Category: Health Concerns

Children’s Health

Raise Healthier Children Naturally

Healthy, Happy Children - Naturally!Children aren’t just “little adults.” Because their bodies are in “fast growth mode,” they have different nutritional requirements than adults.

Because still-growing bodies soak up nutrients like sponges, diet and nutrient deficiencies will have a bigger and more noticeable impact on a child than on an adult. In other words, good nutrition is even more important in childhood and young adulthood that at any other time of life. The nutrition your child receives today will impact him or her for the rest of their life.

While conventional medicine is sometimes necessary to treat certain childhood illnesses, most problems can be better managed through natural means. Less negative side-effects and a true “correction” of underlying problems (instead of just a “band aid” approach) are among the reasons many parents choose natural alternatives over synthetic options.

Children can use many of the “adult” remedies, especially herbs. Here is a convenient equation for adjusting an herb or nutrient dose for a child based on body weight.

Child-Friendly Supplements Health Concerns
of Children
 Children’s Vitamins
 Greens Firse Berry / Red Alert
Similase Jr.
Whey Protein ADD/ADHD
Allergies
Asthma
Attention Deficit
Colds and Flu
Diarrhea
Diarrhea
Parasites

Coconut Oil (Organic, Virgin)

This Oil Should Be in Your Kitchen AND Your Medicine Cabinet

Coconut Oil - A Healthy Oil Of Many UsesCoconut oil is a saturated fat, which means it doesn’t go rancid when heated or when stored for long periods of time.

Essential Fatty Acids (EFA’s) turn into unhealthy “trans fats” when heated, so although you need EFA’s for good health, you should NOT cook with them! Even olive oil, a polyunsaturated fat (PUFA)  should NOT be used for cooking. (Olive oil is NOT an essential fat).

Coconut oil and other saturated fats are heat-stable. For frying and deep-frying, coconut oil is one of the very best oils to use.

In addition to being heat-stable and great for cooking, coconut oil has the following health advantages:

  • Coconut oil contains lauric acid and other a medium-chain triglycerides (MCT’s) with powerful antimicrobial effects against a wide range of bacteria, viruses, fungi / yeasts and protozoa. (1-7)
  • The MCT’s in coconut oil activate the immune system. (8,9)
  • Coconut oil’s MCT’s have proven anti-tumor effects. (10,11)
  • MCT’s in coconut oil aid weight loss three ways: by decreasing hunger, increasing fat-burning and increasing metabolism. (12-19)
  • Lowers cholesterol and improves blood fat levels. (20-22)

If you’ve heard bad things about saturated fats, you should know that it’s all nonsense – bogus B.S. promoted by the soy oil industry and Big Business. (Can you say “Proctor and Gamble”?) Read about the unjustified “bad press” that this miraculous oil has suffered here: Saturated Fat: Another Big, Fat Lie

We offer organic, virgin coconut oil, the finest quality available. Use coconut to cook, make pie crusts or anything that calls for “Crisco” (Crystallized Cottonseed Oil, a product not fit for human consumption).

Use Coconut Oil, two to four tablespoons per day as a food, substituted for whatever oils you currently cook with (except butter which is a true health food). Heck, you can even use coconut oil on your skin as a moisturizer, protectant and anti-microbial!

Coconut Oil (Organic, Virgin) 15 fl. ounces   $15.95

Please Note: Coconut oil is slippery stuff – and it may seep from it’s container during shipment. We have received reports of coconut oil seeping out of still-tightly-sealed jars! We double-bag this product and pack it carefully for shipping but we cannot be responsible for leakage during shipment – there will be no returns or refunds on this product.

References

1.) Antimicrobial activity of potassium hydroxide and lauric acid against microorganisms associated with poultry processing. J Food Prot. 2006 Jul;69(7):1611-5.
2.) In vitro activity of lauric acid or myristylamine in combination with six antimicrobial agents against methicillin-resistant Staphylococcus aureus (MRSA). Int J Antimicrob Agents. 2006 Jan;27(1):51-7. Epub 2005 Nov 28.
3.) Susceptibility of Clostridium perfringens to C-C fatty acids.Lett Appl Microbiol. 2005;41(1):77-81.
4.) Effect of lauric acid and nisin-impregnated soy-based films on the growth of Listeria monocytogenes on turkey bologna. Poult Sci. 2002 May;81(5):721-6.
5.) Inhibition of bacterial foodborne pathogens by the lactoperoxidase system in combination with monolaurin. Int J Food Microbiol. 2002 Feb 25;73(1):1-9.
6.) Fatty acids and derivatives as antimicrobial agents. Antimicrob Agents Chemother. 1972 Jul;2(1):23-8.
7.) Susceptibility of Helicobacter pylori to bactericidal properties of medium-chain monoglycerides and free fatty acids. Antimicrob Agents Chemother. 1996 Feb;40(2):302-6.
8.) Saturated triglycerides and fatty acids activate neutrophils depending on carbon chain-length. Eur J Clin Invest. 2002 Apr;32(4):285-9.
9.) Immunonutrition–supplementary amino acids and fatty acids ameliorate immune deficiency in critically ill patients. Langenbecks Arch Surg. 2001 Aug;386(5):369-76.
10.) Antitumor effect of medium-chain triglyceride and its influence on the self-defense system of the body. Cancer Detect Prev. 1998;22(3):219-24.
11.) Effects of calcitriol, seocalcitol, and medium-chain triglyceride on a canine transitional cell carcinoma cell line. Anticancer Res. 2005 Jul-Aug;25(4):2689-96.
12.) Value of VLCD supplementation with medium chain triglycerides.Int J Obes Relat Metab Disord. 2001 Sep;25(9):1393-400.
13.) The thermic effect is greater for structured medium- and long-chain triacylglycerols versus long-chain triacylglycerols in healthy young women. Metabolism. 2001 Jan;50(1):125-30.
14.) Greater rise in fat oxidation with medium-chain triglyceride consumption relative to long-chain triglyceride is associated with lower initial body weight and greater loss of subcutaneous adipose tissue. Int J Obes Relat Metab Disord. 2003 Dec;27(12):1565-71.
15.) Thermogenesis in humans during overfeeding with medium-chain triglycerides.Metabolism. 1989 Jul;38(7):641-8.
16.) Dietary medium-chain triacylglycerols suppress accumulation of body fat in a double-blind, controlled trial in healthy men and women.J Nutr. 2001 Nov;131(11):2853-9.
17.) Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglyceride. Am J Clin Nutr. 1982 Apr;35(4):678-82.
18.) Medium-chain triglycerides increase energy expenditure and decrease adiposity in overweight men.Obes Res. 2003 Mar;11(3):395-402.
19.) Comparison of diet-induced thermogenesis of foods containing medium- versus long-chain triacylglycerols.J Nutr Sci Vitaminol (Tokyo). 2002 Dec;48(6):536-40.
20.) Effect of dietary medium- and long-chain triacylglycerols (MLCT) on accumulation of body fat in healthy humans. Asia Pac J Clin Nutr. 2003;12(2):151-60.
21.) Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation. Clin Biochem. 2004 Sep;37(9):830-5.
22.) Effect of medium-chain triglycerides on the postprandial triglyceride concentration in healthy men. Biosci Biotechnol Biochem. 2003 Jan;67(1):46-53.

The Bacon and Egg Cure for High Cholesterol

03/15/07

This Week In HealthBeat News:


This is a repeat of last week’s “urgent announcement.” It is SO important that I WANT TO BE SURE EVERYONE SAW IT. If you already took action, good for you and please go enjoy the other articles from this week’s HealthBeat. (And be sure to pass this information along to friends and family)……

More Proof-Positive That Big Pharma Doesn’t Give a Damn
About Your Health

by Dr. Dana Myatt

Breast cancer rates have not changed significantly in the last 50 years with one notable exception. The rates dropped an unbelievable 7% in just one year when the news about the connection between Premarin (Pregnant Mares Urine) hormone therapy and breast cancer finally broke. This was barely mentioned by the media, then it disappeared. I’m not sure if many people really caught the significance of this, so let’s review it in a nutshell.

In 2001, sales of Premarin and Prempro (conventional hormone replacement therapy for post-menopausal women) exceeded $2 billion. In 2002, the huge Women’s Health Initiative Study showed that both Prempro and Premarin significantly increased women’s risks of breast cancer, heart attacks and dementia. (This information was actually known 20 years ago, even before the Women’s Health Initiatit5ve Study, when I was just a medical student. But the news just “broke” to the general public in the last several years). As a result of the study’s findings about these increased health risks, use of Premarin and Prempro plummeted along with sales. Revenues from these poisons fell to less than $1 million per year ($880,000 to be exact) by 2004. That’s a drop of 99.96% in sales and profits if you need a little help with the math.

Benefits of Natural (Bio-identical) Hormone Replacement Therapy

Many women turned from these deadly Big Pharma hormones to natural, aka bio-identical, hormone replacement therapy which so far appears to be MUCH safer than the drug versions of hormones. The big difference is that natural hormone replacement therapy attempts to duplicate a woman’s hormones (replace the same approximate amounts the exact same hormones a woman has when younger), instead of giving un-natural amounts of only the strongest female horse-hormones, which is what the drug versions do. Here is what we know about the benefits of natural hormone replacement therapy (nHRT):

* Natural HRT has been used in the U.S. for almost 25 years without a single related death or complaint

* Unlike synthetic HRT drugs (typically made from horse urine), bio-identical hormones use the same four main sex hormones that the body makes, and in “physiologic” amounts (amounts similar to what the body makes)

* Unlike “one-size-fits-all” horse hormone prescriptions, natural HRT prescriptions are custom-tailored to individual patients

* Natural HRT still requires a doctor’s prescription and supervision

Because the nHRT duplicates the pattern of natural female hormones, they appear to be far safer than conventional HRT. In fact, there is evidence that nHRT may actually help prevent breast cancer instead of causing it. Many women have found relief from menopausal complaints over the past 25 years with this apparently far-safer form of hormone replacement therapy.

Big Pharma Doesn’t Give a Damn About Your Health

In October of 2005, Wyeth Pharmaceuticals, manufacturers of Prempro and Premarin, filed a complaint with the FDA asking that the sale of ALL bio-identical hormones be banned. That’s right —Wyeth, makers of cancer-causing hormones, has petitioned the FDA to outlaw the natural HRT alternatives that are safer, more effective, and cheaper than their dangerous drugs. This should go a long way to preserving the less than one half of one-thousandth the dollars they used to make on these killers. Apparently, Wyeth cares more about protecting the now-miniscule market-share of their line of dismally failing drugs than they do for protecting women’s lives.

Wyeth’s drugs were causing at least 7% of the country’s breast cancers, yet now they want to take away access to the much safer hormone alternative. See how much our lives are worth to Big Pharma?

Why the FDA Sleeps with Big Pharma

Our lives aren’t worth any more to the FDA than they are to Big Pharma. After all, Big Medicine, Big Pharma and their Bed Partner the FDA are about Big Money, not altruistic endeavors. (I hope I’m not popping anyone’s candy-colored bubble here).

The FDA receives “drug user fees,” which totaled over 3 billion dollars in 2004 from pharmaceutical companies for the drugs they sell. The less drugs that Wyeth or any Big Pharma Company sells, the less money goes into the FDA coffers. Natural hormones, made by “compounding pharmacies,” are regulated by the states. The FDA does not receive any money from the sale of natural hormones. No wonder the FDA is just as eager as Wyeth to either outlaw natural hormones OR have compounding pharmacies fall under their (FDA) jurisdiction.

Because the FDA and Big Pharma are bedfellows, an FDA ruling on the matter would have gone in favor of Wyeth last year had it not been for a massive grassroots effort that appeared to put the matter to rest. Now enter the double-dealing “tag on” bill brought to you by our “Also don’t give a damn about the individual” politicians.

Crooked Politicians Aid and Abet The FDA and Big Pharma
(The Sneaky End-Run Around)

Another surprise to some of you, I know, but politicians actually aid and abet this Big Money Machine, not our individual health freedoms or our personal health concerns. Just several days ago, this “tag on” piece of legislation was introduced by Senators Edward Kennedy (D-Mass.), Pat Roberts (R-Kan.) and Richard Burr (R-N.C.), aka “the usual suspects.” It should be noted that Senator Kennedy is # 4 on the list of the top 20 political recipients of Big Pharma money, reporting a total of $221,550 received from the Pharmaceutical Industry in 2006 alone.

“The Safe Drug Compounding Act of 2007,” deftly tacked on the back of a major FDA funding bill, will be voted on the end of this month and will surely pass (so much for our legislators “reigning in” the FDA). What this sneaky “tag” will do is drastically curtail compounding pharmacies and place them under FDA control instead of state control. Expect to kiss your natural (bio-identical) hormone replacement therapy and all other compounded prescriptions
good-bye.

Notice how this “tag” was placed at the last minute (so few people would have time to hear about it, much less respond), and how it was added to a bigger bill that is sure to pass? Evil, dirty, rotten nasty politics. This stinks, but it’s the “modus operandi” of Big Government and other Big Money interests. You and I don’t matter at all to these people except for the money we can put in their collective pockets, and our individual health and freedom be damned.


Take Action Now to Preserve Compounding Pharmacy
and Natural Hormone Replacement Therapy

Remember that I promised to let you know when it was time to take action on an impending health freedom matter? The time is NOW to protect compounding pharmacy and natural hormone replacement therapy.

What You Must Do Today to Protect Your/Our Health Freedom

Since almost no one except HealthBeat readers have even heard about this yet, the opportunity for a grassroots movement to stop this legislation is cutting close. Don’t wait until next week to act. Here is what you need to do if you want to help save compounding
pharmacy and health freedom in general and natural hormone replacement therapy in particular.

You need to write a letter to both your state Senators AND your state Representatives. This letter should be FAXED to their office, not mailed. A fax is far more potent than a phone call (if you can even get through) or an email. It is estimated that each individual fax carries the weight of 13,000 voters (because they figure about one in about 13,000 who care about a particular subject will ever actually contact a representative). Here is what you need to say, and it is short and sweet:

(Please modify this into your own words, but this is the gist of it):
_________________________

Dear Senator BlowHard:

I am vehemently opposed to the proposed “Safe Drug Compounding Act of 2007” and request that you vote “no” on this stealthy tag-on legislation. Leave compounding pharmacy where it belongs, under state jurisdiction. Further, I believe the dysfunctional FDA does
not need more control over drug regulation, they need less.

Please help protect what shred of my health freedom remains by voting “no” on this senseless legislation.

Your Voting Constituent,
Joe Doaks
___________________________

How to locate your representatives:

Locate your representatives by state

Locate your senators by state
_____________________________

Political Action Steps Summary:

1.) Fax your state’s senators and representatives ASAP. If you don’t have a fax machine, http://www.faxzero.com lets you send out 2 free faxes per day. (Hot tip on free faxing courtesy of Steven C.). A fax really is that much more important and worth your time than an email, and a typed or legibly hand-written letter carries a LOT of weight!

2.) Pass this note on to friends, family, anyone who gives a darn about health freedom. (You know, all those people you forward e-mail jokes to). If you have friends who aren’t on e-mail, snail-mail them this information. Encourage them to pass it along to as many people as they can.

Grassroots movements have saved the day on other health freedoms issues in the past decade. We must not underestimate the power of the general citizenry (that’s us!) to slay the dragons that jeopardize our freedom. Since the pen is mightier than the sword, please draw your weapon and let’s see if we can save the day for health freedom once again.

In Pursuit of Health and Freedom,
Dr. Myatt

 

Why Don’t You Bill Insurance?

by Mark Ziemann, R.N.

[Dr. Myatt’s Note: The following commentary is a continuation of Nurse Mark’s Poor, Poor Pitiful Me: Why Some People Will Never Get Well and Would Your Plumber Work This Cheap? from previous weeks’ HealthBeat News. If you haven’t read these articles, you might want to check them out first to see what has gotten my mild-mannered Nurse in such a tizzy. I do believe this is the final installment of Nurse Mark’s indignation! ;-)]

“Why Don’t You Just Bill My Insurance?” This plea usually comes from someone wanting to book an appointment, but who is haggling and chiseling at the cost. “But she is so expensive – I couldn’t possibly afford that much money…” These people almost invariably go elsewhere, usually to their “conventional” doc, who is only too happy to give them a 5 to 10 minute visit, a mandatory drug prescription as a “prize” for visiting, and send them happily on their way. These doctors usually have a bustling office staff devoted to scheduling patients in at ten-minute intervals, and an even busier back-office staff devoted to doing all the preliminary paperwork that goes to the insurance company to generate income for the doctor and his staff. Even with a back-office staff doing much of the prep work, the doctor will still spend several hours each day finishing up his or her part of the insurance paperwork. This really is a major business, and must be run as efficiently as possible if that doctor is to achieve the desired income.

Here is the history behind Dr. Myatt’s decision to “opt out” of the insurance business. As she tells it, it was one of those rare “ah hah” moments in life. Many years ago, while working for a major holistic medical clinic in Phoenix (one that accepted insurance, as most do),
Dr. Myatt came into the office an hour early one morning to plow through the mountain of insurance paperwork that her busy medical practice required. Anyone who does their own income taxes has some idea of what these forms look like, with one notable exception. Each insurance provider has a different form and requirement of what information is needed.

So there sat Dr. Myatt, scratching her head and grinding her way through a mountain of paperwork when in walked one of the clinic nurses, announcing that there was a work-in patient in the ER, here before regular clinic hours with severe breathing difficulty and chest pain. Doctor Myatt was the only physician available (of course she was — it was over an hour before the clinic usually opened)! As The Good Doctor shifted mental gears from paper-pusher to emergency room physician, she found herself for just a moment feeling resentful. After all, how could she get the insurance paperwork completed if she was interrupted with patients? Like a splash of cold water in the face, this thought was immediately replaced with the realization of what the paper-pushing had done to her. Too busy doing insurance paperwork to see a patient? She got up, saw the patient (who was in severe cardiac distress due to a non-functional mitral valve) and decided right then and there that she would never resent seeing a patient for want of more time to fill out insurance forms.
Dr. Myatt “opted out” of insurance and Medicare at that time (it is no longer possible for a physician to “opt out” of Medicare), and has never looked back or regretted her decision. She now spends all of her time on patient care, and her results speak for themselves.

Here at the Wellness Club, we work at a slower pace. We book each patient for a full hour, and visits often run longer. We focus entirely on the patient and on how to make them well, not on how to comply with sometimes-impossible insurance forms.

I recently had a patient (one of our “incurable” success stories) ask me “do you really make any money at this?” and I had to answer honestly. We cover the bills and expenses and we are comfortable, but we are not “rich” and aren’t likely to get rich any time soon unless we hit the lotto.

People measure success by many different markers. Some see success as a big, fancy home (we live in a comfortable but modest straw bale home where we have clean air, clean water, and plenty of outdoors to enjoy). Others measure success by the car they drive (we have an older model van and an older model Saturn wagon). We also have a — you guessed it, older model — RV that allows us to travel to see patients, lecture, and teach. Still other people believe that their success is measured in their 401K’s, retirement pensions and gold-plated medical (sickness) insurance plans. We have no plans to “retire” for as long as we can keep helping people find better health, our “health insurance” is our daily supplement and vitamin regimen (especially Maxi Multis!), clean air, clean water, good food, and modest exercise, and our “retirement plan” is to build a modest home that is completely self-sustainable (no electric company or propane delivery required) and raise our own food.

Dr. Myatt could undoubtedly make more money if we “took insurance.” This would require seeing far more patients for far less time each, and there would be no time for individual “case study,” but it would certainly bring a bigger income.

Would we be “more successful” if we “took” insurance? Not if you calculate success like we do, by the number of people that we have helped. We sleep well at night knowing we are giving our all to each and every patient, and we never find ourselves feeling annoyed that a patient is disturbing our paperwork time. Most importantly, many patients reaffirm our “success” when they thank us for helping them with “incurable” medical problems that conventional medicine has given up on.

Now that’s success in our book!

Cheers,
Nurse Mark

P.S. Here is the information from the “Insurance” page of our website for those who are interested.

How Our Office Handles Insurance

Q: Does Dr. Myatt Accept Medicare or Medicaid?

A: No. Dr. Myatt “opted out” of Medicare years ago. Without a UPN number (universal provider number required by Medicare), there is no way for Medicare to cover Dr. Myatt’s services. Further, Medicare rarely covers the type of progressive, alternative care that Dr. Myatt and other holistic physicians provide.

Q: Does Dr. Myatt accept insurance?

A: No. Services are due and payable on the day they are rendered.

Q: Will Dr. Myatt fill out insurance paperwork if I file a claim myself?

A: Yes. Dr. Myatt will gladly complete any necessary insurance paperwork including writing letters of medical necessity, as required by your insurance company for you to file a claim yourself. However, all time spent completing insurance paperwork or writing such letters is billed at Dr. Myatt’s usual hourly fee of $240. For example, if it takes Dr. Myatt one-half hour to complete insurance paperwork, the patient will be billed $120.

Q: Why does Dr. Myatt charge for filling out insurance paperwork? My other doctor does this for free.

A: Your other doctor spends 5-10 minutes with you and charges for a complete office visit. Dr. Myatt charges for the office visit (typically one hour, the entire time of which is devoted to your care), then spends an average of 2-12 hours in “case study” following your exam or phone consultation. This additional time spent on case study is not charged for but is included in your visit. Very few physicians spend so much time and attention on an individual patient.

Insurance paperwork is incredibly time-consuming. This is valuable time that Dr. Myatt prefers to spend studying the patient’s case in order to get the patient well, not shuffling papers.

When you consider the true amount of time Dr. Myatt spends on an individual case, you will see that her fees are a bargain. When you find yourself recovering from an “incurable” illness, you will further understand why Dr. Myatt’s case-study time is so valuable and why we charge for the non-wellness time spent on paperwork.

Cheers,
Nurse Mark

The Bacon and Egg Cure for High Cholesterol

Is your cholesterol still “too high”? (Above 230, but this depends on what your “good cholesterol,” or HDL levels, are, too).

We get calls and letters literally every day with questions about how to lower high cholesterol. The self-treatment stories we hear include “I only eat good carbohydrates,” or “I almost never eat eggs.” To which we reply, “well no wonder your cholesterol is high!”

You see, what you have probably heard about how to lower cholesterol is completely backwards. If it was correct, you’d see big result in as little as a month. If you’ve been on your cholesterol-avoidance diet for more than a month and haven’t seen dramatic improvements, then you have proof that you are on the wrong track. Clearly, it’s time to try a new approach. Cholesterol levels don’t take that long to change.

I had a telephone follow-up with new patient Kim this week. She’s thrilled because the migraine headaches she originally contacted me about are gone. Not reduced, but completely gone, no drugs needed. As a side-effect, she’s lost 30 pounds and her once-high cholesterol levels have dropped like a rock, back into the normal range for the first time in many years. Her secret? She’s following my advice and having either a Super Shake or bacon and eggs for breakfast, along with following the rest of The Myatt Diet. It wasn’t an easy “sell” to convince her to eat this way, but now she’s an absolute missionary for The Myatt Diet. (You’ll see her testimonial in an upcoming HealthBeat). She also tells me that she’s amazed how her food cravings have completely disappeared, so she’s not missing her former junk food, including “good carbs.”

If you’ve bought into the prevalent but misguided idea that avoiding cholesterol will lower your cholesterol, here’s a hot “biochemical tidbit.” When you lower dietary cholesterol, your liver simply makes more. (Cholesterol comprises 80% of the cell wall of every cell in your body, so it’s a very valuable commodity indeed). Fortunately, your liver knows how to make cholesterol even when you don’t eat it. When you stop eating eggs, your liver detects a “cholesterol famine” and cranks out more of this life-giving fat. Your attempts to outsmart Mother Nature will fail. (You can’t get up early enough to fool Mama Nature)!

Low Cholesterol diets rarely work to lower cholesterol. Eating only “good carbs” rarely works to lower cholesterol. “If you always do what you’ve always done, you’ll always get what you’ve always gotten.” Stop struggling with your cholesterol levels and go have some bacon eggs for breakfast!  — Dr. Myatt

* Calling All Fellow Gardeners! *

Greenest Envy: Make Your Garden The Talk of The Neighborhood
Grow Bigger Flowers, Greener Lawns, Humongous Produce

I like to garden. It pleases me no end to see my front yard filled with bright splashes of color all season long and bring fresh cuttings indoors for a continual warm-weather treat. And really, can you call those tasteless red things from the grocery store a tomato after you’ve tasted home-grown? A juicy red beefsteak still warm from the vine atop fresh-picked lettuce puts me in salad bliss. Not only is home-grown produce far fresher and more convenient, it can be FAR healthier than store-bought produce grown with synthetic fertilizers, insecticides and herbicides, then sprayed with anti-fungal agents, spoilage retardants and Goddess only knows what else so they’ll “keep” longer on the grocery shelf. The toxic spate of chemicals in produce often offsets the value of “eating green” in the first place! For my money and health, homegrown is better whenever I can pull it off. The problem is, how do you fertilize and keep bugs at bay without those nasty chemicals? Much as I hate to use them, there’s no doubt that many of them are effective at what they do.

Fortunately, I’ve found a marvelous gardening secret: Gardens Alive!

Gardens Alive! offers non-toxic solutions for just about every garden problem you can name. Got pests? They have non-toxic solutions that are effective and affordable. Lawn problems? Their seeds and growth enhancers (again, all non-toxic) will give you the greenest lawn on the block with far less effort. Their fruit, vegetable and flower growth enhancers produce bigger, healthier yields without fail. Kill nasty garden pests without harm to yourself or your pets; have an enviably perfect lawn and harvest eye-popping produce with these not-to-be-missed garden solutions. No more nematodes, blossom end-rot or meager yields for me, no siree! Bye bye deer and birds sharing my harvest (it wouldn’t be so bad if they’d eat the whole leaf or fruit instead of pecking one hole in every leaf, huh?). I even get a jump-start on the season with their ingenious little seed starter kits.

I’ve never seen anything like the array of products offered at Gardens Alive! They even have solutions for helping keep your pets healthy. Best of all, these non-toxic solutions are not only more effective than their synthetic counterparts, they are also less expensive in almost every case.

If you do any gardening at all, you owe it to yourself to take a look at these incredible products. Imagine the pride you’ll feel harvesting state-fair quality produce and flowers, or enjoying a golf-course quality lawn that will be the envy of your entire neighborhood! Please be sure to take “before” and after” pictures of your efforts so we can show them off to other gardening readers.

Here are some of my top recommendations:

Gardens Alive! Organic Garden With Seed Got 4’x4′ of space? You can have a complete organic garden with 10 vegetables, easy and weed-free. This kit R-O-C-K-S! I’m setting one up on my deck this summer and I’ll have organic salads all season long.
Vegetables Alive! Fertilizer  Dramatically increase your yield of lettuce, peas, broccoli, cabbage, beans, cucumbers, melons and more.
Turf Alive! Brand Have a thick, green lawn the looks like a lush golf course without the toxic chemicals. Your neighbors will hate you.
Portabella Mushroom Kit Portabellas have a wonderful texture and flavor, plus they’re loaded with nutrients including vitamin B and potassium. They can be difficult to find at the supermarket (and they’re expensive), but with this kit you can grow your own and enjoy fresh mushrooms in 3-5 weeks.
No Fleas, Please! Stop fleas outdoors AND kill ’em indoors. Non-toxic, inexpensive, effective. Outdoor Flea Control and Indoor Flea Control

AND, Here’s a “starter special” for you:
$20 FREE off your first order at Gardens Alive for Wellness Club Members!

Happy Gardening!
— Dr. Myatt

Laughter is Good Medicine : Best Single’s Ad Ever

This has to be one of the best singles ads ever printed. It is reported to have been listed in the Atlanta Journal.

SINGLE BLACK FEMALE seeks male companionship, ethnicity unimportant. I’m a very good girl who LOVES to play. I love long walks in the woods, riding in your pickup truck, hunting, camping and fishing trips, cozy winter nights lying by the fire. Candlelight dinners will have me eating out of your hand. I’ll be at the front door when you get home from work, wearing only what nature gave me. Call (404) 875-XXXX and ask for Lucy, I’ll be waiting…. (Click here to see the punch line):

Cytokines

A Simplified Look At Messenger Molecules

(or… Don’t Shoot the Messenger!)

Let’s get something straight right up front: cytokynes are not a toxin or a disease or something bad to be stamped out. They are just messengers.

Cytokines are not the disease or infection or insult, they are the message that is created by white blood cells (lymphocytes and macrophages), epithelial cells (cells that line internal tissues) and by other cells in lesser degrees, in response to some insult like a bacteria, virus or other infection. They can cause inflammation and are also created in response to inflammation.

Cytokines are the way that cells in distress call other cells for help — like an S.O.S.

When our immune system is fighting pathogens, cytokines call immune cells such as T-cells and macrophages to travel to the site of the infection.

Measuring cytokines gives us an indication of what is going on that would cause our cells to be calling for help.

When we talk about lowering inflammatory cytokines what we really should be talking about is addressing the cause of the inflammation so that cytokine-producing cells no longer feel the need to send out “help me!” messages.

Cytokines work on a “negative feedback” system. When there is a stimulus (a reason for cells to need help), cytokines are produced. The greater the stimulus, the more cytokines are produced. If the stimulus becomes less (when the infection heals or the inflammation subsides), cytokine production decreases because less are needed. Like the gas pedal on your car, to go faster you press harder – if you remove your foot (removing the stimulus) the engine slows down and the car stops.

Occasionally the cytokine response can become unbalanced, entering a sort of positive feedback loop which can easily get out of control – imagine if your car’s gas pedal worked the other way, where you had to keep it pressed down to stop! This has been termed a “cytokine storm” and is a serious medical emergency that can result in organ damage and even death. It is one reason for the deaths of people with otherwise healthy immune systems in pandemics such as the Spanish Flu of 1918 or the more recent Bird Flu and Swine Flu outbreaks.

There are three broad categories of cytokines – they can be grouped according to what they do, though there is also a lot of redundancy and “cross training” going on with cytokines.

First, there are Cytokines involved in innate (as in “born with it”) immunity and inflammation. Most of these cytokines are made by macrophages (important for removing pathogens), mast cells (important to inflammation) and endothelial cells (the cells that line our blood vessels and lymphatic system).

Major players here include:

  • TNF (tumor necrosis factor) and interleukin-1 (IL-1) help to activate endothelial cells.
  • Chemokines serve to attract different kinds of leukocytes (infection-fighting white blood cells)
  • IL-12 and interferon-gamma (IFN-y) are more involved in chronic inflammation.

Then there are cytokines involved in adaptive (as in “acquired in response to an infection or vaccination”) immunity. Most of these cytokines are made by our T helper cells (T cells are a kind of lymphocyte that matures in our thymus gland – hence the ‘T‘).

There are 2 main kinds of T Helper cells:

  • Th1 cells: Type 1 helper T cells make pro-inflammatory cytokines like IFN-y, IL-2, and TNF. These cells are involved in cell-mediated immunity and the cytokines produced by them stimulate the breakdown of microbial pathogens. Several chronic inflammatory diseases like multiple sclerosis, diabetes, and rheumatoid arthritis are considered Th1 dominant diseases.
  • Th2 cells: Type 2 helper T cells produce the cytokines IL-4, IL-5, IL-9, IL-10, and IL-13. Th2 cells are involved in allergy responses. Cytokines like IL-4 stimulate antibodies directed at extracellular parasites and at viruses. IL-5 stimulates eosinophil (a kind of white blood cell) responses, also part of the immune response toward large extracellular parasites. Allergy is considered to be Th2 dominant condition.

While Th1 cells are generally thought to produce inflammatory cytokines and Th2 cells are thought to produce inflammation-mediating cytokines, as you can see here there is “crossover.”

  • IL-2 and IL-4 cytokines tell lymphocytes to proliferate and differentiate (that means to grow, mature, and take on a specialized function).
  • IFN-gamma and IL-5 cytokines send messages that activate other cells.

Then there are cytokines involved in hematopoiesis – a fancy word that means “building new blood cells” – either oxygen-carrying red blood cells or infection-fighting white blood cells. Cells that make these cytokines include endothelial cells, macrophages, and other cells in our immune system. An example of this are colony-stimulating factors like G-CSF (granulocyte-colony stimulating factor) which causes hematopoietic cells to grow.

These are just a few of the more broad classes of cytokines – there are hundreds of these chemical messengers, each with a unique purpose and job to do.

Some of the ones we hear about most often are:

  • TNFa or Tumor Necrosis Factor alpha. While the name sounds ominous, TNF is a vital player in our response to infection. Its primary role is the regulation of immune system cells. TNF is able to induce fever, cause cell death, cause cachexia, initiate inflammation and to inhibit tumor growth and viral replication in response to sepsis or infection.
  • Interleukin 6 (IL-6) is an cytokine that acts as both a pro-inflammatory cytokine and an anti-inflammatory myokine (produced from muscle cells). [could this get any more confusing?] While IL-6 serves to stimulate the inflammatory and auto-immune processes in many diseases it also is anti-inflammatory in that it moderates or mediates inflammation by inhibiting TNF-alpha and IL-1, and by activating other interleukins such as IL-10.
  • Interferon gamma (IFNγ or type II interferon) is a cytokine that is critical for both innate and adaptive immunity against viral and some bacterial and protozoal infections. IFNγ activates macrophages. If IFNγ becomes uncontrolled it can be associated with a number of auto-inflammatory and autoimmune diseases. Its importance in the immune system comes from its ability to inhibit viruses directly, and most importantly from its stimulating and modulating effects on immunity. IFNγ is produced mainly by natural killer (NK) and natural killer T (NKT) cells.
  • Interleukin 10 (IL-10) is an anti-inflammatory cytokine. IL-10 inhibits production of pro-inflammatory cytokines like as IFN-γ, IL-2, IL-3, TNFa and GM-CSF made by cells such as macrophages and T-cells. IL-10 is important for counteracting hyperactive immune responses that can occur with over-stimulation of pro-inflammatory cytokines.

Importantly, we need to remember that many of the inflammatory cytokines are induced by oxidative stress – meaning that antioxidants play an important role in reducing the production of inflammatory cytokines.

Reactive oxygen species (ROS) are chemically reactive molecules containing oxygen that form when cells metabolize oxygen. In normal amounts ROS have important roles in cellular health. In times of stress (exposure to pathogens, toxins, UV or heat, ionizing radiation, etc.), ROS levels may greatly increase which can damage cells. This is known as oxidative stress and ROS are sometimes called “free radicals.”

Also remember that cytokines themselves trigger the release of other cytokines leading to increased oxidative stress. This makes them important in chronic inflammation, as well as other immune responses such as fever.

So, when your doctor presents you with your lab results and says “you have some high cytokines – we need to get those down,” he really means that there are some stresses going on – infection, chronic inflammation, allergy, oxidative stress, toxicity – that are being shown to him by the cytokines that can be measured. These stresses — the cause of elevated cytokines — are what must be dealt with in order to “bring down” the high cytokines, not the other way around. “Bringing down” high cytokines will not correct the insult (infection, toxicity, inflammation, etc.) that is causing the problem in the first place.

Maxi Flavone is formulated to “bring down” high cytokines – but not in a way that a drug might – by simply shutting down important cytokine production. Cytokines are very much a balance, and they are all important – even the inflammatory ones – so shutting down one or several could lead to some serious problems as a delicate balance is upset. Instead, Maxi Flavone, with its flavonoids and antioxidants, addresses the ROS and inflammation that is causing the release of inflammatory cytokines such as TNF-a.

Finding and correcting the reasons for inflammation such as environmental stresses (air pollution, mold, toxic exposure), subtle or sub-clinical infections (candida, chlamydia, amebiasis), personal stresses (job, sleep, relationships), physical stresses (allergies, food intolerances, hormone imbalances) and nutritional deficiencies or excesses is vital to correcting cytokine imbalances.

The truth is, though we talk a lot about cytokines, there are so many of them and their interactions are so complex that we really don’t have a good understanding of the many interactions and ways that they function. Trying to micro-manage cytokines with individual interventions is probably like throwing cups of water into the ocean to make the level rise.

What we DO know is that cytokines become imbalanced in response to identifiable “macro” insults or imbalances in the body: infections (subtle or obvious), stress (external and internal), toxins — anything that creates an alarm reaction in the body.

Instead of pretending that we understand cytokines and their myriad functions and interactions, a more productive path to health and fertility is to balance the body at the higher levels. The cytokines know how to balance themselves when everything “upstream” in the body is in balance and threats to physical health have been removed.

Support:

Th1 Stimulating Supplements:
Immune-boosting herbs such as echinacea, astragulus, licorice root, ashwaganda, panax ginseng, chlorella, grape seed extract, and common immune-boosting medicinal mushroom extracts, like maitake, reishi, and shitake, will stimulate Th1.

Th2 Stimulating Supplements:
Antioxidants like resveratrol, pycnogenol, curcumin from turmeric, genistein, quercetin, and green tea will stimulate Th2.

Vitamin D is increasingly being recognized for it’s importance in managing healthyTh1/Th2 balance and low vitamin D status is associated with an increased risk of Th1 mediated autoimmune diseases. It has been seen that Vitamin D deficient persons have elevated Th1 cell-associated responses and decreased Th2 cell-associated responses. The antiinflammatory effects of vitamin D are very similar to IL-10 – one o fthe most important antiinflammatory cytokines.

Fish Oil – (EPA / DHA) is highly antiinflammatory. EPA (eicosapentaenoic acid) decreases TNF-a.
EPA and DHA (docosahexaenoic acid) each decrease NK cell activity and this effect is synergistic when both EPA and DHA are used together.

References:

Seydel KB1, Li E, Swanson PE, Stanley SL Jr. Human intestinal epithelial cells produce proinflammatory cytokines in response to infection in a SCID mouse-human intestinal xenograft model of amebiasis. Infect Immun. 1997 May;65(5):1631-9

Mullins BJ1, Kicic A, Ling KM, Mead-Hunter R, Larcombe AN.
Biodiesel exhaust-induced cytotoxicity and proinflammatory mediator production in human airway epithelial cells.Environ Toxicol. 2014 Jul 5

Xiong H1, Wei L, Peng B. IL-17 stimulates the production of the inflammatory chemokines IL-6 and IL-8 in human dental pulp fibroblasts.
Int Endod J. 2014 Jul 5

Sundman E, Olofsson PS. Neural control of the immune system. Adv Physiol Educ. 2014 Jun;38(2):135-9

de Vries MA1, Klop B, Janssen HW, Njo TL, Westerman EM, Castro Cabezas M. Postprandial inflammation: targeting glucose and lipids.
Adv Exp Med Biol. 2014;824:161-70

Ciortea R1, Mihu D, Mihu CM. Association between visceral fat, IL-8 and endometrial cancer. Anticancer Res. 2014 Jan;34(1):379-83

Ali Akoum, Christine Jolicoeur, Abdelaziz Kharfi, and Marie Aubé. Decreased Expression of the Decoy Interleukin-1 Receptor Type II in Human Endometriosis. Am J Pathol. Feb 2001; 158(2): 481–489

Margherita T. Cantorna, Sanhong Yu, and Danny Bruce. The paradoxical effects of vitamin D on Type 1 mediated immunity. Mol Aspects Med. Dec 2008; 29(6): 369–375.Published online May 4, 2008. doi: 10.1016/j.mam.2008.04.004 PMCID: PMC2633636 NIHMSID: NIHMS82537

Matheu V1, Bäck O, Mondoc E, Issazadeh-Navikas S. Dual effects of vitamin D-induced alteration of TH1/TH2 cytokine expression: enhancing IgE production and decreasing airway eosinophilia in murine allergic airway disease.J Allergy Clin Immunol. 2003 Sep;112(3):585-92.

Margherita T Cantorna, Yan Zhu, Monica Froicu, and Anja Wittke. Vitamin D status, 1,25-dihydroxyvitamin D3, and the immune system1,2,3,4. 2004 American Society for Clinical Nutrition

Mukaro VR, Costabile M, Murphy KJ, Hii CS, Howe PR, Ferrante A. Leukocyte numbers and function in subjects eating n-3 enriched foods: selective depression of natural killer cell levels. Arthritis Res Ther. 2008;10(3):R57. Epub 2008 May 14.

Ferrucci L, Cherubini A, Bandinelli S, Bartali B, Corsi A, Lauretani F, Martin A, Andres-Lacueva C, Senin U, Guralnik JM. Relationship of plasma polyunsaturated fatty acids to circulating inflammatory markers. J Clin Endocrinol Metab. 2006 Feb;91(2):439-46. Epub 2005 Oct 18.

Sundrarjun T, Komindr S, Archararit N, Dahlan W, Puchaiwatananon O, Angthararak S, Udomsuppayakul U, Chuncharunee S. Effects of n-3 fatty acids on serum interleukin-6, tumour necrosis factor-alpha and soluble tumour necrosis factor receptor p55 in active rheumatoid
arthritis. J Int Med Res. 2004 Sep-Oct;32(5):443-54.

Yamashita N, Sugiyama E, Hamazaki T, Yano S.Inhibition of natural killer cell activity by eicosapentaenoic acid in vivo and in vitro.Biochem Biophys Res Commun. 1988 Jan 15;150(1):497-505.

Yamashita N, Yokoyama A, Hamazaki T, Yano S. Inhibition of natural killer cell activity of human lymphocytes by eicosapentaenoic acid. Biochem Biophys Res Commun. 1986 Aug 14;138(3):1058-67.

Yamashita N, Maruyama M, Yamazaki K, Hamazaki T, Yano S. Effect of eicosapentaenoic and docosahexaenoic acid on natural killer cell activity in human peripheral blood lymphocytes. Clin Immunol Immunopathol. 1991 Jun;59(3):335-45.

Thies F, Nebe-von-Caron G, Powell JR, Yaqoob P, Newsholme EA, Calder PC. Dietary supplementation with eicosapentaenoic acid, but not with other long-chain n-3 or n-6 polyunsaturated fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y. Am J Clin Nutr. 2001 Mar;73(3):539-48.

Cachexia / Catabolism

Natural Support For Unintended Weight Loss

Catabolism means “breaking down” and anabolism means “building up” body tissue. Under normal circumstances, “breaking down” and “building up” are in balance with each other, and a person maintains a consistent weight.

In weight training and weight gain, anabolism or “building up” occurs faster than catabolism, and tissue (fat or muscle) is added to the body. In catabolism, the rate of “breaking down” exceeds the “building up” phase and unintended weight loss results. Cachexia refers to malnutrition and lack of absorption that can cause catabolism.

Causes of cachexia/catabolism include chronic diseases such as tuberculosis and cancer, but catabolism can also occur without the presence of disease. In disease states it is believed that inflammatory substances produced by the body, including interleukin-1 (IL-1), IL-6, interferon gamma and tumor necrosis factor alpha (TNFa) play a role in the progression of cachexia.

Cachexia is a common problem in the elderly. Decreased production of digestive enzymes, plus changes in taste and appetite, often lead to decreased food intake. Total lower calorie consumption results in weight loss.

When the intake of protein falls below critical levels, loss of muscle tissue, including heart muscle, can occur.

When digestion and absorption are decreased, even an adequate amount of calories may not prevent weight loss. Remember, anabolism (“building up”) requires sufficient calories, sufficient protein, and normal digestion and assimilation. The above-listed inflammatory substances may prevent weight gain in spite of adequate caloric nutrition.

Diet And Lifestyle Recommendations

  • Diet MUST include adequate, high quality protein. This is even more important than total calories. High quality protein, especially whey protein, can be added to a “blender drink” to boost protein intake in a highly absorbable form. (See “Dr. Myatt’s Super Shake” recipe).
  • Exercise, especially light weight training, encourages muscle tissue to take up amino acids (protein) from the bloodstream. OVER-exercise is not recommended, but mild to moderate weight training exercise will help build muscle tissue.

Primary Support

  • Maxi Multi: 3 caps, 3 times per day with meals.
  • Protein powder: (alternate between whey and soy or use whey exclusively): 30 grams or more (2 scoops) of protein per day. This can easily (and tastily!) be taken as a “milkshake,” “hot chocolate,” or “pudding.”
  • Similase: 2 caps, 3 times per day with meals. (Digestive enzymes to aid assimilation)
  • L-glutamine: 500-1,000mg, 3 times per day with meals. L-glutamine in powdered form mixes easily with recipes. [Target dose: 3,000-5,000 mg per day].
  • CoQ10 (100mg): 1 cap, 2 times per day with meals.

Additional Support

Dr. Myatt’s Comments (Other Considerations)

A complete physical exam is always in order for unexplained weight loss, since many curable illnesses can cause this problem.

Be sure to have a hormone profile, including thyroid and sex hormones. If you have bowel problems, a Comprehensive Digestive Stool Analysis (CDSA) is in order. Low levels of sex hormones and/or high levels of thyroid or adrenal hormones can cause weight loss. Depending on the results of these tests, your holistic physician may recommend DHEA or other hormones.

How to Calculate Protein & Calorie Requirements

Protein: Multiply your weight by 0.7. This will give you the number of grams of protein you should consume each day. Remember, total protein intake is even more important than total calorie intake, because the body cannot make protein from any other food source (fats or carbohydrates). Protein is necessary for maintenance of muscle mass (including the heart) and for an intact immune system. Excesses of protein can be stored as fat, but excesses of fat, calories, or carbohydrates (starches and sugars) cannot be converted into protein. PROTEIN INTAKE IS OF PRIMARY IMPORTANCE IN CATABOLISM.

Example: 106 pounds (put your body weight here) X 0.7= 74 grams of protein (the amount of protein a 106 pound cachexic person needs each day). Normal or overweight individuals have different protein requirements. Please refer to the “Longevity Protocol” audio tape and paper, page 134 of the Holistic Health Handbook, for precise information on calculating protein and calorie requirements in normal and overweight individuals.

Calories: Multiply your weight in pounds by 18. This will give you the number of calories that you need each day to gain weight. (This number also accounts for a mild to moderate activity level).

Example: 106 pounds (put your body weight here) x 18 = 1908 calories. (Normal or overweight individuals have different calorie requirements. Please refer to the “Longevity Protocol” audio tape and paper for information on calculating protein and calorie requirements in normal and overweight individuals.

REMEMBER: People can survive and be healthy being very lean IF they have sufficient protein to keep muscle mass, heart and the immune system functioning well.

Dr. Myatt’s Final Comment

Non-holistic physicians, upon seeing catabolism in a patient, will often recommend a liquid “milkshake-like” canned “nutritional replacement drink.” These products contain more sugar than protein (you need more protein than sugar) and many artificial additives. They are NOT your “best bet” for restoring body mass. Use your own “Super Shake” with high protein and targeted supplements instead and you can do MUCH better. Whey protein is especially valuable because it contains immune factors and cachexia can cause immune weakness.

Calcium D-Glucarate

Powerful Protection from Environmental Toxins

Calcium D-GlucarateCalcium D-Glucarate, considered to be a longevity booster, is involved in the detoxification of certain xenobiotics, lipid soluble toxins and steroid hormones, and is used for additional support in the Holistic prevention and treatment of breast cancer. Calcium d-glucarate facilitates the excretion of potentially disease-promoting compounds, such as estrogen, and reduces lipid (fat) levels in the blood.

Description- A high-potency natural phytonutrient supplement that supports Phase II glucuronidation pathways.

Suggested dose: 1 – 3 capsules, 3 times daily with meals or as directed.

CANCER


Natural Strategies And Support

Cancer continues to be one fo the most frightening diagnoses that anyone can receive.

Conventional medicine woudl have us believe that there is no possible treatment other than their conventional chemotherapy, radiation, and surgery. No dietary change, no nutritional status improvement, no herb or vitamin, no other treatment can be considered anything but “quackery” and any of those things will be immediately dismissed as useless and even dangerous by most conventional practitioners.

We at the Wellness Club feel differently. We believe that there is no one “magic bullet” to “cure” cancer, and that any approach to cancer must be balanced, rational, and individualized to each person. We believe that in some cases conventional chemotherapy may well be the best treatment. We also believe that conventional treatments, when augmented by natural, holistic treatment, can be made more effective and less toxic.

Leading New Cancer Cases and Deaths – 2013 Estimates

Estimated New Cases*

Estimated Deaths

Male

Female

Male

Female

  1. Prostate
    238,590 (28%)
  2. Lung & bronchus
    118,080 (14%)
  3. Colon & rectum
    73,680 (9%)
  4. Urinary bladder
    54,610 (6%)
  5. Melanoma of the skin
    45,060 (5%)
  6. Kidney & renal pelvis
    40,430 (5%)
  7. Non-Hodgkin lymphoma
    37,600 (4%)
  8. Oral cavity & pharynx
    29,620 (3%)
  9. Leukemia
    27,880 (3%)
  10. Pancreas
    22,740 (3%)

All sites
854,790 (100%)

  1. Breast
    232,340 (29%)
  2. Lung & bronchus
    110,110 (14%)
  3. Colon & rectum
    69,140 (9%)
  4. Uterine corpus
    49,560 (6%)
  5. Thyroid
    45,310 (6%)
  6. Non-Hodgkin lymphoma
    32,140 (4%)
  7. Melanoma of the skin
    31,630 (4%)
  8. Kidney & renal pelvis
    24,720 (3%)
  9. Pancreas
    22,480 (3%)
  10. Ovary
    22,240 (3%)

All sites
805,500 (100%)

  1. Lung & bronchus
    87,260 (28%)
  2. Prostate
    29,720 (10%)
  3. Colon & rectum
    26,300 (9%)
  4. Pancreas
    19,480 (6%)
  5. Liver & intrahepatic bile duct
    14,890 (5%)
  6. Leukemia
    13,660 (4%)
  7. Esophagus
    12,220 (4%)
  8. Urinary bladder
    10,820 (4%)
  9. Non-Hodgkin lymphoma
    10,590 (3%)
  10. Kidney & renal pelvis
    8,780 (3%)

All sites
306,920 (100%)

  1. Lung & bronchus
    72,220 (26%)
  2. Breast
    39,620 (14%)
  3. Colon & rectum
    24,530 (9%)
  4. Pancreas
    18,980 (7%)
  5. Ovary
    14,030 (5%)
  6. Leukemia
    10,060 (4%)
  7. Non-Hodgkin lymphoma
    8,430 (3%)
  8. Uterine corpus
    8,190 (3%)
  9. Liver & intrahepatic bile duct
    6,780 (2%)
  10. Brain & other nervous system
    6,150 (2%)

All sites
273,430 (100%)

 

 

 

 

*Excludes basal and squamous cell skin cancers and in situ carcinoma except urinary bladder.

Data taken from American Cancer Society, Inc., Surveillance Research 2013

Usefull Resources:

Dietary Ketosis In The Treatment of Solid Tissue Malignancy

Prostate Support And PC Spes: A note from Nurse Mark

Botanical and Nutritional Considerations in the Treatment of Prostate Cancer

Prostate Cancer

Breast Cancer Month – And That Little Pink Ribbon Again

Liver Cancer: Is There A One-Pill Treatment?

Cancer Treatment Causes Cancer? Yes!

Cancer Scandal: Poison For Profit

7 Simple Ways to Decrease Your Cancer Risk

Breast Cancer Prevention: Dr. Myatt’s Recommendations

What if you’ve already been diagnosed with cancer? The first thing to remember is — don’t panic. Cancer is not a death sentence. Many good treatments for cancer exist. A few are found in conventional medicine. Many others are available in natural, alternative and “unconventional” medicine. Non-toxic treatments for cancer have been used successfully by many people, with and without conventional treatment.

If you are going to use alternative treatments, OR if you decide to integrate natural and alternative treatments with conventional care, it is best to seek the help of a qualified “integrative” practitioner. (Someone like myself who uses all avenues of medicine, from conventional to natural, with the foremost regard for the patient’s welfare — not the type of treatment used).

The type of cancer, it’s location, the age and health of the patient, all make a difference as to what the best course of action will be. For example, juice fasting has helped some people but should be strictly avoided by others. Certain medications and surgeries are helpful in some types of cancer, useless in others.

All of these questions need to be answered with the assistance of an holistic physician who can help you determine the best course of action to take and will work with you to sort out the legitimate treatments from the “hype.” There is no room for guesswork and inexperience once a diagnosis of cancer has been made. (Please, consider obtaining a consultation with Dr. Myatt).

DIET AND LIFESTYLE RECOMMENDATIONS

  • Eat a low carbohydrate diet with as much organically-produced food as possible. (The primary “fuel” of cancer cells is glucose, or sugar).  Include plenty of “Super Foods,” especially fresh garlic. Do NOT juice fast or undergo other radical diets until you have conferred with an holistic physician.
  • Drink 64 ounces of pure water daily.
  • Exercise moderately if you are able. Walking is one of the best. Your holistic physician can work with you to design an optimal exercise program.
  • Attend a support group. Studies have shown that people fare better with cancer when they attend such support groups.
  • Stop negative health habits immediately! This includes smoking or other tobacco use and alcohol.
  • Practice meditation, relaxation, prayer or your chosen form of spiritually-directed activity.

PRIMARY SUPPORT

  • Maxi Multi: 3 caps, 3 times per day with meals. Optimal (not minimal) doses of antioxidants (ACES), are particularly important. Many nutrients help prevent side effects from chemotherapy and radiation, but be sure to check with your holistic physician to insure that there are no unwanted interactions with various chemotherapy medications.
  • Omega 3 fatty acids:
     Flax seed meal, 2 teaspoons per day with food
    OR
    Flax seed capsules    : 2-4 caps, 3 times per day (target dose range: 6-12 caps per day)
    OR
    Flax seed oil    : 1 tablespoon per day
    OR
    Max EPA     (Omega-3 rich fish oil): 1-2 caps, 3 times per day with meals (target dose: 3-6 caps per day).
  • CoQ10: 50-300mg per day. This powerful antioxidant, produced by the body, diminishes with age. It is especially valuable for all types of heart disease. CHOLESTEROL-LOWERING DRUGS deplete CoQ10.
  • Vitamin C: take an additional 3,000-10,000mg per day in divided doses. Some studies show that IV vitamin C may be more effective.
  • Turmeric: 1-2 caps, 3 times per day with meals
  • Vitamin D: 1,000-5,000IU per day based on blood test results
  • Bromelain: 1-2 caps, 3 times per day between meals
  • Melatonin: 3-20mg at bedtime (DO NOT use in lymphoma or melanoma)

    ADDITIONAL SUPPORT

    For Breast Cancer

  • Calcium D-glucarate: 2-3 caps, 3 times per day with meals or as directed.
  • Diindolymethane (DIM): 2 caps, 2 times per day.

    For Prostate Cancer

  • Lycopene: (15mg): 1 capsule per day with a meal.

    • For all cancers (anti-metastatic)

    Note: If you have been diagnosed with cancer and want to explore your options, it is most important to seek qualified help. DO NOT rely on second-hand stories from well-meaning friends and family members. Good treatments, and combinations of treatments, exist for many types of cancers, but relying on anecdotal stories and unproven “remedies” can be a waste of time and money. More importantly, unproven treatments can lead you away from legitimately helpful treatments.

    Dr. Myatt is available for consultations by telephone. She does extensive research and teaching in the field of both conventional cancer treatment and alternative therapies.

    References

    Low Carbohydrate Diet

    1.) Freedland SJ, Mavropoulos J, Wang A, Darshan M, Demark-Wahnefried W, Aronson WJ, Cohen P, Hwang D, Peterson B, Fields T, Pizzo SV, Isaacs WB. Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis. Prostate. 2008 Jan 1;68(1):11-9.
    2.) Venkateswaran V, Haddad AQ, Fleshner NE, Fan R, Sugar LM, Nam R, Klotz LH, Pollak M. Association of diet-induced hyperinsulinemia with accelerated growth of prostate cancer (LNCaP) xenografts.J Natl Cancer Inst. 2007 Dec 5;99(23):1793-800. Epub 2007 Nov 27.
    3.) Zhou W, Mukherjee P, Kiebish MA, Markis WT, Mantis JG, Seyfried TN. The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer.Nutr Metab (Lond). 2007 Feb 21;4:5.
    4.) Borugian MJ, Sheps SB, Kim-Sing C, Van Patten C, Potter JD, Dunn B, Gallagher RP, Hislop TG. Insulin, macronutrient intake, and physical activity: are potential indicators of insulin resistance associated with mortality from breast cancer? Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1163-72.
    5.) Seyfried TN, Sanderson TM, El-Abbadi MM, McGowan R, Mukherjee P.: Role of glucose and ketone bodies in the metabolic control of experimental brain cancer.Br J Cancer. 2003 Oct 6;89(7):1375-82.
    6.) Muti P, Quattrin T, Grant BJ, Krogh V, Micheli A, Schünemann HJ, Ram M, Freudenheim JL, Sieri S, Trevisan M, Berrino F. Fasting glucose is a risk factor for breast cancer: a prospective study. Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1361-8.
    7.) Meixensberger J, Herting B, Roggendorf W, Reichmann H: Metabolic patterns in malignant gliomas.J Neurooncol 1995, 24:153-161
    8.) Fearon KC.: Nutritional pharmacology in the treatment of neoplastic disease.Baillieres Clin Gastroenterol. 1988 Oct;2(4):941-9.
    9.) Pedersen PL: Tumor mitochondria and the bioenergetics of cancer cells. Prog Exp Tumor Res 1978, 22:190-274.

    Garlic

    1.) Morioka, N., Morton, D.L., and Irie, R.F.: A protein fraction from aged garlic extract enhances cytotoxicity and proliferation of human lymphocytes mediated by interleukin-2 and conavalin. Proc Ann Meet Am Assoc Cancer 34:A3297, 1993.
    2.) Legnani C., Frascaro M., Guazzaloca G., et al.: Effects of a dried garlic preparation on fibrinolysis and platelet aggragation in healthy subjects. Arzneim Forsch Drug Res 43:119-122, 1993.
    3.) Kiesewetter H., et al.: effects of garlic coated tablets in peripheral arterial occlusive disease. Clin Investig 71:383-86, 1993.
    4.) Lau, B.H., Yamasaki, T., and Gridley, D.S.: Garlic compounds modulate macrophage and T-lymphocyte function. Mol Biother 3:103-107, 1991.
    5.) Dausch JG., Nixon DW.: Garlic: a review of its relationship to malignant disease. Prev Med 19:346-61, 1990.
    6.) Kandil O.M., et al.: Garlic and the immune system in humans: its effect on natural killer cells. Fed Proc 46:441, 1987.
    7.) Kandil, O.M. et. al.: Garlic and the immune system in humans: Its effect on natural killer cells. Fed Proc 46:441, 1987.
    8.) Belman S.: Onion and garlic oils prohibit tumor promotion. Carcinogenesis 4(8):1063-5, 1983.
    9.) Kroning, F.: Garlic as an inhibitor for spontaneous tumors in predisposed mice. Acta Unio Inter Contra Cancrum 20(3):855, 1964.

    Super Foods

    1.) Khan N, Afaq F, Mukhtar H. Cancer Chemoprevention Through Dietary Antioxidants: Progress and Promise. Antioxid Redox Signal. 2007 Dec 21 [Epub ahead of print].
    2.) Moreno DA, López-Berenguer C, García-Viguera C. Effects of stir-fry cooking with different edible oils on the phytochemical composition of broccoli. J Food Sci. 2007 Jan;72(1):S064-8.

    Exercise and Cancer

    1.) Valenti M, Porzio G, Aielli F, Verna L, Cannita K, Manno R, Masedu F, Marchetti P, Ficorella C.Physical exercise and quality of life in breast cancer survivors. Int J Med Sci. 2008 Jan 15;5(1):24-8.
    2.) Greenspan SL. Approach to the prostate cancer patient with bone disease. J Clin Endocrinol Metab. 2008 Jan;93(1):2-7.
    3.) Farrell SW, Cortese GM, Lamonte MJ, Blair SN.Cardiorespiratory fitness, different measures of adiposity, and cancer mortality in men.Obesity (Silver Spring). 2007 Dec;15(12):3140-9.
    4.) McBride D. Healthful eating and exercise may lower  mortality after breast cancer. ONS Connect. 2007 Dec;22(12):27.
    5.) Karvinen KH, Courneya KS, North S, Venner P.  Associations between exercise and quality of life in bladder cancer survivors: a population-based study.Cancer Epidemiol Biomarkers Prev. 2007 May;16(5):984-90.
    6.) Kruk J. Physical activity in the prevention of the most frequent chronic diseases: an analysis of the recent evidence. Asian Pac J Cancer Prev. 2007 Jul-Sep;8(3):325-38.
    7.) Lynch BM, Cerin E, Owen N, Aitken JF. Associations of leisure-time physical activity with quality of life in a large, population-based sample of colorectal cancer survivors. Cancer Causes Control. 2007 Sep;18(7):735-42. Epub 2007 May 23.
    8.) Milne HM, Gordon S, Guilfoyle A, Wallman KE, Courneya KS. Association between physical activity and quality of life among Western Australian breast cancer survivors. Psychooncology. 2007 Dec;16(12):1059-68.
    9.) Stevinson C, Faught W, Steed H, Tonkin K, Ladha AB, Vallance JK, Capstick V, Schepansky A, Courneya KS.Associations between physical activity and quality of life in ovarian cancer survivors. Gynecol Oncol. 2007 Jul;106(1):244-50. Epub 2007 May 9.
    10.) Chang SC, Ziegler RG, Dunn B, Stolzenberg-Solomon R, Lacey JV Jr, Huang WY, Schatzkin A, Reding D, Hoover RN, Hartge P, Leitzmann MF. Association of energy intake and energy balance with postmenopausal breast cancer in the prostate, lung, colorectal, and ovarian cancer screening trial. Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):334-41.
    11.) Rogers LQ, Courneya KS, Robbins KT, Malone J, Seiz A, Koch L, Rao K, Nagarkar M. Physical activity and quality of life in head and neck cancer survivors. 1: Support Care Cancer. 2006 Oct;14(10):1012-9. Epub 2006 Mar 15.
    12.) Hanna L, Adams M. Prevention of ovarian cancer. Best Pract Res Clin Obstet Gynaecol. 2006 Apr;20(2):339-62. Epub 2005 Dec 20.
    13.) Pan SY, Ugnat AM, Mao Y. Physical activity and the risk of ovarian cancer: a case-control study in Canada. Int J Cancer. 2005 Nov 1;117(2):300-7.
    14.) Courneya KS, Karvinen KH, Campbell KL, Pearcey RG,  Dundas G, Capstick V, Tonkin KS. Associations among exercise, body weight, and quality of life in a population-based sample of endometrial cancer survivors. Gynecol Oncol. 2005 May;97(2):422-30.
    15.) Vallance JK, Courneya KS, Jones LW, Reiman T. Differences in quality of life between non-Hodgkin’s lymphoma survivors meeting and not meeting public health exercise guidelines. Psychooncology. 2005 Nov;14(11):979-91.
    16.) Zhang M, Xie X, Lee AH, Binns CW.Sedentary behaviours and epithelial ovarian cancer risk. Cancer Causes Control. 2004 Feb;15(1):83-9.

    Support Groups

    1.) Gottlieb BH, Wachala ED. Cancer support groups: a critical review of empirical studies. Psychooncology. 2007 May;16(5):379-400.
    2.) Goodwin PJ. Support groups in advanced breast cancer. Cancer. 2005 Dec 1;104(11 Suppl):2596-601.
    3.) Cunningham AJ, Watson K. How psychological therapy may prolong survival in cancer patients: new evidence and a simple theory. Integr Cancer Ther. 2004 Sep;3(3):214-29.
    4.) Cunningham AJ, Phillips C, Stephen J, Edmonds C. Fighting for life: a qualitative analysis of the process of psychotherapy-assisted self-help in patients with metastatic cancer. Integr Cancer Ther. 2002 Jun;1(2):146-61.

    Stop Tobacco and Alcohol Use

    1.) Kaufman EL, Jacobson JS, Hershman DL, Desai M, Neugut AI. Effect of breast cancer radiotherapy and cigarette smoking on risk of second primary lung cancer. J Clin Oncol. 2008 Jan 20;26(3):392-8.
    2.) Park SM, Lim MK, Jung KW, Shin SA, Yoo KY, Yun YH, Huh BY. Prediagnosis smoking, obesity, insulin resistance, and second primary cancer risk in male cancer survivors: National Health Insurance Corporation Study. J Clin Oncol. 2007 Oct 20;25(30):4835-43.
    3.) Koskinen WJ, Brøndbo K, Mellin Dahlstrand H, Luostarinen T, Hakulinen T, Leivo I, Molijn A, Quint WG, Røysland T, Munck-Wikland E, Mäkitie AA, Pyykkö I, Dillner J, Vaheri A,
    Aaltonen LM. Alcohol, smoking and human papillomavirus in laryngeal carcinoma: a Nordic prospective multicenter study. J Cancer Res Clin Oncol. 2007 Sep;133(9):673-8. Epub 2007 May 8.
    4.) Muwonge R, Ramadas K, Sankila R, Thara S, Thomas G, Vinoda J, Sankaranarayanan R. Role of tobacco smoking, chewing and alcohol drinking in the risk of oral cancer in Trivandrum, India: A nested case-control design using incident cancer cases. Oral Oncol. 2007 Oct 12
    5.) Chen CH, Shun CT, Huang KH, Huang CY, Tsai YC, Yu HJ, Pu YS. Stopping smoking might reduce tumour recurrence in nonmuscle-invasive bladder cancer. BJU Int. 2007 Aug;100(2):281-6; discussion 286. Epub 2007 Apr 5.
    6.) Rieck G, Fiander A.The effect of lifestyle factors on gynaecological cancer. Best Pract Res Clin Obstet Gynaecol. 2006 Apr;20(2):227-51.
    7.) Ford MB, Sigurdson AJ, Petrulis ES, Ng CS, Kemp B, Cooksley C, McNeese M, Selwyn BJ, Spitz MR, Bondy ML.Effects of smoking and radiotherapy on lung carcinoma in breast carcinoma
    survivors. Cancer. 2003 Oct 1;98(7):1457-64.
    8.) van Leeuwen FE, Klokman WJ, Stovall M, Hagenbeek A, van den Belt-Dusebout AW, Noyon R, Boice JD Jr, Burgers JM, Somers R. Roles of radiotherapy and smoking in lung cancer following Hodgkin’s disease. J Natl Cancer Inst. 1995 Oct 18;87(20):1530-7.
    9.) Neugut AI, Murray T, Santos J, Amols H, Hayes MK, Flannery JT, Robinson E. Increased risk of lung cancer after breast cancer radiation therapy in cigarette smokers. Cancer. 1994 Mar
    15;73(6):1541-3.
    10.) Day GL, Blot WJ, Shore RE, McLaughlin JK, Austin DF, Greenberg RS, Liff JM, Preston-Martin S, Sarkar S, Schoenberg JB, et al. Second cancers following oral and pharyngeal cancers: role of tobacco and alcohol. J Natl Cancer Inst. 1994 Jan 19;86(2):131-7.
    11.) Day GL, Shore RE, Blot WJ, McLaughlin JK, Austin DF, Greenberg RS, Liff JM, Preston-Martin S, Sarkar S, Schoenberg JB, et al. Dietary factors and second primary cancers: a follow-up of oral and pharyngeal cancer patients. Nutr Cancer. 1994;21(3):223-32.

    Meditation, Relaxation, Prayer

    1.) Cunningham AJ, Phillips C, Lockwood GA, Hedley DW, Edmonds CV. Association of involvement in psychological self-regulation with longer survival in patients with metastatic
    cancer: an exploratory study. Adv Mind Body Med. 2000 Fall;16(4):276-87.
    2.) Greer S. Improving quality of life: adjuvant psychological therapy for patients with cancer. Support Care Cancer. 1995 Jul;3(4):248-51.

    Multiple Vitamins and Cancer

    1.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival,
    part 1. Altern Ther Health Med. 2007 Jan-Feb;13(1):22-8.
    2.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival,
    Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
    3.) Tsao SM, Yin MC, Liu WH. Oxidant stress and B vitamins status in patients with non-small cell lung cancer. Nutr Cancer. 2007;59(1):8-13.
    4.) Moss RW. Should patients undergoing chemotherapy and radiotherapy be prescribed antioxidants? Integr Cancer Ther. 2006 Mar;5(1):63-82.
    5.) Moyad MA. The use of complementary/preventive medicine to prevent prostate cancer recurrence/progression following definitive therapy. Part II–rapid review of dietary supplements.
    Curr Opin Urol. 2003 Mar;13(2):147-51.
    6.) Moyad MA. Potential lifestyle and dietary supplement options for the prevention and postdiagnosis of bladder cancer. Urol Clin North Am. 2002 Feb;29(1):31-48, viii.
    7.) Kamat AM, Lamm DL. Diet and nutrition in urologic cancer. W V Med J. 2000 May-Jun;96(3):449-54.
    9.) Jatoi A, Daly BD, Kramer G, Mason JB. A cross-sectional study of vitamin intake in postoperative non-small cell lung cancer patients. J Surg Oncol 1998;68:231–6.
    10.) Jatoi A, Daly BD, Kramer G, Mason JB. A cross-sectional study of vitamin intake in postoperative non-small cell lung cancer patients. J Surg Oncol 1998;68:231–6.
    11.) Lamm DL, Riggs DR, Shriver JS, vanGilder PF, Rach JF, DeHaven JI. Megadose vitamins in bladder cancer: a double-blind clinical trial. J Urol. 1994 Jan;151(1):21-6.

    Antioxidants (General) and Cancer

    1.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, part 1. Altern Ther Health Med. 2007 Jan-Feb;13(1):22-8.
    2.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
    3.) Kirsh VA, Hayes RB, Mayne ST, Chatterjee N, Subar AF, Dixon LB, Albanes D, Andriole GL, Urban DA, Peters U; PLCO Trial. Supplemental and dietary vitamin E, beta-carotene, and vitamin C intakes and prostate cancer risk.J Natl Cancer Inst. 2006 Feb 15;98(4):245-54.
    4.) Berger MM. Can oxidative damage be treated nutritionally? Clin Nutr. 2005 Apr;24(2):172-83.
    5.) Ferguson LR, Philpott M, Karunasinghe N. Dietary cancer and prevention using antimutagens. Toxicology. 2004 May 20;198(1-3):147-59.
    6.) Borek C. Dietary antioxidants and human cancer.Integr Cancer Ther. 2004 Dec;3(4):333-41.
    7.) Prasad KN. Multiple dietary antioxidants enhance the efficacy of standard and experimental cancer therapies and decrease their toxicity. Integr Cancer Ther. 2004 Dec;3(4):310-22.
    8.) Heyland DK, Dhaliwal R, Suchner U, Berger MM. Antioxidant nutrients: a systematic review of trace elements and vitamins in the critically ill patient. Intensive Care Med. 2005 Mar;31(3):327-37. Epub 2004 Dec 17.
    9.) Kim YT, Kim JW, Choi JS, Kim SH, Choi EK, Cho NH. Relation between deranged antioxidant system and cervical neoplasia. Int J Gynecol Cancer. 2004 Sep-Oct;14(5):889-95.
    10.) Drisko JA, Chapman J, Hunter VJ. The use of antioxidant therapies during chemotherapy. Gynecol Oncol. 2003 Mar;88(3):434-9.
    11.) Prasad KN, Cole WC, Kumar B, Prasad KC. Scientific rationale for using high-dose multiple micronutrients as an adjunct to standard and experimental cancer therapies. J Am Coll Nutr. 2001 Oct;20(5Suppl):450S-463S; discussion 473S-475S.
    12.) Lamson DW, Brignall MS. Antioxidants in cancer therapy; their actions and interactions with oncologic therapies. Altern Med Rev. 1999 Oct;4(5):304-29.
    13.) Prasad KN, Kumar A, Kochupillai V, Cole WC. High doses of multiple antioxidant vitamins: essential ingredients in improving the efficacy of standard cancer therapy. J Am Coll Nutr. 1999
    Feb;18(1):13-25.
    14.) Lupulescu A. The role of vitamins A, beta-carotene, E and C in cancer cell biology. Int J Vitam Nutr Res. 1994;64(1):3-14.
    15.) Stähelin HB. Critical reappraisal of vitamins and trace minerals in nutritional support of cancer patients. Support Care Cancer. 1993 Nov;1(6):295-7.

    Vitamin A and Carotenes

    1.) Yuan JM, Ross RK, Gao YT, Qu YH, Chu XD, Yu MC. Prediagnostic levels of serum micronutrients in relation to risk of gastric cancer in Shanghai, China. Cancer Epidemiol Biomarkers Prev. 2004 Nov;13(11 Pt 1):1772-80.
    2.) Wu K, Erdman JW Jr, Schwartz SJ, Platz EA, Leitzmann M, Clinton SK, DeGroff V, Willett WC, Giovannucci E.Plasma and dietary carotenoids, and the risk of prostate cancer: a nested case-control study. Cancer Epidemiol Biomarkers Prev. 2004 Feb;13(2):260-9.
    3.) Kamat AM, Lamm DL. Chemoprevention of bladder cancer. Urol Clin North Am. 2002 Feb;29(1):157-68.
    4.) Sato R, Helzlsouer KJ, Alberg AJ, Hoffman SC, Norkus EP, Comstock GW. Prospective study of carotenoids, tocopherols, and retinoid concentrations and the risk of breast cancer. Cancer
    Epidemiol Biomarkers Prev. 2002 May;11(5):451-7.
    5.) Gann PH, Ma J, Giovannucci E, Willett W, Sacks FM, Hennekens CH,Stampfer MJ. Lower prostate cancer risk in men with elevated plasma lycopene levels: results of a prospective analysis. Cancer Res. 1999 Mar 15;59(6):1225-30.
    6.) Giovannucci E, Ascherio A, Rimm EB, Stampfer MJ, Colditz GA, Willett WC. ake of carotenoids and retinol in relation to risk of prostate cancer. J Natl Cancer Inst. 1995 Dec 6;87(23):1767-76.
    7.) Majewski S, Szmurlo A, Marczak M, Jablonska S, Bollag W.: Synergistic effect of retinoids and interferon alpha on tumor-induced angiogenesis: anti-angiogenic effect on HPV-harboring
    tumor-cell lines.Int J Cancer. 1994 Apr 1;57(1):81-5.
    8.) Pastorino U, Infante M, Maioli M, et al. Adjuvant treatment of stage I lung cancer with high-dose vitamin A. J Clin Oncol 1993;11:1216–22.

    Vitamin C

    1.) Wybieralska E, Koza M, Sroka J, Czyz J, Madeja Z. Ascorbic acid inhibits the migration of walker 256 carcinosarcoma cells. Cell Mol Biol Lett. 2008;13(1):103-11. Epub 2007 Oct 29.
    2.) Hanck A. Vitamin C and cancer. Int J Vit Nutr Res 1983;(Suppl #24):87–104 [review].
    3.) Murata A, Morishige F, Yamaguchi H. Prolongation of survival times of terminal cancer patients by administration of large doses of ascorbate. Int J Vit Nutr Res 1982;(Suppl #23):103–14.
    4.) Bussey HJR, DeCosse JJ, Deschner EE, et al. A randomized trial of ascorbic acid in polyposis coli. Cancer 1982;50:1434–9.
    5.) Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: reevaluation of prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA 1978;75:4538–42.
    6.) Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA 1976;73:3685–9.

    Selenium

    1.) Li H, Stampfer MJ, Giovannucci EL, Morris JS, Willett WC, Gaziano JM, Ma J.A prospective study of plasma selenium levels and prostate cancer risk. J Natl Cancer Inst. 2004 May
    5;96(9):696-703.
    2.) Yu M-W, Horng I-S, Hsu K-H, et al. Plasma selenium levels and risk of hepatocellular carcinoma among men with chronic hepatitis virus infection. Am J Epidemiol 1999;150:367–74.
    3.) Knekt P, Marniemi J, Teppo L, et al. Is low selenium status a risk factor for lung cancer? 1998 Nov 15;148(10):975-82.
    4.) Scieszka M, Danch A, Machalski M, Drozdz M. Plasma selenium concentration in patients with stomach and colon cancer in the Upper Silesia. Neoplasma 1997;44:395–7.
    5.) Toma S, Micheletti A, Giacchero A, et al. Selenium therapy in patients with precancerous and malignant oral cavity lesions: preliminary results.Cancer Detection Prev 1991;15:491–3.
    6.) Knekt P, Aromaa A, Maatela J, et al. Serum selenium and subsequent risk of cancer among Finnish men and women. J Natl Cancer Inst 1990;82:864–8.
    7.) Burney PGJ, Comstock GW, Morris JS. Serologic precursors of cancer: serum micronutrients and the subsequent risk of pancreatic cancer. Am J Clin Nutr 1989;49:895–900.
    8.) Helzlsouer KJ, Comstock GW, Morris JS. Selenium, lycopene, alpha-tocopherol, ß-carotene, retinol, and subsequent bladder cancer. Cancer Res 1989;49:6144–8.
    9.) Jaskiewicz K, Marasas WF, Rossouw JE, et al. Selenium and other mineral elements in populations at risk for esophageal cancer. Cancer 1988;62:2635–9.
    10.) Medina D, Morrison DG. Current ideas on selenium as a  chemopreventative agent. Pathol Immunopathol Res 1988;7:187–99.
    11.) Fex G, Pettersson B, Akesson B. Low plasma selenium as a risk factor for cancer death in middle-aged men. Nutr Cancer 1987;10:221–9.
    12.) Medina D. Mechanisms of selenium inhibition of tumorigenesis. Adv Exp Med Biol 1986;206:465–72.
    13.) Willett WC, Polk BF, Morris JS, et al. Prediagnostic serum Selenium and risk of cancer. Lancet 1983;42:130–4.
    14.) Beisel WR. Single nutrients and immunity. Am J Clin Nutr 1982;35:417–68.
    15.) Shamberger RJ, Rukoven E, Lonfield AK, et al. Antioxidants and cancer. Selenium in the blood of normals and cancer patients. J Natl Cancer Inst 1973;4:863–70.

    Omega 3 Essential Fatty Acids

    1.) Colomer R, Moreno-Nogueira JM, García-Luna PP, García-Peris P, García-de-Lorenzo A, Zarazaga A, Quecedo L, del Llano J, Usán L, Casimiro C. N-3 fatty acids, cancer and cachexia: a systematic review of the literature. Br J Nutr. 2007 May;97(5):823-31.
    2.) Zhang W, Long Y, Zhang J, Wang C. Modulatory effects of EPA and DHA on proliferation and apoptosis of pancreatic cancer cells. J Huazhong Univ Sci Technolog Med Sci. 2007 Oct;27(5):547-50.
    3.) Dauchy RT, Dauchy EM, Davidson LK, Krause JA, Lynch DT, Tirrell PC, Tirrell RP, Sauer LA, Van der Riet P, Blask DE. Inhibition of fatty acid transport and proliferative activity in tissue-isolated human squamous cell cancer xenografts perfused in situ with melatonin or eicosapentaenoic or conjugated linoleic acids. Comp Med. 2007 Aug;57(4):377-82.
    4.) Chen J, Power KA, Mann J, Cheng A, Thompson LU. Flaxseed alone or in combination with tamoxifen inhibits MCF-7 breast tumor growth in ovariectomized athymic mice with high circulating levels of estrogen. Exp Biol Med (Maywood). 2007 Sep;232(8):1071-80.
    5.) Kolar SS, Barhoumi R, Callaway ES, Fan YY, Wang N, Lupton JR, Chapkin RS. Synergy between docosahexaenoic acid and butyrate elicits p53-independent apoptosis via mitochondrial Ca(2+) accumulation in colonocytes. Am J Physiol Gastrointest Liver
    Physiol. 2007 Nov;293(5):G935-43. Epub 2007 Aug 23.
    6.) Kato T, Kolenic N, Pardini RS. Docosahexaenoic acid (DHA), a primary tumor suppressive omega-3 fatty acid, inhibits growth of colorectal cancer independent of p53 mutational status. Nutr Cancer. 2007;58(2):178-87.
    7.) Espada CE, Berra MA, Martinez MJ, Eynard AR, Pasqualini ME. Effect of Chia oil (Salvia Hispanica) rich in omega-3 fatty acids on the eicosanoid release, apoptosis and T-lymphocyte tumor infiltration in a murine mammary gland adenocarcinoma. Prostaglandins Leukot Essent Fatty Acids. 2007 Jul;77(1):21-8. Epub 2007 Jul 6.
    8.) Saarinen NM, Power K, Chen J, Thompson LU. Flaxseed attenuates the tumor growth stimulating effect of soy protein in ovariectomized athymic mice with MCF-7 human breast cancer xenografts. Int J Cancer. 2006 Aug 15;119(4):925-31.
    9.) Shirota T, Haji S, Yamasaki M, Iwasaki T, Hidaka T, Takeyama Y, Shiozaki H, Ohyanagi H. Apoptosis in human pancreatic cancer cells induced by eicosapentaenoic acid. Nutrition. 2005
    Oct;21(10):1010-7.
    10.) Schley PD, Jijon HB, Robinson LE, Field CJ. Mechanisms of omega-3 fatty acid-induced growth inhibition in MDA-MB-231 human breast cancer cells. Breast Cancer Res Treat. 2005
    July;92(2):187-95.
    11.) de Deckere EA. Possible beneficial effect of fish and fish n-3 polyunsaturated fatty acids in breast and colorectal cancer. Eur J Cancer Prev. 1999 Jul;8(3):213-21.
    12.) Chang WL, Chapkin RS, Lupton JR. Fish oil blocks azoxymethane-induced rat colon tumorigenesis by increasing cell differentiation and apoptosis rather than decreasing cell
    proliferation. J Nutr. 1998 Mar;128(3):491-7.
    13.) Bagga D, Capone S, Wang HJ, Heber D, Lill M, Chap L, Glaspy JA. Dietary modulation of omega-3/omega-6 polyunsaturated fatty acid ratios in patients with breast cancer. J Natl Cancer Inst. 1997 Aug 6;89(15):1123-31.

    CoQ10

    1.) Caso G, Kelly P, McNurlan MA, Lawson WE. Effect of coenzyme q10 on myopathic symptoms in patients treated with statins. Am JCardiol. 2007 May 15;99(10):1409-12. Epub 2007 Apr 3.
    2.) Premkumar VG, Yuvaraj S, Vijayasarathy K, Gangadaran SG, Sachdanandam P. Effect of coenzyme Q10, riboflavin and niacin onserum CEA and CA 15-3 levels in breast cancer patients undergoing tamoxifen therapy. Biol Pharm Bull. 2007 Feb;30(2):367-70.
    3.) Premkumar VG, Yuvaraj S, Vijayasarathy K, Gangadaran SG, Sachdanandam P. Serum cytokine levels of interleukin-1beta, -6, -8,tumour necrosis factor-alpha and vascular endothelial growth factor in breast cancer patients treated with tamoxifen and supplemented with co-enzyme Q(10), riboflavin and niacin. Basic Clin Pharmacol Toxicol. 2007 Jun;100(6):387-91.
    4.)  Rusciani L, Proietti I, Paradisi A, Rusciani A, Guerriero G, Mammone A, De Gaetano A, Lippa S. Recombinant interferon alpha-2b and coenzyme Q10 as a postsurgical adjuvant therapy for melanoma: a 3-year trial with recombinant interferon-alpha and 5-year
    follow-up. Melanoma Res. 2007 Jun;17(3):177-83.
    5.)  Rusciani L, Proietti I, Rusciani A, Paradisi A, Sbordoni G, Alfano C, Panunzi S, De Gaetano A, Lippa S. Low plasma coenzyme Q10 levels as an independent prognostic factor for melanoma progression. J Am Acad Dermatol. 2006 Feb;54(2):234-41.
    6.)  Langsjoen PH, Langsjoen JO, Langsjoen AM, Lucas LA. Treatment of statin adverse effects with supplemental Coenzyme Q10 and statin drug discontinuation. Biofactors. 2005;25(1-4):147-52.
    7.) Forgionne GA. Bovine cartilage, coenzyme Q10, and wheat grass therapy for primary peritoneal cancer. J Altern Complement Med. 2005 Feb;11(1):161-5.
    8.) Silver MA, Langsjoen PH, Szabo S, Patil H, Zelinger A. Effect of atorvastatin on left ventricular diastolic function and ability of coenzyme Q10 to reverse that dysfunction. Am J Cardiol. 2004 Nov 15;94(10):1306-10.
    9.)  Judy WV. Nutritional intervention in cancer prevention and treatment. American College for Advancement in Medicine Spring Conference, Ft. Lauderdale, FL. May 3, 1998.
    10.) Boik, John: Cancer and Natural Medicine, Oregon Medical Press, 1995,p.71.
    11.)  Lockwood K, Moesgaard S, Folkers K. Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q10. Biochem Biophys Res Commun 1994;199:1504–8.
    12.) Lockwood K, Moesgaard S, Yamamoto T, Folkers K. Progress on therapy of breast cancer with vitamin Q10 and the regression of metastases. Biochem Biophys Res Commun 1995;212:172–7.
    13.)  Lockwood K, Moesgaard S, Hanioka T, Folkers K. Apparent partial remission of breast cancer in ‘high risk’ patients supplemented with nutritional antioxidants, essential fatty acids and coenzyme Q10. Mol Aspects Med. 1994;15 Suppl:s231-40.
    14.)  Folkers K, Brown R, Judy WV, Morita M. Survival of cancer patients on therapy with coenzyme Q10. Biochem Biophys Res Commun. 1993 Apr 15;192(1):241-5.

    Vitamin C – high dose or IV

    1.) Yeom CH, Jung GC, Song KJ. Changes of terminal cancer patients’ health-related quality of life after high dose vitamin C administration. J Korean Med Sci. 2007 Feb;22(1):7-11.
    2.) Shoichiro Ohtani, Arifumi Iwamaru, Wuguo Deng, Kentaro Ueda, Guanglin Wu, Gitanjali Jayachandran, Seiji Kondo, Edward N. Atkinson, John D. Minna, Jack A. Roth and Lin Ji. Tumor Suppressor 101F6 and Ascorbate Synergistically and Selectively Inhibit Non–Small Cell Lung Cancer Growth by Caspase-Independent Apoptosis and Autophagy. Cancer Research 67, 6293-6303, July 1, 2007.
    3.) Sebastian J. Padayatty, Hugh D. Riordan, Stephen M. Hewitt, Arie Katz, L. John Hoffer and Mark Levine. Intravenously administered vitamin C as cancer therapy: three cases. CMAJ
    2006;174(7):937-42.
    4.) Riordan HD, Casciari JJ, González MJ, Riordan NH, Miranda-Massari JR, Taylor P, Jackson JA.A pilot clinical study of continuous intravenous ascorbate in terminal cancer patients. PR
    Health Sci J. 2005 Dec;24(4):269-76.

    Grape Seed Extract (Resveratrol)

    1.) Li T, Fan GX, Wang W, Li T, Yuan YK. Resveratrol induces apoptosis, influences IL-6 and exerts immunomodulatory effect on mouse lymphocytic leukemia both in vitro and in vivo. Int
    Immunopharmacol. 2007 Sep;7(9):1221-31.
    2.) Golkar L, Ding XZ, Ujiki MB, Salabat MR, Kelly DL, Scholtens D, Fought AJ, Bentrem DJ, Talamonti MS, Bell RH, Adrian TE. Resveratrol inhibits pancreatic cancer cell proliferation through transcriptional induction of macrophage inhibitory cytokine-1. J Surg Res. 2007 Apr;138(2):163-9.
    3.) Gill C, Walsh SE, Morrissey C, Fitzpatrick JM, Watson RW.Resveratrol sensitizes androgen independent prostate cancer cells to death-receptor mediated apoptosis through multiple
    mechanisms. Prostate. 2007 Nov 1;67(15):1641-53.
    4.) Chen Y, Tseng SH. Pro- and anti-angiogenesis effects of resveratrol. In Vivo. 2007 Mar-Apr;21(2):365-70.
    5.) Hudson TS, Hartle DK, Hursting SD, Nunez NP, Wang TT, Young HA, Arany P, Green JE. Inhibition of prostate cancer growth by muscadine grape skin extract and resveratrol through distinct mechanisms. Cancer Res. 2007 Sep 1;67(17):8396-405.
    6.) Aziz MH, Nihal M, Fu VX, Jarrard DF, Ahmad N. Resveratrol-caused apoptosis of human prostate carcinoma LNCaP cells is mediated via modulation of phosphatidylinositol
    3′-kinase/Akt pathway and Bcl-2 family proteins. Mol Cancer Ther. 2006 May;5(5):1335-41.
    7.) Delmas D, Lancon, A, Colin, D, Jannin, B, Latruffe N. Resveratrol as a chemopreventative agent: a promising molecule for fighting cancer. Current Drug Targets. 2006 April; 7(4): 423-42.
    8.) Garvin S, Ollinger, K, Dabrosin, C. Resveratrol induces apoptosis and inhibits angiogenesis in human breast cancer xenografts in vivo. Cancer Letters. 2006 Jan; 231(1): 113-22.
    9.) Benitez DA, Pozo-Guisado E, Alvarez-Barrientos A, Fernandez-Salguero PM, Castellón EA. Mechanisms involved in resveratrol-induced apoptosis and cell cycle arrest in prostate
    cancer-derived cell lines. J Androl. 2007 Mar-Apr;28(2):282-93. Epub 2006 Oct 18.
    10.) Horvath Z, Saiko P, Illmer C, Madlener S, Hoechtl T, Bauer W, Erker T, Jaeger W, Fritzer-Szekeres M, Szekeres T. Resveratrol, an ingredient of wine, acts synergistically with Ara-C and tiazofurin in HL-60 human promyelocytic leukemia cells. Nucleosides Nucleotides Nucleic Acids. 2006;25(9-11):1019-24.
    11.) Sexton E, Van Themsche C, LeBlanc K, Parent S, Lemoine P, Asselin E. Resveratrol interferes with AKT activity and triggers apoptosis in human uterine cancer cells. Mol Cancer. 2006 Oct 17;5:45.
    12.) Jazirehi AR, Bonavida B. Resveratrol modifies the expression of apoptotic regulatory proteins and sensitizes non-Hodgkin’s lymphoma and multiple myeloma cell lines to paclitaxel-induced apoptosis. Mol Cancer Ther. 2004 Jan;3(1):71-84.
    13.) Kim YA, Rhee SH, Park KY, Choi YH. Antiproliferative effect of resveratrol in human prostate carcinoma cells. J Med Food. 2003 Winter;6(4):273-80.
    14.) Tyagi A, Agarwal R, Agarwal C. Grape seed extract inhibits EGF-induced and constitutively active mitogenic signaling but activates JNK in human prostate carcinoma DU145 cells: possible role in antiproliferation and apoptosis. Oncogene. 2003 Mar 6;22(9):1302-16.
    15.) ng XZ, Adrian TE. Resveratrol inhibits proliferation and induces apoptosis in human pancreatic cancer cells. Pancreas. 2002 Nov;25(4):e71-6.
    16.) Lin HY, Shih A, Davis FB, Tang HY, Martino LJ, Bennett JA, Davis PJ. Resveratrol induced serine phosphorylation of p53 causes apoptosis in a mutant p53 prostate cancer cell line. J Urol. 2002 Aug;168(2):748-55.
    17.) Ahmad N, Adhami VM, Afaq F, Feyes DK, Mukhtar H. Resveratrol causes WAF-1/p21-mediated G(1)-phase arrest of cell cycle and induction of apoptosis in human epidermoid carcinoma A431 cells. Clin Cancer Res. 2001 May;7(5):1466-73.

    Turmeric (Curcumin)

    1.) Ji C, Cao C, Lu S, Kivlin R, Amaral A, Kouttab N, Yang H, Chu W, Bi Z, Di W, Wan Y. Curcumin attenuates EGF-induced AQP3 up-regulation and cell migration in human ovarian cancer cells.Cancer Chemother Pharmacol. 2008 Jan 23 [Epub ahead of print].
    2.) Steward WP, Gescher AJ. Curcumin in cancer management: Recent results of analogue design and clinical studies and desirable future research. Mol Nutr Food Res. 2008 Jan 9 [Epub ahead of print].
    3.) Shankar S, Ganapathy S, Chen Q, Srivastava RK. Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis, metastasis and angiogenesis. Mol Cancer. 2008 Jan 29;7(1):16 [Epub ahead of print]
    4.) Moiseeva EP, Almeida GM, Jones GD, Manson MM. Extended treatment with physiologic concentrations of dietary phytochemicals results in altered gene expression, reduced growth, and apoptosis of cancer cells. Mol Cancer Ther. 2007 Nov;6(11):3071-9.
    5.) Shankar S, Chen Q, Sarva K, Siddiqui I, Srivastava RK. Curcumin enhances the apoptosis-inducing potential of TRAIL in prostate cancer cells: molecular mechanisms of apoptosis, migration and angiogenesis. J Mol Signal. 2007 Oct 4;2:10.
    6.) Shankar S, Srivastava RK. Bax and Bak genes are essential for maximum apoptotic response by curcumin, a polyphenolic compound and cancer chemopreventive agent derived from turmeric, Curcuma longa. Carcinogenesis. 2007 Jun;28(6):1277-86. Epub 2007 Feb 2.
    7.) Shankar S, Srivastava RK. Involvement of Bcl-2 family members, phosphatidylinositol 3′-kinase/AKT and mitochondrial p53 in curcumin (diferulolylmethane)-induced apoptosis in prostate cancer. Int J Oncol. 2007 Apr;30(4):905-18.
    8.) Somers-Edgar TJ, Scandlyn MJ, Stuart EC, Le Nedelec MJ, Valentine SP, Rosengren RJ. The combination of epigallocatechin gallate and curcumin suppresses ERalpha-breast cancer cell growth in vitro and in vivo. Int J Cancer. 2007 Dec 20 [Epub ahead of print].
    9.) Chen A, Xu J, Johnson AC. Curcumin inhibits human colon cancer cell growth by suppressing gene expression of epidermal growth factor receptor through reducing the activity of the transcription factor Egr-1. Oncogene. 2006 Jan 12;25(2):278-87.
    10.) Wahl H, Tan L, Griffith K, Choi M, Liu JR. Curcumin enhances Apo2L/TRAIL-induced apoptosis in chemoresistant ovarian cancer cells. Gynecol Oncol. 2007 Apr;105(1):104-12. Epub 2006 Dec 15.
    11.) Chen J, Wanming D, Zhang D, Liu Q, Kang J.Water-soluble antioxidants improve the antioxidant and anticancer activity of low concentrations of curcumin in human leukemia cells. Pharmazie. 2005 Jan;60(1):57-61.
    12.) Deeb DD, Jiang H, Gao X, Divine G, Dulchavsky SA, Gautam SC. Chemosensitization of hormone-refractory prostate cancer cells by curcumin to TRAIL-induced apoptosis. J Exp Ther Oncol. 2005;5(2):81-91.
    13.)Dobrovolskaia MA, Kozlov SV.: Inflammation and cancer: when NF-kappaB amalgamates the perilous partnership. Curr Cancer Drug Targets. 2005 Aug;5(5):325-44.
    14.) Deeb D, Jiang H, Gao X, Hafner MS, Wong H, Divine G, Chapman RA, Dulchavsky SA, Gautam SC. Curcumin sensitizes prostate cancer cells to tumor necrosis factor-related apoptosis-inducing gand/Apo2L by inhibiting nuclear factor-kappaB through suppression of IkappaBalpha phosphorylation. Mol Cancer Ther. 2004 Jul;3(7):803-12.
    15.) Van Erk MJ, Teuling E, Staal YC, Huybers S, Van Bladeren PJ, Aarts JM, Van Ommen B. Time- and dose-dependent effects of curcumin on gene expression in human colon cancer cells. J Carcinog. 2004 May 12;3(1):8.
    16.)Ernst P.: The role of inflammation in the pathogenesis of gastric cancer. Aliment Pharmacol Ther. 1999 Mar;13 Suppl 1:13-8
    17.) Menon LG, Kuttan R, Kuttan G. Anti-metastatic activity of curcumin and catechin. Cancer Lett 1999;141:159–65.
    18.) Khafif A, Schantz SP, Chou TC, Edelstein D, Sacks PG. uantitation of chemopreventive synergism between (-)-epigallocatechin-3-gallate and curcumin in normal, premalignant
    and malignant human oral epithelial cells. Carcinogenesis. 1998
    Mar;19(3):419-24.

    Vitamin D

    1.) Lappe J, Travers-Gustafson D, Davies K, Recker R, Heaney R. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. American Journal of Clinical Nutrition. Am J Clin Nutr. 2007 Jun;85(6):1586-91.
    2.) Ma Y, et al. Study presented at the 2007 centennial meeting of the American Association for Cancer Research (AACR), April 14 to 18, 2007, Los Angeles.
    3.)Holick MF.: Vitamin D: Its role in cancer prevention and treatment. Prog Biophys Mol Biol. 2006 Mar 10;
    4.) Schwartz GG, Eads D, Rao A, Cramer SD, Willingham MC, Chen TC, Jamieson DP, Wang L, Burnstein KL, Holick MF, Koumenis C.:Pancreatic cancer cells express 25-hydroxyvitamin D-1
    alpha-hydroxylase and their proliferation is inhibited by the prohormone 25-hydroxyvitamin D3.Carcinogenesis. 2004 Jun;25(6):1015-26. Epub 2004 Jan 23.
    5.) Wietrzyk J, Pelczynska M, Madej J, Dzimira S, Kusnierczyk H, Kutner A, Szelejewski W, Opolski A.: Toxicity and antineoplastic effect of (24R)-1,24-dihydroxyvitamin D3 (PRI-2191).Steroids. 2004 Sep;69(10):629-35.
    6.) Vegesna V, O’Kelly J, Said J, Uskokovic M, Binderup L, Koeffle HP.: Ability of potent vitamin D3 analogs to inhibit growth of prostate cancer cells in vivo. Anticancer Res. 2003
    Jan-Feb;23(1A):283-9.
    7.) Grant WB. An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B radiation. Cancer. 2002 Mar 15;94(6):1867-75.
    8.) Majewski S, Skopinska M, Marczak M, Szmurlo A, Bollag W, Jablonska S.: Vitamin D3 is a potent inhibitor of tumor cell-induced angiogenesis. J Investig Dermatol Symp Proc. 1996
    Apr;1(1):97-101.
    9.) James SY, Mackay AG, Colston KW. Effects of 1,25 dihydroxyvitamin D3 and its analogues on induction of apoptosis in breast cancer cells. J Steroid Biochem Mol Biol. 1996
    Jul;58(4):395-401.
    10.) Schwartz GG, Hill CC, Oeler TA, Becich MJ, Bahnson RR.1,25-Dihydroxy-16-ene-23-yne-vitamin D3 and prostate cancer cell proliferation in vivo. Urology. 1995 Sep;46(3):365-9.
    11.) Majewski S, Szmurlo A, Marczak M, Jablonska S, Bollag W.: Inhibition of tumor cell-induced angiogenesis by retinoids, 1,25-dihydroxyvitamin D3 and their combination.Cancer Lett. 1993
    Nov 30;75(1):35-9.

    Bromelain (anasas comosus)

    1.)Kalra N, Bhui K, Roy P, Srivastava S, George J, Prasad S, Shukla Y.Regulation of p53, nuclear factor kappaB and cyclooxygenase-2 expression by bromelain through targeting mitogen-activated protein kinase pathway in mouse skin.Toxicol Appl Pharmacol. 2008 Jan
    1;226(1):30-7. Epub 2007 Aug 23.
    2.) Báez R, Lopes MT, Salas CE, Hernández M. In vivo antitumoral activity of stem pineapple (Ananas comosus) bromelain. Planta Med. 2007 Oct;73(13):1377-83. Epub 2007 Sep 24.
    3.) Beuth J, Braun JM. Modulation of murine tumor growth and colonization by bromelaine, an extract of the pineapple plant (Ananas comosum L.).In Vivo. 2005 Mar-Apr;19(2):483-5.
    4.) Wallace JM. Nutritional and botanical modulation of the inflammatory cascade–eicosanoids, cyclooxygenases, and lipoxygenases–as an adjunct in cancer therapy. Integr Cancer Ther.
    2002 Mar;1(1):7-37; discussion 37.
    5.) Maurer HR.Bromelain: biochemistry, pharmacology and medical use. Cell Mol Life Sci. 2001 Aug;58(9):1234-45.
    6.) Desser L, Holomanova D, Zavadova E, Pavelka K, Mohr T, Herbacek I. Oral therapy with proteolytic enzymes decreases excessive TGF-beta levels in human blood. Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S10-5.
    7.) Beuth J, Ost B, Pakdaman A, Rethfeldt E, Bock PR, Hanisch J, Schneider B. Impact of complementary oral enzyme application on the postoperative treatment results of breast cancer patients–results of an epidemiological multicentre retrolective cohort study. Cancer
    Chemother Pharmacol. 2001 Jul;47 Suppl:S45-54.
    8.) Tysnes BB, Maurer HR, Porwol T, Probst B, Bjerkvig R, Hoover F. Bromelain reversibly inhibits invasive properties of glioma cells.Neoplasia. 2001 Nov-Dec;3(6):469-79.
    9.) Dale PS, Tamhankar CP, George D, Daftary GV. Co-medication with hydrolytic enzymes in radiation therapy of uterine cervix: evidence of the reduction of acute side effects. Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S29-34.
    10.) Hubarieva HO, Kindzel’s’kyĭ LP, Ponomar’ova OV, Udatova TV, Shpil’ova SI, Smolanka II, Korovin SI, Ivankin VS. Systemic enzymotherapy as a method of prophylaxis of postradiation
    complications in oncological patients] Lik Sprava. 2000 Oct-Dec;(7-8):94-100.
    11.) Eckert K, Grabowska E, Stange R, Schneider U, Eschmann K, Maurer HR. Effects of oral bromelain administration on the impaired immunocytotoxicity of mononuclear cells from mammary tumor patients. Oncol Rep. 1999 Nov-Dec;6(6):1191-9.
    12.) Zavadova E, Desser L, Mohr T. Stimulation of reactive oxygen species production and cytotoxicity in human neutrophils in vitro and after oral administration of a polyenzyme preparation. Cancer Biother. 1995 Summer;10(2):147-52.
    13.) Taussig SJ, Batkin S. Bromelain, the enzyme complex of pineapple (Ananas comosus) and its clinical application. An update. J Ethnopharmacol. 1988 Feb-Mar;22(2):191-203.
    14.) Batkin S, Taussig SJ, Szekerezes J. Antimetastatic effect of bromelain with or without its proteolytic and anticoagulant activity. J Cancer Res Clin Oncol. 1988;114(5):507-8.

    Melatonin

    1.) Lissoni P, Barni S, Mandalà, et al. Decreased toxicity and increased efficacy of cancer chemotherapy using the pineal hormone melatonin in metastatic solid tumour patients with poor clinical status. Eur J Cancer 1999;35:1688–92.
    2.) Lissoni P, Cazzanga M, Tancini G, et al. Reversal of clinical resistance to LHRH analogue in metastatic prostate cancer by the pineal hormone melatonin: efficacy of LHRH analogue plus melatonin in patients progressing on LHRH analogue alone. Eur Urol 1997;31:178–81.
    3.) Lissoni P, Paolorossi F, Tancini G, et al. Is there a role for melatonin in the treatment of neoplastic cachexia? Eur J Cancer 1996;32A:1340–3.
    4.) Lissoni P, Paolorossi F, Tancini G, et al. A phase II study of tamoxifen plus melatonin in metastatic solid tumour patients. Br J Cancer 1996;74:1466–8.
    5.) Lissoni P, Brivio O, Brivio F, et al. Adjuvant therapy with the pineal hormone melatonin in patients with lymph node relapse due to malignant melanoma. J Pineal Res 1996;21:239–42.
    6.) Lissoni P, Barmo S. Meregalli S, et al. Modulation of cancer endocrine therapy by melatonin: a phase II study of tamoxifen plus melatonin in metastatic breast cancer patients progressing under tamoxifen alone. Br J Cancer 1995;71:854–6.
    7.) Reiter RJ, Melchiorri D, Sewerynek E, Poeggeler B, Barlow-Walden L, Chuang J, Ortiz GG, Acuna-Castroviejo D.: A review of the evidence supporting melatonin’s role as an antioxidant.J
    Pineal Res. 1995 Jan;18(1):1-11.
    8.) Neri B, Fiorelli C, Moroni F, et al. Modulation of human lymphoblastoid interferon activity by melatonin in metastatic renal cell carcinoma. Cancer 1994;73:315–9.
    9.) Lissoni P, Barni S, Cazzaniga M, Ardizzoia A, Rovelli F, Brivio F, Tancini G.: Efficacy of the concomitant administration of the pineal hormone melatonin in cancer immunotherapy with low-dose IL-2 in patients with advanced solid tumors who had progressed on IL-2 alone. Oncology. 1994 Jul-Aug;51(4):344-7.
    10.) Lissoni P, Barni S, Ardizzoia A, et al. A randomized study with the pineal hormone melatonin versus supportive care alone in patients with brain metastases due to solid neoplasms. Cancer 1994;73:699–701.
    11.) Lissoni P, Barni S, Tancini G, et al. A randomised study with subcutaneous low-dose interleukin 2 alone vs interleukin 2 plus the pineal neurohormone melatonin in advanced solid neoplasms other than renal cancer and melanoma. Br J Cancer 1994;69:196–9.
    12.) Aldeghi R, Lissoni P, Barni S, et al. Low-dose interlekin-2 subcutaneous immunotherapy in association with the pineal hormone melatonin as a first-line therapy in locally advanced or metastatic hepatocellular carcinoma. Eur J Cancer 1994;30A:167–70.
    13.) Lissoni P, Brivio F, Ardizzoia A, et al. Subcutaneous therapy with low-dose interlekin-2 plus the neurohormone melatonin in metastatic gastric cancer patients with low performance status.
    Tumori 1993;79:401–4.
    14.) Lissoni P, Barni S, Ardizzoia A, et al. Randomized study with the pineal hormone melatonin versus supportive care alone in advanced nonsmall cell lung cancer resistant to a first-line
    chemotherapy containing cisplatin. Oncology 1992;49:336–9.
    15.) Lissoni P, Barni S, Crispino S, et al. Endocrine and immune effects of melatonin therapy in metastatic cancer patients. Eur J Cancer Clin Oncol 1989;25:789–95.

    Calcium D-glucarate

    1.) Singh J, Gupta KP. Induction of apoptosis by calcium D-glucarate in 7,12-dimethyl benz [a] anthracene-exposed mouse skin. J Environ Pathol Toxicol Oncol. 2007;26(1):63-73.
    2.) Hanausek M, Walaszek Z, Slaga TJ. Detoxifying cancer causing agents to prevent cancer. Integr Cancer Ther. 2003 Jun;2(2):139-44.
    3.) Calcium-D-glucarate. Altern Med Rev. 2002 Aug;7(4):336-9.[No authors listed].
    4.) Walaszek Z, Szemraj J, Narog M, Adams AK, Kilgore J, Sherman U, Hanausek M. Metabolism, uptake, and excretion of a D-glucaric acid salt and its potential use in cancer prevention. Cancer Detect Prev. 1997;21(2):178-90.
    5.) Heerdt AS, Young CW, Borgen PI. Calcium glucarate as a chemopreventive agent in breast cancer. Isr J Med Sci. 1995 Feb-Mar;31(2-3):101-5.

    Di-indolymethanes (DIM, IC3)

    1.) Moiseeva EP, Almeida GM, Jones GD, Manson MM.Extended treatment with physiologic concentrations of dietary phytochemicals results in altered gene expression, reduced growth, and apoptosis of cancer cells. Mol Cancer Ther. 2007 Nov;6(11):3071-9.
    2.) Weng JR, Tsai CH, Kulp SK, Wang D, Lin CH, Yang HC, Ma Y, Sargeant A, Chiu CF, Tsai MH, Chen CS. A potent indole-3-carbinol derived antitumor agent with pleiotropic effects on multiple signaling pathways in prostate cancer cells. Cancer Res. 2007 Aug
    15;67(16):7815-24.
    3.) Pappa G, Strathmann J, Löwinger M, Bartsch H, Gerhäuser C. Quantitative combination effects between sulforaphane and 3,3′-diindolylmethane on proliferation of human colon cancer cells in vitro. Carcinogenesis. 2007 Jul;28(7):1471-7. Epub 2007 Feb 28.
    4.) Pappa G, Lichtenberg M, Iori R, Barillari J, Bartsch H, Gerhäuser C. Comparison of growth inhibition profiles and mechanisms of apoptosis induction in human colon cancer cell lines
    by isothiocyanates and indoles from Brassicaceae. Mutat Res. 2006 Jul 25;599(1-2):76-87. Epub 2006 Feb 24.
    5.) Bhuiyan MM, Li Y, Banerjee S, Ahmed F, Wang Z, Ali S, Sarkar FH. Down-regulation of androgen receptor by 3,3′-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in both hormone-sensitive LNCaP and insensitive C4-2B prostate cancer cells. Cancer Res. 2006 Oct 15;66(20):10064-72.
    6.) Aggarwal BB, Ichikawa H. Molecular targets and anticancer potential of indole-3-carbinol and its derivatives. Cell Cycle. 2005 Sep;4(9):1201-15. Epub 2005 Sep 6.
    7.) Chinni SR, Li Y, Upadhyay S, Koppolu PK, Sarkar FH. Indole-3-carbinol (I3C) induced cell growth inhibition, G1 cell cycle arrest and apoptosis in prostate cancer cells. Oncogene. 2001
    May 24;20(23):2927-36.
    8.) Cover CM, Hsieh SJ, Cram EJ, et al. Indole-3-carbinol and tamoxifen cooperate to arrest the cell cycle of MCF-7 human breast cancer cells. Cancer Res 1999;59:1244–51.

    Lycopene

    1.) Parsons JK, Newman VA, Mohler JL, Pierce JP, Flatt S, Marshall J. Dietary modification in patients with prostate cancer on active surveillance: a randomized, multicentre feasibility study. BJU Int. 2008 Jan 24 [Epub ahead of print].
    2.) Wang A, Zhang L.[Effect of lycopene on proliferation and cell cycle of hormone refractory prostate cancer PC-3 cell line]. Wei Sheng Yan Jiu. 2007 Sep;36(5):575-8.
    3.) Gunasekera RS, Sewgobind K, Desai S, Dunn L, Black HS, McKeehan WL, Patil B. Lycopene and lutein inhibit proliferation in rat prostate carcinoma cells. Nutr Cancer. 2007;58(2):171-7.
    4.) Vaishampayan U, Hussain M, Banerjee M, Seren S, Sarkar FH, Fontana J, Forman JD, Cher ML, Powell I, Pontes JE, Kucuk O. Lycopene and soy isoflavones in the treatment of prostate cancer. Nutr Cancer. 2007;59(1):1-7.
    5.) Zhang J, Dhakal I, Stone A, Ning B, Greene G, Lang NP, Kadlubar FF. Plasma carotenoids and prostate cancer: a population-based case-control study in Arkansas. Nutr Cancer. 2007;59(1):46-53.
    6.) Hwang ES, Bowen PE. Effects of lycopene and tomato paste extracts on DNA and lipid oxidation in LNCaP human prostate cancer cells. Biofactors. 2005;23(2):97-105.
    7.) Hantz HL, Young LF, Martin KR. Physiologically attainable concentrations of lycopene induce mitochondrial apoptosis in LNCaP human prostate cancer cells. Exp Biol Med (Maywood). 2005 Mar;230(3):171-9.
    8.) Giovannucci E, Rimm EB, Liu Y, Stampfer MJ, Willett WC. A prospective study of tomato products, lycopene, and prostate cancer risk. J Natl Cancer Inst. 2002 Mar 6;94(5):391-8.
    9.) Levy J, Bosin E, Feldman B, et al. Lycopene is a more potent inhibitor of human cancer cell proliferation than either a-carotene or ß-carotene. Nutr Cancer 1995;24:257–66.
    10.) Giovannucci E. Tomatoes, tomato-based products, lycopene, and cancer: review of the epidemiologic literature. J Natl Cancer Inst 1999;91:317–31.

    Larch arabinogalactin

    1.) Sathisha UV, Jayaram S, Harish Nayaka MA, Dharmesh SM. Inhibition of galectin-3 mediated cellular interactions by pectic polysaccharides from dietary sources. Glycoconj J. 2007 Nov;24(8):497-507. Epub 2007 May 25.
    2.) Choi EM, Kim AJ, Kim YO, Hwang JK. Immunomodulating activity of arabinogalactan and fucoidan in vitro. J Med Food. 2005 Winter;8(4):446-53.
    3.) Larch arabinogalactan. Altern Med Rev. 2000 Oct;5(5):463-6. [NO AUTHORS LISTED].
    4.) Kelly GS. Larch arabinogalactan: clinical relevance of a novel immune-enhancing polysaccharide. Altern Med Rev. 1999 Apr;4(2):96-103.
    5.) Hagmar B, Ryd W, Skomedal H.Arabinogalactan blockade of experimental metastases to liver by murine hepatoma. Invasion Metastasis. 1991;11(6):348-55.
    6.) Beuth J, et al.. Inhibition of liver tumor cell colonization in two animal tumor models by lectin blocking with D-galactose or arabinogalactan. Clin Exp Metastasis 1988;6:115–20.
    7.) Hirai O, Fujitsu T, Mori J, Kikuchi H, Koda S, Fujioka M, Morimoto Y. Antitumour activity of purified arabinogalactan-peptidoglycan complex of the cell wall skeleton of
    Rhodococcus lentifragmentus. J Gen Microbiol. 1987 Feb;133(2):369-73.

    Modified Citrus Pectin

    1.) Sathisha UV, Jayaram S, Harish Nayaka MA, Dharmesh SM. Inhibition of galectin-3 mediated cellular interactions by pectic polysaccharides from dietary sources. Glycoconj J. 2007
    Nov;24(8):497-507. Epub 2007 May 25.
    2.) Jackson CL, Dreaden TM, Theobald LK, Tran NM, Beal TL, Eid M, Gao MY, Shirley RB, Stoffel MT, Kumar MV, Mohnen D. Pectin induces apoptosis in human prostate cancer cells: correlation of apoptotic function with pectin structure. Glycobiology. 2007 Aug;17(8):805-19. Epub 2007 May 19.
    3.) Chen CH, Sheu MT, Chen TF, Wang YC, Hou WC, Liu DZ, Chung TC, Liang YC. Suppression of endotoxin-induced proinflammatory responses by citrus pectin through blocking LPS signaling pathways. Biochem Pharmacol. 2006 Oct 16;72(8):1001-9. Epub 2006 Aug 22.
    4.) Glinskii OV, Huxley VH, Glinsky GV, Pienta KJ, Raz A, Glinsky VV.Mechanical entrapment is insufficient and intercellular adhesion is essential for metastatic cell arrest in distant organs.
    Neoplasia. 2005 May;7(5):522-7.
    5.) Guess BW, Scholz MC, Strum SB, Lam RY, Johnson HJ, Jennrich RI. Modified citrus pectin (MCP) increases the prostate-specific antigen doubling time in men with prostate cancer: a phase II pilot study. Prostate Cancer Prostatic Dis. 2003;6(4):301-4.
    6.) Pratima Nangia-Makker, Victor Hogan, Yuichiro Honjo, Sara Baccarini, Larry Tait, Robert Bresalier, Avraham Raz. Inhibition of Human Cancer Cell Growth and Metastasis in Nude Mice by Oral Intake of Modified Citrus Pectin. J Natl Cancer Inst, Vol. 94, No. 24, December 18, 2002
    7.) Nangia-Makker P, Hogan V, Honjo Y, Baccarini S, Tait L, Bresalier R, Raz A. Inhibition of human cancer cell growth and metastasis in nude mice by oral intake of modified citrus pectin. J Natl Cancer Inst. 2002 Dec 18;94(24):1854-62.
    8.) Pienta KJ, Naik H, Akhtar A, Yamazaki K, Replogle TS, Lehr J, et al. Inhibition of spontaneous metastasis in a rat prostate cancer model by oral administration of modified citrus pectin. J Natl Cancer Inst 1995;87:348–53.
    9.) Hsieh TC, Wu JM. Changes in cell growth, cyclin/kinase, endogenous phosphoproteins and nm23 gene expression in human prostatic JCA-1 cells treated with modified citrus pectin. Biochem Mol Biol Int. 1995 Nov;37(5):833-41.
    10.) Platt D, Raz A. Modulation of the lung colonization of B16-F1 melanoma cells by citrus pectin. J Natl Cancer Inst. 1992 Mar 18;84(6):438-42.

B Vitamins

The “Energy Vitamins”

B vitamins comprise an entire complex or “family” of related but different vitamins. Together, the B vitamins comprise an important group of vitamins with many functions, as seen in the chart below. Although their individual functions differ, all B vitamins are involved in energy production in the body. Deficiencies of B vitamins are common today due to food processing.

B vitamin supplementation is useful for:

  • chronic fatigue
  • overweight and obesity
  • memory loss
  • heart disease
  • depression
  • cataracts
  • neuropathy
  • irritability
  • atherosclerosis
  • anemia and more (see chart below).

Maxi Multi is a comprehensive multi-vitamin and mineral formula that includes high potency B complex vitamins. Click here for a full description of this supplement.

B-12 Extreme

The Most Potent B-12 Formula Available.
A full description of B-12 Extreme can be found here.

B-Complex 50

High-potency vitamin B complex in a hypoallergenic, yeast-free formula.

Each (one) capsule contains:

Vitamin B-1 (Thiamine HCL) 50 mg Biotin 50 mg Vitamin B-2 (Riboflavin) 50 mg Pantothenic acid 50 mg Niacinaminde 50 mg Vitamin B-10 (Para-Aminobenzoic Acid) 50 mg Vitmin B-6 (Pyridoxine HCL) 50 mg Choline (Bitartrate) 50 mg Folic Acid 400 mcg Inositol 50 mg Vitamin B-12 (Cyanocobalamine) 50 mcg

Order B-Complex 50 (100 Capsules) Here $15.90

Hi-B-12/Foliplex

High potency sublingual tablet supplying vitamin B-12 and folic acid.

Each (one) capsule contains:
Vitamin B-12 2500 mcg (Cobalamine concentrate)
Folic Acid 800 mcg

Order Hi-B-12/Foliplex (60 tablets) Here $17.00

The B Vitamin Complex “Family”

vitamin major functions major deficiency associations optimal adult dose range best food sources cautions/
notes

vitamin B1
(thiamine)

energy processes fatigue, mental confusion, neuropathy 5-100 mg eggs, berries, nuts, legumes, liver, yeast Nontoxic.

vitamin B2
(riboflavin)

energy processes, wound healing, activates other B vitamins infection, cataracts, blurred vision, eye surgery 5-100 mg green leafy vegetables, eggs, organ meats Nontoxic. Higher doses will make urine a harmless, bright yellow.

vitamin B3
(niacin)

energy processes depression, tension headaches, memory loss 20-100 mg milk, eggs, fish, whole meal wheat flour Doses greater than 50mg may cause a skin flush. Take high doses only with doctors supervision.

vitamin B5
(pantothenic acid)

energy processes; adrenal gland function allergies, morning stiffness; fatigue; muscle cramps 10-1,000 mg eggs, yeast, liver No known toxicity.

vitamin B6
(pyridoxine)

energy processes; antibody formation insomnia, irritability, atherosclerosis 5-200 mg wheat germ, yeast, whole grains Oral contraceptive use increases need for this vitamin.

Folic acid

red blood cell formation, RNA/DNA synthesis fatigue, depression, atherosclerosis 200-800 mcg beans, green leafy veggies, yeast Do not take with Phenobarbital or dilantin.

vitamin B12

red blood cell formation; energy processes atherosclerosis, memory loss, GI symptoms 10-1,200 mcg fermented soy products; root veggies Nontoxic.

Biotin

energy processes; blood sugar regulation muscle pain, depression 300-600 mcg egg yolks, whole wheat No known toxicity.

Basic Advice

A Short Poem Of Medical Advice

Basic Advice

by

Dr. Dana Myatt

I went to the doctor because I was ill
and asked her to give me the miracle pill
to make me feel better – and please, real quick.
You see, I just hate it whenever I’m sick.

She said “I’m afraid your cure is quite up to you.
Your body is sick from the things that you do.
Your diet’s abhorrent – it’s really quite dire.
And by smoking, your lungs think your house is on fire.

Pushing a pencil is exercise – not,
and the stress that you’re under just thickens the plot.
An antibiotic will not cure your cold
which is caused by a virus – this story’s quite old.”

Somewhere in my head this all made good sense;
however, I put up my strongest defense.
“I can’t change my diet ’till after next week.
My friend’s getting married – you know I must eat.

And life’s too stressful to stop smoking now.
If I quit, and start eating, I’ll gain weight and how!
And if I gain weight I’ll feel even worse.
My fat’s not my fault – it’s an old family curse.

And doctor you really just can’t understand
the pace of my life and how busy I am.
I can’t exercise – I haven’t the time.
So I have a few vices. Is that such a crime?

It was Joe in the office who gave me this cold
or else I’m allergic to house dust and mold.
So please give me something to help me feel better.
I’ll follow your instructions right down to the letter.

“I see,” said the doctor, “I’m not getting through.
Here’s a bottle of pills. Four times daily take two.”
“Four times is a lot when my schedule’s so tight.
Can I just take them twice, each morning and night?”

“Do whatever you want” said the doc with a sigh.
I thought for a moment she was going to cry.
“The state of your health is quite up to you
I can counsel and guide you, but you have to choose.

My studied opinion, my highest advice, is
get ‘back to the basics’ – don’t even think twice.
The choices you make will determine your fate.
Improve your condition before it’s too late.

Pills can be helpful and sometimes can cure,
but your daily routine will affect you for sure.
Now pull out your wallet and pay me my fee.
My advice may be basic, but it doesn’t come free!”

Bio-Identical Hormone Therapy

Bio-identical (Natural) Hormone Replacement Therapy
and Other Natural Hormone-Balancing Therapies

Which One is Right for You?

Index:

Are Your Symptoms Cause by Low or Imbalanced Hormones?

What is Bio-identical Hormone Replacement Therapy (bHRT)?

What are the advantages of bHRT?

Delivery System: Oral Versus Transdermal Hormones

How Best to Address Your Menopausal Symptoms and Concerns?

Dr. Myatt’s “Hormone Balance” Programs: Which One is Right for You?

Are Your Symptoms Caused by Low or Imbalanced Hormones?

Women and men both go through “the climacteric,” a period in mid-life when sex hormone production declines.

In women, this change is called “menopause.” In men, the change is often referred to as “andropause.” Many symptoms of the climacteric are similar in men and women.

In women, peri-menopause (“around the time of menopause”) symptoms can include mood swings, weight gain, fatigue, hot flashes, breast tenderness, vaginal dryness, decreased libido (sex drive), urinary leakage or urgency and sleep difficulties. Menstrual periods may becomes less frequent, irregular and farther apart OR they can become heavier and more frequent. Peri-menopause usually begins in a woman’s 40’s but can start as early as the 30’s or as late as the 50’s.

Menopause symptoms in women are similar to peri-menopause symptoms except that menstrual periods cease. Headaches, heart palpitations, cognitive decline and difficulty sleeping may also occur. Bone mineral loss is often accelerated during this time, leading to osteoporosis.

Andropause symptoms in men can include include night sweats, low libido (sex drive), weight gain, depression, anxiety, hot flashes, gynecomastia (enlarged male breasts), fatigue, irritability, and weight gain. Other male climacteric symptoms include erectile dysfunction, loss of stamina and lean muscle mass, cognitive decline and decreased bone mineral density. Men with lower testosterone have a higher risk of coronary artery disease. (1-4)

The change in men is more gradual than in women and symptoms are often attributed to “natural aging” instead of hormone decline.

What is Bio-identical Hormone Replacement Therapy (bHRT)?

Bio-identical Hormone Replacement Therapy (bHRT) is a way to resolve symptoms and/or restore sex hormones to more youthful levels using hormones that are identical to those produced by the human body. Bio-identical hormone replacement therapy (bHRT) differs from convention HRT (cHRT) which uses horse estrogens (Premarin = Pregnant Mares Urine), synthetic and semi-synthetic hormones that are different from human hormones.

Proponents of bHRT believe that many of the unwanted side effects of conventional HRT are due to the “foreignness” of the molecules, not to hormone replacement therapy itself. This may make bHRT a safer form of hormone replacement therapy. (5-10)

How is Bio-Identical HRT Different from Conventional HRT?

Bio-identical hormone replacement is different from conventional HRT in the following ways.

  1. “Identical to human” hormones are used in bHRT. Conventional HRT typically uses horse hormones and synthetic and semi-synthetic hormones. These hormones are not the same molecules as those produced by the human body.It should be noted that there are bio-identical FDA approved hormones available by prescription. Not all “bio-identical” hormones need to be “compounded,” or made up individually by a compounding pharmacist.
  2. Based on Testing. bHRT is prescribed based on individual hormone test results. Conventional HRT does not use testing but bases treatment on improvement of symptoms.
  3. “Pulsed dosing” is often used in bHRT to duplicate the natural rhythm of hormone production and release. Some studies have shown this pattern of use to be safer and just as effective as continuous HRT. (11-12) Conventional HRT typically uses continuous doses of hormones. Continuous doses are associated with higher risk of breast cancer in some studies. (13)

What are the advantages of bHRT?

Is bHRT Safer than conventional HRT?

Conventional hormone replacement therapy, especially in women, is associated with a number of increased health risks including heart disease, stroke, breast cancer, deep vein thrombosis, gallbladder disease and acid reflux. (14-20) Conventional HRT decreases the risk of osteoporosis and can alleviate some symptoms of menopause including hot flashes and vaginal dryness (21-22) but many experts do not believe these improvements justify the increased risks.

Proponents of bio-identical hormone replacement therapy believe that bHRT is safer than conventional hormone therapy and some studies have shown this. (5-10) However, the number of studies done with bHRT is small compared to the studies done with conventional HRT. Large-scale studies of safety and efficacy of bHRT are lacking.

In spite of a small number of studies confirming safety and efficacy, the case for bio-identical hormones also makes sense in theory. Consider these facts:

Conventional hormone replacement therapy typically employs estrogens from pregnant mare’s urine. Horse hormones are significantly different than human hormones. Conventional hormone replacement also typically uses synthetic progesterone. The difference in synthetic and bio-identical progesterone is  significant. It is therefore believed that most if not all of the negative side effects of conventional hormone replacement is due to their “foreign to humans” molecular structure, not to hormone replacement itself. Some studies on bio-identical versus non-bio-identical progesterone confirm that there is a different effect in humans with natural progesterone appearing to have less risk of associated cancers. (5-10)

Further, conventional hormone replacement is almost always prescribed as a “one-size-fits-all” recommendation without the use of any laboratory testing to verify hormone levels. Practitioners of bio-identical hormone replacement typically start with blood, saliva or urine hormone testing and customize hormone prescriptions based on an individual’s unique requirements. Testing can help guide the prescription and prevent levels of hormones from being excessive.

Finally, risks associated with hormone therapy can be monitored, but this is rarely if ever done in conventional hormone prescribing. However, risks such as total hormone levels, ratios of hormones to each other and hormone metabolites can be potent predictors of heart disease and cancer risks. Even without hormone replacement therapy, these risk factors may be worth monitoring in all middle-aged men and women.

To answer the question of safety, there are theoretical reasons to believe that bio-identical HRT should be safer than conventional HRTand some actual studies show better safety.

Is bHRT Effective?

Studies have verified the effectiveness of bHRT for relieving many of the symptoms of menopause. (7-9, 23-24)

My personal clinical experience over the past 23 years is that bHRT can achieve every positive effect that conventional HRT achieves with less risk of negative side effects. Because I monitor risk factors, I have also seen reductions in cardiac and cancer risk markers and improvements in bone mineral density.

Is bHRT Proven?

Studies have demonstrated the effectiveness of bio-identical hormone replacement therapy. (7-9, 23-28)

Anti-Aging Claims for bHRT

Proponents of bHRT claim that keeping hormones at “youthful” levels can extend life expectancy and help delay the effects of aging. These claims have been popularized by public figures like Suzanne Somers in her book “The Sexy Years.” In spite of these claims, there is no proof that continued use of sex hormones, especially estrogen and progesterone in women, have-extending properties. There IS evidence that DHEA in both men and women (25-28) and testosterone in men (29-33) may have a positive influence on health, longevity and hormone balance.

While claims of living better and longer with bHRT are numerous, proof is lacking. This leaves bHRT and its anti-aging effects in the realm of theory at this point.

Delivery System: Oral Versus Transdermal Hormones

In addition to the “form” (natural or synthetic) of hormone, the method of administration has been shown to make a significant difference in safety and efficacy.

Orally administered hormones, especially estrogens, can increase risk of blood clots and deep vein thrombosis, increase hs-CRP (a marker of inflammation), decrease free testosterone and thyroid hormone and increase cortisol.(34) Oral estrogen is also associated with an increased risk of gallbladder disease and acid reflux. (15,18)

Many hormones used transdermally — applied to the skin or mucous membranes — do not appear to have these unwanted effects. (35) Therefore, when considering bHRT, the form that it is used in is also of importance.

How Best to Address Your Menopausal Symptoms and Concerns?

Symptoms of peri-menopause and menopause in women and andropause in men are a sign from the body that something is “off kilter.” For example, hot flashes in women correspond to an increase in oxidative stress and decreased nitric oxide levels (NO), both risk factors for cardiovascular disease. (36-37)

These symptoms and resulting negative physical changes are not an inevitable part of aging and should not be ignored. They can be addressed and improved through a variety of means, including but not limited to bio-identical hormone replacement therapy.

Diet changes, exercise and personal health practices can all help to improve symptoms of menopause and andropause. (38-39) There are nutritional and herbal supplements are proven to help correct menopause and andropause symptoms. (40-42)  Bioidentical hormone replacement is one way to address declining hormone levels, but it is not the only way.

The decision to use bHRT is a personal one that should be made in conjunction with an holistic physician. Your degree of symptoms, personal thoughts about bHRT, willingness to make other lifestyle changes and use nutritional and herbal supplements should all factor into the “decision equation.” Here are some additional factors to consider when making this decision.

Possible “Pro’s” of bHRT

  1. Faster. Herbs and other factors can help balance hormones, but the effects of bHRT might be more dramatic and faster. (NOTE: I cannot find scientific studies to support this; it is my clinical observation — Dr. Myatt)
  2. Easier. Taking an Rx. may be easier than making lifestyle changes, although any good holistic physician should recommend positive lifestyle changes as part of an overall health program.
  3. Safer. Some studies point to the improved safety of bHRT over conventional HRT. (14-20)
  4. Better hormone balance. Some hormones such as DHEA and testosterone have independent health benefits. (25-33, 43) These hormones are typically not used in conventional HRT but may be prescribed by a physician who uses bHRT.

Possible “Cons” of bHRT

  1. Cost. bHRT is not necessarily expensive and can be as little as $30/month depending on what hormones are needed. However, an Rx. will represent an ongoing expense. Most practitioners prescribing bHRT require initial hormone testing (to customize your Rx.) and follow-up testing to ensure that your hormones are at optimal (safe and effective) levels. Testing plus the Rx. itself will be an ongoing expense.
  2. Safety. Although bHRT appears safer than conventional HRT, there is some evidence that no type of hormone replacement in women has been proven to be “protective” or safer than natural menopause.

Alternatives to bHRT

Hormone Testing: Saliva vs. Blood vs. Urine

Conventional hormone replacement does not use testing. The recommended “end point” (goal of treatment) is alleviation of symptoms. Therefore, when a woman has stopped having hot flashes, for example, the dose is considered to be correct.

Most bHRT practitioners begin treatment with some form of hormone testing, using either saliva, blood or urine to evaluate hormone levels. Although there are many claims about the superiority of one form of testing over another, scientific studies are lacking.

Saliva testing is the least accurate measure of sex hormones. Numerous studies have failed to find a reliable correlation between saliva hormone levels and physiologic (body) hormone levels with the exception of cortisol measurement. (17,44-54)

Blood testing does not reveal the hourly variation and 24-hour cyclical nature of hormone release but it has been better studied. For this reason, blood testing is probably the second-best method of hormone testing.

Twenty-four hour urine testing may be the preferred method of hormone testing. In addition to evaluating hormone output including the 24-hour variation (a “video” instead of a “snapshot,”), urine testing also looks at biochemical intermediates which are independent indicators of hormone levels and hormone metabolism. Some intermediates, such as the 2:16alpha-hydroxyestrone ratio, may be potent predictors of increased risk for hormone-related cancers. (55-56) Fortunately, once known, these risks can be modified.

Dr. Myatt’s Hormone Balance Programs:
Which One is Right for You?

All bHRT programs in both men and women begin with a Brief Telephone Consultation. Together, we determine which program is right for you.

Depending on your age, symptoms, beliefs and what you hope to achieve, we work together to design and implement a complete program to optimize both hormone balance and overall health.

For some men and women, this will include the use of bio-identical hormone replacement therapy, as determined by laboratory testing (24-hour urine). The form may differ depending on which hormones are needed, but usually include both transdermal and oral hormone replacements.

Hormone balance and relief of symptoms can often be achieved without the use of hormone replacement therapy. The decision to use hormones should not be taken lightly and should be made in consultation with a physician who is well-versed in both bHRT and non-hormonal methods of achieving hormone balance.

Which Hormone-Balancing Program is Right for You ?

 The Bronze program is for:

• Peri-menopausal women
• Post-menopausal women
• Men over 35

For women and men desiring better hormone balance  without  the use of
bio-identical hormone replacement.

You will receive a Personalized Health Report and Phone Follow-Up of 60 mins

The Silver program is for:

• Peri-menopausal women
• Post-menopausal women
• Men over 35

For women and men desiring better hormone balance AND bone mineral density protection without using
bio-identical hormone replacement.

You will receive a Personalized Health Report and Phone Follow-Up of 120 mins

The Gold program is for:

• Peri-menopausal women
• Post-menopausal women
• Men over 35

For women and men desiring sex hormone optimization and breast/prostate cancer risk reduction using bHRT.

You will receive a Personalized Health Report and Phone Follow-Up of 360 mins

The Platinum program is for:

• Peri-menopausal women
• Post-menopausal women
• Men over 35

For women and men desiring anti-aging, full-scope endocrine balancing (including sex, thyroid and adrenal hormones) and
breast /prostate cancer risk reduction using bHRT.

You will receive a Personalized Health Report and unlimited Phone Follow-Up

 * saliva hormone testing not available in New York state.

References

1.) Corona G, Rastrelli G, Monami M, Guay A, Buvat J, Sforza A, Forti G, Mannucci E, Maggi M.
Hypogonadism as a risk factor for cardiovascular mortality in men: a meta-analytic study.
Eur J Endocrinol. 2011 Nov;165(5):687-701. Epub 2011 Aug 18.

2.) Corona G, et al “Low testosterone is associated with an increased risk of MACE lethality in subjects with erectile dysfunction” ECE 2010; Poster 149.

3.) Ohlsson C, Barrett-Connor E, Bhasin S, Orwoll E, Labrie F, Karlsson MK, Ljunggren O, Vandenput L, Mellström D, Tivesten A.High Serum Testosterone Is Associated With Reduced Risk of Cardiovascular Events in Elderly Men, J Am Coll Cardiol, 2011; 58:1674-1681

4.) Tivesten A, Mellström D, Jutberger H, Fagerberg B, Lernfelt B, Orwoll E, Karlsson MK, Ljunggren O, Ohlsson C. Low serum testosterone and high serum estradiol associate with lower extremity peripheral arterial disease in elderly men. The MrOS Study in Sweden. J Am Coll Cardiol. 2007 Sep 11;50(11):1070-6. Epub 2007 Aug 24.

5.) Fournier A, Berrino F, Clavel-Chapelon F. Unequal risks for breast cancer associated with different hormone replacement therapies: results from the E3N cohort study. Breast Cancer Res Treat. 2008 Jan;107(1):103-11. Epub 2007 Feb 27.

6.) Fournier A, Berrino F, Riboli E, Avenel V, Clavel-Chapelon F. Breast cancer risk in relation to different types of hormone replacement therapy in the E3N-EPIC cohort. Int J Cancer. 2005 Apr 10;114(3):448-54.

7.) Holtorf K. The bioidentical hormone debate: are bioidentical hormones (estradiol, estriol, and progesterone) safer or more efficacious than commonly used synthetic versions in hormone replacement therapy? Postgrad Med. 2009 Jan;121(1):73-85.

8.) Mahmud K. Natural hormone therapy for menopause. Gynecol Endocrinol. 2010 Feb;26(2):81-5.

9.) Moskowitz D. A comprehensive review of the safety and efficacy of bioidentical hormones for the management of menopause and related health risks. Altern Med Rev. 2006 Sep;11(3):208-23.

10.) Schmidt JW, Wollner D, Curcio J, Riedlinger J, Kim LS. Hormone replacement therapy in menopausal women: Past problems and future possibilities. Gynecol Endocrinol. 2006 Oct;22(10):564-77.

11.) Ichikawa A, Sumino H, Ogawa T, Ichikawa S, Nitta K. Effects of long-term transdermal hormone replacement therapy on the renin-angiotensin- aldosterone system, plasma bradykinin levels and blood pressure in normotensive postmenopausal women. Geriatr Gerontol Int. 2008 Dec;8(4):259-64.

12.) Vilodre LC, Osório Wender MC, Sisson de Castro JA, dos Reis FM, Ruschel S, Magalhães JA,  Spritzer PM. Endometrial response to a cyclic regimen of percutaneous 17beta-estradiol and  low-dose vaginal micronized progesterone in women with mild-to-moderate hypertension.
Gynecol Endocrinol. 2003 Aug;17(4):323-8.

13.) Beral V, Bull D, Reeves G; Million Women Study Collaborators. Endometrial cancer and  hormone-replacement therapy in the Million Women Study. Lancet. 2005 Apr 30-May  6;365(9470):1543-51.

14.) Canonico M, Fournier A, Carcaillon L, et al. Postmenopausal hormone therapy and risk of idiopathic venous thromboembolism: results from the E3N cohort study. Arterioscler Thromb Vasc Biol. 2010;30(2):340-345.

15.) Cirillo DJ, Wallace RB, Rodabough RJ, et al. Effect of estrogen therapy on gallbladder disease. JAMA. 2005;293(3):330-339.

16.)  Eilertsen AL, Høibraaten E, Os I, Andersen TO, Sandvik L, Sandset PM. The effects of oral and transdermal hormone replacement therapy on C-reactive protein levels and other inflammatory markers in women with high risk of thrombosis. Maturitas. 2005;52(2):111-118.

17.)  Files JA, Ko MG, Pruthi S. Bioidentical Hormone Therapy.Mayo Clin Proc. 2011 July; 86(7): 673–680.

18.)  Jacobson BC, Moy B, Colditz GA, Fuchs CS. Postmenopausal hormone use and symptoms of gastroesophageal reflux. Arch Intern Med. 2008;168(16):1798-1804.

19.) Jernström H, Bendahl PO, Lidfeldt J, Nerbrand C, Agardh CD, Samsioe G. A prospective study of different types of hormone replacement therapy use and the risk of subsequent breast cancer: the women’s health in the Lund area (WHILA) study (Sweden). Cancer Causes Control. 2003 Sep;14(7):673-80.

20.)  [No authors listed] Breast cancer and hormone replacement therapy: collaborative reanalysis of data from 51 epidemiological studies of 52,705 women with breast cancer and 108,411 women without breast cancer. Collaborative Group on Hormonal Factors in Breast Cancer. Lancet. 1997 Oct 11;350(9084):1047-59.

21.) de Villiers TJ, Stevenson JC. The WHI: the effect of hormone replacement therapy on fracture prevention. Climacteric. 2012 Jun;15(3):263-6.

22.) Nelson HD, Humphrey LL, Nygren P, Teutsch SM, Allan JD. Postmenopausal hormone replacement therapy: scientific review. JAMA. 2002 Aug 21;288(7):872-81.

23.)  Cramer EH, Jones P, Keenan NL, Thompson BL. Is naturopathy as effective as conventional therapy for treatment of menopausal symptoms? J Altern Complement Med. 2003 Aug;9(4):529-38.

24.)  Ruiz AD, Daniels KR, Barner JC, Carson JJ, Frei CR. Effectiveness of compounded bioidentical hormone replacement therapy: an observational cohort study. BMC Womens Health. 2011 Jun 8;11:27.

25.) Genazzani AR, Pluchino N, Begliuomini S, Stomati M, Bernardi F, Pieri M, Casarosa E, Palumbo M, Genazzani AD, Luisi M. Long-term low-dose oral administration of dehydroepiandrosterone modulates adrenal response to adrenocorticotropic hormone in early and late postmenopausal women. Gynecol Endocrinol. 2006 Nov;22(11):627-35.

26.) Labrie F. DHEA, important source of sex steroids in men and even more in women.
Prog Brain Res. 2010;182:97-148.

27.) Pluchino N, Ninni F, Stomati M, Freschi L, Casarosa E, Valentino V, Luisi S, Genazzani AD, Potì E, Genazzani AR. One-year therapy with 10mg/day DHEA alone or in combination with HRT in postmenopausal women: effects on hormonal milieu. Maturitas. 2008 Apr 20;59(4):293-303. Epub 2008 Apr 3.

28.) Stomati M, Monteleone P, Casarosa E, Quirici B, Puccetti S, Bernardi F, Genazzani AD, Rovati L, Luisi M, Genazzani AR. Six-month oral dehydroepiandrosterone supplementation in early and late postmenopause. Gynecol Endocrinol. 2000 Oct;14(5):342-63.

29.) Aaronson AJ, Morrissey RP, Nguyen CT, Willix R, Schwarz ER. Update on the safety of  testosterone therapy in cardiac disease. Expert Opin Drug Saf. 2011 Sep;10(5):697-704. Epub 2011  Mar 22.

30.) De Maddalena C, Vodo S, Petroni A, Aloisi AM. Impact of testosterone on body fat composition. J Cell Physiol. 2012 Apr 11. doi: 10.1002/jcp.24096. [Epub ahead of print]

31.) Toma M, McAlister FA, Coglianese EE, Vidi V, Vasaiwala S, Bakal JA, Armstrong PW, Ezekowitz  JA. Testosterone supplementation in heart failure: a meta-analysis. Circ Heart Fail. 2012 May

32.) Vermeulen A. Ageing, hormones, body composition, metabolic effects. World J Urol. 2002 May;20(1):23-7.

33.) Vermeulen A, Goemaere S, Kaufman JM. Testosterone, body composition and aging. J Endocrinol Invest. 1999;22(5 Suppl):110-6. 1;5(3):315-21. Epub 2012 Apr 17.

34.)  Shifren JL, Desindes S, McIlwain M, Doros G, Mazer NA. A randomized, open-label, crossover study comparing the effects of oral versus transdermal estrogen therapy on serum androgens, thyroid hormones, and adrenal hormones in naturally menopausal women. Menopause. 2007 Nov-Dec;14(6):985-94.

35.)  L’hermite M, Simoncini T, Fuller S, Genazzani AR. Could transdermal estradiol + progesterone be a safer postmenopausal HRT? A review. Maturitas. 2008 Jul-Aug;60(3-4):185-201. Epub 2008 Sep 5.

36.) Leal M, Díaz J, Serrano E, Abellán J, Carbonell LF. Hormone replacement therapy for oxidative stress in postmenopausal women with hot flushes. Obstet Gynecol. 2000 Jun;95(6 Pt 1):804-9.

37.) Leal Hernández M, Abellán Alemán J, Carbonell Meseguer LF, Díaz Fernández J, García Sánchez FA, Martínez Selva JM. Influence of the presence of hot flashes during menopause on the metabolism of nitric oxide. Effects of hormonal replacement treatment]. Med Clin (Barc). 2000 Jan 22;114(2):41-5.

38.) North American Menopause Society. Treatment of menopause-associated vasomotor symptoms: position statement of The North American Menopause Society. Menopause. 2004 Jan-Feb;11(1):11-33.

39.) McKee J, Warber SL. Integrative therapies for menopause. South Med J. 2005 Mar;98(3):319-26.

40.) Low Dog T. Menopause: a review of botanical dietary supplements. Am J Med. 2005 Dec 19;118 Suppl 12B:98-108.

41.) Kronenberg F, Fugh-Berman A. Complementary and alternative medicine for menopausal symptoms: a review of randomized, controlled trials. Ann Intern Med. 2002 Nov 19;137(10):805-13.

42.) Geller SE, Studee L.Botanical and dietary supplements for menopausal symptoms: what works, what does not. J Womens Health (Larchmt). 2005 Sep;14(7):634-49.

43.) Øverlie I, Moen MH, Holte A, Finset A. Androgens and estrogens in relation to hot flushes during the menopausal transition. Maturitas. 2002 Jan 30;41(1):69-77.

44.) Gröschl M. Current status of salivary hormone analysis. Clin Chem. 2008 Nov;54(11):1759-69. Epub 2008 Aug 29.

45.) Hagen J, Gott N, Miller DR. Reliability of saliva hormone tests. J Am Pharm Assoc . 2003 Nov-Dec;43(6):724-6.

46.) Davison S. Salivary testing opens a Pandora’s box of issues surrounding accurate measurement of testosterone in women. Menopause. 2009;16:630-631.

47.) Flyckt RL, Liu J, Frasure H, Wekselman K, et al. Comparison of salivary versus serum testosterone levels in postmenopausal women receiving transdermal testosterone supplementation versus placebo. Menopause. 2009 Jul-Aug;16(4):680-8.

48.) Granger DA, Shirtcliff EA, Booth A, et al. The “trouble” with salivary testosterone. Psychoneuroendocrinology. 2004 Nov;29(10):1229-40.

49.) Mörelius E, Nelson N, Theodorsson E. Saliva collection using cotton buds with wooden sticks: a note of caution. Scand J Clin Lab Invest. 2006;66(1):15-8.

50.)  6.Lewis JG. Steroid analysis in saliva: an overview. Clin Biochem Rev. 2006 Aug;27(3):139-46.

51.) Stanczyk FZ, Paulson RJ, Roy S. Percutaneous administration of progesterone: blood levels and endometrial protection. Menopause. 2005 Mar;12(2):232-7.

52.) Lewis JG, McGill H, Patton VM, et al. Caution on the use of saliva measurements to monitor absorption of progesterone from transdermal creams in postmenopausal women. Maturitas. 2002 Jan 30;41(1):1-6.

53.) Wren BG, McFarland K, Edwards L, et al. Effect of sequential transdermal progesterone cream on endometrium, bleeding pattern, and plasma progesterone and salivary progesterone levels in postmenopausal women. Climacteric. 2000 Sep;3(3):155-60.

54.) Wood P. Salivary steroid assays – research or routine? . Ann Clin Biochem. 2009 May;46(Pt 3):183-96. Epub 2009 Jan 28.

55.) Kabat GC, Chang CJ, Sparano JA, Sepkovie DW, Hu XP, Khalil A, Rosenblatt R, Bradlow HL.Urinary estrogen metabolites and breast cancer: a case-control study. Cancer Epidemiol Biomarkers Prev. 1997 Jul;6(7):505-9.

56.) Muti P, Bradlow HL, Micheli A, Krogh V, Freudenheim JL, Schünemann HJ, Stanulla M, Yang J, Sepkovic DW, Trevisan M, Berrino F. Estrogen metabolism and risk of breast cancer: a prospective study of the 2:16alpha-hydroxyestrone ratio in premenopausal and postmenopausal women. Epidemiology. 2000 Nov;11(6):635-40.