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Food allergies are the best-known negative reaction to food proteins. In classic food allergies, a protein in certain foods (eg. peanuts, shellfish or egg whites) interacts with an antibody, IgE. Once that reaction occurs, our immune system goes into high gear releasing histamine. Histamine causes an immediate response, and can trigger everything from a scratchy throat and hives to life-threatening swelling of the throat and heart. Because of the rapid and potentially severe response, people with food allergies are usually very aware of them. Repeated exposures to an allergen can also trigger stronger and stronger reactions, which is why it is generally recommended that people with allergies avoid exposure to the food as much as possible.
In food sensitivities, a different antibody, IgG, is involved. IgG activates a much larger and more sophisticated portion of our immune system, when compared to IgE, which causes a greater variety of symptoms, over a longer period of time. Most people with a food sensitivity have some type of digestive complaint, but not always. The classic picture of Irritable Bowel Syndrome – gas, bloating, diarrhea and constipation – can frequently be attributed to an underlying IgG reaction. Food sensitivities can also play a role in major digestive diseases, such as ulcerative colitis and Crohn’s disease. Because of the overall immune activation that happens in food sensitivities, body wide symptoms are also fairly common. Joint pains, difficulty breathing with exertion, and even migraines can all be associated with food sensitivities.
Unlike food allergies, symptoms of food sensitivities typically develop a few days after the exposure. The most common triggers (ie. milk, wheat, corn, soy and eggs) are also common in most diets. Together these facts make tracing food sensitivities more difficult. The two most effective methods for determining a food sensitivity are IgG testing, a blood test, and an elimination or hypoallergenic diet. After a period of avoidance, most people can consume the foods they are sensitive to on a limited basis.
Gluten, a protein in wheat, spelt, rye and some oats, is the culprit behind one of the most serious reactions people can have to protiens, celiac disease. In celiac disease, the antibodies that form in response to gluten also react to lining of the digestive tract. For people with celiac, an exposure to gluten triggers the immune system to attack their digestive tract, which leads to a host of severe digestive complaints. Celiac disease, can be screened for using a blood test for the specific anti-bodies, although a definitive diagnosis involves taking a piece of the small intestine and looking at it under the microscope for specific changes. The treatment for celiac disease is a life-long avoidance of gluten and all gluten containing foods.
The final way the proteins in our food can negatively effects our health is through our nervous system. Some proteins in foods are able to directly affect our nerves. Casein, a protein found in milk, and gluten are both classic examples. These proteins bind onto our endorphin receptors. For most people, eating the protein causes a slight sense of well-being and relaxation. For sensitive individuals, they cause constipation, irritability, mood swings and difficulty concentrating.
Modified Citrus Pectin (MCP) has been advertised as an alternative treatment for advance cancers since the late 1990’s. Normal pectin, the kind found in apples, orange peels and jelly, is a complex carbohydrate. The bacteria in our colons break down pectin into short chain fatty acids, which benefit the cells that line the colon. MCP is a form of pectin that has been chemically broken down to produce a molecule that is about 50x smaller, and can be absorbed by the digestive tract.
The initial research on MCP showed that rats with colon cancer developed fewer liver metastases when MCP was included in their diet. Because of MCP’s novel anti-metastatic properties, there has been a lot of advocacy for it use by patients with advanced cancer. While MCP has had many advocates, it has not had much clinical research. To date only two human clinical trials have been performed.
In the first study, a small group of men with recurrent prostate cancer received MCP every day for a year. 70% of the men saw a positive change in their PSA doubling time, a tumor marker for prostate cancer. Just under half of those men had their PSA doubling time rise above 10 months, which suggests they are less likely to develop metastatic cancer.
In the second trial, 49 people with advanced cancer, who had progressed through conventional cancer treatment, took MCP daily. Just over 20% of the people in the trial saw their disease stabilize within 2 months. Most of them continued to have stable disease for 6 months, when the trial finished.
The limited information suggests that 20-30% of MCP users may halt the progression of their cancer. Unfortunately, we don’t know what separates the people who benefit from those who don’t. At the same time, the benefit of MCP, stabilization of advanced or recurrent cancer, should be noticeable with 2 months of starting it.
MCP, like pectin, is considered a dietary fiber. Most of the reported side-effects: upset stomach, bowel habit changes, gas and nausea, are in line with what would be expected from suddenly increasing the amount of fiber in a diet. The one unexpected side-effect is itchiness, which can be severe enough necessitate medical treatment. All of the side-effects resolve shortly after discontinuing MCP.
Research on MCP continues to progress, and hopefully larger trials can help us identify just who it is that will benefit from MCP. Till that time, individual trials of MCP for patients facing recurrent and metastatic cancer seems like a reasonable inclusion in a comprehensive cancer treatment plan.
Prostate-specific antigen (PSA) is a protein that is produced by the prostate of adult men. A simple blood test is able to measure the small amounts of PSA that circulates through a man’s body. The level of PSA measure in the blood, loosely correlates with the size of the prostate. Bigger prostates produce more PSA, while smaller prostates produce less. Most prostate cancers also produce PSA, which has lead to using the PSA as a screening tool for prostate cancer.
Prostate cancer is the most common type of cancer in men, and the second leading cause of cancer-specific death in men. Medicine has been searching for a way to prevent deaths from prostate cancer. For the last 20 years, conventional wisdom has said the PSA screening and early detection is our best method.
In October of 2011, the US Preventative Services Task Force, the governmental body that reviews medical research and develops practice guideline, reviewed the current literature on using the PSA to screen for prostate cancer with the goal of answering four basic questions.
- Does PSA-Based Screening Decrease Prostate Cancer–Specific or All-Cause Mortality?
- What Are the Harms of PSA-Based Screening for Prostate Cancer?
- What Are the Benefits of Treatment of Early-Stage or Screening-Detected Prostate Cancer?
- What Are the Harms of Treatment of Early-Stage or Screening-Detected Prostate Cancer?
In a best case scenario, the taskforce estimated that 48 men diagnosed with prostate cancer through PSA screening would have to be treated to prevent a single death from prostate cancer, a success rate of just 4%. Depending on the treatment, radiation or surgery, 7-16 of those men would suffer lasting erectile dysfunction. 10 of those men would suffer urinary incontinence. Even more concerning, 1 in 200 men, undergoing surgery will die from surgical complications. The report did not factor in the estimated 3 billion dollars in annual expense that PSA screening costs.
The details of the report are somewhat dense, but the conclusion was clear. The harm to the many, does not justify the benefit to the few. Conventional treatments for prostate cancers detected by PSA screening do not offer a benefit to the vast majority of men.
These results, ultimately, lead the taskforce to recommend against screening men for prostate cancer using PSA. That recommendation ignores the many factors, independent from PSA, that can predict a man’s risk for prostate cancer. Prostate cancer screening should incorporate all aspects of a man’s health: his age, race, physical exam findings, family history, medication and supplement usage, and the PSA.
The findings of the taskforce, also reminds us that conventional treatments for early stage prostate cancer carry a significant risk, without a corresponding benefit.
HPV, the Human Papilloma Virus, was first identified in the late 70s. Over the last 40 years, HPV has been identified as the cause of the most common sexually transmitted disease, genital warts. Current estimates suggest that 1 in 5 people carry an active HPV infection, and that every person is exposed to HPV at least once in their life.
While we talk about HPV as single disease, it is actually group of 130 related viruses. Each virus is able to infect our skin or mucus membranes and causes abnormal growths, or warts. The different strains of HPV are able to infect specific sites of the body. The virus that causes plantar warts is different from the virus that causes genital warts.
Unfortunately, there are about a dozen strains of HPV that cause genital warts. If person is exposed to a single strain and acquires immunity to it, there are still other varieties that can cause a similar infection. There is also second group of HPV known as High-Risk HPV. These strains of HPV can cause warts, but they are also associated with a variety of cancers.
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Different HPV Strains
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| Genital warts: HPV 6, 11, 13, 40, 42, 43, 44, 54, 61, 72, 81 and 89 |
| High-Risk: HPV 16, 18, 31, 33, 35, 39, 45, 52, 58 and 59 |
Infection with a strain of High-Risk HPV in now known to be a required first step in the development of cervical cancer. This realization has caused researchers to look for High-Risk HPV in other types of cancer. The majority of anal cancers show signs of infection with High-Risk HPV, as do some types of oral, esophageal and lung cancers.
Pap smears, a routine screening for cervical cancer, can identify the early changes associated with High-Risk HPV. Depending on the result of a pap smear and the health of the woman, additional testing or treatment can be recommended. Due to the role of High-Risk HPV in anal cancers, anal pap smears are starting to be recommended for men and women who have receptive anal sex, multiple sexual partners, or are HIV+.
Thankfully, our immune systems are very good at eliminating HPV. On average, 90% of people will completely clear an HPV infection within two years without any assistance. Surgical treatment, either cutting off or freezing the warts, can greatly speed up the process. As the body heals from the surgery, the immune system cleans out any remaining infection.
For areas of the body, where surgery isn’t practical or desirable, there are a number of natural therapies that support our immune system’s ability to clear HPV. Anti-viral herbs are able to prevent HPV from replicating or spreading to new cells, while targeted nutritional interventions can strengthen the part of our immune system that attacks HPV and infected cells. Used together, anti-viral herbs and target nutritional therapies can typically clear HPV infections in 3-6 months.
The American Cancer Society has a detailed description of factors that are known to increase a woman’s risk of breast cancer. Many of them relate to estrogen:
- Being a woman
- Beginning menses before age 12
- Going through menopause after age 55
- Using oral contraceptives
- Using hormone replacement therapy
- Being overweight
There are additional factors that reduce a woman’s risk of breast cancer, that again relate to estrogen:
- Breast feeding
- Having children
And a simplistic view, might say that estrogen is “bad” for cancer. If we’re willing to look a little deeper, an interesting trend about estrogens appears, specifically one that opens up a whole avenue of breast cancer treatment and prevention.
When we talk about estrogen, we’re actually talking about a group of related hormones, each with a slightly different origin and different effect. A standard lab test, can tell a woman about the three main forms of estrogen, which are conveniently known as E1, E2 and E3.
E1 (Estrone) is the estrogen that is produced by fat cells – yes, fat cells produce estrogen. E1 is also the backbone for pharmaceutical forms of estrogen that are found in oral contraceptives and hormone replacement therapy. After menopause, E1 is the dominant estrogen in women. E1 is also considered a strong estrogen, because of it’s ability to strongly stimulate cell growth
E2 (Estradiol) is the form of estrogen that is produced by the ovaries. With progesterone, E2 controls the menstrual cycle. E2 serves as the baseline for other estrogens, in terms of being considered strong or weak.
E3 (Estriol) is typically associated with pregnancy. The placenta churns out this relatively weak estrogen throughout pregnancy, and during that time E3 is the dominant form of estrogen in a woman’s body. Outside of pregnancy, the liver produces smaller amounts of E3 as the liver process the other forms of estrogen.
Let’s take a second look at those risk factors, and how they relate to the different forms of estrogen
| Increased Risk |
Beginning menses before age 12 |
Increased E2 |
| Increased Risk |
Going through menopause after age 55 |
Increased E2 |
| Increased Risk |
Using oral contraceptives |
Increased E1 |
| Increased Risk |
Using hormone replacement therapy |
Increased E1 |
| Increased Risk |
Being overweight |
Increased E1 |
| Decreased Risk |
Breast feeding |
Decreased E2 |
| Decreased Risk |
Having children |
Increased E3 |
The trend that starts to emerge suggests that lowering a woman’s E1 and E2, while raising E3 can be an effective intervention for reducing the risk of breast cancer. Admittedly, medicine has yet to prove this approach with the classical multi-center randomized, double-blind study, but there are 40 years of supportive preclinical research.
Most labs, can now report an Estrogen Quotient, a simple number that quantifies the ratio between the different estrogens. A ratio greater than 1, more E3 than E2 and E1, is considered to reduce a woman’s risk of breast cancer. A ratio less than 1, more E1 and E2 than E3, suggests an increased risk of breast cancer.
In 2006, the American Board of Naturopathic Oncology established a board certification to regulate the practice of naturopathic oncology. According to the board:
Naturopathic oncology is the application of the art and science of naturopathic medicine to the field of cancer care and treatment. Naturopathic oncologists work both in hospital oncology settings and in private practices bringing their wisdom, perspective and experience to aid oncology treatment teams that seek the best positive outcomes for their patients.
Naturopathic oncology is the specialty of using natural compounds to treat cancer. Naturopathic oncology blends medical information from conventional western medicine, emerging research and traditional medical systems to support cancer patients through conventional cancer treatment and beyond. The ultimate goal of naturopathic oncology is to address the underlying imbalances that contribute to the development of cancer.
Naturopathic oncologists work with medical, surgical and radiation oncologists to provide comprehensive treatment plans that best support individuals through conventional cancer treatment. Chemotherapy, radiation therapy and surgery each present patients with a unique set of challenges to patients. In this setting, the role of naturopathic oncology is to reduce treatment side effects, to reduce breaks in treatment, and to improve the therapeutic benefits of treatment whenever possible. This ensures that patients receive the best treatment with as little disruption to their daily life as possible.
Outside of conventional treatment the role of naturopathic oncology expands considerably. Conventional oncologists often lack the time or expertise to discuss with patients the myriad of lifestyle factors that can benefit cancer patients and survivors. With their expertise in oncology and natural medicines, naturopathic oncologists are ideally suited to helping patients sort through the sometimes-confusing amount of information regarding natural and alternative cancer treatments. Looking at all levels of scientific evidence, a naturopathic oncologist can help determine which complementary and alternative therapies are best for each individual. Using this eclectic approach, naturopathic oncology has something to offer all people struggling with cancer.
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