis for this patient would have been certain eventual mortality for her metastasized aggressive cancer.  However, she achieved a complete response and has been in remission and designated NED or No Evidence of Disease for many years now.   This is a patient who most likely would not be alive today without the advent of PD1 -PDL-1 inhibitor therapy.

The problem with this class of drugs is that their use is very unskillful and very unpredictable. Some patients will respond with a modicum of mild to moderate systemic autoimmune inflammation while other patients will be disabled by furious, extreme, and damaging autoimmune syndromes.  Some patients may die from extreme autoimmune activity.  I had one patient who developed myocarditis and died within a few days of receiving his first dose.  This was a prostate cancer patient whose sudden death was completely unexpected and not predicted.   

These patients require a health model and safe, effective modulation of extreme auto-immune inflammation not provided by their oncology teams. 

Some patients will have immune activation similar to a nice warm burning ember.  They get the therapeutic benefit without extreme adverse effects.  While other patients will respond with a forest fire of inflammation that must be suppressed aggressively with steroid medications for long periods of time.  The adverse effects of long-term steroid therapy then become part of the clinical picture and challenge for these patients.  In these circumstances, it IS reasonable to ask if the cure is worse than the disease itself? 

My patient developed such severe colitis (a common adverse effect) that she visited the emergency room multiple times for fluid and electrolyte replacement due to extreme persistent watery diarrhea.  Additionally, the nutritional status of this patient was also compromised and she became depleted in both calories and nutrients and developed sarcopenia.

Many cancer patients receiving PD1 and PDL 1 inhibitors are left with lifelong autoimmune disease.   Most common are autoimmune arthritis, colitis, thyroiditis, dermatitis, pneumonitis, and associated loss of normal tissue and organ function.  Some patients suffer ongoing chronic inflammatory pain syndromes.

Less prevalent, but also part of the long list of adverse effects are myocarditis, pericarditis, nephritis, hepatitis, pancreatitis, neuritis, vasculitis. Essentially, any tissue or organ can be impacted with associated loss of function and sequelae.

It is my practice to screen and monitor patients receiving cancer immunotherapies for the development of autoimmune syndromes and intervene early.  If I have a patient with a history of inflammatory or autoimmune disorders I can predict that such patients are more likely to develop adverse effects. 

Additionally, high levels of inflammation not only lead to pain syndromes but are also contributors to ongoing chronic fatigue as well as agitation,  cognitive changes, sleep disruption, anxiety, and depression, and the stress of living not only as a cancer survivor but with a chronic and distressing autoimmune syndrome difficult to control and manage.  It is my firm goal that Quality of Life must be a goal in all treatment plans for cancer patients and survivors.

 If a patient has NO inflammatory adverse effects it is assumed that the patient is not going to benefit from the PD1/PDL1 inhibitor because there is no sign or symptom indicating immune activation.   I always tell patients we should celebrate if they develop a rash or diarrhea because we know the drug is working!   

In fact, it is my observation over many years of following patients who have received these therapies that when the course of immunotherapy treatment is completed those patients who continue to have low levels of inflammation continue to have the therapeutic benefit of tumor control.  This is only an empirical observation on my part.  For example, the endometrial cancer patient described above continues to have mild colitis and has remained in remission.  Before the availability of these therapies, we would expect this patient to have a recurrence and to die of her advanced stage 4 metastatic disease within a few years of her diagnosis.   Patients such as this with lung metastases historically had very poor prognoses and very high mortality rates.  Patients with powerful and manageable responses to PD1 and PDL1 inhibitors may live a long time.  While some patients do recur, some have not.  We have not had decades of time to follow these patients as these treatments are relatively new.  If nothing else, these treatments do extend the life of many patients.

How can we modulate the auto-immune adverse effects of these potentially curative immunotherapy treatments?   I have taken the approach that we employ in Functional and Naturopathic Medicine in the management of auto-immune syndromes to turn down the volume on the immune inflammation just enough to reduce extreme side effects, damage, and loss of function without losing the therapeutic benefit of these immunotherapy treatments.   

While we can rely on studies that have demonstrated that Omega 3 Fatty Acids, Vitamin D3, and Curcumin and a healthy microbiome can modulate auto-immune inflammation, there is a paucity of research on managing autoimmune syndromes related to immunotherapy adverse effects with the exception of steroids. (See selected references below.)

I share with you here my empirical clinical experience.  I have employed this approach with several hundred patients since immunotherapies have come into wider use in oncology.  Clinicians experienced in managing autoimmune syndromes will recognize the basic principles of care.

  • Anti-Inflammatory, Low Antigen Diet
  • Support for the healthy intestinal microbiome 
  • Specific Nutriceutical-Phytochemical Interventions
    • Omega 3 Fatty Acids (EPA DHA)  recommended dose 4-6 grams daily SPMs Specialized ProResolving Mediators can also be considered 1-2grams daily
    • Fat soluble Curcumin recommended dose 2-6 grams daily
    • Vitamin D3 5,000-25,000iu daily  (125mcg-625mcg). 
      • Consider a loading dose of 50,000iu (1.25mg)

I always start at the lower end of the dose range and spread the dosing out into 3-4 doses over the day.  The goal is to MODULATE but not SUPPRESS the therapeutic impact.  It is also important to be mindful of the anticoagulant/platelet aggregation inhibitory effect of such an approach and to determine which patients may NOT be a candidate for high dosing due to thrombocytopenia or anticoagulant pharmaceutical therapies.

This approach has few negative drug-nutrient interactions. I have continued these inflammation-modulating therapies continuously for many years with most patients.  Dosing is highly individualized to each patient towards the goal of supporting and promoting healthy function and quality of life.

For front-line clinicians interested in supporting the health of cancer patients and cancer survivors and learning and implementing my OutSmart Cancer® System developed over 35 years in practice, I encourage you to join our training program, Foundations of Integrative Oncology, self-paced online training with clinical supervision and mentoring.  Go to aiiore.com.  

There is a huge population of patients whose lives have been touched by cancer searching for a health model and skilled and knowledgeable clinicians.

Selected References:

Vitamin D and autoimmune diseases.
Illescas-Montes R, Melguizo-Rodríguez L, et al Life Sci. 2019 Sep 15;233:116744. doi: 10.1016/j.lfs.2019.116744. Epub 2019 Aug 8. PMID: 31401314 

Vitamin D intake is associated with decreased risk of immune checkpoint inhibitor-induced colitis.
Grover S, Dougan M, et al Cancer. 2020 Aug 15;126(16):3758-3767. doi: 10.1002/cncr.32966. Epub 2020 Jun 22. PMID: 32567084

Therapeutic Potential of omega-3 Polyunsaturated Fatty Acids in Human Autoimmune Diseases.
Li X, Bi X, Wang S, Zhang Z, Li F, Zhao AZ.
Front Immunol. 2019 Sep 27;10:2241. doi: 10.3389/fimmu.2019.02241. eCollection 2019.  PMID: 31611873 

Resolvins: Emerging Players in Autoimmune and Inflammatory Diseases.
Abdolmaleki F, Kovanen PT, et al 
Clin Rev Allergy Immunol. 2020 Feb;58(1):82-91. doi: 10.1007/s12016-019-08754-9. PMID: 31267470 

Curcumin in Autoimmune and Rheumatic Diseases.
Yang M, Akbar U, Mohan C.
Nutrients. 2019 May 2;11(5):1004. doi: 10.3390/nu11051004.
PMID: 31052496 

Curcumin and autoimmune disease.
Bright JJ.
Adv Exp Med Biol. 2007;595:425-51. doi: 10.1007/978-0-387-46401-5_19. PMID: 17569223  

Curcumin as an Adjuvant to Cancer Immunotherapy.
Paul S, Sa G.
Front Oncol. 2021 Aug 16;11:675923. doi: 10.3389/fonc.2021.675923. eCollection 2021.
PMID: 34485117 

Gut Bacteria Influence Effectiveness of a Type of Immunotherapy. https://www.cancer.gov/news-events/cancer-currents-blog/2018/gut-bacteria-checkpoint-inhibitors. Feb 2018  NCI Staff

brain-cancer

Brain Cancer: Resolving Cancer Related Cognitive Impairment

Did you know that 45% of all cancer patients self-report a decline in cognitive function after completing chemotherapy?

Brain Cancer-related cognitive impairment is attributed to both cancer as well as treatment-related changes in cytokine profiles, blood brain barrier permeability, genetic susceptibility, hormonal factors and mitochondrial dysfunction.

Both the disease itself and the treatments, can impact attention, memory and executive functions, as well, as brain structure and anatomy.

As many as 20% of all patients report continued persistent changes in cognitive function as many as 10-20 years after completing successful treatment.

Eight Nutraceuticals and Phytochemicals that Promote Neuron Repair and Support Restoration of the Blood Brain Barrier and Cognitive Function

 

Brain Cancer


1. Melatonin (10-20mg hs) -
Maintains Blood Brain Barrier Integrity and Permeability

  • Inhibits Matrix Metalloproteinase-9 (MMP-9)
  • Inhibits NADPH oxidase-2
  • Activates SIRT1 Silent Information Regulator 1
  • Activates AMP Activated Protein Kinase (AMPK)

2. Astragalus (1-6g/day) - Decreases Blood Brain Barrier Permeability

  • Inhibition of MMP-9 Neuro-Immuno-regulation
  • Control of Oxidative Stress
  • Control of Neuro-inflammation
  • Regulation of Neuro-apoptosis
  • Inhibition of p53 Modulation of the Bcl-2/Bax

3. Resveratrol (1000mg bid x 52 weeks) - Regulates Neuro-Inflammation

  • Decreases CSF MMP9
  • Modulates neuro-inflammation
  • Induces adaptive immunity
  • Activates SIRT1

4. Pterobstilbene (50-100mg/d) - Attenuates Learning and Memory Impairment

  • Inhibitory effect on microglia activation
  • Protective effect on neuronal injury
  • Decreases production of NO, TNF-α and IL-6 in microglial cells
  • More lipophilic than Resveratrol

5. Unique Probiotic Blend (KLAIRE Target gb-X 1 packet/day) - Targets Gut-Brain Axis

  • Strengthening of the gut barrier function
  • Modulation of cytokines and inflammatory response
  • Production of potentially neuroprotective metabolites
  • Shift away from macrophage-produced cytokines to T-lymphocyte-produced cytokines
  • Reduction in circulating lipopolysaccharide endotoxins
  • Marked reduction in transcription of hippocampal genes related to HPA regulation

6. Curcumin (3-6g/day) - Improves Cognitive Function

  • Crosses Blood Brain Barrier
  • Supports Axonal Regeneration
  • Increases Brain Derived Neurotrophic Factor
  • Reduces NeuroInflammation linked to mood dysregulation and cognitive function
  • Stimulates Clearance of beta amyloid plaques

7. Omega-3 Fatty Acids (1.8g/d) - Protects Neurons From Toxic Effects of Chemotherapy

  • Opposing actions of omega-3 fatty acids and added sugars on cognitive function, neuroinflammation, and adult hippocampal neurogenesis
  • A diet rich in long-chain, marine-derived omega-3 fatty acids and low in added sugars may be an ideal pattern for preventing or alleviating neuroinflammation and oxidative stress

8. Lion's Mane Mushroom (3-5g/d) - Enhances Cognition

  • Strengthens Memory and Concentration
  • Stimulates the synthesis of Nerve Growth Factor Promotes and Accelerate Myelination
  • Immune Modulation
cancer-patient

VITAL TALK: Learn to Communicate Effectively with Patients Experiencing Serious Illness

“Just as no doctor is born knowing how to handle a scalpel, the same is true for how to communicate effectively with seriously ill patients and their families. We believe every clinician can become a better communicator.”

dr-tony

I met oncologist Dr. Tony Back, MD at a meditation retreat focused on working skillfully and mindfully with patients with serious, life changing illnesses as well as end of life care.  Dr. Back is affiliated with the Center to Advance Palliative Care at Fred Hutchinson Cancer Center in Seattle, Washington and has combined his years of clinical oncology experience with his recognition that patients and clinicians require more skillful and effective conversations in the midst of emotionally charged and medically complex discussions. Dr. Back has developed online and in person trainings called Vital Talk for clinicians to LEARN TO COMMUNICATE EFFECTIVELY WITH PATIENTS EXPERIENCING SERIOUS ILLNESS. His mission is “To Elevate Patient Care with better communication”.

Dr. Back and the Vital Talk mission is “that every seriously ill patient will be surrounded by clinicians who can speak about what matters most and match care to values.”

Vital Talk Trainings help clinicians to Master Tough Conversations

Whether in person or online, clinicians feel safe practicing newly learned skills through VitalTalk’s evidence-based training methodologies.

Some tips from a Vital Talk trained physician

Dr. Nalini

  • Give yourself grace
  • Lean in with emotion, heart and feeling
  • Respond with empathy.  
  • Explore and ask the patient to tell you more.  
  • Ask permission to talk about a topic (scan results, disease progression, end of life care)

[READ MORE]

EVIDENCE-BASED SKILLS Vital Talk TRAINING COURSES 

  • Elevate patient care with better communication
  • Explore best-practice communication methodologies and tools, as well as our rich community of support to better serve the needs of patients with serious illness and their families.
  • Support clinicians in learning to communicate effectively and compassionately with patients living with serious illness. 

We are living in the midst of an aging patient population in the United States. Therefore our patients are increasingly at risk of developing more serious illnesses, experiencing co-morbidities and facing many life changes of loss and limitation, frailty and mortality.   Cancer patients of all ages face immense challenges and must redefine their sense of self and examine their values and relationship to life, suffering, death and dying. These challenges may be turned into gateways to transformation.  I counsel my patients to reframe their cancer journey so that the challenges that they face become opportunities for growth, insight and wisdom and not just suffering, grief and loss.   These conversations require clinicians to develop greater communications skills and the ability to be comfortable engaging in these dialogues.

It is my experience that clinicians who are inspired to work with cancer patients are motivated by the drive towards making a difference, the intellectual challenge of the complexity of cancer and the deep meaning that arises in meeting patients at the edge where  the rawness and overwhelm of being a cancer patient can be transformed into a profound healing journey of awareness and transformation.   

I highly recommend that all clinicians continue to develop their clinical skills so that they can be fully present, capable and comfortable for participating in these most tender, human and meaningful conversations.   

I always feel it is a privilege and an honor to be allowed to accompany a patient and their family on their journey and to be able to guide them into deeper meaning and a greater sense of connection to each other and to all of life.

I encourage you to explore The Vital Talk website where you will find information on their programs and trainings but also Free Downloadable Tools and Guides to get you started

https://www.chooseyourpath.vitaltalk.org/

https://www.vitaltalk.org/resources/

Please do share your stories with us!!  

Cancer-SARS

Inflammation, Cancer and SARS-CoV2

Managing Inflammation and Inflammasome in both the Cancer Terrain and SARS-Cov2

There is a subset of cancer patients who suffer significantly more inflammation as well as the sequela of increased inflammation including ongoing cancer related fatigue, increased pain, cognitive deficits.   Similarly there is a subset of COVID-19 patients who suffer a cytokine storm and the wildfire of inflammation that leads to respiratory distress syndrome and mortality. Identifying patients with a higher risk of increased inflammation can be assessed by taking a thorough history in search of historical tendencies and patterns and an analysis of single nucleotide polymorphisms (SNPs).  Patients with IL1B, IL6 and NFkB  SNPs are more prone to developing greater inflammation in both syndromes.

inflammationThe inflammatory drivers and cytokines are similar in both cases: NFkB, TNFa, IL1, IL6, IL8, Inflammasone NLRP3, TGFb1, STAT3, JAK2, p38MAPK, Nrf2, AMPK

Activation of Inflammasome NLRP3 is correlated with the development of the SARS CoV2 cytokine storm.  Inflammasome activation is an important component of innate immunity which enhances inflammation.  Inflammasome activity is correlated with destructive inflammation particularly in viral diseases.  Inflammsome NLRP3  increases IL-1B is also  upregulated in the cancer terrain, particularly in metastatic lung cancer, breast cancer, fibrosarcoma and gastric carcinoma.

curcuminCurcumin exhibits anti-inflammatory and anti-inflammasome properties and can be used in both syndromes.  Curcumin impacts all of the above named inflammatory drivers along with inhibition of COX2 transcription.    Furthermore curcumin acts as an antioxidant increasing control of reactive oxygen species present with increased inflammation.

I recommend Designs for Health Curcumevail, Thorne Research Meriva and Euromedica Curapro.  In managing both the cancer terrain and the SARS CoV2 terrain the dose range is 2g-6g curcuminoids per day.

Another actor, Nrf2, is a nuclear transcription factor that increases the presence of antioxidant proteins when cells are stressed.   Management of the cancer terrain also includes support for normal function of Nrf2.  Nrf2 is highly expressed in the lungs and is responsible for inhibiting the activity of Inflammasome NLRP3.  Sulforaphanes include Di-indole methane, Indole-3-Carbinol and  Sulforaphane glucosinolate.  Broccoli, broccoli sprouts and kale are dietary sources of sulforaphanes.  

antioxidant

I recommend Designs for Health Broccoprotect and Thorne Research Crucera for a high quality source of sulforaphane glucosinolate 50mg twice daily.

Ultimately we may find that the core foundation and targeted supplements used in the OutSmart Cancer System for managing the cancer terrain ALSO protect our patients in the midst of a viral pandemic.

Selected References 

Rajendra Karki et al Inflammasomes and Cancer                                                                                                             PMID: 28093447 DOI: 10.1158/2326-6066.CIR-16-0269

Saeedi‐Boroujeni  et al COVID‐19: A Case for Inhibiting NLRP3 Inflammasome, Suppression of Inflammation with Curcumin?  Ali  https://doi.org/10.1111/bcpt.13503 Volume128, Issue1 January 2021 Pages 37-45

Howrylak JA, Nakahira K. 

Inflammasomes: Key Mediators of Lung Immunity. 

Annu Rev Physiol. 2017;79:471‐494. doi:10.1146/annurev-physiol-021115-105229

James W.Pinkertona1Richard Y.Kima1Avril A.B.RobertsonbJeremy A.HirotacLisa G.WoodaDarryl A.KnightaMatthew A.CooperbLuke A.J.O’NeilldJay C.Horvata1Philip M.Hansbroa  Inflammasomes in the Lung

Molecular Immunology Volume 86, June 2017, Pages 44-55         

Shih-Yi Chuang,1,2 Chih-Hung Lin,3,4 and Jia-You Fang

Natural Compounds and Aging: Between Autophagy and Inflammasome

Biomed Research Int. Volume 2014 |Article ID 297293 | 10 pages | https://doi.org/10.1155/2014/297293                                                    

József Tőzsér1 and Szilvia Benkő

Natural Compounds as Regulators of NLRP3 Inflammasome-Mediated IL-1β Production

Mediators of Inflammation Volume 2016 |Article ID 5460302 | 16 pages                                               https://doi.org/10.1155/2016/5460302

turmeric

Tumeric Prevents Chemotherapy Induced Hand Foot Syndrome

Xeloda (Capecitabine) is the oral form of  chemotherapy agent 5-Fluorouracil  (5-FU) which is administered intravenously. 

Both drugs are widely used in a broad range of cancers. The mechanism of action is inhibition of mitosis (cell division).   

One of the most common side effects of these drugs is HAND-FOOT SYNDROME or palmar-plantar erythrodysesthesia.  Hand-Foot syndrome presents with redness, swelling and pain, tingling, burning and sensitivity to touch on the palms of the hands and the soles of the feet. Severe cases may include cracked, flaking or peeling skin, painful blisters, ulcers or sores, severe pain and difficulty walking or using the hands.

While etiology is not certain it is hypothesized that these drugs cause capillary fragility and subsequent leakage of drugs into and damage of  the surrounding tissue.

fhs

Other commonly used chemotherapy agents  which result in Hand - Foot syndrome include 5-Fluorouracil, Capecitabine, Cytarabine, Docetaxel, Doxorubicin, Doxil and Paclitaxel. These drugs are widely used in Breast, Ovarian and Gastrointestinal Cancers.  

Not all patients who receive these drugs develop Hand-Foot Syndrome. The symptoms typically appear with the first dose administration in 40-50 percent of patients at grade 2 or higher.

turmeric-as-cure

Grade 1: painless erythema or dysesthesia, no impairment

Grade 2: painful erythema, swelling, tingling, numbness, dryness, cracking, Desquamation, activity is impaired

Grade 3: strong pain, ulceration, blistering, erythema, limited self-sufficiency

For drugs administered via IV infusion, cold (Ice) gloves and booties that constrict capillaries reduce local exposures in the hands and feet and must be worn during infusions and for several therapy to hands and feet concurrently with chemotherapy infusions. 

Capcetabine increases COX-2 expression in both tumors and healthy tissues.

A double blind placebo controlled study in which oral COX2 inhibitor celecoxib was administered to patients over a 2 year period while receiving capecitabine or capecitabine plus oxaliplatin demonstrated a significant decrease in the incidence and intensity of symptoms.

The phytochemical curcumin derived from Rhizoma Curcuma longa interacts with over 100 genes that impact tumor cell behavior and metabolism. Curcumin is known to decrease COX2 expression along with expression of  pro-inflammatory NFkB, TNFa, IL1B, IL6 and IL8.  

foot-hand-syndromeIn a human study researchers administered turmeric at a dose of 4 g/day (2 pills 12 hours apart) starting at the beginning of capecitabine treatment and lasting six weeks. The study included 40 patients whose mean age was 62 years. Most were female (80%), 52% had breast cancer, and 47.5% had GI tumors. After the first cycle of capecitabine treatment, 11 of 40 patients developed HFS (27.5%; 95% CI [15, 42]), whereas four patients developed HFS equal or superior to grade 2 (10%; 95% CI [3.3, 23]).. The study concluded that  turmeric combined with capecitabine seems to produce a lower rate of HFS, especially grade 2 or higher. 

Comments

  • There were no contra-indications to utilizing turmeric concurrently with capecitabine
  • A significant therapeutic dose of 4 grams per day was used.   In my practice I prefer to use the more concentrated isolate curcumin and dose at 2-4 grams per day.  This would yield more inflammation control.   
  • Turmeric falls into the category of herbs that “Move Stagnant Blood” in Chinese Medicine.  One of the properties of curcumin is inhibition of platelet aggregation.

References:

Curcuma longa (Turmeric) for Prevention of Capecitabine-Induced Hand-Foot Syndrome: A Pilot Study

Vanessa Armenio Scontre , MD,Janine Capobiango Martins , MD, et al 

Jnl Diet Supp Pages 606-612 | Published online: 02 Nov 2017

 https://doi.org/10.1080/19390211.2017.1366387 PMID: 2909565

The effect of COX-2 inhibitor on capecitabine-induced hand-foot syndrome in patients with stage II/III colorectal cancer: a phase II randomized prospective study.Zhang RX, Wu XJ, Lu SX, Pan ZZ, Wan DS, Chen G.
J Cancer Res Clin Oncol. 2011 Jun;137(6):953-7. doi: 10.1007/s00432-010-0958-9. Epub 2010 Nov 27.
PMID: 21113620 Clinical Trial.

stress-cancer

Does Stress Cause Cancer?

 

Lifestyle Factors That Impact Breast Cancer Risk

cancer-and-stress

  • Alcohol:  Drinking Alcohol Increases Risk of Breast Cancer
  • Weight and Body Composition: Excess body fat increases risk for post-menopausal breast cancer. Lean muscle, low body fat decreases risk of pre-menopausal breast cancers
  • Physical Activity: Sedentary behavior is linked to increased risk of breast cancer, while being active decreases the risk of breast cancer 

Vigorous activity decreases the risk for pre-menopausal breast cancer.

Moderate activity decreases risk for post-menopausal breast cancer.

Some evidence indicates that people who are physically active (both before and after diagnosis) have a greater chance of surviving breast cancer.

  • Breastfeeding: Reduces risk of both pre- and post-menopausal breast cancer
  • Sleep: Women who report sleeping less than 5 hours per night  before diagnosis have an increased risk of dying from breast cancer compared to women whose  pre-diagnosis sleep pattern was 7-8 hours per night.  Women who have disrupted circadian rhythms due to night shift work have an increased risk of breast cancer.

cancer-cells

Does Stress Cause Cancer?

Maladaptive and ongoing responses to stress mediated by the Autonomic Nervous System and Hypothalamic Pituitary Axis promote a tumor microenvironment that favors inflammation, oxidative stress, poor glycemic control, carcinogenesis, proliferation, angiogenesis and metastasis

Physiological Pathways, Bio-behavioural Processes and Oncogenesis:

  • Environmental and social processes activate interpretive processes in the central nervous system (CNS) that can subsequently trigger fight-or-flight stress responses in the autonomic nervous system (ANS) or defeat/withdrawal responses through the activation of the hypothalamic–pituitary–adrenal axis (HPA)
  • Individual differences in perception and evaluation of external events (coping) creates variability in individual ANS and HPA activity levels.
  • Over long periods of time, these neuroendocrine dynamics can alter various physiological processes involved in tumorigenesis, including oxidative metabolism, DNA repair, oncogene expression by viruses and somatic cells, and production of growth factors and other regulators of cell growth.
  • Once a tumour is initiated, neuroendocrine factors can also regulate the activity of proteases, angiogenic factors, chemokines and adhesion molecules involved in invasion, metastasis and other aspects of tumour progression.
  • CNS processes can also shape behavioural processes that govern cancer risk (for example, smoking, transmission of oncogenic viruses or exposure to genotoxic compounds).


Integrated Model of Bio-behavioral Influences on Cancer Pathogenesis Through Neuro-Endocrine Pathways

chart

In this model, bio-behavioural factors such as life stress, psychological processes and health behaviours (blue panel) influence tumour-related processes (green panel) through the neuroendocrine regulation of hormones, including adrenaline, noradrenaline and glucocorticoids (red panel). 

Central control of peripheral endocrine function also allows social, environmental and behavioural processes to interact with biological risk factors such as genetic background, carcinogens and viral infections to systemically modulate malignant potential (red panel). 

Direct pathways of influence include effects of catecholamines and glucocorticoids on tumour-cell expression of genes that control cell proliferation, invasion, angiogenesis, metastasis and immune evasion (green panel). 

Stress-responsive neuroendocrine mediators can also influence malignant potential indirectly through their effects on oncogenic viruses and the cellular immune system (red panel). 

These pleiotropic hormonal influences induce a mutually reinforcing system of cellular signals that collectively support the initiation and progression of malignant cell growth (green panel). 

Furthermore, neuroendocrine deregulation can influence the response to conventional therapies such as surgery, chemotherapy and immunotherapy (green panel). 

In addition to explaining bio-behavioural risk factors for cancer, this model suggests novel targets for pharmacological or behavioural intervention. 

(CTL, cytotoxic T lymphocytes; IL, interleukin; MRD, minimal residual disease; NKC, natural killer cell; TGFβ, transforming growth factor-β; TNFα, tumour-necrosis factor-α; TSH, thyroid-stimulating hormone.)

Dr. Nalini’s Adrenal Stress-Immune Support Protocol 

DAYTIME

Designs for Health Adrenotone   2/3x/day. With meals

All-in-one synergistic adrenal support formula. 

Metagenics Immucore 1/3x/day. With meals

Multidimensional Support for Healthy Immune Function

BEDTIME

Integrative Therapeutics  Cortisol Manager 2 caps one hour  before bedtime

  • Safe for use every night
  • Stress reducing sleep aid
  • Reduces cortisol levels for stress reduction and restful sleep.

https://us.fullscript.com/protocols/chilkov-dr-nalin-s-adrenal-stress-immune-support-kit

Treatment Plan should include 

Patient Teaching, Lifestyle and Dietary Guidelines and ongoing behavior change support

  • Dietary Guidelines -Nutrient Repletion-Glycemic Control
  • How to nurture parasympathetic tone
  • Sleep Hygeine
  • Self Regulation-Resilience- Stress and Mood Management guidelines
  • Monitoring Heart Rate Variability
  • Encourage Meditation-Tai Chi-Yoga-Deep Relaxation, Time in Nature
  • Acupuncture
  • Massage
  • Importance of Social Support
green tea extracts

Green Tea Extract Reduces Severity of Radiation-Induced Dermatitis

Breast cancer is the most common cancer affecting women worldwide. Radiation dermatitis affects nearly all women receiving radiotherapy for breast cancer.  http://repoceuticals.dk/pipeline/radiation-dermatitis/

new-breast-cancer

RID may result in less tolerance to treatment and even discontinuation of treatment. The patient may have skin changes ranging from faint erythema (reddening) and desquamation (peeling skin) to skin necrosis (death of skin cells) and ulceration, depending on the severity of the reaction.  Several studies demonstrate that topical green tea extract may be an effective prophylactic treatment.  

To make a strong hot water extract:  Place 8 tea bags of organic green tea into 1 cup of filtered or distilled water. Bring to a boil and simmer covered for 20 minutes. Place extract into sterile glass dropper bottle. (Available at most pharmacies).   Spray skin liberally before and after radiotherapy treatment.

The National Cancer Institute (USA) has developed 4 criteria for the classification of acute radiation dermatitis:

  • Grade 1 – Faint erythema or desquamation.
  • Grade 2 – Moderate to brisk erythema or patchy, moist desquamation confined to skin folds and creases. Moderate swelling.
  • Grade 3 – Confluent, moist desquamation greater than 1.5 cm diameter, which is not confined to the skin folds. Pitting oedema (severe swelling).
  • Grade 4 – Skin necrosis or ulceration of full-thickness dermis (middle layer of skin).

Hymes SR, Strom EA, Fife C. Radiation dermatitis: Clinical presentation, pathophysiology and treatment 2006. J Am Acad Dermatol 2006; 54:28-46. PubMed 

https://dermnetnz.org/topics/radiation-dermatitis

Epigallocatechin-3-gallate ameliorates radiation-induced acute skin damage in breast cancer patients undergoing adjuvant radiotherapy

In a study using topical Epigallocatechin-3-gallate forty nine patients topical EGCG was applied daily during radiotherapy treatment.  “Topical EGCG was applied daily, starting when grade I dermatitis appeared and ending two weeks after radiotherapy. The maximum dermatitis observed during the EGCG treatment was as follows: Grade 1 toxicity, 71.4% (35 patients); grade 2 toxicity, 28.6% (14 patients); there were no patients with grade 3 or 4 toxicity. The majority of the radiation-induced dermatitis was observed 1 week after the end of radiotherapy. EGCG reduced the pain in 85.7% of patients, burning-feeling in 89.8%, itching in 87.8%, pulling in 71.4%, and tenderness in 79.6%.”

Zhu W et al Oncotarget. 2016 Jul 26;7(30):48607-48613. doi: 10.18632/oncotarget.9495. PMID: 27224910; PMCID: PMC5217042.

Efficacy of Epigallocatechin-3-Gallate in Preventing Dermatitis in Patients With Breast Cancer Receiving Postoperative Radiotherapy: A Double-Blind, Placebo-Controlled, Phase 2 Randomized Clinical Trial 

A total of 180 eligible patients were enrolled, of whom 165 (EGCG, n = 111; placebo, n = 54) were evaluable for efficacy (median [range] age, 46 [26-67] years). The occurrence of grade 2 or worse RID was significantly lower (50.5%; 95% CI, 41.2%-59.8%) in the EGCG group than in the placebo group (72.2%; 95% CI, 60.3%-84.1%) (P = .008). The mean RIDI in the EGCG group was significantly lower than that in the placebo group. Furthermore, symptom indexes were significantly lower in patients receiving EGCG. Four patients (3.6%) had adverse events related to the EGCG treatment, including grade 1 pricking skin sensation (3 [2.7%]) and pruritus (1 [0.9%]).

Prophylactic use of EGCG solution significantly reduced the incidence and severity of RID in patients receiving adjuvant radiotherapy for breast cancer.

Zhao H, Zhu W,  et al. JAMA Dermatol. 2022 Jul 1;158(7):779-786. doi: 10.1001/jamadermatol.2022.1736. PMID: 35648426; PMCID: PMC9161122.

tea-extracts

The effects of tea extracts on proinflammatory signaling

Tea extracts supported the restitution of skin integrity. 

Tea extracts inhibited proteasome function and suppressed cytokine release. 

NF-kappaB activity was altered by tea extracts in a complex, caspase-dependent manner, which differed from the effects of epigallocatechin-gallate. 

Additionally, both tea extracts, as well as epigallocatechin-gallate, slightly protected macrophages from ionizing radiation

Pajonk F, et al, BMC Med. 2006 Dec 1;4:28. doi: 10.1186/1741-7015-4-28. PMID: 17140430; PMCID: PMC1698929.

doi: 10.1186/1741-7015-4-28. PMID: 17140430; PMCID: PMC1698929.

JAMA Derma

environmental-toxins

All Cancers Linked to Environmental Toxins

Making Environmental Health A Part of Health Care

Each month of the year is devoted to awareness of one or more cancers. September is devoted to multiple cancers.  

What do all of these cancers have in common?

There is an increasing volume of compelling evidence linking all types of cancer to environmental exposures.

Our knowledge of mechanisms linking exposures of toxicants to specific cancers is also increasing.  

environmental-pollution

There are two reasons that we as clinicians and care providers must be aware of the many contributing offenders and how to identify, assess, mitigate risk and safely remove body burden or toxicants in our patients.

Additionally, it is my practice to engage in patient education and patient teaching on the first or second visit to increase patient and family awareness about the importance of taking control of and reducing their toxic exposures as many toxicants are ubiquitous our homes, workplaces and communities.  Many toxicants include the use of common everyday products.    I also refer patients to these very reliable and up to date websites:  Environmental Working Group where foods, cleaning supplies, garden supplies are rated and their secondary site  Skin Deep Cosmetics Database for self-care and baby care products, including safe sunscreens.  They also have many downloadable publications for patients including 12 Hormone-Altering Chemicals and How to Avoid Them

Taking a good “ toxic exposures history” is important in all patients.  Of course, the very diagnostic methods and treatment modalities used in oncology are sources of toxic exposure as well!!  Many clinicians feel taking such a history from their patients will open us a Pandora’s box.

sewer-pollution

However, in the context of oncology, it is essential to do so, if only to bring awareness and to address the risk and health status not only of the patient, but also their family members.

My go to experts in this area include Dr. Walter Crinnion ND and Joseph Pizzorno, ND, both seasoned researchers and clinicians. They have recently published a well researched book  Clinical Environmental Medicine, which I consider required reading for all clinicians, especially those working with cancer patients.  There is a version for patients as well The Toxin Solution: How Hidden Poisons in the Air, Water, Food, and Products We Use Are Destroying Our Health--AND WHAT WE CAN DO TO FIX IT Dr. Crinnion’s has an excellent downloadable Toxic Exposure Questionnaire.  

The  American Academy of Environmental Medicine is an excellent resource for education and training and conferences where world-class experts convene.

Most in the patients control is their home environment and their food and water.

Fran Drescher’s Cancer Schmancer website has instructions for how to host a Detox Your Home Party.   

The first step is avoidance, avoidance, avoidance to reduce body burden, followed by appropriate supplements to help the body deal with what is there and finally safe and appropriate cleansing and detoxification interventions. Patients must also understand how to avoid re-exposure.

Resources:

Recommended Laboratories for Assessing Body Burden of Toxins 

(This is not a complete list and I have no financial relationship with any of these labs)

  • Great Plains Laboratory (heavy metals, environmental exposures, mycotoxins, glyphosate)
  • Genova Diagnostics (heavy metals, environmental chemicals)
  • RealTime Labs (Mold and Mycotoxins)
  • IMS Laboratory (Mold and Mycotoxins)
  • Quicksilver Scientific (Mercury)

*from a headline published in the New York Times