Cancer: Can testosterone improve patients’ quality of life?

Cachexia is a condition characterized by loss of body mass — including muscular atrophy — that is usually accompanied by severe weakness and fatigue. Many people who go through cancer experience this.

Studies have noted that “[a]pproximately half of all patients with cancer experience cachexia,” severely impairing their quality of life.

It appears to be “responsible for the death of 22 [percent] of cancer patients.”

What exactly causes this condition — which appears in some patients but not in others — remains unclear, and options to manage and address it are scarce.

But recently, researchers from the University of Texas Medical Branch in Galveston — led by Dr. Melinda Sheffield-Moore, from the Department of Health and Kinesiology — have been investigating the potential of administering testosterone in addition to chemotherapy in order to ameliorate the impact of cachexia.

“We hoped to demonstrate these [cancer] patients [who received testosterone treatment] would go from not feeling well enough to even get out of bed to at least being able to have some basic quality of life that allows them to take care of themselves and receive therapy.”

Dr. Melinda Sheffield-Moore

The researchers’ findings — now published in the Journal of Cachexia, Sarcopenia and Muscle — confirm that administering testosterone to individuals experiencing cachexia can, in fact, improve their quality of life to some extent, by restoring some independence of movement.

Adjuvant testosterone shows promise

The most widely used approach to manage cachexia is special nutrition treatments, but these often fail to prevent or redress the loss of body mass.

So, Dr. Sheffield-Moore and team decided to investigate the potential of testosterone based on existing knowledge that this hormone can help build up muscle mass.

“We already know that testosterone builds skeletal muscle in healthy individuals,” she says, “so we tried using it in a population at a high risk of muscle loss, so these patients could maintain their strength and performance status to be able to receive standard cancer therapies.”

In order to test this theory, the scientists worked — for 5 years — with volunteers who had been diagnosed with squamous cell carcinoma, which is a type of skin cancer.

The patients received chemotherapy, radiotherapy, or both, in order to treat the cancer. For 7 weeks during their treatment, some also received a placebo (the control cohort), while others received testosterone.

Dr. Sheffield-Moore and colleagues noticed that the participants who had been given extra testosterone had maintained total body mass and actually increased lean body mass (body mass minus body fat) by 3.2 percent.

“Patients randomized to the group receiving testosterone as an adjuvant to their standard of care chemotherapy and/or radiation treatment also demonstrated enhanced physical activity,” she continues.

“They felt well enough to get up and take care of some of their basic activities of daily living, like cooking, cleaning, and bathing themselves,” says Dr. Sheffield-Moore.

This effect could make a world of difference to people with cancer, as it allows them to maintain more autonomy.

At present, she and her team are looking to describe cancer patients’ muscle proteomes — the totality of proteins found in skeletal muscles — so as to understand how cancer in general, and specifically cachexia, affects their composition.

According to Dr. Sheffield-Moore, “What the proteome tells us is which particular proteins in the skeletal muscles were either positively or negatively affected by testosterone or by cancer, respectively.”

“It allows us to begin to dig into the potential mechanisms behind cancer cachexia,” she claims.

The scientists’ ultimate goal is to be able to support individuals likely to experience cachexia in continuing to support standard cancer treatment, and maintaining, as much as possible, their quality of life.

Article Source: https://www.medicalnewstoday.com/articles/322487.php?utm_source=dlvr.it&utm_medium=gplus

Published Tuesday 17 July 2018

By Maria Cohut

Fact checked by Jasmin Collier

 

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Report: Industry hid decades-old study showing sugar’s unhealthy effects

Big Sugar seems to have copied the Big Tobacco playbook, a new report contends.

More than four decades ago, a study in rats funded by the sugar industry found evidence linking the sweetener to heart disease and bladder cancer, the paper trail investigation reports.

The results of that study were never made public.

Instead, the sugar industry pulled the plug on the study and buried the evidence, said senior researcher Stanton Glantz, a professor of medicine and director of the University of California, San Francisco (UCSF) Center for Tobacco Control Research and Education.

Glantz likened this to suppressed Big Tobacco internal research linking smoking with heart disease and cancer.

“This was an experiment that produced evidence that contradicted the scientific position of the sugar industry,” Glantz said. “It certainly would have contributed to increasing our understanding of the cardiovascular risk associated with eating a lot of sugar, and they didn’t want that.”

In response to the investigation, The Sugar Association issued a statement calling it “a collection of speculations and assumptions about events that happened nearly five decades ago, conducted by a group of researchers and funded by individuals and organizations that are known critics of the sugar industry.”

The new paper focuses on an industry-sponsored study referred to as Project 259 in documents generated by the Sugar Research Foundation and its successor, the International Sugar Research Foundation, and dug up decades later by Glantz and his colleagues.

Researchers at the University of Birmingham in England conducted Project 259 between 1967 and 1971, comparing how lab rats fared when fed table sugar versus starch. The scientists specifically looked at how gut bacteria processed the two different forms of carbohydrate.

Early results in August 1970 indicated that rats fed a high-sugar diet experienced an increase in blood levels of triglycerides, a type of fat that contributes to cholesterol.

Rats fed loads of sugar also appeared to have elevated levels of beta-glucuronidase, an enzyme previously associated with bladder cancer in humans, the researchers said.

Months after receiving these results, the International Sugar Research Foundation failed to approve an additional 12 weeks of funding that the Birmingham researchers needed to complete their work, according to the authors behind the new investigation.

“The investigator they funded came back to them with preliminary results, which were showing these adverse effects of sugar and said, ‘I need a few more weeks to finish the study,'” Glantz said. “They just looked at it and said no, and shut the whole thing down. As far as we can tell, nothing was ever published.”

Project 259’s timing was critical, said Glantz and lead author Cristin Kearns, a postdoctoral fellow with the UCSF School of Medicine who reportedly discovered the industry documents.

During that period, the U.S. Food and Drug Administration was weighing whether to take a hard line on high-sugar foods.

“Had those results been made public, sugar would have gotten a lot more scrutiny than it did,” Kearns said.

The Sugar Association says Project 259 was significantly delayed and over budget, “and the delay overlapped with an organizational restructuring with the Sugar Research Foundation becoming a new entity, the International Sugar Research Foundation,” according to its own review of archive material.

“There were plans to continue the study with funding from the British Nutrition Foundation, but, for reasons unbeknown to us, this did not occur,” the industry trade group’s statement says.

“Throughout its history, the Sugar Association has embraced scientific research and innovation in an attempt to learn as much as possible about sugar, diet and health,” the statement continues. “We know that sugar consumed in moderation is part of a balanced lifestyle, and we remain committed to supporting research to further understand the role sugar plays in consumers’ evolving eating habits.”

Nutritionist Sharon Zarabi is director of the bariatric program at Lenox Hill Hospital in New York City. She said the new investigation reveals “the power food industry lobbyists have on government guidelines that instruct us on what to eat.”

Zarabi noted that “most research studies that support specific foods are funded by industry and this oftentimes skews the results.”

Although these revelations might produce a media furor, they’re unlikely to change the recommendations coming from dietitians, said Kelly Hogan, clinical nutrition and wellness manager at the Mount Sinai Dubin Breast Center in New York City.

That’s because subsequent research has revealed the effect that diets high in sugar can have on long-term health. People need to follow a balanced diet if they want to eat healthy, and that doesn’t mean just focusing on added sugars, she said.

“You can’t point out one single thing and blame that on any sort of health crisis, either now or 40 years ago,” Hogan said. “It’s never just one thing, whether that’s sugar or saturated fat or whatever the trendy thing might be.”

The new paper was published online in November in the journal PLOS Biology. It was funded by a grant from the U.S. National Cancer Institute, among others.

Article Source: http://www.chicagotribune.com/lifestyles/health/sc-hlth-industry-hid-effects-of-sugar-1129-story.html

Written By: Dennis Thompson

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From Causing Cancer To Treating Depression, 6 Little-Known Facts About Oral Sex

Before the Clinton years and well after the Michael Douglas days, the notion of oral sex has been considered taboo. Now, oral sex is more openly discussed in movies, TV shows, and magazines as a pleasurable part of a healthy adult relationship. However, there’s much about oral sex that sexually active people should know before performing fellatio or cunnilingus on their partner.

In the U.S., 27 percent of men and 19 percent of women have had oral sex in the past year, according to a 2010 National Survey of Sexual Health and Behavior (NSSHB).  Meanwhile in 2012, two-thirds of young Americans aged 15 to 24 have engaged in oral sex. Most of these young adults have tried oral sex before they engage in intercourse because of the popular misconception that oral sex is “risk-free,” but that’s not the case.

The surprising facts below will clarify misinformation surrounding sex, especially oral sex, and what can happen to the human body.

1. Men give oral sex as much as they receive it, especially older men.

Contrary to popular belief, men, especially older men, give as much oral sex to women as women give to men. A 2010 study published in The Journal of Sexual Medicine found only 55 percent of men in the 20 to 24-year-old range admitted to giving oral sex in the past year compared to 75 percent of women. In the 30 to 39 age range, 69 percent of men have given women oral sex compared to 59 percent of women. This pattern suggests that the more you age, the more reciprocal you are in oral sex.

2. Giving oral sex can lower the risk of preeclampsia.

Pregnant women who perform oral sex on their male partner can lower their risk of preeclampsia. A 2000 study published in the Journal of Reproductive Immunology found women a strong correlation between a diminished incidence of preeclampsia and the frequency at which a woman practices oral sex. If a woman had relatively little prior exposure to the father’s semen, she would have a higher risk of developing the condition compared to if she performed oral sex and swallowed his semen.

The researchers believe this occurs because of the development of immunological tolerance via oral insertion and gastrointestinal absorption of the semen. This supports the notion that a greater frequency of sex with the same partner who is the father of a woman’s child, can significantly decrease her chances of developing preeclampsia. The pregnancy complication is characterized by high blood pressure, and can sometimes be accompanied by fluid retention and proteinuria.

3. Swallowing semen during oral sex can ease pregnancy morning sickness.

Typically, the nausea that occurs during the first few months of pregnancy, morning sickness, can be remedied with a teaspoon of ginger or mint. However, a 2012 paper written by SUNY-Albany psychologist Gordon Gallup suggests pregnant women who swallow the father’s semen can actually cure their episodes of morning sickness.  The woman’s body will first reject the father’s semen upon ingestion as an infection and then react to it by vomiting, according to Gallup. After this, the woman’s body will build up a tolerance to it and alleviate the morning sickness symptoms.

4. Sperm via oral sex can lower the risk of depression.

Semen’s mood altering chemicals can elevate mood, increase affection, and ward off depression. A 2012 studypublished in the journal Archives of Sexual Behavior found seminal fluid may contain antidepressant properties and may significantly lower depression in women who had oral sex and sexual intercourse. The researchers also noted women who described themselves as “promiscuous” yet used condoms, were as depressed as women who practice absinthe. This implies how it’s not the semen, not the sex that made the women in this study happy.

5. Oral sex can give you cancer.

The link between oropharynx cancers and HPV has been growing overtime in the U.S. A 2011 study published in the Journal of Clinical Oncology found the proportion of cancers associated with human papillomavirus (HPV) rose from 16 percent to 72 percent from the late 1980s to the early 2000s, particularly among Caucasian middle-age men. The sexually transmitted disease (STI) can cause genital warts or present itself without symptoms. If it’s left untreated, it can also cause cancers including cervix, anus, penis, vagina, and head and neck, among many others.

6. You can get STDs from oral sex.

STDs are commonly transmitted through vagina and anal sex, but unprotected oral sex can also put you at risk for them. HPV, gonorrhea, syphilis, herpes, and hepatitis B can all be spread through oral sex. According to Planned Parenthood, the human immunodeficiency virus is less likely to be transmitted through this.

Oral sex is still sex and should always be performed with caution and preferably with a condom on to reduce the transmission of STDs.

Written By: Lizette Borreli

Article Source: http://www.medicaldaily.com/causing-cancer-treating-depression-6-little-known-facts-about-oral-sex-343010

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Muscles Fight Cancer – The Science Behind Outmuscling Cancer

Written by: Colin Champ, MD

Several years back a scientific article revealed that those of us with high “muscular strength” have a lower risk of becoming a victim to cancer – a 40% lower risk to be exact.¹ After assessment of almost 9,000 men aged 20-82, scientists found that men with a stronger one-rep max on bench press and leg press have a 40% reduction in their risk of dying from cancer. They adjusted for body mass index (BMI), body fat, and cardiorespiratory fitness and the results still held strong (pun intended).² In other words, there is something about simply being stronger that can lower our risk of getting cancer. Many felt as though there was something innately healthy about having more muscles, but another study associated weak hand grip strength with an increased risk of cancer, even regardless of muscle size.³ So is it all about strength or do muscles fight cancer?

Strength goes beyond lowering our risk of dying from cancer; it lowers our risk of dying from most major health issues. For instance, men exhibiting a lower vertical leap, less sit-ups, and decreased grip strength have a higher risk of dying period.⁴Men and women with moderate and high bench press and sit-up scores have lower risks of death,⁵ while men with a higher 1-repetition bench and leg press apparently live longer (even when we account for other health issues, like cardiovascular disease, smoking, obesity, etc.).⁶

Muscles Fight Cancer – More Muscles = More Health?

The first thought that comes to mind is that more muscles means more strength, and both are a result of more exercise. Sure enough, when we take a close look through these studies, we do see that the strongest among us have less body fat, are in better shape, and have better “good” cholesterol values with lower blood sugar and triglycerides.¹ This is not surprising.

However, in nearly all these “muscles fight cancer” studies, other health issues were adjusted for and the findings still held. In other words, these studies seem to suggest that strength is independently associated with a lower risk of cancer and a higher change of avoiding an untimely death, regardless of age, smoking, alcohol usage, or other health issues. But as we know, associations can only take us so far, before we must explore the mechanism that support these associations.

Muscles Fight Cancer – It’s the Muscles!

In the study above, the scientists found some intriguing results: the benefits of muscular strength overlap with cardiovascular fitness, but the benefits of muscular strength in decreasing the risk of cancer death work through different mechanisms.¹Perhaps the synergy exists, or in other words, having more muscle and strength is good, and exercising them is better.

For instance, we know that exercising our muscles leads to:

• Improved insulin sensitivity (less insulin needed to remove sugar from our blood)
• More sugar extracted from our blood by skeletal muscle and used for energy during exercise
• Less cancer-promoting sugar and insulin floating around our blood
• A decrease in the levels of hormones that, over a prolonged period, can lead to cancer. For instance, resistance training increases IGFBP-3, which binds to insulin-like growth factor (IGF), decreasing its ability to promote cancer (growth factors are normal within the human body, but too many can lead to excessive cellular growth, including cancer growth)⁷
• Decreased inflammation (which when present, serves as a fertilizer for cancer)
• Increased antioxidant defense, which helps fight potential cancer-causing free-radicals
• Less inflammation-producing body fat

However, recent studies have changed much of our thinking when it comes to muscle. There are many organs in our body that respond to stimuli and secrete hormones, which serve as messages to direct remote parts of the body. We are recently starting to find some more unconventional organ-like structures in the body. For instance, it is now well-established that our adipose tissue works like an endocrine organ – albeit a bad one – secreting inflammatory hormones and an excess of potentially cancer-stimulating hormones.⁸ Take estrogen for example, which is a hormone that both men and women require to function normally. However, when supplied in higher than physiologically normal amounts from excess body fat, it can increase a woman’s risk of breast cancer. When women lose theses additional pounds through dietary changes and exercise, estrogen levels decrease.⁹

Studies have now shown that fat is not the only recently discovered endocrine organ. Muscle may act similarly, though this time to the benefit of our health. The metabolic muscular organ within us secretes IL-6, an important cytokine that was once felt to be a bad guy that caused inflammation. Newer studies reveal that IL-6 has a healthy role and is actually a myokine, which is an endocrine hormone produced by muscle (myo = muscle) and released during contraction. In other words, while fat secretes harmful hormones, muscles squeeze out some healthy hormones during lifting.

Muscles Fight Cancer – The Physiologic Benefits of Having More Muscle

As discussed above, exercise has plenty of benefits. However, contracting our muscles during running, resistance training, or simply heavy lifting provides benefits that are entirely separate from those of exercise.

For instance, while fat tissue secretes the pro-inflammatory cytokine TNF-α (which stands for tumor necrosis factor since our immune cells secrete it in the presence of tumor cells), our muscles secrete IL-6, which fights inflammation. As bad as fat is generally considered, muscle seems to stand in direct opposition to fat physiologically, and TNF versus IL-6 further embodies this difference.

• Adipose-derived TNF is inflammatory, while muscle-derived IL-6 is anti-inflammatory.
• Muscle-derived IL-6 signals to our body to break down lipids and burn fat.¹⁰
• Adipose-derived TNF causes insulin resistance and impairs glucose uptake by our cells (both leading to increased blood sugar).¹¹
• While serious and often fatal events like septic shock cause a sudden release of TNF, excess adipose tissue causes the chronic release of harmful TNF.
• Muscle-derived IL-6 helps regulate AMPK (while muscle contraction directly activates AMPK), which stimulates the breakdown of fat and cholesterol, stimulates our mitochondria, and potentially fights cancer.¹²

 

AMPK, or AMP-activated protein kinase, is an enzyme extensively expressed in our muscles, liver, and brain. It serves as an energy sensor and regulator and closely monitors changes in energy status based on our dietary and lifestyle habits. ATP, the energy currency of our cells, is broken down to AMP by our cells. ATP has three phosphates (the T is for tri) and when it loses one becomes ADP (the D is for di, or two) and when it loses two phosphates it becomes AMP (the M is for mono). Without dipping too deep into boredom territory:

ATP → ADP + P

ATP → AMP + 2P

AMPK works to supply more ATP and increase our available energy molecules. AMPK achieves this through several mechanisms described in the picture below. The dark blue mechanisms involve breaking down glucose (sugar) to burn for energy. This can be done by pulling glucose out of our blood stream and into our cells to be consumed. The aqua circles represent the breaking down of cholesterol and fat to be used as an efficient source of energy. The purple includes building more mitochondria to use these fats and sugars to make more energy, and the light blue mechanisms turn off cell building and replication.

 

Basically, AMPK signals to our body and cells that it is not a time for building, but rather for breaking down.

AMPK and Cancer

 

AMPK is, in essence, the antithesis of cancer. While cancer cells are burning large amounts of glucose and nutrients, this is mostly to build up biomass – or simply put to keep growing and spreading. AMPK, on the other hand, shuts off this process, blocking cancer growth so we can feed our own cells.^12,13 As you can see in the picture to the right, AMPK actually blocks mTOR, a pathway that leads to cancer survival and growth.¹⁴ This is the same pathway that is blocked with targeted cancer drugs. You will also notice that the pathways are all affected by intermittent fasting, labeled as “IF,” as this is a state of energy scarcity.  You may also notice that increased insulin sensitivity, which happens though exercise and muscle contraction, also appears to upregulate AMPK.

AMPK and Warburg

The Warburg hypothesis is something that comes up often when dealing with cancer and metabolism. Briefly put, Warburg showed that regardless of the presence of oxygen, cancer cells prefer to use glucose for energy derivation (through a process known as glycolysis). In our normal cells, preference is given to the mitochondria for energy production, as it is significantly more efficient. While AMPK may stop several pro-cancer pathways, newer data shows that it actually blocks the Warburg Effect, by blocking the ability of cancer cells to use sugar for energy.¹⁵

AMPK is upregulated via several mechanisms (in no apparent order):

1. Muscle contraction during exercise,^16,17 with the more intense exercise resulting in increased expression of AMPK¹⁸
2. Carbohydrate restriction (with or without fasting and even in the face of an increase in calories)¹⁹
3. Intermittent fasting²⁰

Inflammation is the fertilizer of cancer cells; it fosters an environment where normal cells can turn cancerous and cancer cells can grow with less effort. Inflammation has recently been labeled a “hallmark of cancer cells.”²¹ Any method to decrease this inflammation can provide health benefits, and even decrease the risk of cancer. When muscles are contracted, they release IL-6 and several other hormonal signals that act to decrease inflammation. These “signals” alert other organs that energy status is down, stimulating processes like AMPK,²² leading to a state of breaking down components for energy instead of stimulating growth processes like cancer. In other words, our muscles are creating signals that act at distant places within the body. These signals are plenty, but one of the more famous is when muscles signal to our bones to grow stronger²³ – one of the many reasons why weight training strengthens bones.²⁴ In a sense, the way in which our muscles “talk” with the rest of our body is only one of the many ways in which they improve our health, and ultimately, help in the fight against cancer.

Muscles Fight Cancer – The Physiologic Benefits of Lifting Weights

While our muscle cells (myocytes) secrete IL-6 at baseline, exercise increases this release up to 100 times.²⁵ Those of us that exercise and contract our muscles frequently experience a sensitization to IL-6 when not exercising and at rest.²⁶ While excess fat tissue desensitizes us to the action of insulin (i.e. more insulin is needed to get rid of extra blood sugar), increasing harmful amounts of blood sugar, contracting our muscle sensitizes us to the benefits of muscle-derived IL-6.

The amount of IL-6 produced depends on several factors,²⁷ including:

• Intensity of the exercise
• Duration of the exercise
• Endurance capacity
• Size of muscle contracting

As a side note, carb-loading before exercise appears to oppose this effect, blunting IL-6 release from the muscle, perhaps paying homage to our ancient times of exercise, which was often hunting for wild game on an empty stomach.²⁸

Countering the benefits of weight-lifting are the harms of inactivity, which, much like excess body fat, increases background inflammation.²⁹ Exercise is such a powerful anti-inflammatory, that it offsets the potential inflammatory damage from injection of the toxin E. coli into healthy volunteers. For instance, while E. coli normally causes doubling or tripling of harmful TNF, when injected during exercise, no increase occurs.³⁰ Not surprisingly, trained athletes have lower levels of several inflammatory factors.³¹

Inflammation is the likely cause of or contributor to many diseases, including atherosclerosis, diabetes, and cancer. Oxidative (free radical) damage is also considered a major cause of disease and cancer.³² Much like inflammation, high levels of free radicals can damage our cells and DNA, exposing us to a higher risk of cancer. To counter this potential damage, our cells have spent millions of years developing a defense mechanism against free radicals – known as the antioxidant defense system – that creates a plethora of antioxidant compounds that can offset the harm of radicals.

When we place men on a regimen of muscle-activating resistance training twice a week, many of these antioxidant defense mechanisms are activated. For instance, glutathione peroxidase, which defuses the potential damage from free radicals that are bound to lipids, is increased. Mitochondrial and cytosolic superoxide dismutase – which break apart, or dismutase the potentially harmful free radical superoxide – are amplified. Interestingly, when weight lifting was compared to endurance training, the latter antioxidant mechanism was only increased by weight training.³³ Muscle biopsies of legs after unilateral resistance training shows similar findings, that antioxidant defense mechanisms are boosted.³⁴

Finally, while muscle and fat can be considered opposites by the hormones they produce, the same can be said about stimulated muscle versus inactivity. Muscle contraction releases large amounts of IL-6, which sensitizes our cells to its effect, resulting in less IL-6 circulating at rest. In other words, our cells get better at dealing with IL-6 and inflammation from exercise. Muscle-derived IL-6 is beneficial, but a constantly elevated amount of IL-6 can be inflammatory.

High levels of adipose tissue and inactivity lead to an opposite state when it comes to insulin. Both decrease insulin sensitivity, or in other words, more insulin is required to rid the blood of sugar, which eventually results in chronically elevated levels of circulating insulin and sugar within our blood. Both are unhealthy and can lead to cancer.³⁵ Further closing the loop of association, exercise-derived IL-6 increases insulin sensitivity and can prevent this damaging state from inactivity and excessive body fat.

Muscles Fight Cancer – A Final Comment of Exercise, Blood Sugar and Cancer

Many people have recently questioned the benefit of exercise before or after a cancer diagnosis since it can result in elevated levels of blood glucose. This occurs when our body mobilizes available stores of glucose (from glycogen within the liver and muscles). As increased blood glucose levels correlate with an increased risk of several cancers,³⁶ this may seem concerning on the surface. Furthermore, while IL-6 secreted from muscle increases the breakdown of fats and activation of the AMPK energy sensor can reduce the risk of cancer,^37–39 the increase in PI3K, another pro-cancer pathway, is concerning.

Yet, these changes primarily occur in the muscle, which is using the mobilized glucose. Furthermore, the rise in blood sugar is transient (glucose levels drop by 30 minutes afterwards⁴⁰), and as exercise and resistance training increases insulin sensitivity, overall we are left with a lower blood glucose and insulin level.⁴¹ The multitude of other physiologic changes that occur listed above provide an overwhelming anti-cancer benefit. This has played out in several recent studies, showing a decreased risk of breast cancer in women who exercise, with some data suggesting additional benefit from strenuous exercise.^42,43 The benefits appear to be similar for women who were already diagnosed with breast cancer.⁴⁴

Muscles Fight Cancer – Conclusions

Muscles fight cancer and strength is associated with a decreased risk of cancer. The conclusions are obvious: if you are physically able, lift more weights, build more muscle, and increase your strength. Do it safely, do it right, and do it periodically to ensure that you are “health cost averaging.” Flex your muscles and squeeze out the anti-inflammatory beneficial messengers that direct the rest of our body to be healthy.

I hope this article has convinced you to lift (or throw around) some weights, put on some muscle, and fight cancer. The added benefits are stronger bones, a better physique, and hopefully, a longer life.

It looks like muscles fight cancer, but to do so, they must be put to work.

Muscles Fight Cancer References

1. Ruiz JR, Sui X, Lobelo F, et al. Muscular strength and adiposity as predictors of adulthood cancer mortality in men. Cancer Epidemiol Biomarkers Prev. 2009;18(5):1468-1476. doi:10.1158/1055-9965.EPI-08-1075.
2. Ramírez-Vélez R, Correa-Bautista JE, Lobelo F, et al. High muscular fitness has a powerful protective cardiometabolic effect in adults: influence of weight status. BMC Public Health. 2016;16(1):1012. doi:10.1186/s12889-016-3678-5.
3. Gale CR, Martyn CN, Cooper C, Sayer AA. Grip strength, body composition, and mortality. Int J Epidemiol. 2007;36(1):228-235. doi:10.1093/ije/dyl224.
4. Fujita Y, Nakamura Y, Hiraoka J, et al. Physical-strength tests and mortality among visitors to health-promotion centers in Japan. J Clin Epidemiol. 1995;48(11):1349-1359. http://www.ncbi.nlm.nih.gov/pubmed/7490598. Accessed January 3, 2017.
5. FitzGerald SJ, Barlow CE, Kampert JB, Morrow JR, Jackson AW, Blair SN. Muscular Fitness and All-Cause Mortality: Prospective Observations. J Phys Act Heal. 2004;1(1):7-18. doi:10.1123/jpah.1.1.7.
6. Ruiz JR, Sui X, Lobelo F, et al. Association between muscular strength and mortality in men: prospective cohort study. BMJ. 2008;337.
7. Izquierdo M, Ibañez J, González-Badillo JJ, et al. Differential effects of strength training leading to failure versus not to failure on hormonal responses, strength, and muscle power gains. J Appl Physiol. 2006;100(5).
8. Siiteri PK. Adipose tissue as a source of hormones. Am J Clin Nutr. 1987;45(1):277-282. http://www.ajcn.org/content/45/1/277.abstract. Accessed January 24, 2017.
9. Campbell KL, Foster-Schubert KE, Alfano CM, et al. Reduced-calorie dietary weight loss, exercise, and sex hormones in postmenopausal women: randomized controlled trial. J Clin Oncol. 2012;30(19):2314-2326. doi:10.1200/JCO.2011.37.9792.
10. Hall G van, Steensberg A, Sacchetti M, et al. Interleukin-6 Stimulates Lipolysis and Fat Oxidation in Humans. J Clin Endocrinol Metab. July 2013. http://press.endocrine.org/doi/abs/10.1210/jc.2002-021687. Accessed September 30, 2015.
11. Plomgaard P, Bouzakri K, Krogh-Madsen R, Mittendorfer B, Zierath JR, Pedersen BK. Tumor necrosis factor-alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation. Diabetes. 2005;54(10):2939-2945. http://www.ncbi.nlm.nih.gov/pubmed/16186396. Accessed January 27, 2017.
12. Shackelford DB, Shaw RJ. The LKB1-AMPK pathway: metabolism and growth control in tumour suppression. Nat Rev Cancer. 2009;9(8):563-575. doi:nrc2676 [pii]10.1038/nrc2676.
13. Green AS, Chapuis N, Maciel TT, et al. The LKB1/AMPK signaling pathway has tumor suppressor activity in acute myeloid leukemia through the repression of mTOR-dependent oncogenic mRNA translation. Blood. 2010;116(20):4262-4273. doi:blood-2010-02-269837 [pii] 10.1182/blood-2010-02-269837.
14. Champ CE, Baserga R, Mishra M V, et al. Nutrient Restriction and Radiation Therapy for Cancer Treatment: When Less Is More. Oncologist. 2013;18(1):97-103. doi:10.1634/theoncologist.2012-0164.
15. Faubert B, Boily G, Izreig S, et al. AMPK is a negative regulator of the Warburg effect and suppresses tumor growth in vivo. Cell Metab. 2013;17(1):113-124. doi:10.1016/j.cmet.2012.12.001.
16. Vavvas D, Apazidis A, Saha AK, et al. Contraction-induced changes in acetyl-CoA carboxylase and 5’-AMP-activated kinase in skeletal muscle. J Biol Chem. 1997;272(20):13255-13261. http://www.ncbi.nlm.nih.gov/pubmed/9148944. Accessed January 16, 2015.
17. Winder WW, Hardie DG. Inactivation of acetyl-CoA carboxylase and activation of AMP-activated protein kinase in muscle during exercise. Am J Physiol. 1996;270(2 Pt 1):E299-304. http://www.ncbi.nlm.nih.gov/pubmed/8779952. Accessed January 16, 2015.
18. Rasmussen BB, Winder WW. Effect of exercise intensity on skeletal muscle malonyl-CoA and acetyl-CoA carboxylase. J Appl Physiol. 1997;83(4):1104-1109. http://www.ncbi.nlm.nih.gov/pubmed/9338417. Accessed January 16, 2015.
19. Draznin B, Wang C, Adochio R, Leitner JW, Cornier MA. Effect of Dietary Macronutrient Composition on AMPK and SIRT1 Expression and Activity in Human Skeletal Muscle. Horm Metab Res. 2012;44(9):650-655. doi:10.1055/s-0032-1312656.
20. Cantó C, Jiang LQ, Deshmukh AS, et al. Interdependence of AMPK and SIRT1 for metabolic adaptation to fasting and exercise in skeletal muscle. Cell Metab. 2010;11(3):213-219. doi:10.1016/j.cmet.2010.02.006.
21. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646-674.
22. Hardie DG. Sensing of energy and nutrients by AMP-activated protein kinase. Am J Clin Nutr. 2011;93(4):891S-6. doi:ajcn.110.001925 [pii]10.3945/ajcn.110.001925.
23. Hamrick MW. A role for myokines in muscle-bone interactions. Exerc Sport Sci Rev. 2011;39(1):43-47. doi:10.1097/JES.0b013e318201f601.
24. Layne JE, Nelson ME. The effects of progressive resistance training on bone density: a review. Med Sci Sports Exerc. 1999;31(1):25-30. http://www.ncbi.nlm.nih.gov/pubmed/9927006. Accessed January 29, 2017.
25. Pedersen BK, Steensberg A, Keller P, et al. Muscle-derived interleukin-6: lipolytic, anti-inflammatory and immune regulatory effects. Pflügers Arch Eur J Physiol. 2003;446(1):9-16. doi:10.1007/s00424-002-0981-z.
26. Keller P, Keller C, Carey AL, et al. Interleukin-6 production by contracting human skeletal muscle: autocrine regulation by IL-6. Biochem Biophys Res Commun. 2003;310(2):550-554. doi:10.1016/j.bbrc.2003.09.048.
27. Pedersen BK, Febbraio MA. Muscle as an Endocrine Organ: Focus on Muscle-Derived Interleukin-6. Physiol Rev. 2008;88(4):1379-1406. doi:10.1152/physrev.90100.2007.
28. Febbraio MA, Steensberg A, Keller C, et al. Glucose ingestion attenuates interleukin-6 release from contracting skeletal muscle in humans. J Physiol. 2003;549(Pt 2):607-612. doi:10.1113/jphysiol.2003.042374.
29. Gratas-Delamarche A, Derbré F, Vincent S, Cillard J. Physical inactivity, insulin resistance, and the oxidative-inflammatory loop. Free Radic Res. 2014;48(1):93-108. doi:10.3109/10715762.2013.847528.
30. Starkie R, Ostrowski SR, Jauffred S, Febbraio M, Pedersen BK. Exercise and IL-6 infusion inhibit endotoxin-induced TNF-alpha production in humans. FASEB J. 2003;17(8):884-886. doi:10.1096/fj.02-0670fje.
31. Lira FS, Rosa JC, Pimentel GD, et al. Endotoxin levels correlate positively with a sedentary lifestyle and negatively with highly trained subjects. Lipids Health Dis. 2010;9:82. doi:10.1186/1476-511X-9-82.
32. Oberley TD. Oxidative damage and cancer. Am J Pathol. 2002;160(2):403-408. doi:10.1016/S0002-9440(10)64857-2.
33. García-López D, Häkkinen K, Cuevas MJ, et al. Effects of strength and endurance training on antioxidant enzyme gene expression and activity in middle-aged men. Scand J Med Sci Sports. 2007;17(5):595-604. doi:10.1111/j.1600-0838.2006.00620.x.
34. Parise G, Phillips SM, Kaczor JJ, Tarnopolsky MA. Antioxidant enzyme activity is up-regulated after unilateral resistance exercise training in older adults. Free Radic Biol Med. 2005;39(2):289-295. doi:10.1016/j.freeradbiomed.2005.03.024.
35. Lehrer S, Diamond EJ, Stagger S, Stone NN, Stock RG. Increased serum insulin associated with increased risk of prostate cancer recurrence. Prostate. 2002;50(1):1-3. http://www.ncbi.nlm.nih.gov/pubmed/11757030. Accessed December 24, 2015.
36. Crawley DJ, Holmberg L, Melvin JC, et al. Serum glucose and risk of cancer: a meta-analysis. BMC Cancer. 2014;14:985. doi:10.1186/1471-2407-14-985.
37. Klement RJ, Champ CE. Calories, carbohydrates, and cancer therapy with radiation: exploiting the five R’s through dietary manipulation. Cancer Metastasis Rev. January 2014:1-13. doi:10.1007/s10555-014-9495-3.
38. Klement RJ, Fink MK. Dietary and pharmacological modification of the insulin/IGF-1 system: exploiting the full repertoire against cancer. Oncogenesis. 2016;5:e193. doi:10.1038/oncsis.2016.2.
39. Fine EJ, Champ CE, Feinman RD, Márquez S, Klement RJ. An Evolutionary and Mechanistic Perspective on Dietary Carbohydrate Restriction in Cancer Prevention. J Evol Heal. 2016;1(1). doi:10.15310/2334-3591.1036.
40. Goodwin ML. Blood glucose regulation during prolonged, submaximal, continuous exercise: a guide for clinicians. J Diabetes Sci Technol. 2010;4(3):694-705. http://www.ncbi.nlm.nih.gov/pubmed/20513337. Accessed January 29, 2017.
41. Adams OP. The impact of brief high-intensity exercise on blood glucose levels. Diabetes Metab Syndr Obes. 2013;6:113-122. doi:10.2147/DMSO.S29222.
42. Bernstein L, Henderson BE, Hanisch R, Sullivan-Halley J, Ross RK. Physical Exercise and Reduced Risk of Breast Cancer in Young Women. JNCI J Natl Cancer Inst. 1994;86(18):1403-1408. doi:10.1093/jnci/86.18.1403.
43. Carpenter CL, Ross RK, Paganini-Hill A, Bernstein L. Lifetime exercise activity and breast cancer risk among post-menopausal women. Br J Cancer. 1999;80(11):1852-1858. doi:10.1038/sj.bjc.6690610.
44. Bradshaw PT, Ibrahim JG, Khankari N, et al. Post-diagnosis physical activity and survival after breast cancer diagnosis: the Long Island Breast Cancer Study. Breast Cancer Res Treat. 2014;145(3):735-742. doi:10.1007/s10549-014-2966-y.

 

Article Source:  http://colinchamp.com/muscles-fight-cancer/

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The Promising Potential of Medical Marijuana

 

Medical marijuana is now legal in several U.S. states, but it’s still incredibly difficult for scientists to legally study it. The possible therapeutic uses of marijuana are vast, but more research is still needed. Read on to learn about the most promising potential applications of medical marijuana and the current state of marijuana research.

Marijuana is the term commonly used for the Cannabis sativa plant. (1) Despite being legal in 23 states and Washington, D.C., cannabis is still federally classified as a Schedule I drug, meaning that it has a high abuse potential and no medical use currently accepted by the U.S. government. (2) Other Schedule I drugs include heroin and 3,4-methylenedioxymethamphetamine (ecstasy), while cocaine and methamphetamine (meth) are Schedule II drugs, since they have an officially recognized medical use. (2)

As crazy as this may sound, it’s harder for scientists to conduct studies on marijuana than on cocaine or meth. College students routinely administer methamphetamine to rodents in their science classes, but if they are caught with cannabis, they may face serious disciplinary—or even legal—consequences.

The differences between cannabis, CBD, and THC

The terms “marijuana” and “cannabis” both refer to any of the subspecies of the whole, unprocessed Cannabis sativa plant and its basic extracts. (3) Cannabidiol (CBD) and delta-9-tetrahydrocannibidol (THC) are chemical compounds found in the cannabis plant that are of particular medical interest. These chemicals and those that resemble them are known as cannabinoids. (3) THC is the psychoactive chemical in cannabis responsible for much of the “high” that users feel; CBD, however, is non-psychoactive and does not produce the physiological responses that THC does. (4, 5)

While using unprocessed cannabis as medicine remains unapproved by the Food and Drug Administration (FDA), the FDA has approved two synthetic cannabinoid medications. These medications are dronabinol and nabilone, both of which are approved for the treatment of nausea caused by chemotherapy and to increase appetite in patients with extreme weight loss caused by AIDS. (3) However, there are numerous other areas in which cannabis and cannabinoids could prove beneficial to people’s health and well-being.

Four promising uses for medical marijuana

Endocannabinoid receptors suggest potential targets and applications for medical cannabis

The human brain contains endocannabinoid receptors. Cannabinoids can induce either an inhibitory or excitatory response from the affected neuron by acting on these endocannabinoid receptors. These receptors bind not only the chemicals found in cannabis but also endogenous compounds—i.e., compounds that are naturally produced in the body. (6) The known functions of our bodies’ endogenous cannabinoids and endocannabinoid receptors suggest possible therapeutic targets for medical cannabis.

Endocannabinoid receptors have been linked to the regulation of appetite, pain management, neuroprotection, central regulation of motor functions, sleep, regulation of nausea and vomiting, reward-driven neurocircuitry, intraocular pressure, memory, tumor growth, and gastrointestinal motility. (7)

One specific type of endocannabinoid receptor, CB1, is known to stimulate appetite and ingestive behaviors. (7) This effect is responsible for the snacking behavior—or “munchies”—caused by recreational cannabis use. It is also the reason that cannabis can be used medically to increase the appetites of patients with AIDS or those who are undergoing chemotherapy, as mentioned before, while also reducing nausea and vomiting among those groups. Cannabis’s appetite-stimulating effects could also be used to treat age-induced anorexia in the elderly in general, and specifically for those with Alzheimer’s disease. (8) Cannabinoids may also be able to slow the disease process of Alzheimer’s by preventing inflammatory effects induced by the beta-amyloid deposition that is a hallmark of the disease. (9)

Endocannabinoid receptors have been shown to reduce pain from a variety of causes. The analgesic effects of acetaminophen can be prevented by blocking specific cannabinoid receptors. (10) Cannabis extracts containing THC alone and THC with CBD have proved effective at reducing chronic and neuropathic pain. (11) Many people with multiple sclerosis (MS) who use cannabis report a reduction in symptoms, including muscle spasticity, pain in extremities, tremor, bowel dysfunction, and walking and balance dysfunction. (12) This may be due to cannabis’s role in pain, motor control, and gastrointestinal motility.

Conditions for which medical cannabis shows the most promise

1. PTSD. While anti-drug crusaders frequently cite the detrimental effects of cannabis on memory (13), there are certain populations for which this effect would be a good thing. People suffering from post-traumatic stress disorder (PTSD) could benefit from the memory-weakening effects of the drug. Nabilone, the cannabinoid drug approved for the treatment of anorexia and nausea among cancer and AIDS patients, is associated with a cessation or reduction in the intensity of nightmares in a majority of PTSD patients surveyed. (14) New Mexico was the first state to allow usage of medical cannabis to treat PTSD, and one study done within in the state revealed a 75 percent reduction in symptoms among participants with PTSD. (15)

2. Cancer. Cancer and AIDS patients are the two populations for which medical cannabis or cannabinoid use has become most widely accepted. Nabilone and dronabinol have been approved for treatment of anorexia, cachexia, nausea, and vomiting in cancer patients undergoing chemotherapy since the 1980s. (16) Newer research has revealed an even more exciting use of cannabis for cancer patients: cannabis may be able to treat the cancer cells themselves. Cannabinoids induce cell death, inhibit cell growth, and slow metastasis in tumor cells without harming the surrounding non-cancerous cells. (16) In a mouse model, pure THC and CBD were shown to prime glioma cells—a cell found in certain types of brain cancer—for radiation therapy, making them more sensitive to and easily destroyed by irradiation. (17) Studies like these show that cannabis may have a broader application for cancer patients than previously thought.

3. Multiple sclerosis (MS). Cannabis can provide relief for multiple symptoms of MS, as discussed above, but it has shown the most promise for treating spasticity. Spasticity refers to the feelings of stiffness and involuntary muscle contractions experienced by people with MS, and it is one of the most common symptoms of the disease. (18) The endogenous cannabinoid system may be active in controlling spasticity, as indicated by exacerbation of this symptom in a mouse model of MS following blockage of endocannabinoid receptors. (19) In humans with MS, both whole plant cannabis-based medicine and an extract combining THC and CBD may reduce the number and severity of spastic episodes. (20, 21) Despite being one of most common symptoms of MS, spasticity has remained difficult to treat with most drugs currently on the market, making cannabis a very intriguing option for treatment.

4. Treatment-resistant epilepsy. Cannabis has been used for millennia in the treatment of epilepsy, but it has only recently been investigated seriously by scientists for safety and effectiveness in this use. In particular, research has focused on cannabis use for childhood epilepsy that has shown resistance to current treatments. While cannabinoids have produced mixed results in animal models of epilepsy (22), CBD has been associated with a decrease in seizure frequency in a recent human study among participants with childhood-onset treatment-resistant epilepsy. (23) Additionally, the safety profile of CBD makes it an attractive treatment for epilepsy in children and young adults. The side effects of antiseizure drugs can be brutal for kids, and a growing number of parents have turned to CBD as an effective and much better tolerated alternative. More research and clinical trials are needed on this application of medical cannabis, but more than 4,000 years of anecdotal support for its efficacy in treating seizures have provided hope for many.

A changing legal and social environment

Once a niche area with limited scientific interest, the field of cannabis research has expanded rapidly in the last decade. Much of the research continues to focus on cannabinoids, rather than whole, unprocessed cannabis. Support for the use of whole cannabis comes from anecdotal evidence as much as from empirical scientific research, but research is slowly beginning to confirm or disprove those anecdotal claims. Cannabis’s current classification as a Schedule I drug by the U.S. government, as well as the attached social stigma, continues to limit the ability and willingness of researchers to investigate all of its possible uses. But as more states approve cannabis for medical and/or recreational use, research and funding will likely continue to expand.

The National Institutes of Health (NIH) currently provides funding to more than forty active projects in the category of Therapeutic Cannabinoid Research. (24) Projects include investigations into the potential of transdermal CBD to reduce the chance of relapse in abstinent alcoholics (25), the ability of vaporized cannabis and dronabinol to reduce neuropathic back pain (26), and the role of the endocannabinoid system in radiation and chemotherapy-induced cognitive impairment and possible methods for prevention or treatment (27), among many others.

Article Source: https://chriskresser.com/the-promising-potential-of-medical-marijuana

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Weight loss plus vitamin D reduces inflammation linked to cancer, chronic disease

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For the first time, researchers at Fred Hutchinson Cancer Research Center have found that weight loss, in combination with vitamin D supplementation, has a greater effect on reducing chronic inflammation than weight loss alone. Chronic inflammation is known to contribute to the development and progression of several diseases, including some cancers.

Results of the randomized, controlled clinical trial — which involved more than 200 overweight, postmenopausal women who had insufficient levels of vitamin D at the beginning of the study — are published online ahead of the July print issue of Cancer Prevention Research, a journal of the American Association for Cancer Research.

“We know from our previous studies that by losing weight, people can reduce their overall levels of inflammation, and there is some evidence suggesting that taking vitamin D supplements can have a similar effect if one has insufficient levels of the nutrient,” said lead and corresponding author Catherine Duggan, Ph.D., a principal staff scientist in the Public Health Sciences Division at Fred Hutch. However, it has not been known whether combining the two — weight loss and vitamin D — would further boost this effect. “It’s the first study to test whether adding vitamin D augments the considerable effect of weight loss on inflammatory biomarkers,” she said.

To explore this question, Duggan and colleagues recruited 218 healthy, overweight older women who had lower-than-recommended levels of vitamin D (less than 32 ng/mL). The women then took part in a 12-month diet and exercise program (including 45 minutes of moderate-to-vigorous exercise five days a week). Half of the study participants were randomly selected to receive 2,000 IU of vitamin D daily for the duration of the year-long trial, and the other half received an identical-appearing placebo, or dummy vitamin. Biomarkers of inflammation were measured at the beginning and end of the study. The researchers then compared changes in these levels between the two groups.

At the end of the study, all of the participants had reduced levels of inflammation, regardless of whether they took vitamin D, “which highlights the importance of weight loss in reducing inflammation,” Duggan said. However, those who saw the most significant decline in markers of inflammation were those who took vitamin D and lost 5 to 10 percent of their baseline weight. These study participants had a 37 percent reduction in a pro-inflammatory cytokine called interleukin-6, or IL-6, as compared to those in the placebo group, who saw a 17.2 percent reduction in IL-6. The researchers found similar results among women in the vitamin D group who lost more than 10 percent of their starting weight. While IL-6 has normal functions in the body, elevated levels are associated with an increased risk of developing certain cancers and diabetes and may be implicated as a cause of depression, Duggan said.

“We were quite surprised to see that vitamin D had an effect on an inflammation biomarker only among women who lost at least 5 percent of their baseline weight,” Duggan said. “That suggests vitamin D can augment the effect of weight loss on inflammation.”

Vitamin D is a steroid hormone that has multiple functions beyond its widely recognized role in regulating calcium levels and bone metabolism. Vitamin D receptors are found in more than 30 cell types and the research focus around this nutrient recently has shifted from bone health to vitamin D’s effect on cancer, cardiovascular health and weight loss, among other health issues.

Inflammation occurs when the body is exposed to pathogens, such as bacteria or viruses, which puts the immune system in overdrive until the “attack” ceases and the inflammatory response abates. Overweight or obese people, however, exist in a state of chronic inflammation. This sustained upregulation of the inflammatory response occurs because fat tissue continually produces cytokines, molecules that are usually only present for a short time, while the body is fighting infection, for example.

“It is thought that this state of chronic inflammation is pro-tumorigenic, that is, it encourages the growth of cancer cells,” she said. There is also some evidence that increased body mass “dilutes” vitamin D, possibly by sequestering it in fat tissue.

“Weight loss reduces inflammation, and thus represents another mechanism for reducing cancer risk,” Duggan said. “If ensuring that vitamin D levels are replete, or at an optimum level, can decrease inflammation over and above that of weight loss alone, that can be an important addition to the tools people can use to reduce their cancer risk.”

Duggan encourages women to speak to their health care providers about measuring their levels of vitamin D to determine the most appropriate dosage.

###

The Breast Cancer Research Foundation, Susan G. Komen for the Cure, National Institutes of Health, Seattle Cancer Consortium Breast Cancer Specialized Program in Research Excellence, Fred Hutchinson/University of Washington Cancer Consortium and Safeway Foundation funded the research.

Editor’s note: To obtain a copy of the Cancer Prevention Research paper, “Effect of vitamin D3 supplementation in combination with weight loss on inflammatory biomarkers in postmenopausal women: a randomized controlled trial,” or to arrange an interview with corresponding author Catherine Duggan, please contact: Kristen Woodward in Fred Hutch media relations, kwoodwar@fredhutch.org or 206-667-5095.

Fred Hutch: 40 years of cures 1975-2015

At Fred Hutchinson Cancer Research Center, home to three Nobel laureates, interdisciplinary teams of world-renowned scientists seek new and innovative ways to prevent, diagnose and treat cancer, HIV/AIDS and other life-threatening diseases. Fred Hutch’s pioneering work in bone marrow transplantation led to the development of immunotherapy, which harnesses the power of the immune system to treat cancer with minimal side effects. An independent, nonprofit research institute based in Seattle, Fred Hutch houses the nation’s first and largest cancer prevention research program, as well as the clinical coordinating center of the Women’s Health Initiative and the international headquarters of the HIV Vaccine Trials Network. Private contributions are essential for enabling Fred Hutch scientists to explore novel research opportunities that lead to important medical breakthroughs. For more information visit fredhutch.org or follow Fred Hutch on Facebook, Twitter or YouTube.

Glutathione: The Mother of All Antioxidants

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Glutathione: The Mother of All Antioxidants

By: Mark Hyman, MD

It’s the most important molecule you need to stay healthy and prevent disease — yet you’ve probably never heard of it. It’s the secret to prevent aging, cancer, heart disease, dementia and more, and necessary to treat everything from autism to Alzheimer’s disease. There are more than 89,000 medical articles about it — but your doctor doesn’t know how address the epidemic deficiency of this critical life-giving molecule …

What is it? I’m talking about the mother of all antioxidants, the master detoxifier and maestro of the immune system: GLUTATHIONE (pronounced “gloota-thigh-own”).

The good news is that your body produces its own glutathione. The bad news is that poor diet, pollution, toxins, medications, stress, trauma, aging, infections and radiation all deplete your glutathione.

This leaves you susceptible to unrestrained cell disintegration from oxidative stress, free radicals, infections and cancer. And your liver gets overloaded and damaged, making it unable to do its job of detoxification.

In treating chronically ill patients with Functional Medicine for more than 10 years, I have discovered that glutathione deficiency is found in nearly all very ill patients. These include people with chronic fatigue syndrome, heart disease, cancer, chronic infections, autoimmune disease, diabetes, autism, Alzheimer’s disease, Parkinson’s disease, arthritis, asthma, kidney problems, liver disease and more.

At first I thought that this was just a coincidental finding, but over the years I have come to realize that our ability to produce and maintain a high level of glutathione is critical to recovery from nearly all chronic illness — and to preventing disease and maintaining optimal health and performance. The authors of those 76,000 medical articles on glutathione I mentioned earlier have found the same thing!

So in today’s blog I want to explain what glutathione is, why it’s important and give you 9 tips that will help you optimize your glutathione levels, improve your detoxification system and protect help yourself from chronic illness.

What is Glutathione?

Glutathione is a very simple molecule that is produced naturally all the time in your body. It is a combination of three simple building blocks of protein or amino acids — cysteine, glycine and glutamine.

The secret of its power is the sulfur (SH) chemical groups it contains. Sulfur is a sticky, smelly molecule. It acts like fly paper and all the bad things in the body stick onto it, including free radicals and toxins like mercury and other heavy metals.

Normally glutathione is recycled in the body — except when the toxic load becomes too great. And that explains why we are in such trouble …

In my practice, I test the genes involved in glutathione metabolism. These are the genes involved in producing enzymes that allow the body to create and recycle glutathione in the body. These genes have many names, such as GSTM1, GSTP1 and more.

These genes impaired in some people for a variety of important reasons. We humans evolved in a time before the 80,000 toxic industrial chemicals found in our environment today were introduced into our world, before electromagnetic radiation was everywhere and before we polluted our skies, lakes, rivers, oceans and teeth with mercury and lead.

That is why most people survived with the basic version of the genetic detoxification software encoded in our DNA, which is mediocre at ridding the body of toxins. At the time humans evolved we just didn’t need more. Who knew we would be poisoning ourselves and eating a processed, nutrient-depleted diet thousands of years later?

Because most of us didn’t require additional detoxification software, almost of half of the population now has a limited capacity to get rid of toxins. These people are missing GSTM1 function — one of the most important genes needed in the process of creating and recycling glutathione in the body.

Nearly all my very sick patients are missing this function. The one-third of our population that suffers from chronic disease is missing this essential gene. That includes me. Twenty years ago I became mercury poisoned and suffered from chronic fatigue syndrome due to this very problem. My GSTM1 function was inadequate and I didn’t produce enough glutathione as a result. Eventually, my body broke down and I became extremely ill …

This is the same problem I see in so many of my patients. They are missing this critical gene and they descend into disease as a result. Let me explain how this happens …

The Importance of Glutathione in Protecting Against Chronic Illness

Glutathione is critical for one simple reason: It recycles antioxidants. You see, dealing with free radicals is like handing off a hot potato. They get passed around from vitamin C to vitamin E to lipoic acid and then finally to glutathione which cools off the free radicals and recycles other antioxidants. After this happens, the body can “reduce” or regenerate another protective glutathione molecule and we are back in business.

However, problems occur when we are overwhelmed with too much oxidative stress or too many toxins. Then the glutathione becomes depleted and we can no longer protect ourselves against free radicals, infections, or cancer and we can’t get rid of toxins. This leads to further sickness and soon we are in the downward spiral of chronic illness.

But that’s not all. Glutathione is also critical in helping your immune system do its job of fighting infections and preventing cancer. That’s why studies show that it can help in the treatment of AIDS.(i)

Glutathione is also the most critical and integral part of your detoxification system. All the toxins stick onto glutathione, which then carries them into the bile and the stool — and out of your body.

And lastly, it also helps us reach peak mental and physical function. Research has shown that raised glutathione levels decrease muscle damage, reduce recovery time, increase strength and endurance and shift metabolism from fat production to muscle development.

If you are sick or old or are just not in peak shape, you likely have glutathione deficiency.
In fact, the top British medical journal, the Lancet, found the highest glutathione levels in healthy young people, lower levels in healthy elderly, lower still in sick elderly and the lowest of all in the hospitalized elderly. (ii)

Keeping yourself healthy, boosting your performance, preventing disease and aging well depends on keeping your glutathione levels high. I’ll say it again … Glutathione is so important because it is responsible for keeping so many of the keys to ultimate wellness optimized.

It is critical for immune function and controlling inflammation. It is the master detoxifier and the body’s main antioxidant, protecting our cells and making our energy metabolism run well.

And the good news is that you can do many things to increase this natural and critical molecule in your body. You can eat glutathione-boosting foods. You can exercise. And you can take glutathione-boosting supplements. Let’s review more specifics about each.

9 Tips to Optimize your Glutathione Levels

These 9 tips will help you improve your glutathione levels, improve your health, optimize your performance and live a long, healthy life.

Eat Foods that Support Glutathione Production

1. Consume sulfur-rich foods. The main ones in the diet are garlic, onions and the cruciferous vegetables (broccoli, kale, collards, cabbage, cauliflower, watercress, etc.).

2. Try bioactive whey protein. This is great source of cysteine and the amino acid building blocks for glutathione synthesis. As you know, I am not a big fan of dairy. But this is an exception — with a few warnings. The whey protein MUST be bioactive and made from non-denatured proteins (“denaturing” refers to the breakdown of the normal protein structure). Choose non-pasteurized and non-industrially produced milk that contains no pesticides, hormones, or antibiotics. Immunocal is a prescription bioactive non-denatured whey protein that is even listed in the Physician’s Desk Reference.

Exercise for Your Way to More Glutathione

3. Exercise boosts your glutathione levels and thereby helps boost your immune system, improve detoxification and enhance your body’s own antioxidant defenses. Start slow and build up to 30 minutes a day of vigorous aerobic exercise like walking or jogging, or play various sports. Strength training for 20 minutes 3 times a week is also helpful.

Take Glutathione Supporting Supplements

One would think it would be easy just to take glutathione as a pill, but the body digests protein — so you wouldn’t get the benefits if you did it this way. However, the production and recycling of glutathione in the body requires many different nutrients and you CAN take these. Here are the main supplements that need to be taken consistently to boost glutathione. Besides taking a multivitamin and fish oil, supporting my glutathione levels with these supplements is the most important thing I do every day for my personal health.

4. N-acetyl-cysteine. This has been used for years to help treat asthma and lung disease and to treat people with life-threatening liver failure from Tylenol overdose. In fact, I first learned about it in medical school while working in the emergency room. It is even given to prevent kidney damage from dyes used during x-ray studies.

5. Alpha lipoic acid. This is a close second to glutathione in importance in our cells and is involved in energy production, blood sugar control, brain health and detoxification. The body usually makes it, but given all the stresses we are under, we often become depleted.

6. Methylation nutrients (folate and vitamins B6 and B12). These are perhaps the most critical to keep the body producing glutathione. Methylation and the production and recycling of glutathione are the two most important biochemical functions in your body. Take folate (especially in the active form of 5 methyltetrahydrofolate), B6 (in active form of P5P) and B12 (in the active form of methylcobalamin).

7. Selenium. This important mineral helps the body recycle and produce more glutathione.

8. A family of antioxidants including vitamins C and E (in the form of mixed tocopherols), work together to recycle glutathione.

9. Milk thistle (silymarin) has long been used in liver disease and helps boost glutathione levels.

So use these nine tips and see how they work to help you optimzie your glutathione levels. When you do, you will take one more step to lifelong vibrant health.

Now I’d like to hear from you…

Had you ever heard of this important nutrient before?

Have you tried any of the advice in this article?

What effects have you noticed on your health?

Please leave your thoughts by adding a comment below.

To your good health,

Mark Hyman, M.D.

References

(i) De Rosa SC, Zaretsky MD, Dubs JG, Roederer M, Anderson M, Green A, Mitra D, Watanabe N, Nakamura H, Tjioe I, Deresinski SC, Moore WA, Ela SW, Parks D, Herzenberg LA, Herzenberg LA. N-acetylcysteine replenishes glutathione in HIV infection. Eur J Clin Invest. 2000 Oct;30(10):915-29

(ii) Nuttall S, Martin U, Sinclair A, Kendall M. 1998. Glutathione: in sickness and in health. TheLancet 351(9103):645-646

Are Women Causing Cancer in Men?

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Research now suggests that excess estrogen may be culprit in causing prostate cancer in men.

At Boston Testosterone Partners, we are one of the few Age Management Clinics that erases Low Testosterone, stimulates natural testosterone production, while at the same time, modulates every patient’s estrogen level into the preferred low area of the reference range.  No other clinic in New England offers that type of Testosterone Replacement Therapy.  So why do we place so much importance on making sure every one of our patients lower estrogens and maintains natural testosterone production as well?

Liike women, men also make estrogens such as estradiol, although (usually) in much lower amounts than women.

Even the characteristically “male” hormone testosterone can be converted into estradiol via the hormone aromatase – which is found in higher concentrations in fat tissue.

While this process of testosterone-to-estrogen conversion is necessary for proper bone density and quality in men, for instance, it may also contribute to prostate growth and malignancy.

Fortunately, testosterone is also antagonist to estrogens like estradiol, which may explain why men with low testosterone are at greater risk of prostate cancer.

It may be, also, that men are being exposed to hidden sources of estrogen from the environment.

Estrogen-mimicking chemicals such as bisphenol-A, PFOA and phthalates are disturbingly widespread; as are soy foods that contain high levels of phytoestrogens, which are capable of mimicking estrogens and/or disrupting their cellular receptor sites.

Not only that, but a wide range of heavy metals have been identified to have powerfully estrogenic properties.

These “metalloestrogens,” as they are called, include aluminium, antimony, arsenite, barium, cadmium, chromium (Cr(II)), cobalt, copper, lead, mercury, nickel, selenite, and tin.

Recently, an interesting new theory has been proposed that suggests another route of estrogen exposure in men: water contaminated by women’s birth control pills. Could this be the culprit in the rising number of prostate cancer cases?

Drug Residues Common in Drinking Water

Many waterways in the United States contain residues of birth control pills, antidepressants, painkillers, and many other chemical compounds. This has been known for many years now.

Most of them enter water supplies from human and animal waste that enter rivers from sewage treatment plants, leach into groundwater from septic systems, or run off into groundwater. Even drugs thrown into the trash can wind up in your drinking water, as when it enters a landfill its contents can and do mingle with other trash and its surrounding environment, including water supplies.

The drug industry, while admitting that pharmaceuticals are clearly contaminating water supplies, maintains that the levels are too low to cause any harm. Yet, it’s known that drugs in waterways can harm fish and other aquatic species, and laboratory studies show human cells do not grow normally when exposed to even trace amounts of certain drugs.

Many drugs in the water supply are known to have dangerous side effects when taken in normal prescription doses, not to mention that some people are now exposed to traces of multiple drugs at one time, in addition to other harmful metals and chemicals in their water. Further, people are now being exposed to combinations of drugs that should never be combined, leading to unknown consequences.

Birth Control Pills in Water Supply Linked to Men’s Prostate Cancer

Using data from the International Agency for Research on Cancer and the United Nations World Contraceptive Use report, which spanned 100 countries, researchers analyzed rates of prostate cancer and prostate cancer deaths, as well as oral contraceptive use among women.

The report concluded that the areas with a high rate of oral contraceptive use also had a high rate of prostate cancer. In addition, the researchers speculated that higher environmental levels of estrogen — and by implication, higher cumulative estrogen exposures in men — may be to blame.

In the United States alone, over 82 percent of women aged 15-44 have used oral contraceptives, according to the U.S. Centers for Disease Control and Prevention (CDC). Typically, hormonal birth control methods like The Pill work by releasing estrogen and progestin into a woman’s body, preventing her ovaries from releasing eggs.

While it’s argued that only a small amount of additional estrogen is excreted by a woman using this form of contraception, this “small amount” is compounded by millions of women, many of whom use the pill for long periods of time. Also, synthetic estrogen and progesterone (progestin) – being unnatural – does not biodegrade as rapidly and is far harder to remove through conventional water purification systems – resulting in greater accumulation in the environment.

While this latest study did not prove cause and effect — that is, it did not prove that environmental estrogen from women’s oral contraceptive use causes prostate cancer in men — it did find a significant association between the two that deserves further investigation, especially in light of estrogen’s well established role in a wide range of cancers.

Estrogen Already Proven to Cause Breast Cancer

The guidelines for preventing and treating prostate cancer are almost identical to those for treating breast cancer (more on those shortly), which is why it’s worth noting that causative factors — like estrogen — may also be similar. It is, in fact, already known that breast cancer is closely tied to estrogen exposure.

According to a study published online in the Journal of the National Cancer Institute, breast cancer rates for women dropped in tandem with decreased use of hormone replacement therapy (HRT), which exposed women to synthetic estrogen. In Canada, between 2002 and 2004 HRT use dropped by 7.8 percent. In fact, it was no coincidence that, during that same time, breast cancer rates also fell by 9.6 percent.

However, after remaining stable at around 5 percent between 2004 and 2006, breast cancer rates then began to rise again, even though HRT use remained lower. The researchers claim this is an indication that HRT simply speeds up tumor growth, as opposed to directly causing it.

It’s also important to consider that you are exposed to a large number of estrogen-like compounds daily, called xenoestrogens. Estrogen pollution is increasingly present all around you, from plastics to canned food and drinks, food additives, household cleaning products, and pesticides. And estrogen levels are rising in our waterways, not only as pollution from birth control use but as a result of the runoff from confined animal feeding operations (CAFOs).

So whether it’s a promoter or a causative factor (likely it’s both), there’s a wealth of evidence supporting excess estrogen exposure as a risk factor for cancer.

By Dr. Mercola

Food to Prevent Cancer: Vegetables With Proven Cancer Fighting Abilities

Add some of these veggies to your plate daily for added cancer fighting protection.  Many people will say they don’t like vegetables, but there are many ways to cook and flavor veggies, the possibilities are endless.  You don’t have to stick with just one kind, mix it up for a variety of flavors and colors.  Vegetables are low in calories, high in fiber and have many other  benefits besides cancer fighting.  It seems like vegetables could be a wonder food.   In the world full of processed foods, obesity and diseases at high rates, doing what you can to help your body stay in great health should be important and easy.  Adding vegetables to every meal is an easy way to help protect your body.  Most importantly, your body will thank you.

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A growing number of studies are discovering foods to prevent cancer, and several types of vegetables are gaining a reputation as reliable cancer fighters. On this page, we’ll outline research related to vegetables that scientists have labeled foods to prevent cancer.

 

Cruciferous vegetables

Cruciferous vegetables (brocolli, brussel sprouts, cauliflower, cabbage, collard greens, bok choy and kale) have been identified by the American Institute for Cancer Research (AICR) as clearly reducing the likelihood of cancer of the mouth, pharanx, larynx, esophagus and stomach. AICR issued this claim in its 2007 report, Food, Nutrition, Physical Activity, and the Prevention of Cancer.

 

Several components of cruciferous vegetables– glucosinolates, crambene, indole-3-carbinol, isothiocynates and sulforaphane– have been shown by researchers to lower cancer risk, according to the AICR. Laboratory studies have found that compounds in cruciferous vegetables stop the growth of cancer cells and tumors in the breast, lung, colon, liver, cervix and endometrium. A research project conducted in Seattle and published in 2000 found that men who ate three or more servings of crucierous vegetables a week were 41 percent less likely to develop prostate cancer than men who at less than one serving of cruciferous vegetables a week.

This group of foods to prevent cancer also is high in fiber, which has been shown in numerous studies to be important in reducing risk for colon cancer. One cup of cooked cabbage contains 4 grams of fiber, one cup of cauliflower is 3 grams of fiber, and a cup of brocolli has 2 grams. The American Cancer Society recommends that cruciferous vegetables regularly be included in your diet.

 

Foods to prevent cancer – Carrots

These orange root vegetables are one of the richest sources of cartenoids (including beta-carotene), which are linked to lower risk for cancer of the colon, bladder, cervix, prostate, larynx, esophogus and breast (in post-menopausal women). Researchers have also demonstrated that the compounds in carrots can help lungs withstand the damage from smoking and may have protective properties against lung cancer.

One cancer-fighting compound in carrots, called falcarinol, is more effective when carrots are cooked whole, rather than sliced before cooking. In June 2009, scientists at Newcastle University in England released their findings that cooked whole carrots contained 25 percent more falcarinol than carrots that were chopped before cooking. Individuals who participated in a taste test also said they preferred the taste of the carrots cooked whole.

 

Mushrooms including Reishi, Shiitake and Maitake

For centuries, Eastern medicine has used mushrooms for healing. It turns out modern science has concluded mushrooms are indeed healers and researchers have added them to the list of foods to prevent cancer.

The traditional healing mushrooms– Reishi, Shiitake and Maitake– all contain a component called 1,3-beta-glucan, which has been shown in animal studies to slow the growth of tumors and boost the immune system. The Shiitake mushroom also contains a similar component called lentinan, which has a demonstrated ability to stop or slower tumor growth. A study released in 2006 found that White button mushrooms contain phytochemicals that are protective against breast and prostate cancer. The common white button mushroom is rich in selenium, which lowers the risk for lung, stomach, colon and prostate cancer, according to the American Institute for Cancer Research.

A study published in March 2009 that involved 2,000 Chinese women showed that women who ate fresh or dried mushrooms were less likely to have breast cancer. Women who consumed at least 10 grams of fresh mushrooms daily were 64 percent less likely to have breast cancer than women who ate no mushrooms. Participants who ate 4 grams of dried mushrooms every day were 47 percent less likely to have breast cancer compared to women who never ate dried mushrooms. Results were similar in pre-menopausal and post-menopausal women.

 

Beans/Legumes

Beans, lentils and peas are included in the AICR’s list of foods to prevent cancer. Beans contain saponins, protease inhibitors and phytic acid, which have been linked to cancer prevention. Saponins are able to stop cancer cells from reproducing and slow the growth of tumors.Protease inhibitors can slow the division of cancer cells and stop cancer cells from destroying nearby healthy cells. And phytic acid has been shown to slow the growth of tumors.

In addition, beans are one of the most fiber-rich foods available. A high-fiber diet has been clearly associated with a significantly reduced risk for colon cancer and a somewhat reduced risk for esophogus cancer. A diet high in legumes has been linked to a decreased probability of stomach and prostate cancer.

 

Dark, leafy green vegetables

It’s not surprising to find leafy green vegetables are cancer fighters, we’ve always been told they are good for you. The AICR says that spinach, kale, romaine lettuce, leaf lettuce, mustard greens, collard greens, chicory and Swiss chard contain the cancer-inhibiting cartenoids, as well as folate and fiber.

Cartenoids, also found in carrots, are associated with lower risk for cancer of the mouth, pharynx and larynx. Laboratory projects have found that inhibit the growth of breast, skin, lung and stomach cancer.

Intake of foods high in folate can reduce the incidence in pancreatic cancer, AICR reports, and eating a diet high in fiber can lower the risk of colorectal cancer.

 

Garlic and onions – Foods to prevent cancer

Garlic and onions belong to the vegetable family, which also includes scallions, leeks and chives. The AICR reports that intake of allium vegetables is associated with reduced risk for stomach cancer, and eating garlic in particular may reduce the incidence of colon cancer.

Researchers have been avidly studying the healing properties of garlic and have discovered that components in garlic have stopped or slowed the growth of tumors in the prostate, bladder, colon and stomach. In lab studies, one particular garlic phytonutrient, diallyl disulfide, guarded against cancer of the skin, colon and lung. In lab studies, this component also killed leukemia cells.

Animal studies have revealed that phytochemicals in allium vegetables can slow the growth of cancer in the breast, stomach, esophogus, lung and colon.

 

Red Sweet Peppers

These colorful veggies have significant amounts of beta-cryptoxanthin, a cartenoid that has been linked to lower levels of lung cancer. In January 2004, the journal Cancer Epidemiology Biomarkers and Prevention reported that individuals who ate the most foods with beta-cryptoxanthin reduced their lung cancer risk by more than 30%, compared to those who ate the least of the cartenoid.

 

Tomatoes

This vegetable has been identified as one of the foods to prevent cancer, specifically prostate cancer. Tomatoes contain lycopene, which gives them their red color. AICR reports that eating foods high in lycopene can protect against cancer of the prostate. Animal studies have shown that comsumption of tomato components decreased prostate cancer risk. A Harvard University study involving 47,000 men discovered that men who ate 10 servings of tomato products a week (tomatoes, tomato sauce, tomato juice, pizza) developed 45 percent fewer cases of prostate cancer than men who ate fewer than two servings of tomato products weekly.

Tomato components, including lycopene, have also been shown in lab studies to halt cancer cells in the breast and lung.

 

written by: http://www.foods-that-heal.com

 

 

STAY HEALTHY!

 

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