Microscopes and Hodgkin's Lymphoma - Understanding the Pathophysiology of a Common Cancer

First off What is Lymphoma?

We have to first define what lymphoma is before discussing Hodgkin’s disease. Lymphoma is a cancer that develops from cells in the body known as “lymphocytes.” Lympocytes are a subcategory of white blood cells. There are two different types of lymphocytes: B-cells and T-cells. Almost all lymphomas, including Hodgkin’s disease, stem from B-cells.

In Hodgkin’s lymphoma a B-cell, for unknown reasons, becomes cancerous. The cell then makes many many clones of itself. These cells bundle together to form a solid tumor known as a lymphoma. There are several hypotheses for why these cells become cancerous in Hodgkin’s. One belief is that infection with Epstein-Barr virus (EBV, the same virus that causes infectious mononucleosis) can cause the cells to turn malignant in genetically susceptible people. Other theories are that certain genetic translocations may be the underlying factor. As of yet, no particular theory has significant supporting data to call it the “cause.” In fact, there may be multiple unrelated causes.

Types

There are different subcategories of Hodgkin’s lymphoma. They are based on several microscopic characteristics, and are important in determining prognosis. The features the pathologist is looking for are the number of Reed-Sternberg cells, as well as the number of lymphocytes present in the biospy specimen. A Reed-Sternberg cell is a funny shaped cell with two nuclei that looks like owl’s eyes.

The first subcategory, and most common type, is nodular sclerosing Hodgkin’s lymphoma. In this type there are very few Reed-Sternberg cells with a moderate number of lymphocytes. It commonly occurs in younger individuals, and with treatment, the prognosis is excellent.

The second subcategory is mixed cellularity Hodgkin’s lymphoma. This type has many Reed-Sternberg cells and a moderate number of lymphocytes when viewed under the microscope. It has an intermediate prognosis.

The third subcategory is lymphocyte predominant Hodgkin’s. It has very few Reed-Sternberg cells and many lymphocytes. It occurs most commonly in males less than 35 years of age. It is also one of the few types that is not associated with Epstein-Barr virus infection.

The last subcategory is lymphocyte depleted. It is the rarest form of Hodgkin’s lymphoma. It typically affects older males. Unfortunately it has the worst prognosis of the four types.

Skin Problem - Melanoma

Johnnie Powell’s face had a small spot that looked different. It was purple and white and itched. That spot started because a melanocyte had grown a cancerous tumor. He was told by his family doctor that he had a melanoma.

Melanocytes are the cells that produce melanin. Melanin gives dark or tan color to the skin. But, when one of these cells gets out of control, it can produce one of the most dangerous cancers known. And more than 53,0605 people are told that they have melanoma every year just inside the United States of America.

Risks for getting Melanoma

The most common risk factor for melanoma known is too much ultraviolet rays. When melanoma was first studied, it was found that people who labored out of doors were those who tended to show up with melanoma. Furthermore, those who had gotten a sunburn causing blisters were those who tended to go on to get a malignant melanoma.

People with light skin are much more likely to get melanoma. This might likely be related to the fact that they are more likely to get skin damage by sun exposure. But, this is not set in stone.

Those who have lots of nevi (moles) are at higher risk for melanoma, particularly those who have over 50. Also, those who have a particular type of mole called a dysplastic nevus are at higher risk.

Some people have had other skin cancers successfully treated including squamous cell carcinoma. Those people are more likely to get melanoma.

If you have had other people in your family that had melanoma, then you are more likely to get a melanoma as well.

Finally, those who have a weakended immune system get malignant melanomas more frequently. Whether a person has AIDS, an organ transplant needing medications to curtail the immune system or others using those medications, that person will have a higher risk.

One published case highlighted the role of genetics in melanoma. A man who was a chimera got melanoma. A chimera is someone who has two different types of DNA on each side of the body. This may occure when twins are formed and somehow join into one body. The man in the journal article had large metastatic lumps of melanoma tumors on one side of his body and none at all on the other!

How to Identify a Malignant Melanoma

The only way to be sure whether a bump on your skin is a melanoma or not is to have your doctor take it off and get it studied by a pathologist. However, there are some ways to know if you should be suspicious of one of those lumps or bumps.

Irregular Border – A melanoma will usually have an uneven border. The average mole has a sharp border. You can point to any spot on your skin and say for sure whether it is part of the mole or not. This is not the case with melanoma.

Assymetric Shape – The melanoma lesions typically have two halves that look different.

Different Color – Malignant Melanomas often will have different parts of the tumor that have different colors.

Size – most melanomas are larger than other moles. And they also tend to grow and may bleed or itch.

If you have something suspicious on your skin that you have a question about, get it examined by your dermatologist early. By removing the melanoma while it is just getting started gives you a much better chance of a cure. Particularly when the bump is still tiny.

The Lymphomas

Malignant lymphomas are a diverse group of cancers derived from the immune system, which result from neoplastic proliferation of B or T lymphocytes. These tumors may arise anywhere in the physique, most commonly inside lymph nodes but occasionally in other organs in which lymphoid components reside. 1 subtype of lymphomas that are composed of mixtures of cellular kinds having a unique biology is called Hodgkin’s lymphomas, whereas all other kinds of lymphomas are referred to as non-Hodgkin’s lymphomas.

Several elements are associated with the improvement of non-Hodgkin’s lymphoma. These consist of congenital or acquired immunodeficiency states for example AIDS or iatrogenic immunosuppression utilized in organ transplantation. Viruses are related to the pathogenesis of some types. For instance, most instances of Burkitt’s lymphoma that happen in Africa (endemic kind) are associated with Epstein-Barr virus (EBV), whereas Burkitt’s lymphoma manifesting in temperate zones is associated with EBV in only 30% of cases. Human T-cell leukemia-lymphoma virus I (HTLV-I) plays a causative role in the genesis of adult T-cell leukemia-lymphoma, in which the malignant cells contain the integrated virus. Human herpesvirus-8 (HHV-8) have been related to physique cavity-based lymphoma, a uncommon B-cell lymphoma that occurs predominantly in patients with AIDS. Chronic immune stimulation may be a causal system in the development of lymphomas too. For instance, chronic gas tritis secondary to Helicobacter pylori infection may give go up to gastric mucosa-associated lymphoid tissue (MALT) lymphomas. Resolution of gastric MALT lymphoma might occur in the majority of patients with localized disease who’re dealt with with antibiotics efficient against H pylori.

The classification of lymphomas has evolved over several decades. The newest distinction was devised by an international group of lymphoma specialists for that Globe Health Organization. The new scheme characterizes non-Hodgkin’s lymphomas according towards the cellular of origin utilizing a combination of criteria: medical and morphologic features, cytogenetics, and immunoreactivity with monoclonal antibodies that recognize B-cell and T-cell antigens, too as genotypic determination of B-cell and T-cell receptor rearrangements. Most non-Hodgkin’s lymphomas originate in B tissue and express on their surface CD20, a B-cell marker. Their monoclonal origin could be inferred by characterization from the particular class of light chain that is expressed: Either kappa or lambda B-cell lymphomas are further classified as malignant expansions of tissue from your germinal center, mantle zone, or marginal zone of normal lymph nodes.

Somatic gene rearrangements occur normally during B-cell and T-cell differentiation. The genes for variable and continual regions of the immunoglobulin weighty and light chains are discontinuous in the B-cell germline DNA but are blended by somatic rearrangement to create a functional antibody molecule. The T-cell receptor gene is analogous to the immunoglobulin molecule in that discontinuous sections of this gene also undergo somatic rearrangement early in T-cell development. DNA hybridization by Southern blot analysis permits recognition of a band of electrophoretic mobility that serves being a fingerprint for a monoclonal population of lymphoma tissue.

Most non-Hodgkin’s lymphomas exhibit karyotypic abnormalities. The most prevalent translocations consist of t(8;14), t(14;18), and t(11;14). Each translocation requires the immunoglobulin weighty chain gene locus at chromosome 14q32 with an oncogene. Identification and cloning of the breakpoints have identified 8q24 as c-myc, 18q21 as bcl-2, and 11q13 as bcl-1. The proximity of these oncogenes to the immunoglobulin gene results in deregulation and elevated expression from the oncogene product.

Representative subtypes of non-Hodgkin’s lymphoma include the indolent lymphomas for example follicular lymphoma, marginal zone lymphomas, and also the intense lymphomas for example mantle cell lymphoma, diffuse large-cell lymphoma, and Burkitt’s lymphoma.

Follicular lymphomas are low-grade tumors that may be insidious within their presentation. The translocation t(14;18)(q32;q21) is found in more than 90% of follicular lymphomas. The mutation results in overexpression from the bcl-2 protein by these tissue. The bcl-2 is an oncogene that codes for a protein that blocks apoptosis when overexpressed. The absence of bcl-2 translocation as assessed through the highly sensitive polymerase chain reaction test may be a marker for full remission standing in sufferers whose lymphomas harbor this translocation. Spontaneous regression of lymph node size is typical in sufferers with follicular lymphomas. Nevertheless, this class of lymphoma is not curable with standard chemotherapy; although the affected person with follicular lymphoma tends to possess an indolent clinical course, transformation to some a lot more aggressive grade of lymphoma happens in 40-50% of patients by 10 years.

An important subtype of limited area lymphomas would be the MALT lymphomas, which might originate within the stomach, lungs, epidermis, parotid gland, thyroid, breasts, along with other extranodal websites, where they characteristically align themselves with epithelial cells. A close association has been set up between gastric MALT lymphomas and H pylori infection.

Mantle mobile lymphoma presents histologically being a monotonous populace of small to medium-sized atypical lymphoid cells having a nodular or diffuse pattern that is composed of little lymphoid tissue with irregular nuclear outlines. The diagnosis of mantle mobile lymphoma is depending on morphologic requirements with confirmation by monoclonal antibody staining against cyclin D1 (bcl-1). The t(11;14) translocation seen in the majority of cases of mantle mobile lymphoma results in juxtaposition from the PRAD1 gene on chromosome 11 with the immunoglobulin heavy chain gene on chromosome 14. This outcomes in overexpression from the PRAD1 gene item, cyclin D1. Cyclin D1 binds to and activates cyclin-dependent kinases, which are believed to facilitate cell cycle progression through the G1 phase of the cell cycle. This illness occurs more frequently among older males and presents with adenopathy and hepatosplenomegaly. Mantle mobile lymphomas are significantly a lot more resis tant to remedy with mixture chemotherapy than follicular lymphomas and are also incurable.

Diffuse large-cell lymphoma is probably the most prevalent subtype of non-Hodgkin’s lymphoma. One third of presentations involve extranodal sites, particularly the head and neck, abdomen, epidermis, bone, testis, and nervous program. Diffuse big B-cell lymphomas frequently harbor mutations or rearrangements from the BCL6 gene.

Virtually all instances of Burkitt’s lymphoma are associated with alterations of chromosome 8q24, resulting in overexpression of c-myc, an oncogene that encodes a transcriptional regulator of mobile proliferation, differentiation, and apoptosis. Adults presenting with higher tumor burdens and elevated serum lactate dehydrogenase have a bad prognosis. Disease with a large tumor burden may be connected with a hypermetabolic syndrome that is triggered by remedy as the tumor undergoes sudden lysis. This syndrome may result in life-threatening hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia.

Anaplastic large-cell lymphoma is characterized through the proliferation of extremely atypical cells that express the CD30 antigen. These tumors usually communicate a T-cell phenotype and are connected using the chromosomal translocation t(a couple of;five)(p23;q35), producing in the nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) fusion protein. Activation of the ALK receptor tyrosine kinase results in an unregulated mitogenic signal.

Another kind of T-cell lymphoma may be the adult T-cell leukemia-lymphoma, an intense illness connected with HTLV-I infection that is characterized by generalized adenopathy, polyclonal hypergammaglobulinemia, hypercalcemia, and lytic bone lesions.

Lastly, Hodgkin’s lymphoma is distinguished by the presence of the Reed-Sternberg giant cell of B-cell lineage, which can be regarded the malignant cell kind in this neoplasm. The Reed-Sternberg cell constitutes only 1-10% of the total number of tissue in pathologic specimens of this illness and is connected with an infiltrate of nonneoplastic inflammatory cells.

Low Fat Diet Menu Reduces Common Skin Cancers

If you have a history of skin cancer, or are looking for ways to reduce your risk, you might want to adopt a low fat diet menu according to research just out of Australia. The findings tie high intakes of total fat to increased risk of a form of skin cancer known as squamous cell carcinoma among those who have a history of the disease. The research appears in the International Journal of Cancer.

“In addition to protecting the skin from sunlight, people who have a history of skin cancer would benefit from lowering their total fat intake,” says Dr. Torukiri I. Ibiebele of the Queensland Institute of Medical Research in Australia.

Though intakes of dietary fat have been associated with skin cancer in the past, until now there was sparse, inconsistent evidence of any link between the two.

The team studied the diet of 457 men, 600 women aged 25-75 years old, computing their daily intake of saturated, monounsaturated and polyunsaturated fats in meats, fried foods, breads, veggies and what’s used in cooking.

The subjects all lived in the sub-tropical area of Nambour, Queensland, a place with high exposure to ultraviolet sunlight. Findings stand up even after allowing for factors that could be linked to cancer such as where a subject lived and their level of exposure to the sun.

Basic information about diet, skin color and sun exposure was collected using a questionnaire in 1992.

The follow up to the study lasted 11 years, during which time 267 of the study subjects developed a total of 664 basal cell skin tumors – the worlds most common skin cancer.

Another 127 subjects developed a total of 235 squamous cell skin tumors – the second most common form of skin cancer. These two forms of non-melanoma skin cancer account for the vast majority of skin cancers. These are readily and successfully treated when caught early.

The Australian study found there was no significant association between the amount of fat a subject consumed each day and the overall risk of either basal cell or squamous cell cancers.

However, if a subject had a prior history of skin cancer, higher total fat intake was associated with an almost twofold increased risk of squamous cell cancers.

This supports a body of work that shows that prior skin cancers make high fat diets a no-no.

Eating a low fat diet isn’t as hard as you might think. You need to start by being aware of what you’re putting in your body.

Get into the habit of reading food labels, watch for the hidden fats in those processed and baked goodies and don’t neglect the fats and oils used in cooking. Keep your goals realistic, that means don’t cut everything all at once.

Be sure that you stock your fridge and cabinets with healthy options – whole grain pastas, breads and grains, plus lots of fresh veggies and fruits.

You can also work to make substitutions – leaner cuts of meat, adding more chicken or fish (once or twice per week), fresh veggies and fruits to your menu. Always eat breakfast, as this will keep your blood sugar levels stable till lunch, making you less likely to snack.

Water is super helpful, as it aids digestion and keeps you feeling fuller, longer. It’s also important to watch the portion sizes on all your meals, as what you’ve become accustomed to seeing on restaurant plates is usually quite a bit bigger than a true serving.

Remember, deciding to choose a low fat diet menu doesn’t mean depriving yourself. Some fat is good, and you can certainly enjoy a treat once in a while, but cutting the unnecessary fats in your daily intake can certainly be helpful for skin cancer patients, and the rest of us too.

A Guided Imagery While Undergoing Cancer Treatments

“When we practice dying, We are learning to identify less with Ego and more with Soul.” Ram Dass

The cancer literature that I had read said to envision the cancer cells as the enemy. The books said to imagine destroying the “bad” invasive cells by blowing them up. Envisioning the annihilation of my cancer cells seemed to me like I was dividing myself against my own body. These particular cancer cells were mine, my body had created them. I saw them as a benign part of nature. I simply could not use this suggested method of annihilation. I longed for options and prayed for guidance. The night before my first cancer treatment I received my answer expressed in the form of the most vivid dream I could ever recall.

She began her journey to the hospital as she climbed into the small red car with the person that first revealed her suspected cancer. She was startled to see hundreds of starfish-like creature emanating sheer glee for the love of life alone. They displayed exquisitely vivid multi colors. They were friendly, cheerful and fun albeit noisy as they were all trying to communicate with her at once. The woman felt overwhelming love and compassion for these odd, beautiful little creatures. They made her laugh. She beseeched the driver not to move the car until she could get the little ones to depart. They were everywhere, on the seats, under the seats, in the glove compartment, hanging off the mirror and the doors both inside and outside of the car. They were beneath the tires. They had no sense of the impending danger. They would be smashed to bits if the driver moved the car. The woman felt deeply connected and protective of these curious little creatures and intuitively knew th at they meant no harm. They were simply and totally self-absorbed in the maintenance of their own life force akin to self-centered teenagers. She did not want them to die any more than she herself wanted to die from their invasion into her body. The woman awoke feeling strong, refreshed and humored by another of nature’s endless surprises.

When I awoke I was filled with delight. Smiling, I pondered the wondrous nature of cells and the innate intelligence of these body building blocks, of which there are some 50 trillion, give or take a million here or there. Inherent in the life of the cell is an intricate process of cell division. It is somewhere within the cycle of cell division that a cancer cell runs amok.

All possible explanations aside, we now have a cell with a behavioral problem. A cell that does not play well with others, and in fact, is mutating into a type of aggressive gang member mentality that rapidly MUTATES and CLONES itself into more gang members. Their adventures eventually lead to invasion of neighboring turfs. Part of this “gang” mentality is to ignore agreed upon social rules which govern their old community of cells. They totally disregard cooperation and how a “community” should be formed and maintained for the highest good of the entire system. They do not understand the impact of their choices on neighboring communities or that eventually these renegade cells will cause their own demise. Dr. Lewis Thomas says that “Disease usually results from inconclusive negotiations for symbiosis, an overstepping of the line by one side or the other, a biologic misinterpretation of borders”.

Turning inward as I lay upon the hospital bed, I felt peaceful and deeply grateful for having had this delightful dream. The nurse prepared to administer the chemo treatment through the catheter-type device previously implanted in my chest, as I continued listening to the beautiful piece of music that I had brought along. I visualized angels standing just to the right of me. In my mind’s eye, the angels were holding large soft nets made of the finest silk. I explained to the delightful shimmering creatures, vibrant with spectacular colors, that they were in great danger of being eliminated by incoming poison. They had to vacate my body at once. I envisioned guiding them on their way out of my body into the loving arms of awaiting angels holding silk nets.

Six years have passed since my mastectomy. I am thriving in all areas of my life. I still smile when I think of those joyous little creatures that I believe are part of God’s creation. I remember their blessings as they showered me with colors more beautiful and vivid than seen in the movie Avatar. My friends constantly remark on how colorful I dress these days reminding me of the usual blacks, browns and tans that I used to wear. I just smile unless I know them well and then I say, “Yes, one of the many gifts from my cancer cells.”

Cervical Cancer and Having Children Later

Will I be able to have children after surgery? Do I have to have a hysterectomy? These are both natural questions women ask when they’re told they have to have surgery for cervical cancer. The answer to the second question is: it depends. It depends on how early your cancer was caught. If it’s still just local and smaller than 2 cm (which is a little less than an inch), then you should be able to avoid a hysterectomy. The answer to the second question is: it depends, but probably yes as long as you don’t have a hysterectomy.

Surgery to remove a small, localized cervical cancer will require one of these surgeries: LEEP, cone biopsy or trachelectomy. Sometimes you may have more than one, like a LEEP followed by a cone biopsy. The reason for two surgeries is because you may have a LEEP to remove severe dysplasia, and they find a small tumor in the tissue. Then you may have a followup cone biopsy to make sure it was all removed.

Okay, now your surgery is over, you have waited 6 months to a year to heal, can you have children? Provided you don’t have any other reason to be infertile, you should be able to, but you might encounter a few hurdles. These hurdles are cervical stenosis (or stiffness of the cervix), decreased cervical mucus, blocked fallopian tubes and incompetent cervix. You may not have any of these, or you may have all of them.

I had micro-invasive cervical cancer, and after 3 surgeries, I had a baby five years later. I was terrified that I would suffer from preterm labor because all the doctors warned about that due to the dreaded “incompetent cervix.” That is when your cervix won’t stay closed to keep the baby inside. It can happen because your cervix is shorter after the surgeries, but, interestingly, the length of your cervix may still be long enough. An “incompetent cervix” is more likely to happen to women who are born with short cervixes or who have a genetic defect in the shape of their uterus.

Nobody can guarantee that you won’t have premature dilation of your cervix, so you will go see a perinatologist once you get pregnant, and the doctor can measure your cervix length on ultrasound. The doctor will see you once a month once you’re about 3 months pregnant, and if your cervix looks like it’s shortening, you may need a cerclage to keep it closed.

A cerclage is a fancy word for a stitch in the cervix. Literally, they put in a stitch to close the cervix. That stays in until about 2 weeks before you’re due to have the baby. I think the important thing to know is that there is life after cervical cancer, and it can include having children if you catch the cancer early. Go to your doctor for regular Pap smears and pelvic exams! Whether or not you have children later is something that you should get to decide, not have cancer decide it for you.

Prostate Cancer - The Basic Facts

Prostate Cancer has unfortunately presented itself as one of the most common male cancers within the western world. There is much information about this disease on the Internet – some of this is helpful – some less so.

It is therefore essential that the patient seeks out the facts and is regular contact with their doctor

What is it?

The Prostate, or sex gland as it is often termed, is actually one of the more unusual aspects of the male reproductive system. The Prostate is essentially responsible for producing the sperm nourishing prostatic fluid found in semen. Cancer of the prostate gland develops when cells in the area begin to multiply at an uncontrollable rate.

Although in its early stages, it presents minimal complications, this slow growing cancer does need to be treated before it spreads to the bones located outside the prostate.

Who is affected?

Relatively little is actually known about the gland, although we do know that Prostate Cancer is the most common cause of cancer in men. It is responsible for a huge 25% of newly diagnosed cases of cancer in England and Wales. It is actually more common in men aged over 65 and in men from an African Caribbean or African descent. Within the UK prostate cancer is responsible for the death of approximately 9,000 men every year.

What are the symptoms?

Most men with early prostate cancer will actually exhibit little or no symptoms.

However, if you do experience any of the following symptoms it is important that you visit your Doctor.

o Needing to urinate more often, especially at night

o Having to rush to the toilet, so that you may even leak urine at times

o A difficulty in attempting to pass urine.

o A weak urine flow

o Dribbling when urinating

o Pain when passing urine.

o New pain in the lower back, hips or pelvis

What causes it?

There is actually no single cause that can be identified for the onset of this disease. However there are risk factors that can affect the genetic material of prostate cells and encourage subsequent cancerous activity.

Whilst factors such as age, ethnic group, and family history are impossible to control, cancer specialist have noted that a diet high in diary products and red meat can increase the risk of developing the condition.

* How is it treated?

Following your Doctor making a referral to a multi Disciplinary Team ( MDT) an assessment will be undertaken to establish whether the cancer is localized (i.e. only affecting the prostate), or in an advanced stage (the cancer has moved outside the prostate)

Treatments that can be utilized for localized Prostate Cancer can include one or more of the following:

o Active Surveillance – where the state of the cancer is closely observed and treatment is only commenced if absolutely necessary.

o External Beam radiotherapy – where radiation is used to kill cancer cells.

o Radical Prostatectomy – where the prostate is removed.

o Brachytherapy – here radioactive seeds are implanted into the prostate.

o High Dose Rate Brachytherapy – here temporary sources of radiation are targeted daily at the prostate.

If the cancer is locally advanced or advanced, you may instead be offered hormone therapy, radiotherapy and chemotherapy[y. At this point, it is actually no longer possible to actually cure the disease.

Instead treatments are aimed at the prolonging of life and relieving of symptoms.

* What are the likely side effects of Treatment?

Prostate Cancer Treatment is unfortunately often uncomfortable mainly due to the side effects experienced by patients. Post surgical effects can include urinary incontinence and sexual dysfunction, while radio and chemotherapy can cause tiredness, nausea and hair loss.

These are important considerations but are put in context by the possibility of a greater return – that vitally important all clear diagnosis!

The Top Three Ways to Prevent Cancer Naturally

If you wonder how you can prevent cancer naturally, either in your life, or in the life of your loved ones, you are not alone. The good news is, most cancer is completely preventable, according to the National Institute of Health, and there are many things you can do to reduce your risk of developing that frightening disease.

Following are three of the most important changes you can make in order to prevent cancer from affecting your life.

1. Eliminate processed foods from your diet. Used to eating boxed and/or frozen dinners, sodas, store-bought sweets and flour-based foods (such as bread and pasta)? How about cold cereals, pasteurized milk, snack chips and canned vegetables?

If so, you are eating yourself into bad health. Processed foods not only have little to no nutritional value, but can actually cause nutritional deficiencies. In addition, they are likely to contain toxic substances, and more than you think: the FDA allows food manufacturers to put as many as 15,000 different chemicals in food without having to list them on the label! Many of these toxic chemicals are carcinogenic-or, can cause cancer-and the more that accumulate in your system, the higher your risk of developing cancer.

2. Eat more fruits and vegetables. Fruits and vegetables are nutrient-dense, filled with vitamins, minerals, phytonutrients and antioxidants. All of these substances work against disease, and the more you eat, the lower your risk of developing all sorts of disease. Aim for at least seven servings daily.

3. Take an antioxidant supplement. I usually eat eight or nine servings of fruits and vegetables every day. Sometimes, I eat as many as eleven. Yet, my blood recently showed more free radicals than is considered healthy, and I was told to boost my antioxidant intake. So, your healthy diet may not be sufficient to supply the antioxidants you need.

I recommend a 100% pure juice from one of the superberries, such as goji, Noni, or aca’i, or a mixture of such juices. Many antioxidant supplements come in a powder form, and those have lost up to two-thirds of their antioxidant value.

There are many other lifestyle changes you can make to help prevent cancer naturally. However, if you had to choose three, these would be the three I would recommend.