Saturday, March 29, 2014

The Remarkable Anti-Cancer Properties of Vitamin K

Reposted from Life Extension

By Felix DiFara
The Remarkable Anticancer Properties of Vitamin K
For most of mankind’s existence, scientists wallowed in lethal ignorance regarding the critical need for humans to supplement with enough vitamin D.

We fear the same knowledge deficit exists today regarding vitamin K.
In this article, you will discover remarkable findings on vitamin K and its rapidly emerging anti-cancer profile. You’ll learn of newly identified mechanisms by which vitamin K exerts its potent effects. You will also understand why interest is growing among scientists and even some mainstream physicians about vitamin K’s role in combating cancer at multiple stages.

Vitamin K: A New Frontier in Cancer Prevention

Vitamin K2 (menaquinone) has been shown to safely suppress growth and invasion of human hepatocellular carcinoma, a common and deadly form of liver cancer.1,2 It exerts multiple effects on these tumors, modifying growth factors and their receptor molecules in a way that makes them less able to stimulate tumor growth and progression.2-4 It freezes the cell cycle, blocking further replication.5 And it triggers programmed cell death by apoptosis through several distinctive mechanisms.6

Vitamin K: A New Frontier in Cancer Prevention
Lab studies demonstrate tremendous potential for vitamin K in many other cancer types as well.7 Vitamin K2 induces certain kinds of human leukemia cells to differentiate, or turn into normal white blood cells.8 In cells from certain brain tumors, in stomach cancer, and in colorectal cancer lines, vitamin K halts the reproductive cell cycle and induces apoptosis.9-11 Vitamin K also triggers a DNA-degrading protein that cancer cells normally suppress; thereby preventing tumor cells from repairing themselves effectively.12

Lung cancers are notoriously aggressive and difficult to treat. In several different types of lung cancer, including small cell, squamous cell, and adenocarcinomas, vitamin K induces apoptosis through activation of a “suicide protein.”13 Clinical trials of newer chemotherapy agents have been disappointing, but when vitamin K was added to one newer drug, imatinib mesylate, it rapidly suppressed growth in all lung cancer cell lines tested.14 Vitamin K exhibits similarly synergistic effects in bladder and liver cancers as well.15,16

A unique mechanism of vitamin K’s activity is so-called “oncosis,” a form of stress-activated ischemic cell death to which tumor cells are particularly susceptible.17 Because of their high growth rate, tumor cells consume vast amounts of glucose. And because they can rapidly outgrow their blood supplies, that high metabolism means they use up oxygen rapidly, making them especially vulnerable to oxidant stress—much more so than the healthy tissues around them. Vitamin K targets tumor cells for destruction by stimulating oxidative stress, without toxicity to healthy tissues.18

Another unique mechanism, demonstrated recently in bile duct cancers and leukemia, is autophagy, in which cancer cells essentially “eat” themselves by releasing their own digestive enzymes internally.19,20 By still another unique mechanism, vitamins C and K in combination contribute to cancer cell death by autoschizis, whereby cells simply split open, spilling their contents.21

Finally, three of vitamin K’s synergistic anticancer mechanisms have recently been identified. Vitamin K3 inhibits DNA-building enzymes.22 Vitamins K2 and K3 block new blood vessel formation essential to support the rapid growth of tumor tissue.22-24 And vitamin K3 disrupts crucial intracellular communications networks composed of microtubules, preventing the cells from proliferating in a coordinated fashion.25
Why Are Doctors So Slow to Catch On?
Despite more than 2.4 million papers published on cancer research to date, conventional medicine has largely failed to identify safe, low-cost, effective methods of cancer intervention and prevention.1
At the core of the problem is a pervasive arrogance and apathy within the field of oncology. Physicians unquestioningly rely on cookie-cutter treatments (chemotherapy, radiation) that do as much harm as good—and sometimes inflict hideous suffering on patients without improving their chances for survival. Worse, this “one-size-fits-all” mentality bars admittance to novel findings on nutritional strategies that combat cancer at multiple stages in its development.
Don’t expect to hear much from your doctor about vitamin K. It may be ten years before the medical establishment catches on to the remarkable properties of this low-cost nutrient.

Liver and Prostate Cancer: Improving Survival Rates

Vitamin K’s promise in managing a variety of advanced solid tumors has been established in vitro and in animal studies, with benefits shown in lung cancers but not in gastrointestinal cancers, when combined with traditional chemotherapy.26,27 Other studies had already demonstrated that massive doses of vitamin K2, up to more than 2.5 grams given IV per day, were safe and caused no enhancement of the chemotherapy toxicity.28

Additional positive findings came in the form of two case reports, also from Japan. In the first, a 72 year-old woman with leukemia who had failed standard therapy experienced complete remission after vitamin K2 was added to her therapeutic regimen.29 In the second, an 85 year-old man with hepatocellular carcinoma after hepatitis C infection chose to take vitamin K but no chemotherapy.30 His tumor markedly regressed by CT scan, and his tumor markers in blood all normalized.

A study from Uruguay demonstrated that serum markers in a group of prostate cancer patients indicated tumor cell destruction following supplementation with vitamins C and K.31

Recently published studies have revealed vitamin K’s power to reduce recurrence of liver cancer—extending and even saving lives. The first reported on 61 patients documented to be free of their cancers following surgical treatment. Thirty-two were assigned to receive a vitamin K2 analogue called menatetrenone, while 29 received placebo.32 The supplemented group had recurrence of tumors of 12.5% at 12 months, 39.0% at 24 months, and 64.3% at 36 months. In the control group the recurrence rates were significantly higher: 55.2%, 83.2%, and 91.6%, respectively. And 100% of the supplemented group survived a full year, with 87% still alive at 36 months; among controls those numbers were 96.4% and a dismal 64%, respectively.
What You Need to Know: Vitamin K and Cancer
  • Microscopic image of lung carcinoma
    Cancer remains a deadly threat for millions of aging Americans, despite decades of aggressive research.
  • Standard cancer medications can only help after a cancer is discovered, and even then they are limited by toxicity.
  • Standard cancer treatments attack only one or a few biochemical steps in the long cascade of events leading to tumor development.
  • Long associated only with blood clotting, vitamin K is now known to have effects on tissues throughout the body, including most of the steps leading up to cancer.
  • Recent discoveries about vitamin K illustrate the tremendous breadth of its targets, spanning virtually every phase in cancer’s deadly progress.
  • A solid base of laboratory science is complemented by compelling clinical evidence that vitamin K can prevent, and in some cases treat, a variety of common and dangerous cancers.
In a smaller study with 45 patients,33 rates of recurrence were only 33.3% in patients treated with vitamin K compared with 50% in controls. And survival rates tended to be modestly higher in treated patients.

A 2007 study provided some additional support, showing a significant reduction in tumor recurrence, but not survival rates, over a 3-year period in supplemented patients.34 More studies are needed.
Vitamin K2 also induces MDS cells to differentiate into healthy white blood cells
Studies of combination therapies have now provided strong evidence favoring vitamin K2 both in liver and prostate cancer. A group of US urologists studied the combination of vitamin K3, 50 mg per day, plus vitamin C at 5,000 mg per day in treating prostate cancer patients who had failed standard therapy.35 They showed that treatment significantly decreased the velocity of rise in PSA, the serum marker of disease, while increasing the time it took for PSA levels to double. And only one patient in this group of advanced cancer patients died in the 14 months of treatment. This finding demonstrates vitamin K’s disease-fighting credentials in a particularly compelling fashion, when combined with another readily available supplement.

The combination of vitamin K2 plus a drug in the ACE-inhibitor category (both of which reduce tumor blood vessel growth) also produced a marked decrease in recurrence of hepatocellular carcinoma.36 The same research group showed that they could use that combination to stop a precancerous nodule from developing into liver cancer in a patient with hepatitis C-related cirrhosis.37

Vitamin K2 in Action: The Case of Myelodysplastic Syndrome

“Myelodysplastic syndrome” (MDS) is a disorder related to leukemia; in fact it was formerly known as “pre-leukemia.”38,39 In patients with MDS, the bone marrow begins churning out increasingly young white blood cells of various kinds. In most cases it goes on to full-blown leukemia, with all of the disastrous consequences of that disease. But unlike leukemia, MDS cells, at least early on, can be induced to develop into mature normal blood cells.39,40 And that’s where vitamin K comes in.
Vitamin K2 in Action: The Case of Myelodysplastic Syndrome
Vitamin K treatment of bone marrow cells from MDS patients potently induces apoptosis (programmed cell death) of the leukemic cells, with the effect much more prominent on blast cells than on mature white cells.41,42 Vitamin K2 also induces MDS cells to differentiate into healthy white blood cells, even when full-blown leukemia has developed.43

Successful therapy of MDS with vitamin K2 was first reported in 1999, in an 80-year-old woman with persistent anemia from the disease. Prior to treatment she had required regular blood transfusions; 14 months later she was independent of them.44 Similar benefits were found in a small group of MDS patients with refractory anemia in 2002.45 And some improvements were also found in MDS patients with low white blood counts compared with those receiving no treatment.46

The combination of vitamin K2 with vitamin D3 achieved good differentiation in a lab study of leukemia cells, suggesting that it might be effective therapy for both MDS and leukemia.47 In a clinical study in mid-2010, the addition of vitamin D3 to vitamin K2 more than doubled the response rate of MDS patients with refractory anemia and low white blood counts, from 13% to 30%. Those are big numbers for conditions traditionally difficult to treat with standard chemotherapy!48
Why You Need Vitamin K: The Triage Theory
Bruce Ames of the Children’s Hospital in Oakland, CA, is noted for substantive, evidence-based reflections on cancer and the human condition. Together with colleague Joyce McCann, Ames has developed the so-called “Triage Theory,” which has surprising relevance to our discussion of Vitamin K and cancer.49 According to the theory, the body prioritizes micronutrient use, favoring functions required for short-term survival over those needed for longevity. Ames and McCann recently applied this thinking to the many newly-discovered roles of vitamin K in our bodies, including cancer prevention.
Here’s an example: our cave-dwelling predecessors were constantly threatened by large predators (think saber-toothed tigers). Get mauled by one of those big cats, and you’d better have good blood clotting systems if you’re going to survive. You’d need at least enough vitamin K to prevent bleeding to death. But your chances of living to a ripe old age—hungry felines or otherwise—was quite low in those days. So it didn’t really matter if you had enough vitamin K on board to prevent cancer—you just weren’t going to get that old.
The reality in today’s world is rather different, when in the absence of a bad accident most of us are quite safe from bleeding to death. So if we get only enough vitamin K to assure proper blood coagulation, we’ll not get nearly enough to prevent cancer and other chronic conditions, such as osteoporosis or atherosclerosis, that rarely threatened our ancestors. McCann and Ames concluded their 2009 summary of this idea as follows: “much of the population… may not receive sufficient vitamin K for optimal function of vitamin K-dependent proteins that are important to maintain long-term health.”


Cancer remains a deadly threat for millions of aging Americans, despite decades of aggressive research. Standard cancer medications can only help after a cancer is discovered, and even then they are limited by toxicity. Standard cancer treatments attack only one or a few biochemical steps in the long cascade of events leading to tumor development.

Long associated only with blood clotting, vitamin K is now known to have effects on tissues throughout the body, including most of the steps leading up to cancer. Recent discoveries about vitamin K illustrate the tremendous breadth of its targets, spanning virtually every phase in cancer’s deadly progress. A solid base of laboratory science is complemented by compelling clinical evidence that vitamin K can prevent, and in some cases treat, a variety of common and dangerous cancers.
If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.
1. Mizuta T, Ozaki I. Clinical application of vitamin K for hepatocellular carcinoma. Clin Calcium. 2007 Nov;17(11):1693-9.
2. Otsuka M, Kato N, Shao RX, et al. Vitamin K2 inhibits the growth and invasiveness of hepatocellular carcinoma cells via protein kinase A activation. Hepatology. 2004 Jul;40(1):243-51.
3. Nishikawa Y, Wang Z, Kerns J, Wilcox CS, Carr BI. Inhibition of hepatoma cell growth in vitro by arylating and non-arylating K vitamin analogs. Significance of protein tyrosine phosphatase inhibition. J Biol Chem. 1999 Dec 3;274(49):34803-10.
4. Yamamoto T, Nakamura H, Liu W, et al. Involvement of hepatoma-derived growth factor in the growth inhibition of hepatocellular carcinoma cells by vitamin K(2). J Gastroenterol. 2009;44(3):228-35.
5. Kuriyama S, Hitomi M, Yoshiji H, et al. Vitamins K2, K3 and K5 exert in vivo antitumor effects on hepatocellular carcinoma by regulating the expression of G1 phase-related cell cycle molecules. Int J Oncol. 2005 Aug;27(2):505-11.
6. Matsumoto K, Okano J, Nagahara T, Murawaki Y. Apoptosis of liver cancer cells by vitamin K2 and enhancement by MEK inhibition. Int J Oncol. 2006 Dec;29(6):1501-8.
7. Kim HJ, Mun JY, Chun YJ, Choi KH, Ham SW, Kim MY. Effects of a naphthoquinone analog on tumor growth and apoptosis induction. Arch Pharm Res. 2003 May;26(5):405-10.
8. Sakai I, Hashimoto S, Yoda M, et al. Novel role of vitamin K2: a potent inducer of differentiation of various human myeloid leukemia cell lines. Biochem Biophys Res Commun. 1994 Dec 15;205(2):1305-10.
9. Sun L, Yoshii Y, Miyagi K, Ishida A. Proliferation inhibition of glioma cells by vitamin K2. No Shinkei Geka. 1999 Feb;27(2):119-25.
10. Tokita H, Tsuchida A, Miyazawa K, et al. Vitamin K2-induced antitumor effects via cell-cycle arrest and apoptosis in gastric cancer cell lines. Int J Mol Med. 2006 Feb;17(2):235-43.
11. Ogawa M, Nakai S, Deguchi A, et al. Vitamins K2, K3 and K5 exert antitumor effects on established colorectal cancer in mice by inducing apoptotic death of tumor cells. Int J Oncol. 2007 Aug;31(2):323-31.
12. Taper HS, Jamison JM, Gilloteaux J, Gwin CA, Gordon T, Summers JL. In vivo reactivation of DNases in implanted human prostate tumors after administration of a vitamin C/K(3) combination. J Histochem Cytochem. 2001 Jan;49(1):109-20.
13. Yoshida T, Miyazawa K, Kasuga I, et al. Apoptosis induction of vitamin K2 in lung carcinoma cell lines: the possibility of vitamin K2 therapy for lung cancer. Int J Oncol. 2003 Sep;23(3):627-32.
14. Yokoyama T, Miyazawa K, Yoshida T, Ohyashiki K. Combination of vitamin K2 plus imatinib mesylate enhances induction of apoptosis in small cell lung cancer cell lines. Int J Oncol. 2005 Jan;26(1):33-40.
15. Kassouf W, Highshaw R, Nelkin GM, Dinney CP, Kamat AM. Vitamins C and K3 sensitize human urothelial tumors to gemcitabine. J Urol. 2006 Oct;176(4 Pt 1):1642-7.
16. Wei G, Wang M, Hyslop T, Wang Z, Carr BI. Vitamin K enhancement of Sorafenib-mediated HCC cell growth inhibition in vitro and in vivo. Int J Cancer. 2010 Jun 7.
17. Scott GK, Atsriku C, Kaminker P, et al. Vitamin K3 (menadione)-induced oncosis associated with keratin 8 phosphorylation and histone H3 arylation. Mol Pharmacol. 2005 Sep;68(3):606-15.
18. Verrax J, Taper H, Buc Calderon P. Targeting cancer cells by an oxidant-based therapy. Curr Mol Pharmacol. 2008 Jan;1(1):80-92.
19. Enomoto M, Tsuchida A, Miyazawa K, et al. Vitamin K2-induced cell growth inhibition via autophagy formation in cholangiocellular carcinoma cell lines. Int J Mol Med. 2007 Dec;20(6):801-8.
20. Yokoyama T, Miyazawa K, Naito M, et al. Vitamin K2 induces autophagy and apoptosis simultaneously in leukemia cells. Autophagy. 2008 Jul 1;4(5):629-40.
21. Verrax J, Cadrobbi J, Delvaux M, et al. The association of vitamins C and K3 kills cancer cells mainly by autoschizis, a novel form of cell death. Basis for their potential use as coadjuvants in anticancer therapy. Eur J Med Chem. 2003 May;38(5):451-7.
22. Matsubara K, Kayashima T, Mori M, Yoshida H, Mizushina Y. Inhibitory effects of vitamin K3 on DNA polymerase and angiogenesis. Int J Mol Med. 2008 Sep;22(3):381-7.
23. Taper HS. Altered deoxyribonuclease activity in cancer cells and its role in non toxic adjuvant cancer therapy with mixed vitamins C and K3. Anticancer Res. 2008 Sep-Oct;28(5A):2727-32.
24. Yoshiji H, Kuriyama S, Noguchi R, et al. Combination of vitamin K2 and the angiotensin-converting enzyme inhibitor, perindopril, attenuates the liver enzyme-altered preneoplastic lesions in rats via angiogenesis suppression. J Hepatol. 2005 May;42(5):687-93.
25. Acharya BR, Choudhury D, Das A, Chakrabarti G. Vitamin K3 disrupts the microtubule networks by binding to tubulin: a novel mechanism of its antiproliferative activity. Biochemistry. 2009 Jul 28;48(29):6963-74.
26. Tetef M, Margolin K, Ahn C, et al. Mitomycin C and menadione for the treatment of lung cancer: a phase II trial. Invest New Drugs. 1995;13(2):157-62.
27. Tetef M, Margolin K, Ahn C, et al. Mitomycin C and menadione for the treatment of advanced gastrointestinal cancers: a phase II trial. J Cancer Res Clin Oncol. 1995;121(2):103-6.
28. Margolin KA, Akman SA, Leong LA, et al. Phase I study of mitomycin C and menadione in advanced solid tumors. Cancer Chemother Pharmacol. 1995;36(4):293-8.
29. Fujita H, Tomiyama J, Tanaka T. Vitamin K2 combined with all-trans retinoic acid induced complete remission of relapsing acute promyelocytic leukaemia. Br J Haematol. 1998 Nov;103(2):584-5.
30. Nouso K, Uematsu S, Shiraga K, et al. Regression of hepatocellular carcinoma during vitamin K administration. World J Gastroenterol. 2005 Nov 14;11(42):6722-4.
31. Lasalvia-Prisco E, Cucchi S, Vazquez J, Lasalvia-Galante E, Golomar W, Gordon W. Serum markers variation consistent with autoschizis induced by ascorbic acid-menadione in patients with prostate cancer. Med Oncol. 2003;20(1):45-52.
32. Mizuta T, Ozaki I, Eguchi Y, et al. The effect of menatetrenone, a vitamin K2 analog, on disease recurrence and survival in patients with hepatocellular carcinoma after curative treatment: a pilot study. Cancer. 2006 Feb 15;106(4):867-72.
33. Hotta N, Ayada M, Sato K, et al. Effect of vitamin K2 on the recurrence in patients with hepatocellular carcinoma. Hepatogastroenterology. 2007 Oct-Nov;54(79):2073-7.
34. Kakizaki S, Sohara N, Sato K, et al. Preventive effects of vitamin K on recurrent disease in patients with hepatocellular carcinoma arising from hepatitis C viral infection. J Gastroenterol Hepatol. 2007 Apr;22(4):518-22.
35. Tareen B, Summers JL, Jamison JM, et al. A 12 week, open label, phase I/IIa study using apatone for the treatment of prostate cancer patients who have failed standard therapy. Int J Med Sci. 2008;5(2):62-7.
36. Yoshiji H, Noguchi R, Toyohara M, et al. Combination of vitamin K2 and angiotensin-converting enzyme inhibitor ameliorates cumulative recurrence of hepatocellular carcinoma. J Hepatol. 2009 Aug;51(2):315-21.
37. Yoshiji H, Noguchi R, Yamazaki M, et al. Combined treatment of vitamin K2 and angiotensin-converting enzyme inhibitor ameliorates hepatic dysplastic nodule in a patient with liver cirrhosis. World J Gastroenterol. 2007 Jun 21;13(23):3259-61.
38. Fisher WB, Armentrout SA, Weisman R, Jr., Graham RC, Jr. “Preleukemia”. A myelodysplastic syndrome often terminating in acute leukemia. Arch Intern Med. 1973 Aug;132(2):226-32.
39. Albitar M, Manshouri T, Shen Y, et al. Myelodysplastic syndrome is not merely “preleukemia”. Blood. 2002 Aug 1;100(3):791-8.
40. Cazzola M, Malcovati L. Prognostic classification and risk assessment in myelodysplastic syndromes. Hematol Oncol Clin North Am. 2010 Apr;24(2):459-68.
41. Yaguchi M, Miyazawa K, Otawa M, et al. Vitamin K2 selectively induces apoptosis of blastic cells in myelodysplastic syndrome: flow cytometric detection of apoptotic cells using APO2.7 monoclonal antibody. Leukemia. 1998 Sep;12(9):1392-7.
42. Nishimaki J, Miyazawa K, Yaguchi M, et al. Vitamin K2 induces apoptosis of a novel cell line established from a patient with myelodysplastic syndrome in blastic transformation. Leukemia. 1999 Sep;13(9):1399-405.
43. Miyazawa K, Yaguchi M, Funato K, et al. Apoptosis/differentiation-inducing effects of vitamin K2 on HL-60 cells: dichotomous nature of vitamin K2 in leukemia cells. Leukemia. 2001 Jul;15(7):1111-7.
44. Takami A, Nakao S, Ontachi Y, Yamauchi H, Matsuda T. Successful therapy of myelodysplastic syndrome with menatetrenone, a vitamin K2 analog. Int J Hematol. 1999 Jan;69(1):24-6.
45. Abe Y, Muta K, Hirase N, et al. Vitamin K2 therapy for myelodysplastic syndrome. Rinsho Ketsueki. 2002 Feb;43(2):117-21.
46. Takami A, Asakura H, Nakao S. Menatetrenone, a vitamin K2 analog, ameliorates cytopenia in patients with refractory anemia of myelodysplastic syndrome. Ann Hematol. 2002 Jan;81(1):16-9.
47. Iguchi T, Miyazawa K, Asada M, Gotoh A, Mizutani S, Ohyashiki K. Combined treatment of leukemia cells with vitamin K2 and 1alpha,25-dihydroxy vitamin D3 enhances monocytic differentiation along with becoming resistant to apoptosis by induction of cytoplasmic p21CIP1. Int J Oncol. 2005 Oct;27(4):893-900.
48. Akiyama N, Miyazawa K, Kanda Y, et al. Multicenter phase II trial of vitamin K(2) monotherapy and vitamin K(2) plus 1alpha-hydroxyvitamin D(3) combination therapy for low-risk myelodysplastic syndromes. Leuk Res. 2010 Sep;34(9):1151-7.
49. McCann JC, Ames BN. Vitamin K, an example of triage theory: is micronutrient inadequacy linked to diseases of aging? Am J Clin Nutr. 2009 Oct;90(4):889-907.

Wednesday, March 26, 2014

Ever Heard of a Fat Cleanse?

Reposted from Dr. Mercola (Facebook Post)

Last rant was about healthy pasture-fed cows vs industrial feed-lot corn-fed cows on hormones and anti-biotics. The fat profile of the two animals is completely different. People who eat one or the other often have remarkably different physical results too. Those who consume industrialized cheese, butter, milk and meat tend towards excess weight and early onset of cardiovascular disease, to name a few. When the switch is made to grass-fed, man...y report weight loss and other benefits such as bad cholesterol dropping.

Which brings me to the point about people attempting low-fat diets to lose fat. See, if you eat foods your body wasn't designed for, it can only end badly. This practice is so widespread though that I suspect many of us need to change the way we think about food. People should ask themselves- what's real food? What's fake food?

Here's a thought. Do any of you know of a cow that produces skim milk? I don't. Mother nature produces a perfect food, a BALANCED food which will take a newborn calf from tiny to big and full of life, and we are so clever we think we can improve on it. Oooooh, let's take the fat out, because lots of people are fat. Trouble is, now you have a fake food. An IMBALANCED food. And if you drink or eat such stuff, your body will react. ("Where's my fat? Better save up what I have, looks like a shortage.")

Flip the coin over. Eat real food. Normal food has some ‘made-by-nature’ fats in it. Healthy fats. Not fats made in a food chemicals lab. Healthy fats get RID of other fats. Arteries get cleared. What do you dissolve grease with? Water, or an oil-based solvent? Grease-cutters are themselves made from grease. Water won't dissolve oils and fats. (Think skim milk, remember?) So even foods with quite a bit of fats in 'em like nuts and avocados, do NOT make us fat (unless we are stuffing ourselves).

Our bodies react by slowing down fat retention because there's plenty coming in. Plus, your brain which is comprised of 2/3rd’ fat needs them!

Resist the Fat Famine lie!

Acetaminophen: More Dangerous Than You Ever Suspected

Reposted from Dr. Mercola

By Dr. Mercola
Acetaminophen, sold under the brand name Tylenol, among others, may be among the most dangerous medicines on the market. I'm sure this comes as a surprise to most of you, as virtually every single household keeps a bottle on hand for the occasional ache and pain, and doesn't think twice about taking it.
Not thinking, it turns out, could cost you dearly... Acetaminophen overdose is actually the leading cause for calls to Poison Control Centers across the US—more than 100,000 instances per year—and, each year, is responsible for:1
  • More than 56,000 emergency room visits
  • 2,600 hospitalizations
  • An estimated 458 deaths due to acute liver failure
In fact, according to data from the Acute Liver Failure Study Group registry, acetaminophen poisoning is responsible for nearly HALF of ALL acute liver failure cases in the US.2 As stated in a paper published in the journal Hepatology3 an entire decade ago:
"[Acetaminophen] is heavily marketed for its safety compared to nonsteroidal analgesics.
By enabling self-diagnosis and treatment of minor aches and pains, its benefits are said by the Food and Drug Administration to outweigh its risks. It still must be asked: Is this amount of injury and death really acceptable for an over-the-counter pain reliever?"

Acetaminophen—More Dangerous Than You Ever Suspected

In the program above, originally aired by ThisAmericanLife.org4 in September of last year, host Ira Glass recounts the story of Sarah Erush.
Sarah is a pharmacist at the Hospital of the University of Pennsylvania who was contacted by the Food and Drug Administration (FDA) about a number of cases of acetaminophen overdosing at her hospital. The FDA encouraged her to sit down and collate the data, and when she did, some very interesting, and disturbing, patterns emerged. As Ira Glass reports:
"Erush was surprised by how little over the recommended dose of the drug resulted in liver damage and, for three patients, death.
One of the country's most popular over-the-counter painkillers — acetaminophen, the active ingredient in Tylenol — also kills the most people, according to data from the federal government. Over 150 Americans die each year on average after accidentally taking too much. And it requires a lot less to endanger you than you may know."
As it turns out, acetaminophen can be toxic to your liver even at recommended doses when taken daily for just a couple of weeks.5
Previous research6 has also shown that taking just a little more than the recommended dose over the course of several days or weeks (referred to as "staggered overdosing") is far more risky than taking one large overdose. Your risk of severe liver injury and/or death increases if you:
  1. Take more than one regular strength (325 mg) acetaminophen when combined with a narcotic analgesic like codeine or hydrocodone
  2. Take more than the prescribed dose of an acetaminophen-containing product in a 24-hour period
  3. Take more than one acetaminophen-containing product at the same time. Make sure to read the list of ingredients on any other over-the-counter (OTC) or prescription drug you take in combination. Beware that many cold remedies also contain acetaminophen at varying dosages, and you must add all of these amounts together. Certain prescription painkillers, such as Vicodin and Percocet, also contain acetaminophen and should therefore not be mixed with other acetaminophen-containing medications.
  4. Drink alcohol while taking an acetaminophen product. Recent research7 suggests that acetaminophen also significantly increases your risk of kidney dysfunction if taken with alcohol—even if the amount of alcohol is small.8 Combining alcohol with acetaminophen was found to raise the risk of kidney damage by 123 percent, compared to taking either of them individually. Besides alcoholics,9 young adults are particularly at risk as they're more likely to consume both.

Deaths Cast Doubt on Widely Used OTC Pain Reliever

Last year, PBS News10 reported that 1,500 deaths over the past 10 years have been linked to taking a little bit more acetaminophen than the recommended dosage. A major problem, as PBS points out, is that while acetaminophen is considered safe when taken as recommended, the margin between a safe dose and a potentially lethal one is disturbingly small. According to their report:
"Taken over several days, as little as 25 percent above the maximum daily dose - or just two additional extra strength pills a day - has been reported to cause liver damage, according to the [Food and Drug Administration]. Taken all at once, a little less than four times the maximum daily dose can cause death...
Warnings on liver damage were added to the drug's label in 2009 by the FDA, 32 years after an expert panel convened by the agency advised it was 'obligatory' to do so. The recommendation was a part of a broader safety review of acetaminophen, which the report says has not yet been completed." [Emphasis mine]
An FDA advisory panel actually recommended adding a warning label about liver damage to acetaminophen as early as 1977, yet the FDA kept dragging its feet. Last year, reporter Sean Cole noted in an interview with ThisAmericanLife.org11:
"The drug approval process is usually slow but not usually this slow. The FDA began with acetaminophen over 40 years ago in 1972. In that time, science has mapped the human genome, eradicated smallpox, we've cloned a sheep. And yet we still have not come up with final rules for safe usage and labeling of one of the most popular drugs in the country, of which more than 20 billion doses are sold each year."

FDA Admits: Too Much Acetaminophen Can Cause Liver Damage

On January 14, this year, the FDA finally issued a statement12, 13 urging doctors and other health professionals to discontinue prescribing and dispensing prescription combination drug products that contain more than 325 milligrams (mg) of acetaminophen per tablet, capsule, or other dosage unit. According to the FDA, there's no evidence suggesting that taking more than 325 mg of acetaminophen provides any benefit that might outweigh the increased risk of severe liver damage.
The FDA also notes that while more than half of manufacturers have voluntarily complied by reducing the amount of acetaminophen per dose, prescription products that contain more than the recommended maximum of 325 mg of acetaminophen still remain on the market. So please, always check the label before you take any medication containing acetaminophen, to make sure you're not getting too much.
"In the near future FDA intends to institute proceedings to withdraw approval of prescription combination drug products containing more than 325 mg of acetaminophen per dosage unit that remain on the market," the FDA noted.

Also Beware of Fatal Skin Reactions

While rare, it's also worth noting that acetaminophen has been linked to very serious skin reactions. After reviewing data from the FDA Adverse Event Reporting System (FAERS), the FDA found 107 cases of serious skin reactions linked to acetaminophen products between 1969 and 2012. Sixty-seven of them required hospitalization; 12 died. The data, coupled with several cases documented in medical literature, has prompted the FDA to require a warning about potential skin reactions be added to prescription acetaminophen products.14 The skin reactions linked to acetaminophen include:
  • Stevens-Johnson Syndrome (SJS): This reaction begins with flu-like symptoms that progress into a painful purple or red rash that blisters and causes the top layer of your skin to slough off. This can lead to serious infections, blindness, damage to internal organs, permanent skin damage, and even death.
  • Toxic Epidermal Necrolysis (TENS): TENS also typically begins with flu-like symptoms (cough, headache, aches, and fever) and progresses into a blistering rash. Layers of the skin may peel away in sheets, and hair and nails may fall out. TENS is often fatal, typically as a result of infection.
  • Acute Generalized Exanthematous Pustulosis (AGEP): This skin eruption causes numerous pustules to appear on the skin, often accompanied by fever. This condition typically resolves within two weeks once the acetaminophen is stopped.
While the main cause of SJS, TENS, and AGEP is the consumption of certain acetaminophen-containing medications, no one knows exactly why it occurs, or what makes certain people more at risk. What is particularly alarming is that it can occur at any time, even if you've taken the medication in the past without issue. According to the FDA,15 there's no way to predict who might be at increased risk for such side effects. For this reason, I strongly advise you to heed the FDA's recommendation:
"If you've ever had a skin reaction when taking acetaminophen, don't take the drug again."

NAC Helps Counteract Acetaminophen Hazards

N-acetyl cysteine (NAC) is a supplement used in cases of acetaminophen overdose.16 It's a standard part of care, approved in 1985 by the FDA as an antidote for acetaminophen toxicity. The approval of NAC for this purpose was based on a research program by the Rocky Mountain Poison and Drug Center, which "clearly demonstrated the efficacy of acetylcysteine, when used early in the course of treatment, in reducing morbidity and virtually eliminating mortality associated with acetaminophen overdose," according to the published treatment guidelines.17
Here, I can't help but note the irony of the situation, as a nutritional supplement—NAC is the rate-limiting nutrient for the formation of the intracellular antioxidant glutathione—is prescribed as the antidote to a pharmaceutical drug... This goes back to the conversation about the extraordinary safety, and wide-ranging benefits, of dietary supplements. Yet, Big Pharma promoters like Dr. Paul Offit and Senator Dick Durbin are going to great lengths to try to paint supplements as a dangerous scourge that has no place in good medicine.
The case of NAC (N-acetyl cysteine) is just one of many examples where a supplement can be a lifesaver after conventional medicine has wrought havoc on your body. Another potent example is CoQ10, which is absolutely crucial if you're taking a statin drug. If Senator Durbin and the drug industry get their way, lifesaving supplements (like NAC and CoQ10) would have to go through extensive and extremely costly drug testing, which might make them unavailable—at least temporarily, and if they were available, they would be far more expensive.
But back to my main point: while I generally do not recommend using acetaminophen-containing drugs for minor aches and pains, given the health risks discussed above, they are sometimes necessary to temporarily suppress severe pain, such as post-surgical pain. For those instances, I recommend taking it along with NAC.
It is believed that the liver damage acetaminophen causes is largely due to the fact that it can deplete glutathione, an antioxidant compound secreted by your liver in response to toxic exposure. Glutathione also helps protect your cells from free radical damage. If you keep your glutathione levels up, the damage from the acetaminophen may be largely preventable. As noted above, mortality due to acetaminophen toxicity has been shown to be virtually eliminated when NAC is promptly administered in cases of acetaminophen overdose.
So whether you are taking Tylenol in prescription or over-the-counter form, I strongly suggest taking NAC along with it. Bear in mind that while this may help prevent liver damage from occurring, I'm not aware of any evidence supporting its use for the prevention of kidney toxicity and/or potential skin reactions.

Avoiding the Painkiller Trap

It's important to remember that just because a drug is sold without prescription does not mean it is completely harmless. This is particularly important to remember if you're using OTC drugs for your children. There have been tragic cases of acetaminophen overdosing when an infant is given children's brand Tylenol, at an older child's recommended dosage. Always make sure to check the dosage recommendations for the age of your child!
Whether you're trying to address acute or chronic pain, please know that there are many other safer yet still effective alternatives to prescription and over-the-counter painkillers. For an extensive list of recommendations, please see this recent article on acetaminophen alternatives.
One potent alternative I'd encourage you to investigate is K-Laser therapy, which can be an excellent choice for many painful conditions, including acute injuries. By addressing the underlying cause of the pain, you will no longer need to rely on regular doses of painkillers.
Also, for long-term relief, I strongly recommend taking a high-quality, animal-based omega-3 fat like krill oil, as omega-3 fats are precursors to mediators of inflammation called prostaglandins. Addressing your diet by eliminating or radically reducing most grains and sugars (including fructose) is also important, as avoiding grains and sugars will lower your insulin and leptin levels. Elevated insulin and leptin levels are one of the most profound stimulators of inflammatory prostaglandin production. That is why eliminating sugar and grains is so important to controlling your pain.
I also recommend optimizing your production of vitamin D by getting regular, appropriate sun exposure, which will work through a variety of different mechanisms to reduce your pain. Along with these strategies, be sure you are also addressing any emotional elements. EFT is particularly useful for this—whether your pain is chronic or acute. In both instances, your level of stress, your anxiety, and your perceptions of pain all play a role in how you experience pain, and addressing these elements can go a long way toward providing effective pain relief.  

Tuesday, March 18, 2014

Saturated Fat Doesn't Cause Heart Disease

Reposted from Daily Mail Online

Guidelines urging people to avoid ‘unhealthy’ fat to stave off heart disease are wrong, according to a major study.

After decades of advice on the harm done by saturated fat such as butter, scientists have found no evidence of a link with heart problems.

A ‘mega’ study which analysed a huge amount of existing data also said so-called healthy polyunsaturated fats, such as sunflower oil, had no general effect on the risk of heart disease.

In contrast, a dairy fat called margaric acid ‘significantly reduced’ risk, while two kinds of saturated fat found in palm oil and animal products had only a ‘weak link’ with heart disease.

Two types of omega-3 fatty acid found in oily fish – EPA and DHA – and the omega-6 fat arachidonic acid were linked to a lower risk of heart disease. But omega-3 and omega-6 supplements appeared to have no benefit.

This study comes in the wake of growing controversy over the relative importance of sugar and fat in the diet.

Fats have long been blamed for obesity and heart disease, but some scientists now say there is evidence that fat may have been unfairly demonised and sugar is really to blame.

Lead researcher Dr Rajiv Chowdhury, from Cambridge University, said: ‘These are interesting results that potentially stimulate new lines of scientific inquiry and encourage careful reappraisal of our current nutritional guidelines.

‘Cardiovascular disease, in which the principal manifestation is coronary heart disease, remains the single leading cause of death and disability worldwide. In 2008, more than 17million people died from a cardiovascular cause globally.

‘With so many affected, it is critical to have appropriate prevention guidelines which are informed by the best available scientific evidence.’
Two types of omega-3 fatty acid found in oily fish were linked to a lower risk of heart disease
Two types of omega-3 fatty acid found in oily fish were linked to a lower risk of heart disease
The team, whose results appear in the journal Annals Of Internal Medicine, conducted a ‘meta-analysis’ of data from 72 studies involving 600,000 participants in 18 countries.
The technique can reveal trends that may be masked in individual small studies but become obvious when they are amalgamated.

A key finding was that total saturated fat, whether measured in the diet or the bloodstream, showed no association with heart disease.

The study fails to ‘yield clearly supportive evidence for ... guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of saturated fats’.
'Healthy' oils, such as sunflower oil, do not improve heart health
'Healthy' oils, such as sunflower oil, do not improve heart health
Almost four decades ago advice began to emerge from scientific and medical bodies to cut back on saturated fats found in cream, butter and less lean meat. Last year, however, London cardiologist Dr Aseem Malhotra told the British Medical Journal it was time to bust the myth of the role of saturated fat in heart disease, which was based on faulty interpretation of scientific studies.

He said yesterday: ‘This huge and important study provides even more evidence that our focus purely on saturated fat as the number one dietary villain in causing heart disease has been misplaced when we should be focusing on food groups.
‘Our over-consumption of processed food is what is driving much of the increasing burden of chronic disease currently plaguing the Western world.
‘Poor diet is responsible  for more disease than physical inactivity, alcohol and  smoking combined.

‘Furthermore, nutritional supplements have no proven benefit for the vast majority of people. It’s better for the body to gain essential nutrients from just eating real food.’

Professor Jeremy Pearson, associate medical director at the British Heart Foundation which co-funded the study, said: ‘This analysis of existing data suggests there isn’t enough evidence to say that a diet rich in polyunsaturated fats but low in saturated fats reduces the risk of cardiovascular disease.

‘But large-scale clinical studies are needed, as these researchers recommend, before making a conclusive judgment.’

The industry-backed Health Supplements Information Service said that while the study showed only a modest protective effect of omega-3 fats, the trials involving omega-3 supplements nearly all involved non-healthy participants, which was likely to give misleading results.

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Sunday, March 16, 2014

Make Your Own Natural Toothpaste

Reposted from Food Matters

By Michelle Schoffro Cook, Care 2

Most toothpaste contains sugar, fluoride, artificial colors, and other harmful ingredients that are best avoided.  Instead of using the toxic commercial varieties, why not make your own?  It’s simple and quick.  Once you have the essential oils needed you can use them to make the toothpaste or tooth powder, which more accurately describes it, for years to come.
Here’s how:

Natural Tooth Powder Recipe

  • ½ cup baking soda
  • 10 drops pure peppermint essential oil (this is not the same as peppermint extract or fragrance oil.  Also, it should be a high quality food grade essential oil, which is available from many health food stores)
  • 5 drops pure myrrh essential oil (optional, also available in many health food stores)
Mix all ingredients in a small jar with a lid, cover, and shake well to disperse oils throughout. Use a small amount on a damp toothbrush the way you would use toothpaste.
The peppermint essential oil helps freshen breath, kill bacteria, and clear sinuses.  The myrrh oil is highly antibacterial and anti-fungal.  It is often used in the ancient healing arts of Ayurvedic Medicine.  The baking soda restores a natural, slightly alkaline pH balance to the teeth and gums and helps to whiten teeth.


Study: Antioxidants Present in Virgin Coconut Oil Inhibits Inflammation Associated with Arthritis

Reposted from Health Impact News Daily

by Brian Shilhavy
Health Impact News

In what may the first study of its kind, researchers in India extracted the antioxidants unique to virgin coconut oil from the oil and injected them into rats with induced arthritis. They found that the unique coconut oil antioxidants reduced inflammation associated with arthritis more effectively than current pharmaceutical drugs.

The authors of the study write that their motivation to examine the antioxidants present in virgin coconut oil in relation to inflammation caused by arthritis is due to the ineffectiveness and serious side effects of current pharmaceutical drugs prescribed for arthritis:

 Arthritis is one of the most pervasive diseases that cause disability. Arthritis encompasses over 120 diseases and conditions that affect joints, surrounding tissues and connective tissues. Rheumatoid arthritis (RA) is characterized by chronic inflammation of synovial joints and subsequent progressive erosive destruction of articular cartilage. The consequent morbidity and mortality have a substantial socioeconomic impact and epidemiology of arthritis in female:male is 3:1. Most of the patients with aggressive disease evolution become clinically disabled within 20 years.
At present the drug used to treat RA range from non-steroidal antiinflammatory drugs (NSAIDs) to more potent disease modifying antirheumatic drugs (DMARDs) [3]. The lack of reliable treatment for early RA is a major problem in modern medicine. Most of these treatments cause severe side effects such as stomach problems, heartburn, ulcers and bleeding in the case of NSAIDs and cataracts, high blood pressure, sleep problems, muscle loss, bruising, thinning of the bones (osteoporosis), weight gain and susceptibility to infections in the case of DMARDs. There is therefore a need to develop effective antiinflammatory drugs with fewer side effects. The main objective of the present study is to evaluate the antioxidant and anti-inflammatory effect of polyphenolic fraction isolated from virgin coconut oil (VCO) on experimental arthritis.
The study found that antioxidants extracted from virgin coconut oil were more effective in reducing the inflammation in arthritis induced in rats, than Indometacin, a popular prescription nonsteroidal anti-inflammatory drug (NSAID) often prescribed for arthritis.

While this study was obviously motivated to create new patent-able drugs or supplements from virgin coconut oil antioxidants, it should encourage those who consume virgin coconut oil, knowing the effectiveness of the unique antioxidants present in some virgin coconut oils has wonderful health benefits. This is yet another benefit of virgin coconut oil that can be added to the already impressive long list of benefits associated with coconut oil, much of it related to the medium chain fatty acids, such as lauric acid.

It is important to note, however, that when discussing antioxidants present in coconut oil, that not all coconut oils are equal in amounts of antioxidants present. Refined coconut oils would have little or none, and not all virgin coconut oils are produced the same way to have the highest amounts of antioxidants. The virgin coconut oil used in this study was produced using the wet-milling method and heat.

Previous research has shown that antioxidants are most present in virgin coconut oils produced using the wet-milling method, and that they are released in more abundance into the coconut oil when some heat is used in the processing. Many virgin coconut oils on the market today are actually produced with no heat, or “cold pressed.” While this is an advantage in the olive oil industry, it is a disadvantage in producing high quality coconut oils. For more information, see:  What Type of Coconut Oil is Best? How to Choose a Coconut Oil.


Polyphenolics isolated from virgin coconut oil inhibits adjuvant induced arthritis in rats through antioxidant and anti-inflammatory action.

Friday, March 14, 2014

Is Processed Fructose a Poison?

Reposted from Life Extension

By Michael A. Smith, MD

What is a poison? Well, interestingly, there are different theories as to what makes something a poison. But most of them go something like this:

"A dangerous chemical, natural or unnatural, enters the blood through the skin, gut or lungs and travels to the liver, the primary organ of detoxification."

The liver attempts to “detoxify” the chemical creating metabolites — sometimes the metabolites are less toxic and sometimes they’re not — in order to excrete the chemical and any remnants of it out of the body.

So for us to believe that fructose is a poison, it needs to follow, in some respects, the pathway I just described — and we’ll get to that soon.

But first, let’s clarify something...

Natural vs. Unnatural Fructose

Natural fructose is a sugar found in fruits. It’s chemically distinct from glucose and does not require insulin to enter into cells. Once inside cells, it can be used, like glucose, in cell energy pathways.

Unnatural fructose is stripped of naturally occurring fibers resulting in a crystalline form of fructose that can be used in the manufacturing of processed sweeteners and syrups. The processed, fiber-stripped fructose is found in many everyday packaged foods, cereals, breads, and drinks.

The Difference Comes Down to Quantity

I am writing about fructose — whether it is natural or unnatural. The effect on the body, as you will see, is the same. With one important exception though: quantity.

Unnatural fructose absorbs into your blood unabated by the missing natural fibers. For example, all 15 grams of fructose from a glass of orange juice or two slices of white bread absorb into your bloodstream. In contrast, the fibers found in fruits will minimize the absorption of natural fructose limiting the net influx of fructose into your circulatory system.

Bottom line: Serving for serving, higher amounts of unnatural, fiber-stripped fructose absorb into your body than natural fructose. Processed sugars and syrups containing unnatural fructose are more dangerous to your body than natural fructose, based solely on quantity.

The Pathological Effects of Fructose

Fructose is metabolized primarily by the liver, just like most poisons. The liver cell begins by taking a phosphate group from ATP, adenosine triphosphate, and adds it to fructose. The result is fructose-1-phosphate and ADP, adenosine diphosphate.

First, let’s follow what happens to ADP. Excessive fructose consumption requires such a tremendous amount of ATP that it decreases the availability of phosphate groups, known as “sequestering of phosphates.” This means that the ADP formed initially doesn't have phosphate groups readily available to convert back to ATP.1

Without phosphate groups, ADP catabolizes into AMP, adenosine monophosphate, and eventually into IMP or inosine-5-monophosphate. IMP is the initiating compound for uric acid production. In high concentrations, uric acid crystallizes causing the painful joint disorder known as gout.1
Additionally, it inhibits nitric oxide (NO) production which can raise blood pressure.2 So as a result of fructose inside the liver and the production of uric acid, we see two possible negative outcomes: gout and hypertension.

Remember, this isn’t going to happen by drinking one soda with high fructose corn syrup. It takes excessive (daily) consumption of soda — which actually characterizes most Americans! — or other sources of fructose to accumulate uric acid.

The Fate of Fructose-Phosphate

What happens to fructose-1-phosphate? Some of it is metabolized into pyruvate, a compound used to initiate cell energy production.

However, in excessive amounts, it converts into xylulose-5-phosphate which then activates pathways that produce fat, called lipogenesis.3 This can increase the number and size of fat cells, along with raising blood triglycerides levels - a marker of metabolic disease and a known risk factor of heart disease.

And the Verdict Is…?

Well, let’s review the facts:

  • Fructose (natural or unnatural) enters the liver because that’s the primary organ that can metabolize it.
  • The liver cell converts fructose into metabolites (uric acid and xylulose-5-phosphate) that are known to have negative health effects in high concentrations: gout, hypertension, body fat, and high blood triglycerides.
So, is fructose a poison?

Or, more specifically, is unnatural, fiber-stripped fructose a poison?

You be the judge!


  1. Champe, P. (2008). Biochemistry, 2nd edition. New York, New York: Lippincott Williams & Wilkins (Pages 128, 350).
  2. Nitric Oxide. 2013 Aug;1(32):36-42. doi: 10.1016/j.niox.2013.04.003. Epub 2013 Apr 23.
  3. Endocr J. 2008 Aug;55(4):617-24. Epub 2008 May 19.

Wednesday, March 12, 2014

St. John's Wort Eases Depression

Reposted from Newsmax Health

by Dr. David Brownstein

St. John’s Wort is a flowering plant, indigenous to Europe, which has been used for thousands of years in treating depressive symptoms. It is thought to work through the same mechanism as selective serotonin reuptake inhibitors (SSRIs), by impeding the reabsorption of serotonin in the
presynaptic area of the neuron.
There have been many studies comparing St. John’s Wort to commonly prescribed SSRI medications. The Cochrane Collaboration — an independent, nonprofit healthcare study group — found that St. John’s Wort was superior to placebo in patients with major depression, and compared favorably to SSRIs and older tricyclic medications.
Furthermore, St. John’s Wort was found to have 75 percent fewer side effects than standard anti-
depressive medications.
I have used St. John’s Wort to help wean patients off SSRIs. However, you have to be very careful when taking the two together. If you are taking an SSRI, consult your healthcare provider before using St. John’s Wort.
While St. John’s Wort can be helpful in treating depression, I believe other methods — including exercise, psychotherapy, cleaning up the diet, and drinking adequate water — are more effective, and, in the end, better options.
Today, 10 percent of the American population is on some kind of antidepressant medication, most of which come with harmful, if not dangerous, side effects.
This is hard for me to fathom. It also suggests that something is terribly wrong with the way the medical establishment handles depression.The truth is that you do not have to suffer from depression and you do not have to suffer from side effects of antidepressant medications.
While there are some patients who do benefit from antidepressants, for the vast majority of patients, natural therapies are safer and more effective against depression.
More information can be found in my book, Drugs That Don’t Work and Natural Therapies That Do.

Meta-analysis finds reduced mortality among breast cancer patients with sufficient vitamin D levels

Reposted from Life Extension

Tuesday, March 11, 2014. The results of a meta-analysis conducted by a team from the Naval Health Research Center and the University of California, San Diego reveal a protective effect for higher levels of vitamin D against the risk of dying from breast cancer. The findings were reported in the March 2014 issue of the journal Anticancer Research.
For their analysis, Cedric F. Garland and associates selected five observational studies conducted between 2009 and 2013 that included a total of 4,443 women, among whom there were 471 cases of breast cancer. For women whose serum 25-hydroxyvitamin D levels were among the highest categories, a lower risk of dying from breast cancer was observed. In a pooled analysis of all participants, subjects whose vitamin D levels were categorized as high at an average of 30 nanograms per milliliter (ng/mL) experienced a 44% reduction in breast cancer mortality risk when compared to those whose levels were low at 17 ng/mL.
Concerning the findings, Dr Garland explained that "Vitamin D metabolites increase communication between cells by switching on a protein that blocks aggressive cell division. As long as vitamin D receptors are present tumor growth is prevented and kept from expanding its blood supply. Vitamin D receptors are not lost until a tumor is very advanced. This is the reason for better survival in patients whose vitamin D blood levels are high."
"There is no compelling reason to wait for further studies to incorporate vitamin D supplements into standard care regimens since a safe dose of vitamin D needed to achieve high serum levels above 30 nanograms per milliliter has already been established," he added.
The authors suggest the initiation of a clinical trial to test the effect of 10,000 international units (IU) per day of vitamin D3.
What's Hot

Higher vitamin D levels correlated with improved breast cancer prognosis

What's Hot
An article published online on October 9, 2013 in Breast Cancer Research and Treatment reports the results of a meta-analysis conducted by Canadian researchers which found an association between higher serum levels of vitamin D and better prognosis for women with early stage breast cancer.
For their analysis, Pamela J. Goodwin of the University of Toronto and her colleagues selected eight studies involving a total of 5,691 women diagnosed with breast cancer from 1973 to 2010. Blood samples were collected, on average, within 90 days of diagnosis or shortly before treatment. Deficient levels of vitamin D were uncovered in 38.6% of the subjects.
When the lowest versus highest categories of serum vitamin D were compared in a pooled analysis, women whose levels were low had a risk of recurrence that was more than double that of subjects whose levels were high and a risk of death that was 76% higher. The authors remark that vitamin D, when activated, can alter the transcription and expression of specific genes, resulting in growth arrest, apoptosis, aromatase suppression, decreased inflammation, and inhibition of angiogenesis, invasion and metastasis, all of which help combat cancer.
"These findings support an association of low levels of vitamin D with increased risk of recurrence and death in early stage breast cancer patients," the authors conclude. "Given the observational nature of the included studies, it cannot be concluded that this association is causal. Further research is warranted to investigate the potential beneficial effects of vitamin D in breast cancer."