1. Optimal Health Hour – Voice of America

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    The Optimal Health Hour

    Tuesday at 2 PM Pacific

    December 27, 2016: Manage Stress During The Holidays

    The holidays are an opportunity for reflection, joy and peace. Then why do we feel stressed and why does any stress we already have seem more pronounced? Stop the madness and make your holidays joyful. This week we will talk with an expert on how you can manage and reduce stress, especially during the holiday season. This is a topic you don’t want to miss. Join us for the next Optimal Health Hour episode.
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    Loran Thompson

    An expert in stress management with over 25 years of experience, Loran Thompson is a corporate trainer, health coach, national speaker and founder of “The Wellness Edge”. Loran’s powerful and energetic message teaches her audience and clients how to reduce their stress and make healthier choices. Her willingness to share stories about overcoming her own obstacles, brings a refreshingly, “real” perspective to her presentations which include: Stress Management at Work, Achieving Balance at Work and Home, and Adopting a Healthy Lifestyle. Loran is dedicated and committed to her mission of empowering individuals to make healthy, positive changes in their lives. With an amazing ability …..
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  2. Optimal Health Hour – Voice of America

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    The Optimal Health Hour

    Tuesday at 2 PM Pacific

    December 13, 2016: Medical Marijuana and The FDA’s stance on the medical marijuana industry

    This week we will explore the scientific reasons behind medical Marijuana protocol and why it is so effective for treating illness. We will talk with a leading medical marijuana industry expert about medical marijuana protocol for a wide array of illnesses. You will learn about new research, where the FDA regulations are heading for medical marijua-na and what it means for patients that it can help. This is a hot topic you don’t want to miss. Join us for the next Optimal Health Hour episode.
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    Featured Guest

    Dr. Stuart Titus, Ph.D

    Stuart Titus, Ph.D. is a cannabis industry icon and innovator and the co-founder and President of General Hemp, LLC. He has a broad background in all aspects of the medical marijuana and industrial hemp industries. His passion is to help others by supporting the greater cannabis industry. He practiced as a British Physiotherapist for over fifteen years, specializing in integrative pain management and injury rehabilitation, treating over 40,000 patients. His first-hand experience with therapeutic hemp oil products as nutritional supplements drive him to continue to support the emerging cannabis medical marijuana and industrial hemp industries in the United States and abroad. A…..
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  3. Is Cancer Due to ‘Bad Luck’, Faulty Genes or Lifestyle Factors?

    Daniel Weber from Panaxea comments:

    The below article suggests that the stress hormone Corticotropin Releasing Factor (CRF) promotes breast cancer cell motility and invasiveness. CRF stimulates breast cancer progression and may stimulate metastasis. Another reason to work with your BCa patients to help them de-stress and take up those activities that calm the mind and spirit.

    Cancer cells secrete bioactive peptides that act in an autocrine or paracrine fashion affecting tumor growth and metastasis. Corticotropin-releasing factor (CRF), a hypothalamic neuropeptide that controls the response to stress, has been detected in breast cancer tissues and cell lines. CRF can affect breast cancer cells in an autocrine or paracrine manner via its production from innervating sympathetic neurons or immune cells.
    Overall, the data from Androulidaki et al., (2009) suggests that CRF stimulates cell motility and invasiveness of breast cancer cells most probably via induction of FAK phosphorylation and actin filament reorganization and production of prostaglandins via Cox1. Based on these findings they postulate that the stress neuropeptide CRF present in the vicinity of tumors (either produced locally by the tumor cells themselves or by nearby normal cells or secreted from the innervations of surrounding tissues) may play an important role on breast tumor growth and metastatic capacity, providing a potential link between stress and tumor progression.
    Source
    Corticotropin Releasing Factor promotes breast cancer cell motility and invasiveness. Mol Cancer. 2009 Jun 2;8:30. doi: 10.1186/1476-4598-8-30.

    Is Cancer Due to ‘Bad Luck’, Faulty Genes or Lifestyle Factors?

    A study published in Science in early 2015 reported that most cancers aren’t preventable and are simply a case of “bad luck”. That study said some tissue types give rise to human cancers millions of times more often than other tissue types. Although this has been recognized for more than a century, it has never been explained. Tomasetti & Vogelstein (2015) show that the lifetime risk of cancers of many different types is strongly correlated (0.81) with the total number of divisions of the normal self-renewing cells maintaining that tissue’s homeostasis.
    These results suggest that only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to “bad luck,” that is, random mutations arising during DNA replication in normal, noncancerous stem cells. This is important not only for understanding the disease but also for designing strategies to limit the mortality it causes.
    A year on, however, and a study published in Nature has come to the opposite conclusion: that external factors such as tobacco, sunlight and human papilloma virus play a greater part in whether or not a person gets cancer.
    So what does cause cancer: bad luck, or avoidable lifestyle choices and environmental factors?

    Why bad luck?
    The “bad luck” study, by Tomasetti and Vogelstein from Johns Hopkins University, was based on two facts.
    First, it is not the case that cancer is equally likely to occur in all the various organs and tissues of the body. Some cancers, such as colon cancer, are relatively common, while others, such as bone cancer, are much rarer for reasons that the study aimed to discover.
    Second, various types of tissues have different numbers of dividing cells, called stem cells, which serve to replace cells that have become old or damaged. How often these divide varies depending on where in the body they are located and how often the cells need to be replaced.

    According to one school of thought, cancer arises when stem cells go out of control.
    Every time a cell divides in two, it needs to make an accurate copy of its entire DNA. This copying process is usually accurate but mistakes can occur leading to spontaneous random mutations in the new cells. When mutations occur in genes that keep cell division under control, their tumour-suppressing job is prevented. The result is cancer.
    Tomasetti and Vogelstein proposed that every time a cell divides the random inaccuracy in DNA copying could result in a cancer-causing mutation. If individual cells divide more frequently, or if there are more cells dividing overall, then there is an increased chance of such mutations occurring.
    They looked at the behaviour of stem cells from various tissues, and in particular the number of stem cells and how often they divide in a human’s life. Based on how these numbers vary for different tissues, they inferred that the risk of developing a particular type of cancer was closely related to the number of times stem cells have divided in that tissue. This reflects the “intrinsic risk” that frequent DNA copying carries.

    Why environment?
    In the more recent study, researchers at Stony Brook University (SBU) in New York took another look at the data used by Tomasetti and Vogelstein. They noted that even when you take into account the total number of stem cell divisions, some cancers were still more likely to occur than others. More common cancers, they inferred, must have some additional external cause, such as the environment, lifestyle or genetic makeup.
    When they re-analysed the data on this basis they found that for many cancers, including some of the most common ones, such as lung and liver cancers, less than 10% of the risk was traceable to random copying errors.

    What to believe?
    The two studies have some things in common but differ substantially in their estimates of how much intrinsic and extrinsic risks contribute to cancer. Notably, the SBU team have backed up their argument with evidence that wasn’t included in Tomasetti and Vogelstein’s study.
    First of all, the SBU team highlight the vast array of evidence that points to a substantial contribution of environmental factors and lifestyle choices to cancer risk. For example, it’s well-known that colon cancer is comparatively rare in Japan but that Japanese immigrants in the USA and their descendants have an even higher risk of getting colon cancer than European Americans.
    health concept – cloud of related words and topicsThe SBU team also looked at the types of mutations that various cancers carry. Some mutations are seen more often in tumours from older patients. This fits with the “bad luck” model, where the key factors behind cancer occurrence are the errors that accumulate each time a cell divides.
    However, cancers also contain many other types of mutations that can occur because of specific carcinogens, for instance, the sunlight-triggered mutations in skin cancer. How often these cancer-causing changes occur depends much more on the amount of exposure a person has to carcinogens, rather than on age.
    Finally, they also showed that the known error rate for copying DNA is not high enough to be the sole determinant for the risk of developing the cancers both teams examined.
    Although we know what causes some types of cancer – such as smoking causing lung cancer – in many cases it’s more complicated than finding one simple cause. We are only just teasing apart many of the factors involved. While chance has a role in determining who gets cancer and who does not, it’s very clear that lifestyle, environment and our genes can change the odds considerably.

    Sources
    Allinson S. Oncology Network. Jan 12 2016 http://oncologynews.com.au/why-most-cancer-isnt-due-to-bad-luck/

    Tomasetti C & Vogelstein B. Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science 02 Jan 2015: Vol. 347, Issue 6217, pp. 78-81 DOI: 10.1126/science.1260825

  4. Optimal Health Hour – Voice of America

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    The Optimal Health Hour

    Tuesday at 2 PM Pacific

    December 06, 2016: Breast Cancer Conquero’s Amazing Journey

    Annie W. Brandt was diagnosed with advanced-stage breast cancer on Friday the 13th of July, 2001. It was found it in her lymphatic system, metastatic breast cancer was the diagnosis. The doctor immediately booked her for a double mastectomy, chemo and radiation. However due to her dysfunctional immune syndrome, she knew traditional chemo and radiation would kill her. Her doctor said if she did not do it she would be dead in 6 months. From this amazing journey Annie has gifted us a blueprint to build your own cure, “The Healing Platform”. We will discover what thousands have done to conque
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    Tuesday at 2 PM Pacific Time on VoiceAmerica Health and Wellness Channel
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    Annie Brandt

    Annie Brandt was diagnosed 15 years ago with cancerous tumors/lesions in her breast, lymph, brain, and lungs. She was given 3-5 months to live. Rather than get her affairs in order, she decided to research and devise a path for survival. Every day, cancer patients ask Annie how to be a survivor. She founded the Best Answer for Cancer Foundation to improve the quality of life and treatment of cancer patients with a holistic platform, targeted cancer therapies, and a patient-centered approach. Best Answer for Cancer Foundation (BAFC) believes the best standard of cancer care is one that provides the best quality of life during treatment and the best outlook for a long, vital life. Annie …..
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  5. If testosterone were the cause of prostate cancer, why dont 20 y.o. men have PCa

    Daniel Weber (PHD, MSC) comments on the article below:

    Historical perspective reveals that there is not now-nor has there ever been-a scientific basis for the belief that T causes PCa to grow. Discarding this modern myth will allow exploration of alternative hypotheses regarding the relationship of T and PCa that may be clinically and scientifically rewarding (Morgentaler, 2006).
    Testosterone supplementation after prostate cancer?
    At some point in their 40s, mens testosterone production begins to slow. By some estimates, levels of this hormone drop by about 1% a year. As men get into their 50s, 60s, and beyond, they may start to have signs and symptoms of low testosterone. These include reduced sex drive and sense of vitality, erectile dysfunction, decreased energy, lower muscle mass and bone density, and anaemia. When severe, these signs and symptoms characterise a condition called hypogonadism.

    Researchers estimate that hypogonadism affects two to six million men in the United States. Yet it is an underdiagnosed problem, with only about 5% of those affected receiving treatment, according to the FDA. Deciding which patients should receive testosterone supplementation has proved tricky, however. For example, little consensus exists on what constitutes low testosterone. (The Endocrine Society considers a man to have low testosterone if the blood level is less than 300 ng/dl; some physicians set higher or lower benchmarks.) In addition, some men may have low blood levels of testosterone but not experience any symptoms. And few large, randomised studies on the long-term risks or benefits of testosterone supplementation have been completed.

    One of the most heated debates centres on whether testosterone fuels prostate cancer. If thats true, say some experts, then why do men develop prostate cancer when they are older, at the same time their testosterone levels are dropping? (Harvard University, 2011)

    Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk
    Testosterone plays a central role in male development and health. Likewise, androgen deficiency, or hypogonadism, is associated with a variety of symptoms including decreased energy, diminished libido and erectile dysfunction, among others. Male androgen levels steadily decline with age, and, in a subset of symptomatic older men, can result in late-onset hypogonadism (LOH). Over the last decade, increased awareness of hypogonadism among patients and providers has led to a significant rise in the use of testosterone replacement therapy (TRT) for hypogonadism, and especially in LOH. Accompanying the rise in TRT are concerns of potential adverse effects, including cardiovascular risks and the promotion of prostate cancer. The androgen hypothesis asserts that prostate cancer development and progression is driven by androgens, and thus TRT has the theoretical potential to drive prostate cancer development and progression.

    While there is significant evidence that androgens promote prostate cancer in experimental systems. However, there is no clear evidence that elevations in endogenous testosterone levels promote the development of prostate cancer in humans.As a result of experimental and historical data on the progression of prostate cancer following TRT, there has been widespread belief that TRT will promote disease progression in prostate cancer patients. Despite these fears, there are a growing number of studies demonstrating no increase in prostate cancer incidence among men on TRT. Furthermore, in studies involving a small number of patients, there has been no discernible increase in disease progression in prostate cancer patients on TRT (Michaud et al., 2015).
    Sources
    Harvard University. http://www.harvardprostateknowledge.org/testosterone-supplementation-after-prostate-cancer
    Michaud JE, Billups KL, Partin AW. Ther Adv Urol. 2015 Dec; 7(6): 378387. doi: 10.1177/1756287215597633
    Morgentaler A. Testosterone and prostate cancer: an historical perspective on a modern myth. Eur Urol. 2006 Nov;50(5):935-9.