When the Cure Is Worse Than the Disease

by Bill Sardi by Bill Sardi

DIGG THIS

Mary wonders why the new young doctor she visited recently says to nearly every patient, after examining their throat, that it looks like their esophagus is being eroded by stomach acid and they need to start taking acid-blocking pills. He hands patients free samples provided by pharmaceutical companies. The patients are oblivious to the fact that if they begin using the drug, they may never be able to stop taking it without experiencing an excruciatingly painful bout of rebound heartburn.

One way to build an income in private medical practice is to hook patients on drugs that continually require re-examination, testing and prescription renewal.

For example, blood thinners require prothrombin tests to determine how long it takes the blood to clot. Blood pressure pills require monitoring of blood pressure. And in the example above, once patients start taking acid-blocking medications they will find it is nearly impossible to stop taking them because withdrawal will provoke rebound acidity with throat-gripping pain.

Since the early 1990s it has been known that acid-blocking (histamine blocking) drugs commonly prescribed for heartburn create dependency. Withdrawal from the drug will create rebound hyper-acidity that causes the patient to reach for the antacid pills in desperation again. [1] , [2] To make matters worse, acid blockers may induce more, not less, disease. Stomach acid is a defense against invading pathogenic bacteria that enter the gut in food (foods are not sterile, but have low bacteria and mold counts that stomach acid normally kills). The habitual use of acid blockers may result in infection and even cancer. [3]

Most drugs don’t work, are inappropriate or are designed to make things worse

Critical examination of the effectiveness of prescription drugs reveals that there is (1) convincing data that most prescription drugs are not only ineffective but may worsen the condition being treated (yet are approved by the FDA), that (2) some of these medications appear to be designed to create life-long dependency upon the drug (drug withdrawal exacerbates symptoms), and that (3) some long-standing drugs that are the hallmarks of modern medicine have begun to lose their biological punch.

There are many examples of this:

It has recently been shown that asthma symptoms worsen upon withdrawal of the drug Accolate (zafirlukast), with benefits lasting only for the first five weeks and then symptoms return soon thereafter. The FDA approved this drug based upon short-term use data. Benefits are seen for only the first five weeks, after which symptoms return to their original state within seven weeks. Side effects range from diarrhea to liver damage. With no long-term benefits, the drug is only problematic for users. [4]

Other asthma drugs, such as albuterol, ventolin and salbutamol, work in the short term to relax airways, but over the long term over-sensitize the body and make the drugs less effective. Then airways become more sensitive to asthma triggers. [5]

Quetiapine, a drug commonly used in nursing homes to treat agitation and related symptoms in people with Alzheimer’s disease, actually worsens their condition and speeds the rate of their mental decline. [6]

First-line drugs used to treat Alzheimer’s do not stop the progression of the disease and are largely disappointing, [7] and side effects caused by second-line treatments (like Quetiapine) for Alzheimer’s-related psychosis, aggression and agitation, offset any modest advantages of first-line drugs. [8] Drugs like these ensure your loved ones will never make it out of the Alzheimer’s care facility.

Diabetes rates are exploding in America. Millions of Americans are being placed on anti-diabetic drugs. But nearly all anti-diabetic drugs result in weight gain and eventual total dependency upon insulin injections. [9] , [10] This is another example of drugs locking patients into inevitably more severe disease.

Disease substitution, not disease treatment

All too frequently, drugs substitute one disease for another. For example, most anti-psychotic drugs induce weight gain and diabetes. [11] , [12] This is so typical that many people believe a pudgy body always accompanies mental disorders.

Another example of disease substitution is the treatment of high blood pressure with diuretics which can induce a vitamin B1 (thiamine) deficiency that results in heart failure. One study found a third of patients hospitalized for heart failure, who are often treated with diuretics, were vitamin B1 deficient. [13] Vitamin therapy is uncommon in hospital settings.

Blood pressure drugs: inappropriate treatment

Consider drug therapy for high blood pressure, what doctors call hypertension. The idea is to lower blood pressure with medications and reduce the risk for a stroke. But no single blood pressure pill seems to work. More than one drug is often needed, and there are few if any studies that prove combination therapies are safe and effective. [14]

Most blood pressure drugs do not address the cause of the disease, which commonly are age-related changes in blood sugar or hardening of the arteries, resulting in inability of the blood vessels to dilate (widen) upon physical or mental exertion or stress.

Age-related inability to control blood sugar levels is generally caused by insulin resistance (inability of insulin to enter cells) which is induced by iron overload, [15] , [16] , [17] and hardening of the arteries by calcification which impairs dilation.

Diabetics experience buildup of underlying calcium in their arteries, which largely explains diabetic hypertension. [18]

Calcification of the inside wall of arteries induces coronary artery disease and hypertension, which can be measured by a CT scan. [19] Rats that spontaneously develop hypertension exhibit calcified aortas (the aorta is the first blood vessel outside the heart). [20]

Once the aorta stiffens due to calcification, then the heart must pump harder against this resistance, and hypertension develops. Societies that consume the most calcium have the highest rates of cardiovascular disease. Presently used calcium blocker drugs are not so satisfactory, but fortunately nature provides a component in whole grains (IP6 phytate, bran factor), which dissolves calcifications, but IP6 goes unused by modern medicine. [21]

The lack of HDL u201Cgoodu201D cholesterol, the alleged cause of artery disease, is just a marker of arterial calcification. [22] , [23]

But instead of employing agents that will reduce the iron load or calcifications, like IP6 [24] rice bran, vitamin D, [25] vitamin K [26] or magnesium, [27] other inappropriate medications are used, such as:

Beta blockers, which slow the heart rate to control blood pressure, but an overly fast heart rate is not the common cause of hypertension. Beta blockers induce a form of heart failure, cause fatigue and impotence and breathing problems, another example of disease substitution.

ACE inhibitors (angiotensin converting enzyme), which are employed to control blood pressure, but again, hypertension is not commonly caused by an excess of this enzyme.

Diuretics (water pills), which are prescribed for hypertension, but again, chronic elevated blood pressure is not caused by too much fluid in the circulatory system. The depletion of water will artificially lower blood pressure, but also deplete the body of essential minerals (electrolytes) required for proper heart rhythm and deplete vitamin B1 (thiamine) which then induces heart failure and mental problems, as previously mentioned.

Calcium blockers are more appropriate for the treatment of hypertension but are fraught with side effects, while magnesium is a natural calcium blocker that goes unused. [28] , [29]

Statin drugs help to lower blood pressure, [30] but not by their ability to reduce cholesterol, but because they modestly increase vitamin D levels, which is an anti-calcifying agent. [31]

Adults at risk for cardiovascular disease are warned they will experience a heart attack if they don’t take their cholesterol-lowering drugs. Yet with millions of Americans taking these drugs, the number of heart attacks remains about the same. There is simply no evidence that statin drugs, the most commonly used drug for cholesterol reduction, reduce mortality rates. [32]

It is said statin drugs lower the risk for a heart attack by 30% (relative number), but in hard numbers the risk reduction is almost imaginary, with only 1-in 70 high-risk individuals, and in maybe 1-in 300 healthy individuals, averting a non-mortal heart attack, and these imaginary benefits are weighed against the real risk for liver damage, memory loss, muscle damage and other side effects. (Ask yourself how the FDA could possibly approve such a class of ineffective drugs.)

Paul J. Rosch, Clinical Professor of Medicine and Psychiatry at New York Medical College, has recently said:

The belief that coronary artery atherosclerosis (plaque) is due to high cholesterol from increased saturated fat intake originated from experiments in herbivorous animals. It was reinforced by reports allegedly demonstrating this sequence of events in various populations but ignoring contradictory data. The idea has been perpetuated by powerful forces using similar tactics to preserve the profit and the reputations of those who promote this doctrine. Opponents find it difficult to publish their scientifically supported opinions. The advent of statins has further fuelled this fallacious lipid hypothesis, despite compelling evidence that their effect is not due to cholesterol lowering and that serious side effects have been suppressed and alleged benefits have been hyped. The adverse effects of the cholesterol campaign on health, quality of life, the economy and medical research are inestimable. It is imperative that public health officials, physicians and patients are apprised of proof that it is misguided, malicious and malignant. [33]

This outspoken opinion was aired in a medical journal published outside the U.S.

Drugs losing their punch

Add to all these aforementioned problems with prescription medications the fact that the u201Cmagic bulletsu201D of modern medicine, the antibiotic drugs, are becoming less and less effective due to germ resistance. Germs are now developing resistance against vancomycin, the antibiotic of last resort, which is reserved for use when other antibiotics fail. Reports are increasing that vancomycin is unable to kill off Staphylococcus aureus that causes pneumonia, which can be mortal. [34] An estimated 33—55% of Staphylococcus aureus infections in U.S. hospitals are now resistant to first-line antibiotic therapy. [35] Repeated use of antibiotics pushes patients to the day when they will develop an infection and not be able to recover from it.

In the cancer treatment arena, resistance to chemotherapy is believed to cause treatment failure in over 90% of patients with metastatic (spreading) cancer. [36] One study shows chemotherapy works to produce 5-year survival in less than 3% of cases. [37] Chemotherapy does temporarily shrink tumors by 50%, but leaves the patient with a totally impaired immune system. Furthermore, chemotherapy cannot penetrate solid tumors (breast, prostate, lung, colon, pancreas, brain, liver, etc), which represent the majority of tumors in humans. Most cancer patients succumb to side effects caused by treatment before they do from their tumors.

Summary

The major classes of prescription drugs are failures. Of concern is the realization most drugs are never designed to address the underlying biochemical causes of disease and may intentionally be designed to create life-long dependency.

Adjectives that could be used to describe modern pharmacology range from u201Cdisappointing, unacceptable, ineffective,u201D to u201Cimmoral, despicable, shameful, appalling, wicked, dreadful.u201D The Food & Drug Adminstration approval of such drugs gives false credence to medical therapies that were never designed for cure but rather to keep patients in a state of chronic disease and drug enslavement. This report begs for a follow-up report on safe and effective alternatives to prescription drugs, which is forthcoming.

Nearly all anti-diabetic drugs cause a person to become overweight and totally dependent upon insulin.

Asthma drugs sensitize the body to triggers that worsen this condition.

There is no evidence that cholesterol-lowering drugs reduce mortality rates.

All cancer chemotherapy drugs result in tumor resistance.

None of the many drugs prescribed to control high blood pressure address the cause of hypertension.

Antacid u201Cheartburnu201D drugs induce greater problems when withdrawing from them, locking patients into lifetime use.

Of the many drugs used to treat age-related senility, none stop the progression of mental decline and some hasten it.

To an increasing degree, man-made antibiotics produce germ-resistance and mortality rates are rising from infections once conquered by these drugs.

References

[1] Nwokolo CU, Smith JT, Rebound intragastric hyperacidity after abrupt withdrawal of histamine H2 receptor blockade. Gut 1991 Dec; 32(12):1455-60.

[2] Fullatron GM, Macdonald AM, McColl KE, Rebound hypersecretion after H2-antagonist withdrawal — a comparative study with nizatidine, ranitidine and famotidine. Aliment Pharmacological Therapy 1991 Aug; 5(4):391-8.

[3] Waldum HL, Brenna E, Sandvik AK, Long-term safety of proton pump inhibitors: risks of gastric neoplasia and infections. Expert Opinion Drug Safety. 2002 May; 1(1):29-38.

[4] Reid DW, Misso NL, Aggarwal S, Tolerance and rebound with zafirlukast in patients with persistent asthma. Journal of Negative Results in BioMedicine 2008, 7:3.

[5] Drugs make asthma worse, BBC NEWS: August 17, 2003: McGraw DW, Almoosa KF, Paul RJ, Kobilka BK, Liggett SB, Antithetic regulation by beta-adrenergic receptors of Gq receptor signaling via phospholipase C underlies the airway beta-agonist paradox. Journal Clinical Investigation 2003 Aug; 112(4):619-26.

[6] Ballard C, Margallo-Lana M, Juszczak E, et. al., Quetiapine and rivastigmine and cognitive decline in Alzheimer’s disease: randomised double blind placebo controlled trial. British Medical Journal 2005 Apr 16; 330(7496):874.

[7] Ringman JM, Cummings JL, Current emerging pharmacological treatment options for dementia. Behavioral Neurology 2006; 17(1):5-16.

[8] Schneider LS, Tariot PN, Dagerman KS, Effectiveness of atypical antipsychotic drugs in patients with Alzheimer’s disease. New England Journal Medicine 2006 Oct 12; 355(15):1525-38.

[9] Krentz AJ, Management of type 2 diabetes in the obese patient: current concerns and emerging therapies. Current Medical Research Opinion 2008 Feb; 24(2):401-17.

[10] Nichols GA, Gomez-Caminero A, Weight changes following the initiation of new anti-hyperglycaemic therapies. Diabetes Obesity Metabolism 2007 Jan; 9(1):96-102.

[11] Ramaswamy K, Masand PS, Nasrallah HA, Do certain atypical antipsychotics increase the risk of diabetes? A critical review of 17 pharmacoepidemiologic studies. Annals Clinical Psychiatry. 2006 Jul-Sep; 18(3):183-94.

[12] Dibben CR, Kalavalapalli SS, Linnington HE, et. al., Diabetes associated with atypical antipsychotic treatment may be severe but reversible: case report. International J Psychiatry Medicine 2005; 35(3):307-11.

[13] Hanninen SA, Darling PB, Sole MJ, Barr A, Keith ME, The prevalence of thiamin deficiency in hospitalized patients with congestive heart failure. J American College Cardiology 2006 Jan 17; 47(2):354-61.

[14] Neutel JM, Prescribing patterns in hypertension: the emerging role of fixed-dose combinations for attaining BP goals in hypertensive patients. Current Medical Research Opinion 2008 Jul 9.

[15] Sharifi F, Nasab NM, Zadeh HJ, Elevated serum ferritin concentrations in prediabetic subjects. Diabetes Vascular Disease Research 2008 Mar; 5(1):15-8.

[16] Tsimihodimos V, Gazi I, Kalaitxidis R, Elisaf M, Siamopoulos KC, Increased serum ferritin concentrations and liver enzyme activities in patients with metabolic syndrome. Metab Syndr Relat Disord. 2006 Fall; 4(3):196-203

[17] Mojiminiyi OA, Marouf R, Abella NA, Body iron stores in relation to the metabolic syndrome, glycemic control and complications in female patients with type 2 diabetes. Nutrition Metabolism Cardiovascular Disease 2007 Dec 4.

[18] Soor GS, Vukin I, Leong SW, et. al., Peripheral vascular disease: who gets it and why? A histomorphological analysis of 261 arterial segments from 58 cases. Pathology. 2008 Jun; 40(4):385-91.

[19] Husmann L, Scheffel H, Valenta I, et. al., Impact of hypertension on the diagnostic accuracy of coronary angiography with computed tomography. International Journal Cardiovascular Imaging. 2008 Mar 28

[20] Kanemaru K, Seya K, Miki I, et. al., Calcification of aortic smooth muscle cells isolated from spontaneously hypertensive rats. Journal Pharmacology Science 2008 Feb;106(2):280-6.

[21] Seely S, Is calcium excess in western diet a major cause of arterial disease? International Journal Cardiology 1991 Nov; 33(2):191-8.

[22] Orakzai SH, Nasir K, Blaha M, et. al., Non-HDL cholesterol is strongly associated with coronary artery calcification in asymptomatic individuals. Atherosclerosis. 2008 Mar 25.

[23] Allison MA, Wright CM, A comparison of HDL and LDL cholesterol for prevalent coronary calcification. Int J Cardiol. 2004 May;95(1):55-60.

[24] Grases F, Sanchis P, Perello J, Isern B, Prieto RM, Fernandez-Palomeque C, Fiol M, Bonnin O, Torres JJ. Phytate (Myo-inositol hexakisphosphate) inhibits cardiovascular calcifications in rats. Frontiers Bioscience 2006 Jan 1; 11:136-42.

[25] Grases F, Sanchis P, Perell J, Isern B, Prieto RM, Fernndez-Palomeque C, Torres JJ. Effect of crystallization inhibitors on vascular calcifications induced by vitamin D: a pilot study in Sprague-Dawley rats. Circulation Journal 2007 Jul; 71(7):1152-6.

[26] Jie KS, Bots ML, Vermeer C, Witteman JC, Grobbee DE. Vitamin K intake and osteocalcin levels in women with and without aortic atherosclerosis: a population-based study. Atherosclerosis. 1995 Jul; 116(1):117-23.

[27] Rayssiguier Y, Mbega JD, Durlach V, Gueux E, Durlach J, Giry J, Dalle M, Mazur A, Laurant P, Berthelot A. Magnesium and blood pressure. I. Animal studies. Magnesium Research 1992 Jun; 5(2):139-46.

[28] Touyz RM. Magnesium supplementation as an adjuvant to synthetic calcium channel antagonists in the treatment of hypertension. Medical Hypotheses. 1991 Oct; 36(2):140-1

[29] Touyz RM, Laurant P, Schiffrin EL. Effect of magnesium on calcium responses to vasopressin in vascular smooth muscle cells of spontaneously hypertensive rats. J Pharmacology Experimental Therapeutics 1998 Mar; 284(3):998-1005.

[30] Kjeldsen SE, Jamerson KA, Bakris GL, Predictors of blood pressure response to intensified and fixed combination treatment of hypertension: the ACCOMPLISH study. Blood Pressure 2008;17(1):7-17.

[31] Prez-Castrilln JL, Vega G, Abad L, Sanz A, Chaves J, Hernandez G, Dueas A. Effects of Atorvastatin on vitamin D levels in patients with acute ischemic heart disease. American Journal Cardiology 2007 Apr 1;99(7):903-5.

[32] Abramson J, Wright J (2007). "Are lipid-lowering guidelines evidence-based?" Lancet 369 (9557): 168-9.

[33] Rosch PJ, Cholesterol does not cause coronary heart disease in contrast to stress. Scandinavian Cardiovascular Journal 2008 Apr 1:1-6.

[34] Sakoulas G , Moellering RC Jr, Increasing antibiotic resistance among methicillin-resistant Staphylococcus aureus strains.Clinical Infectious Disease 2008 Jun 1; 46 Suppl 5:S360-7.

[35] Appelbaum PC, MRSA — the tip of the iceberg. Clinical Microbiology Infection 2006 Apr;12 Suppl 2:3-10.

[36] Longley DB, Johnston PG, Molecular mechanisms of drug resistance. Journal Pathology 2005 Jan; 205(2):275-92.

Bill Sardi Archives