~ Dying From Neglect

Dying From Neglect

by William Faloon

I regret having to write this editorial. The reason being that it forces me to discuss elementary medicine instead of cutting-edge science. The problem is that conventional medicine has regressed to a point where I am compelled to alert members about a life-threatening situation that is supposed to be taken care of by doctors.[1] The result of this physician neglect is that tens of thousands of people are needlessly dying because an easy-to-treat disorder is being ignored.

Most people think that modern medicine properly diagnoses and treats anemia. The startling fact is that 24% to 40% of hospitalized patients over age 65 are anemic.[2] Compared to non-anemic people, these blood deficient individuals have high mortality rates from diseases such as heart failure, stroke and cancer.

When the oxygen carrying capacity of the blood is impaired (i.e. anemia), people with reduced blood flow to any organ (such as those with coronary artery disease) are at a much greater risk for infirmity and death. Cancer cells thrive in a low oxygen environment and even borderline anemia predicts higher mortality.

Anemia can be detected by a standard CBC blood test, yet busy doctors are often accepting anemia as being a normal state in aged people and are failing to treat it. Since drugs used to treat severe anemia (such as Procrit) are very expensive, many insurance companies are not paying for these drugs unless blood oxygen carrying capacity is far below the standard reference range. This means that those most in need of these anti-anemia drugs (such as cancer and congestive heart failure patients) are being denied access. Anemia greatly increases all-cause mortality risk. Health insurance companies are thus saving big dollars by denying Procrit to their sickest policyholders.

The neglect of doctors in ignoring tests that reveal anemia, coupled with insurance company refusal to pay for anti-anemia drugs, amounts to widespread euthanasia being inflicted upon the elderly. In this editorial, you will learn about natural and pharmaceutical approaches to reversing anemia.

Anemia Predicts Who Will Die From Acute Heart Attack

In a recent New England Journal of Medicine study,[2] doctors looked at heart attack victims presenting at the hospital. Anemia was a strong predictor of who was most likely to die.

One of the tests used in this study was the hematocrit. The hematocrit measures the percentage of whole blood that is made up of red blood cells. Normal hematocrit ranges are between 36% to 50%. Below 36% indicates anemia. What follows are the shocking findings revealed in the New England Journal of Medicine study:

Heart Attack Patients Hematocrit Percentage Odds Of These Patients Dying Within 30 Days
5.0 to 24.0% 78%
24.1 to 27.0% 52%
27.1 to 30.0% 40%
30.1 to 33.0% 31%
Over 33.1% (No increased risk)

The statistics presented above show that anemia sharply increases the risk that a heart attack victim will die within 30 days. The doctors also found a high prevalence of anemia among these elderly heart attack patients.

Blood Transfusion Reduces Mortality

The doctors who published the New England Journal of Medicine study then evaluated the effects of a blood transfusion to reverse the anemic state in this large group of heart attack victims.

A blood transfusion was associated with a significant reduction in mortality in heart attack patients with low hematocrit (below 33%). In patients with very low hematocrit (below 24%), transfusion was associated with a 64% reduction in mortality. In patients with hematocrit between 24.1 and 27.0, transfusion reduced mortality by 31%. Mortality was reduced by transfusion by 25% in those with a hematocrit between 27.1 and 30.

These numbers show that the greater the severity of anemia, the more likely a heart attack patient will benefit from a blood transfusion. Mortality actually increased when transfusions were administered to non-anemic patients, possibly a result of transfusion-related complications.

Despite numerous published studies showing the lethal effects of anemia in heart attack patients, only 4.7% of the elderly patients in this study received a blood transfusion. The doctors concluded that "more aggressive use of transfusion in the management of lower hematocrit levels in elderly patients with acute coronary disease may be warranted."

Blood Tests That Detect Anemia

When you obtain a CBC/Chemistry blood test, there are several indicators that measure the number and quality of red blood cells, along with the oxygen carrying capacity of these cells. The three most important that indicate an anemic state are:

  Reference Range
Reference Range
Red Blood Cell Count 4.10 to 5.60 (x 10-6/uL) 3.80 to 5.10 (x 10-6/uL)
12.5 to 17 (g/dL) 11.5 to 15.0 (g/dL)
Hematocrit 36 to 50% 34 to 44%

If your blood test results indicate even borderline anemia, seek professional assistance to ascertain the underlying cause. Since aging itself predisposes people to anemia, consider specific supplements, hormones and/or drugs that help boost blood cell production. What can be done to reverse anemia is discussed later in this article.

Anemia and Cancer

Anemia is common in cancer patients. Conventional cancer therapies (chemotherapy, radiation, testosterone blockade, etc.) often induce anemia. Elevated levels of cytokines seen in cancer patients (such as tumor necrosis factor-alpha) also suppress red blood cell formation.

When we talk to oncologists on behalf of Foundation members, we inquire about the patient’s hematological condition. Since cancer cells thrive in a low oxygen environment (hypoxia), we want to make sure the cancer patient’s red blood cell count, hematocrit and hemoglobin are in the upper one-third range of normal.

The importance of avoiding anemia is well established in the scientific literature. A recent study was conducted to systematically review and obtain an estimate of the effect of anemia on survival in cancer patients.[3] This study found that the increased risk of mortality in cancer patients who were anemic was an astounding 65%!

Despite this data, most oncologists fail to adequately treat for anemia. One reason for this is that insurance companies refuse to reimburse for expensive anti-anemia drugs unless the patient is severely anemic (often 25% below the lowest number on the standard reference range).

Since anemia predisposes cancer patients to greatly increased mortality, it is in the economic interest of the insurance companies to deny reimbursement for anti-anemic drugs like Procrit. In fairness, it is important to note that the cost of Procrit is so prohibitively expensive, that if everyone in need were allowed to have these kinds of drugs, many health insurance companies could go bankrupt. So part of this problem gets back to the outrageously high cost of prescription drugs that only exists because of today’s FDA-protected monopoly.[4]

It should be noted that the sickest cancer patients are often the most anemic, which makes our case even stronger that anti-anemic drug therapy should be used more often. We do not usually recommend blood transfusions for cancer patients because of potential immune-suppressing effects. Cancer patients need to maintain healthy immune function.

Anemia Predicts Mortality

Anemia is a strong predictor of early death in the elderly. In a recent study, anemic individuals aged 70 to 79 were 28% more likely to die over a five year time period.[5] Anemic people aged 80 to 89 were 34% more likely to die, while those aged 90 to 99 were 48% more likely to die over a five year period. Cerebrovascular disease (stroke) was the most common disease associated with anemia. If you are over age 65, it is a life or death matter to correct an anemia state.

Don’t Let Doctors Bleed You To Death

Two centuries ago, doctors treated sick people by draining their blood (bloodletting). Based on what we now know, those who could afford the bloodletting procedure died much sooner than those who avoided doctors.

Medicine has not changed much over the past 200 years. Here we are in the year 2002 and most doctors still do not take anemia seriously. It is shocking to have a member send us their blood results, complain of the symptoms of anemia, and then hear that their doctor said not to worry about their low hematocrit, red blood count, etc.

Conventional doctors often tell their elderly patients that anemia is “normal.” While it is true that anemia is epidemic in the elderly, this is not an excuse to leave it untreated.

I strongly urge all Foundation members to have an annual CBC/Chemistry blood test that can detect anemia and a host of other correctable life-threatening abnormalities. Those who have health insurance can sometimes have this test done for free at their own doctor’s office. Members can order this test directly by calling 1-800-208-3444. The cost at this time is only $26.00.

If the blood test reveals that you are anemic, follow the recommendation in the section entitled "How To Correct Anemia" (below).

Americans are routinely dying from a deficiency of oxygenated blood, yet doctors are failing to recommend supplements, prescribe transfusions and anti-anemia drugs to elderly people most in need.

To avoid becoming a victim of this appalling neglect by the medical establishment, have your blood tested annually and if necessary, aggressively pursue the anti-anemia strategies that have been outlined in this article.

How To Correct Anemia

You or your doctor can determine if you are anemic by taking a standard CBC/Chemistry blood test. This test measures red blood cell count, hematocrit, hemoglobin and other hematological indicators of an anemic state.

If it is determined you are anemic, it is important that your doctor determine what is causing it. Sometimes anemia is the first sign of cancer or serious internal bleeding.

It is often the aging process itself, however, that causes people to become anemic. Aged men are usually deficient in testosterone and testosterone deficiency can induce anemia.[6] Aged women and men usually secrete low levels of melatonin, and melatonin deficiency has been linked with anemia.[7]

Low levels of folic acid, vitamin B12 and other nutrients can induce anemia.[8] Excess levels of the pro-inflammatory cytokines can also induce an anemic state by attacking the blood cell forming proteins (erythropoietin).[9] Supplements that suppress these dangerous cytokines include the DHA fraction of fish oil, vitamin K, DHEA and nettle leaf extract.[10] The prescription drug pentoxifylline is also effective in suppressing the pro-inflammatory cytokines that can reduce red blood production in the body.[11]

If supplements such as melatonin, folic acid, B12 and DHA fish oil fail to correct anemia, then testosterone replacement and pentoxifylline drug therapies should be considered.

If anemia continues to persist, see if your doctor will prescribe the drug Procrit. The high cost of Procrit will keep most people from being able to afford it unless their health insurance will pay for it. If you are prescribed Procrit, it is especially important that most people take supplemental iron, as Procrit will cause iron to be utilized to help form new red blood cells. Some people fail on Procrit because their doctor forgets to prescribe an iron supplement.

It is important to note that when treating life-threatening anemia, the only effective therapy is immediate blood transfusion, as it can take six weeks for Procrit or Epogen to reverse the anemic state.

You should refer to our Anemia protocols for additional suggestions. You can also review information about testosterone replacement and the off-label use of the drug pentoxifylline on our website. If you do not have access to the Internet, call 1-800-226-2370 and we will mail Foundation members these protocols at no charge.


1. The era of modern hematology is considered to have begun at Harvard Medical School with the work of George Richards Minot (1885-1950) and his assistant, William Parry Murphy (1892-1987) who, between 1924 and 1926, found that patients who suffered from pernicious anemia could be successfully treated with large quantities of raw liver in their diets. Minot and Murphy shared the 1934 Nobel Prize for their discovery. From this point on, the investigation of anemia revolved around phenomena at the molecular level, which is where we are today. http://www.neosoft.com/~uthman/unanemia/unanemia_ch1.html (http://www.neosoft.com/)

2. Wu WC, et.al. Blood transfusion in elderly patients with acute myocardial infarction. New England Journal of Medicine, Oct 25, 2001, pp. 1230-1236.

3. Caro JJ, et. al. Anemia as an independent prognostic factor for survival in patients with cancer: a systemic, quantitative review. Cancer 2001 Jun 15;91(12):2214-21.

4. Life Extension magazine, “Are Offshore Drugs Dangerous?,” Sept. 2001, pp. 11-14. Life Extension magazine, “Drugs The FDA Says You Can’t Have,” July 2001, pp. 7-11. Life Extension magazine, “What’s Wrong With The FDA,” May 2001, pp. 24-29. Life Extension magazine, “Life Extension Wins In The House And Senate,” Sept. 2000, pp. 7-9. Life Extension magazine, “Big Bucks,” July 2000, pp. 32-34. Life Extension magazine, “The Great American Rip-Off—High Drug Prices...Courtesy of the FDA,” June 1999, pp. 7-8. Life Extension magazine, “The Plague Of FDA Regulation,” May 1999, pp. 7-8. Life Extension magazine, “They Want You Brain Dead,” Dec. 1998, pp. 7-8.

5. Kikuchi M, et al., Five-year survival of older people with anemia: variation with hemoglobin concentration. J Am Geriatr Soc 2001 Sep;49(9):1226-8.

6. Abbasi AA, et al. Gonadal function abnormalities in sickle cell anemia. Studies in adult male patients. Ann Intern Med 1976 Nov;85(5):601-5. Bain J. Andropause. Testosterone replacement therapy for aging men. Can FamPhysician 2001 Jan;47:91-7. Gao RL, et al. Clinical study of 63 patients with aplastic anemia by using in vitro culture of BFU-E, CFU-E, CFU-GM and of the relation between pathogenesis and treatment. Zhonghua Nei Ke Za Zhi 1991 May;30(5):268-72, 316. Kraft D. Long-term treatment of renal anaemia with mesterolone. Dtsch Med Wochenschr 1980 Jun 6;105(23):830-2. Landefeld CS, et al. Clomiphene-responsive hypogonadism in sickle cell anemia. Ann Intern Med 1983 Oct;99(4):480-3. Luo XS. Correlation between traditional Chinese medicine classification of 53 patients with aplastic anemia and varieties of hemopoietic progenitor cells in vitro culture. Zhongguo Zhong Xi Yi Jie He Za Zhi 1992 Mar;12(3):139-41, 131. Pavlatos AM, et al. Review of oxymetholone: a 17alpha-alkylated anabolic-androgenic steroid. Clin Ther 2001 Jun;23(6):789-801; discussion 771. Prasad AS, et al. Effect of zinc supplementation on serum testosterone level in adult male sickle cell anemia subjects. Am J Hematol 1981;10(2):119-27. Radtke HW, et al. Serum erythropoietin concentration in anephric patients. Nephron 1978;22(4-6):361-5. Singhal A, et. al. Testosterone deficiency and extreme retardation of puberty in homozygous sickle-cell disease. West Indian Med J 1995 Mar;44(1):20-3. Zitzmann M, Nieschlag E. Hormone substitution in male hypogonadism. Mol Cell Endocrinol 2000 Mar 30;161(1-2):73-88.

7. Foldes C, et al, 1988. Congenital dyschromia with erythrocyte, platelet and tryptophan metabolism abnormalities. J Am Acad Dermatol Oct;19(4):642-55. Herrera J, et al, 2001. Melatonin prevents oxidative stress resulting from iron and erythropoietin administration. Am J Kidney Dis Apr;37(4):750-7. Vaziri ND, et al,1996. Dysregulation of melatonin metabolism in chronic renal insufficiency: role of erythropoietin-deficiency anemia. Kidney Int Aug;50(2):653-6.

8. Andres E, et al, 2000. Anemia caused by vitamin B 12 deficiency in subjects aged over 75 years: new hypotheses. A study of 20 cases. Rev Med Interne Nov;21(11):946-54. Baik HW, et al, 1999. Vitamin B12 deficiency in the elderly. Annu Rev Nutr 19:357-77. Brinch L, et al, 1990. Folic acid deficiency can cause severe anemia and pancytopenia. Tidsskr Nor Laegeforen May 30;110(14):1830-1. Pentimone F, et al, 1992. Clinical evaluation of anemia in the aged. Minerva Med Jan-Feb;83(1-2):35-9. Remacha AF, et al, 1997. Serum erythropoietin and erythroid activity in vitamin B12 deficiency. Haematologica Jan-Feb;82(1):67-8. Rodriguez RM, et al, 2001. Nutritional deficiencies and blunted erythropoietin response as causes of the anemia of critical illness. J Crit Care Mar;16(1):36-41. Smith DL, et al, 2000. Anemia in the elderly. Am Fam Physician Oct 1;62(7):1565-72. Zarazaga A, et al, 1991. Folates in human nutrition. Different clinical situations in which folate deficiencies exist. Nutr Hosp Jul-Aug;6(4):207-26.

9. Bron D, et al, 2001. Biological basis of anemia. Semin Oncol Apr;28(2 Suppl 8):1-6. Eckarat KY, 2001. Anemia in critical illness. Wien Klin Wochenschr Feb 15;113(3-4):84-9. Pertosa G, et al, 2000. Clinical relevance of cytokine production in hemodialysis. Kidney Int Suppl Aug;76:S104-11. Ratajzak MZ, et al, 1997. In vitro studies on anemia in chronic inflammatory disease: influence of interleukin-6 on human erythropoietin. Pol Merkuriusz Lek Jan;2(9):172-5.

10. Calder PC, 1997. n-3 polyunsaturated fatty acids and cytokine production in health and disease. Ann Nutr Metab;41(4):203-34. Calder PC, et al, 2001. Polyunsaturated fatty acids and rheumatoid arthritis. Curr Opin Clin Nutr Metab Care Mar;4(2):115-21. De Caterina R, et al, 1994. The omega-3 fatty acid docosahexaenoate reduces cytokine-induced expression of proatherogenic and proinflammatory proteins in human endothelial cells. Arterioscler Thromb Nov;14(11):1829-36. Eichbaum FW, et al, 1979. Anti-inflammatory effect of warfarin and vitamin K1. Naunyn Schmiedebergs Arch Pharmacol Jun 18;307(2):185-90. James MJ, et al, 2000. Dietary polyunsaturated fatty acids and inflammatory mediator production. Am J Clin Nutr Jan;71(1 Suppl):343S-8S. Kelley DS, et al, 1999. Docosahexaenoic acid ingestion inhibits natural killer cell activity and production of inflammatory mediators in young healthy men. Lipids Apr;34(4):317-24. Khalfoun B, et al, 1996. Docosahexaenoic and eicosapentaenoic acids inhibit human lymphoproliferative responses in vitro but not the expression of T cell surface activation markers. Scand J Immunol Mar;43(3):248-56. Kipper-Galperin M, et al, 1999. Dehydroepiandrosterone selectively inhibits production of tumor necrosis factor alpha and interleukin-6 [correction of interlukin-6] in astrocytes. Int J Dev Neurosci Dec;17(8):765-75. Klingelhoefer S, et al, 1999. Antirheumatic effect of IDS 23, a stinging nettle leaf extract, on in vitro expression of T helper cytokines. J Rheumatol Dec;26(12):2517-22. Loria RM, 1997. Antiglucocorticoid function of androstenetriol. Psychoneuroendocrinology 22 Suppl 1:S103-8. Mantzioris E, et al, 2000. Biochemical effects of a diet containing foods enriched with n-3 fatty acids. Am J Clin Nutr Jul;72(1):42-8. Matsuda M, et al, 1999. Clinical roles of vitamins in hematopoietic disorders. Nippon Rinsho Oct;57(10):2349-55. Menta AB, et al, 1998. Haematological disorders in liver disease. Forum (Genova) Jan-Mar;8(1):8-25. Mc Cann ME, et al, 2000. Effect of intravenous infusion of omega-3 and omega-6 lipid emulsions on equine monocyte fatty acid composition and inflammatory mediator production in vitro. Shock Aug;14(2):222-8. Obertreis B, et al, 1996. Ex-vivo in-vitro inhibition of lipopolysaccharide stimulated tumor necrosis factor-alpha and interleukin-1 beta secretion in human whole blood by extractum urticae dioicae foliorum. Arzneimittelforschung Sep;46(9):936. Reddi K, et al, 1995. Interleukin 6 production by lipopolysaccharide-stimulated human fibroblasts is potently inhibited by naphthoquinone (vitamin K) compounds. Cytokine Apr;7(3):287-90. Riehemann K, et al, 1999. Plant extracts from stinging nettle (Urtica dioica), an antirheumatic remedy, inhibit the proinflammatory transcription. FEBS Lett Jan 8;442(1):89-94. Somers SD, et al, 1994. Alteration of tumor necrosis factor-alpha production by macrophages from mice fed diets high in eicosapentaenoic and docosahexaenoic fatty acids. Cell Immunol Feb;153(2):287-97. Soyland E, et al, 1994. Dietary supplementation with very long-chain n-3 fatty acids in man decreases expression of the interleukin-2 receptor (CD25) on mitogen-stimulated lymphocytes from patients with inflammatory skin diseases. Eur J Clin Invest Apr;24(4):236-42. Straub RH, et al, 2000. Replacement therapy with DHEA plus corticosteroids in patients with chronic inflammatory diseases—substitutes of adrenal and sex hormones. Z Rheumatol 59 Suppl 2:II/108-18. Straub RH, et al, 1998. Serum dehydroepiandrosterone (DHEA) and DHEA sulfate are negatively correlated with serum interleukin-6 (IL-6), and DHEA inhibits IL-6 secretion from mononuclear cells in man in vitro: possible link between endocrinosenescence and immunosenescence. J Clin Endocrinol Metab Jun;83(6):2012-7. Straub RH, et al, 1998. Association of humoral markers of inflammation and dehydroepiandrosterone sulfate or cortisol serum levels in patients with chronic inflammatory bowel disease. Am J Gastroenterol Nov;93(11):2197-202. Teucher T, et al, 1996. Cytokine secretion in whole blood of healthy subjects following oral administration of Urtica dioica L. plant extract. Arzneimittelforschung Sep;46(9):906-10. Tomobe YI, et al, 2000. Dietary docosahexaenoic acid suppresses inflammation and immunoresponses in contact hypersensitivity reaction in mice. Lipids Jan;35(1):61-9. Yam D, et al, 2001. Suppression of tumor growth and metastasis by dietary fish oil combined with vitamins E and C and cisplatin. Cancer Chemother Pharmacol 47(1):34-40.

11. Aihara K, et al, 2001. Successful combination therapy—flunarizine, pentoxifylline, and cholestyramine—for spur cell anemia. Int J Hematol Apr;73(3):351-5. Navarro JF, et al, 1999. Effects of pentoxifylline on the haematologic status in anaemic patients with advanced renal failure. Scand J Urol Nephrol Apr;33(2):121-5.

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