List of citations and foot notes from Before You Take That Pill

These are additional citations for facts presented in the book that were not listed
in the book itself due to space constraints. Citatations for the most important
studies are in the book and not listed here; this is supplementary material

Chapters

Chapter 1. The Drug Problem
Chapter 2. Arthritis Medications
Chapter 3. Acne Treatments
Chapter 4. Cholesterol Lowering Medications
Chapter 5. Anti-hypertensives
Chapter 6. Diet Pills
Chapter 7. Asthma and Allergy Medications
Chapter 8. Enlarged Prostate
Chapter 9. Treatments of Ulcers and Gastric Reflux
Chapter 10. Antibiotics and Vaccines
Chapter 11. Osteoporosis Drugs
Chapter 12. Hormone Replacement Therapy and Oral Contraceptives
Chapter 13. Diabetes Drugs
Chapter 14. Dementia Drugs
Chapter 15. Antidepressants
Chapter 16. Insomnia
Chapter 17. Drugs for Sexual Dysfunction
Chapter 18. Vitamins and Supplements
Chapter 19. Medication in Kids
Chapter 20. How to Keep Yourself and Your Family Safe

Chapter 1. The Drug Problem

“Today we are faced with what may be the single greatest drug safety catastrophe in the history
of this country or the history of the world… In my opinion, the FDA has let the American people down,
and sadly, betrayed a public trust.”(Graham 2004).

The answer [to delays in drug approval] was essentially legislation allowing pharmaceutical companies
to pay the salaries of the staff at the FDA (Hilts 2003)

Eight of the nine doctors who formed a committee in 2001 to advise the government on cholesterol
guidelines for the public were making money from the very same companies that made the cholesterol
lowering drugs that they were urging millions of Americans to take (2004).

For example, one of the committee members, Dr. H. Bryan Brewer, was the Chief of the Molecular Disease
Branch at the National Institute of Health. He worked as a consultant or speaker for 10 different
pharmaceutical companies, making over $100,000 over three years while he was on the committee, and
sat on one of their boards (Willman 2004).

Dr. Curt D. Furberg, a former head of clinical trials at the National Heart, Lung, and Blood Institute
and now a professor at Wake Forest University in North Carolina, explained how information on expert
guidelines reached physicians: “The [company] reps tell the doctors, ‘You should follow these guidelines,’
implying that you're not a good doctor if you don't follow these guidelines."(Willman 2004).

Approval time for drugs decreased from 20 months to six months right after the law changed. However,
the number of drugs that had to be later withdrawn also increased from 2% of drugs to 5% of drugs (Okie 2005).

Half of Americans take prescription drugs and 81% take at least one kind of pill everyday (Kaufman, Kelly et al. 2002).

One study showed that 54% of the time doctors will prescribe a specific brand and type of medication
if patients ask for it (Kravitz, Epstein et al. 2005).

One hundred thousand Americans die every year from the effects of prescription medications (Lazarou, Pomeranz et al. 1998).

Over a million Americans a year are admitted to the hospital because they have had a bad reaction
to a medication (Lazarou, Pomeranz et al. 1998).

About a quarter of the prescriptions that doctors write for the elderly have a potentially life
threatening error (Liu and Christensen 2002).

Janet Woodcock, Deputy Commissioner of Operations at the FDA, said that the nation’s drug safety system
had, “pretty much broken down.” She went on to say that “the keystone of the current system is the
prescriber, and that person is the one who decides if the benefits of a drug outweigh the risks for
that patient. This system has obviously broken down to some extent as far as the fully informed provider
and the fully informed patients.” She charged that neither doctors nor patients had enough information
about the side effects of drugs to make informed decisions about taking them. Dr. Woodcock went on to say
that, “the bottom line is that a lot of drug safety problems are actually preventable, [because] most
adverse events are from known side effects.”(Harris 2005).

Drug companies often recruit former college cheerleaders for this job (Saul 2005).

Drug companies also buy information about the medications that doctors prescribe from major chain drug
stores like CVS, and then use this information to reward doctors who prescribe their drugs frequently,
with trips to resorts and other perks (Kassirer 2005).

Research studies show that, although doctors deny that the perks have any effect on their prescribing
practices, there are changes in objective measures, like how often a doctor will try to have a drug
from that particular company put on his hospital’s formulary (Wazana 2000).

In a survey of 13 industrialized nations, the US was found to be last in many health-related measures,
and overall was 2nd to the last (Starfield 2000).

Studies have shown that peasants in Indian villages with the diagnosis of schizophrenia who get
intermittent doses of chlorpromazine, the original antipsychotic that is dirt cheap, together with
support from their family, actually do better in terms of having fewer psychotic symptoms than Americans
who get expensive new generation anti-psychotics and traditional Western psychiatric care (Jablensky, Sartorius et al. 1992).

Nexium, “the purple pill,” works no better for gastric reflux than the older medications like Prilosec,
even though it costs much more (Gillson 2005).

Billy Tauzin, President of the Pharmaceutical Research and Manufacturer’s Association (PhaRMA), the
lobbying organization for the drug companies, in response to efforts to regulate the content of TV
ads for drugs, said “We don't make ice cream or handbags or automobiles, we make products that save lives."(Pear 2005).

A whopping 80% of drug company budgets is used for marketing (Goozner 2004).

The newer antidepressant drugs like Prozac have never been shown to work better than the older
tricyclic antidepressant drugs (Kirsch, Moore et al. 2002).

The Economist reported in 2004 that less than 50% of us perceive drug companies as “favorable.” That’s
only slightly above the low favorable ratings we give oil and tobacco companies (2004).

Daniel Troy, the Chief Counsel for the FDA under George W. Bush in 2004 was a political appointee who
formerly worked in a Washington law firm defending the interests of pharmaceutical companies. He worked
as a “friend of the court” on cases where pharmaceutical companies had been sued for drug safety problems.
The logic was that the FDA approved the drug and therefore had an interest in the outcome (2004).

Research studies show that one out of four medical information web sites offer information that is
inaccurate or misleading, and only one out of five are authored by identifiable medical experts (Beredjiklian, Bozentka et al. 2000).

Chapter 2. Arthritis Medications

Based on data released to the FDA, it was later discovered that in the second six months there was
an increase in heart attack risk in CLASS. The editor of the journal was understandably perturbed
when told about this after the fact, as she expressed in an editorial in her journal (DeAngelis 2006).

Polyps do not necessarily proceed to gastrointestinal cancer, and at least five times as many people
on a coxib will have a cardiac events as will develop gastrointestinal cancer if they don’t take a coxib (Psaty and Potter 2006).

A study randomized 202 patients with osteoarthritis of the knee to three years of treatment with
glucosamine or placebo. Placebo treated patients had a greater degree of joint space narrowing as
measured by X-ray than glucosamine (-.19 mm v +.04 mm). There were statistically significantly greater
reductions in glucosamine for measures of pain self ratings (-2 v -1.3) as well as measures of
stiffness and function (Pavelka, Gatterova et al. 2002).

Chapter 3. Acne Treatments

After a while less than 20% of patients treated with Accutane met the original criteria for the
treatment of acne (Goulden, Layton et al. 1995; Cunliff, van der Kerkhof et al. 1997).

Soon after its introduction as a treatment for cystic acne, troubling reports of depression and
suicide associated with Accutane’s use started to surface (Byrne, Costello et al. 1998; Jick, Kremers et al. 2000; Wysowski, Pitts et al. 2001; Bremner 2003).

The cases of Accutane-related depression and suicide reported to the World Health Organization and
the Food and Drug Administration were much higher than for reports of these events related to other
treatments for acne, such as antibiotics (Middelkoop 1999; Wysowski, Pitts et al. 2001).

By the year 2000 Accutane earned the distinction of having the most reported side effects to agencies
like the World Health Organization (WHO) of any drug in the world (Middelkoop 1999; Wysowski, Pitts et al. 2001).

Arctic explorers from the 19th Century who lived almost exclusively on polar bear liver, an extremely
rich source of Vitamin A, developed symptoms of confusion and psychosis. Large doses of Vitamin A
can have a number of other neurological and mental effects including fatigue, decreased interest,
headache, and double vision (Rodahl and Moore 1943; Bass 1959; Restak 1972) aggression, personality
changes, depression, psychosis (Restak 1972; McCance-Katz and Price 1992; Fishbane, Frei et al. 1995)
and a swelling of the brain, called pseudotumor cerebri that can be fatal
(Marie and See 1954; Stimson 1961; Restak 1972; Seigel and Spackman 1972; Lombaert and Carton 1976;
Selhorst, Waybright et al. 1984; Spector and Carlisle 1984; Gomber and Chellani 1996).

Many patients who recovered from depression after stopping the drug became depressed again
after restarting it (Meyskens 1982; Hazen, Carney et al. 1983; Bigby and Stern 1988;
Villalobos, Ellis et al. 1989; Scheinman, Peck et al. 1990; Bravard, Krug et al. 1993; Duke and Guenther 1993; Middelkoop 1999).

Some patients’ behavior became bizarre, even psychotic (Villalobos, Ellis et al. 1989; Duke and Guenther 1993).

Internal memos in 1984 (just two years after Accutane hit the market) between the FDA and Roche stated
that there “probably” was a relationship in some patients (McCoy 2004).

In 1986 Roche changed the package insert to include information that some patients had reported
depression on Accutane. The company’s public spokespersons, however, still publicly denies that
there is a “causal relationship” between Accutane and depression (McCoy 2004).

In 1997 Dr. Peter Schifferdecker, a doctor working for Roche in Switzerland, wrote in a report for
the FDA that Accutane “probably caused” depression, doctors and patients should be warned, and
patients should be monitored for the development of depression. The company’s US marketing team
“re-wrote” his report because of concerns about the “impact on marketing strategy and product
liability,” removing the language about how Accutane could cause depression in some patients (McCoy 2004).

My study looking at the effects of Accutane on brain function using brain imaging was first
presented in November of 2004. If Accutane affected the brain and caused depression in that way,
we should be able to detect it with brain imaging. In our research, we did in fact find that
Accutane caused a decrease in function in the orbitofrontal cortex. This was identical to what
we found in patients who developed depression (Bremner, Fani et al. 2005).

This showed that Accutane was affecting brain areas that were known to underlie depression. It
also countered the argument that Accutane couldn’t be causing depression because it doesn’t go into the brain; it is an acne drug (2000).

Other work funded by Mr. Grant showed that Accutane inhibited the growth of neurons in a brain
area called the hippocampus that is involved in memory and emotion (Crandall, Sakai et al. 2004).

This brain area is smaller in patients with depression, suggesting atrophy (Sheline, Wang et al. 1996; Bremner, Narayan et al. 2000).

In fact, antidepressants promote growth of neurons in the hippocampus, which is thought to
underlie how antidepressants work to treat depression (Duman, Heninger et al. 1997).

Other studies showed that Accutane caused abnormalities in behavior in animals (Ferguson, Cisneros et al. 2004).

Roche strangely continued to state publicly in December of 2004 there is no “causal relationship”
between Accutane and depression, at the same time that Martin Huber, Roche's global head of drug
safety, testified under oath in a deposition that Roche’s internal assessments showed Accutane
"probably caused" depression and other psychiatric ailments in some users, and that the rate of
depression among Accutane users was 1.5 times higher than among non-users (McCoy 2004).

Although the prevalence of depression (meaning that it occurred at some time in your life) is
16% (Kessler, Berglund et al. 2003) the actual incidence (developing new onset depression)
during any given year is only 1.6% (Eaton, Kramer et al. 1989).

Therefore in the four month period of an isotretinoin trial, about 0.5% of patients would
spontaneously develop depression. Estimates of the incidence of depression following treatment
with isotretinoin range from 1% (Hull and Demkiw-Bartel 2000) to 4% (Scheinman, Peck et al. 1990) to 6% (Hazen, Carney et al. 1983).

Over six million patients have been treated with Accutane; if 3% of patients treated with
Accutane would develop depression while taking isotretinoin that otherwise would not have;
this means that 180,000 people could have developed depression from Accutane since its introduction.
This is higher than the estimated numbers of patients with heart attack from Vioxx (Topol 2004).

Half of all “Accutane babies” have a reduction in IQ (Windhorst and Nigra 1982; Bigby and Stern 1988; Maden and Holder 1992; 2000; Wilson, Gale et al. 2003).

Accutane causes severe headaches in about 20% of patients (Hull and Demkiw-Bartel 2000).

Accutane more rarely pseudotumor cerebri (a swelling of the brain that can be fatal) (Roytman, Frumkin et al. 1988; Alemayehu 1995; Lee 1995).

Chapter 4. LDL Cholesterol Lowering Medications (Statins)

“I’ve studied the human heart my whole life. I trust Lipitor to help keep my heart healthy.”
– Dr Robert Jarvik, inventor of the Jarvik artificial heart. www.lipitor.com

Studies suggest that high levels of HDL cholesterol reduce your risk of heart attack (Wilson, Abbott et al. 1988).

Too much LDL cholesterol, a condition known as Hypercholesterolemia, can clog your arteries and
increase your risk of heart attack and stroke (Campos, Genest et al. 1992).

Fibrates were found to lower LDL cholesterol and prevent heart disease, but they were also found
to actually increase overall mortality by as much as 47% (Smith and Pekkanen 1992; Huttunen, Heinonen et al. 1994).

The guidelines of the National Cholesterol Education Program provide a series of “points” based
on various risk factors for heart disease (high LDL or low HDL cholesterol, smoking, diabetes,
family history of someone dying young from a heart attack, uncontrolled high blood pressure) (NCEP 2001).

There has been a recent push to give statins to people even if their LDL cholesterol is normal,
pushing LDL levels to extremely low levels (Sever, Dahlof et al. 2003).

Very low cholesterol concentrations have been linked to depression and suicide, possibly because
of the impairment in the ability to maintain neurons in the brain (Chen, Peto et al. 1991;
Engelberg 1992; Brown, Salive et al. 1994; Cadeddu, Fioravanti et al. 1995; Rozzini, Bertozzi et al. 1996;
Brunner, Parhofer et al. 2003; Steffens, McQuoid et al. 2003; Papakostas, Ongur et al. 2004).

When the national guidelines for who should take a statin were compared across different countries,
the guidelines which called for the most liberal use of statins (you guessed it, the U.S.) which
called for 25% of the population to be on statins, saved no more lives than the guidelines for
one of the most restrictive countries, New Zealand, which would treat 13% of the population (Manuel, Kwong et al. 2006).

And statins are not without their risks. A paper published in the Journal of the American College of Cardiology
in 2007 found that when cholesterol levels were pushed to very low concentrations (LDL<100) using the high doses of
statins currently in vogue with many US doctors, there was a statistically significant increase in cancer rates (Alsheikh et al. 2007).

. Some analyses combining data from multiple studies have shown no statistically significant
increases in cancer with statins (Baigent, Keech et al. 2005; Dale, Coleman et al. 2006).

Because of concerns about Crestor, a consumer group urged the FDA not to approve Crestor in
the US in 2003. The FDA approved it anyway. Since that time there have been 65 cases of
rhabdomyolysis reported to the FDA with Crestor, some of them fatal (Wolfe 2004).

Studies have shown that myalgia can be associated with changes in the muscle tissue (2007).

There have been recommendations not to use statins in patients over 70 because of risk of muscle
pain (myopathy) or breakdown (rhabdomyolysis). However these guidelines are not followed,
either due to lack of knowledge about the guidelines or for other reasons, e.g. 21% of
patients prescribed statins were shown to be over 70 (Florentius, Heerdink et al. 2004).

A large body of research including large studies with tens of thousands of patients have
shown that vitamins do not prevent heart disease (Morris and Carson 2003; Vivekananthan, Penn et al. 2003).

Studies have found that replacement of animal fat by soy results in a reduction of LDL
cholesterol of 13% (Anderson, Johnstone et al. 1995).

Studies of coenzyme Q10 have shown only some modest changes in measures of cardiovascular
function that were not directly related to clinical function (Morisco, Trimarco et al. 1993; Watson, Scalia et al. 1999).

There are also “non-medical” factors not directly related to lifestyle that increase the risk
for heart disease, like low income, lack of social support, depression, marginalization in
society, and stress in childhood (Anda, Williamson et al. 1993; Raphael 2002; Anda, Felitti et al. 2006).

Following the low fat diet advocated by the National Cholesterol Education Program lowers LDL
cholesterol equally well as treatment with a statin, with no side effects (Jenkins, Kendall et al. 2005).

It is often pointed out that ancient diets had a ratio of omega-3 to omega-6 of 1:1 whereas
current diets have much higher amounts of omega-6, largely through the substitution of calories
in the forms of leafy plants with grains and seeds (Pollan 2006).

Chapter 5. Anti-hypertensives

In ALLHAT rates of heart attacks were the same between chlorthalidone, amlodipine or lisinopril (a href="#ALLHAT 2002). Chapter 6. Diet Pills

One in four Americans is obese, defined by a body mass index or BMI [calculated as weight in kilograms
divided by the square of height in meters] of over 30. In 1999 and 2000 more than 64% of Americans were
overweight or obese, as defined by a BMI of 25 (Flegal, Carroll et al. 2002).

You may not be surprised that one death out of five each year is caused by cigarette smoking, but
did you know that an equal number of deaths are caused by obesity? (Nestle 2002).

The recent rapid increase in obesity parallels the widespread availability of fast food outlets
like McDonalds, Wendy’s, Burger King, Subway and Hardees, as well as the chain restaurants like Olive
Garden and Outback Steakhouse, that serve mega-portions of food (Flegal, Carroll et al. 2002; Olshansky, Passaro et al. 2005).

Every day one out of four Americans eats at a fast food restaurant, 43% of the time at McDonalds (Schlosser 2001; Spurlock 2005).

Convenience food makers try to increase our desire for the items we crave most (fat, sugar, and salt)
in order to sell products, even if it kills us (Schlosser 2001).

The National Institute of Health recommends that most obese Americans should undergo drug treatment,
which means 100 million Americans could be on drugs for obesity (Pi Sunyer, Becker et al. 1998).

Heidi Connolly, MD, of the Mayo Clinic in Rochester, Minnesota assessed the risk of getting PPH following
treatment with diet pills. She found that there is a 6-fold increase in risk of PPH with diet pills.
Pills that were included in this assessment of risk were dexfenfluramine, fenfluramine, diethylpropion,
clobenzorek, fenproporek, phemetrazine, and other compounds. Patient taking diet pills for more than
3 months face a 23-fold increased risk (Connolly and McGoon 1999).

Dr. Connolly and colleagues also found other life threatening side effects with diet pills, notably
the dangerous effects of “fen-phen” (fenfluramine-phentermine) on the heart. The doctors performed
ultrasound examinations of the heart and found abnormalities of the heart valves in 24 women, five of
whom required cardiac surgery for valve repair (Connolly, Crary et al. 1997).

Multiple studies have not shown evidence that Meridia (or any other weight loss drug for that matter)
reduces obesity related death or disease, like heart disease, stroke, and hypertension (Arterburn, Crane et al. 2004).

Reports of these side effects led Sidney Wolfe, MD, Director of Public Citizen, a Washington DC based
organization devoted to drug safety that is an offshoot of Ralph Nader’s consumer rights related organization,
to petition for the removal of Meridia from the market (Wolfe, Sasich et al. 2005).

A variety of products are sold in stores as natural weight loss aids, most of which have not been
scientifically evaluated (Saper, Eisenberg et al. 2004).

Seven percent of Americans are using over the counter weight loss products, and most are young women (Blanck, L.K. et al. 2001).

Ephedra has been associated with several deaths, including a pitcher for the Baltimore Orioles, which
led to the unusual (for a supplement) step of the FDA banning it in 1994 (Haller and Benowitz 2000).

Chapter 7. Asthma & Allergy Medications

There is evidence for an association between obesity and asthma related to the fact that obese people
have a smaller area for the lungs to expand, higher levels of the hormone leptin (which is released
from fat and is also higher in asthmatics), and higher levels of inflammatory markers (which may contribute to airway reactivity) (Ford 2005).

Although blood levels of IgE are normal in non-allergic asthma, a similar type of inflammatory response
takes place in the airways, for reasons that are not fully understood (Romanet-Manent, Charpin et al. 2002; Jayaratnam, Corrigan et al. 2005).

Clarinex is merely a metabolite (breakdown product) of its precursor, Claritin. That means that 20 minutes
after you take Claritin, you will be getting Clarinex, but you’ll be paying much less for it than if you took Clarinex (Lowe 2002).

Claritin and Clarinex as far as you are concerned are the same drug (Lowe 2002).

About 20% of patients using OTC inhalers have severe asthma that needs medical care (Dickinson, Altman et al. 2000).

Thirteen deaths, mostly cardiovascular, have been reported to be associated with the use of OTC inhalers
over the last 20 years (Dickinson, Altman et al. 2000).

A long acting beta agonist drug marketed in New Zealand was associated with an increase in asthma related
deaths and was pulled from the market there in 1976 (Wolfe, Sasich et al. 2005).

As proof of this the website of the Asthma and Allergy Foundation of America (www.aafa.org) states that,
“Exercise—frequently in cold air—is a frequent asthma trigger.” Although the site notes that children can
exercise with appropriate management, nowhere does it mention the beneficial effects of exercise. All
of the treatments listed are medications, and under prevention it lists “take your medication as prescribed”
and “identify and minimize contact with your asthma triggers” (one of which is “running, playing, or
exercising”!) Why such an emphasis on drugs instead of viable alternatives? The fact that 72% of this
particular non-profit foundation’s revenue comes from pharmaceutical companies might have something to do with it (2002).

Chapter 8. Enlarged Prostate

Fifty percent of men over 50 and 90% of men older than 80 have BPH (Dull, Reagan et al. 2002).

In half of cases BPH reduces quality of life for men. Thirty six percent of spouses of BPH men surveyed
reported that BPH caused a lack of physical intimacy in their relationships (2007).

Alpha adrenergic receptor blocker medications, including doxazosin (Cardura), prazosin (Minipress),
alfuzosin (Uroxatral), and terazosin (Hytrin), cause a relaxation of prostate smooth muscle and increase
urine flow (Lepor, Williford et al. 1996; McConnell, Roehrborn et al. 2003).

Saw Palmetto was shown in one controlled trial to be efficacious in the treatment of BPH (Gordon and Shaughnessy 2003).

Chapter9. Gastric Reflux and Ulcer Drugs

If you have a negative H. Pylori test and you don’t take aspirin, NSAIDs or Cox 2 inhibitors it is unlikely
you have an ulcer (Talley, Phung et al. 2001).

The PPIs have been shown to be more effective than placebo in promoting the healing of ulcers and decreasing symptoms of GERD (Salas, Ward et al. 2002).

A review of 21 randomised controlled trials of PPIs in patients with proven peptic ulcers showed no effect
on mortality, but a reduction in re-bleeding and repeat surgery of about 50% (Leontiadis, Sharma et al. 2005).

After its introduction in 1998, sales of Prilosec continued to rise year after year until it reached sales
of one billion dollars a year in 1995 and peaked at 4 billion dollars a year in 2000 when it was the most
popular drug in the world (Prakash 2002).

It was an effective campaign: by 2002 the company had weaned one in six former Prilosec users off of Prilosec and onto Nexium (Prakash 2002).

Irritable bowel syndrome (IBS) is a common disorder which is very disabling affecting as many as 20% of people in the US (2007).

IBS accounts for 20-50% of visits to gastroenterologists (Mitchell and Drossman 1987).

IBS is characterized by symptoms including abdominal pain, altered bowel function, bloating, distension,
and feelings of incomplete evacuation (like you didn’t get rid of everything when you sat on the toilet) (Farthing 2005).

Tegaserod (Zelnorm) is a 5-HT-4 serotonin receptor partial agonist that promotes contractions of the colon
that is effective in women with constipation predominant IBS (Schoenfeld 2004).

It has also been linked more rarely with ischaemic colitis, with 20 cases reported to the FDA from 2002 to 2004 (Brinker, Mackey et al. 2004).

Two controlled studies showed an improvement in IBS symptoms with cromolyn sodium compared to placebo
treatment (Bolin 1980; Lunardi, Bambara et al. 1991).

One controlled study showed that itopride, a dopamine D2 agonist, was superior to a placebo in improving
symptoms of functional dyspepsia (Holtmann, Talley et al. 2006).

A number of herbs, supplements, and food products are commonly used as self treatments by patients suffering
from gastrointestinal disorders like IBS, FD and GERD (Tillisch and Tan 2005).

Patients with IBS commonly can’t tolerate a number of foods, including milk, wheat, eggs, and fresh fruits and
vegetables. IBS patients do not however have an increase in lactase deficiency (the enzyme that digests dairy
products) or an inability to absorb sugars (like fructose) when measured in the laboratory, although they may
have more symptoms when exposed to these compounds (Spanier, Howden et al. 2003).

At least three randomized placebo controlled trials have shown that peppermint improves symptoms of IBS (while
two did not show an effect) (Dew, Evans et al. 1984; Liu, Chen et al. 1997; Pittler and Ernst 1998; Spanier, Howden et al. 2003).

One study showed that peppermint helped symptoms of dyspepsia (May, Kohler et al. 2000).

Artichoke (Cynara scolymus) leaf extract (ALE) has been promoted as a treatment for dyspepsia. One study of 244
patients randomized to ALE or placebo showed an improvement in dyspepsia symptoms and quality of life scores
compared to placebo after 6 weeks of ALE therapy (Holtmann, Adam et al. 2003).

Although ginger has been promoted for nausea treatment, controlled studies have shown that it does not decreases
post-operative nausea (Spanier, Howden et al. 2003) although it has been shown to work for sea sickness
(Grontved, Brask et al. 1988) and nausea with pregnancy (Fischer-Rasmussen, Kjaer et al. 1991).

Probiotics are used more commonly in Europe than the US, and are most popular in France; 3 percent of French
people will take probiotics on any given day (Goossens, Ferech et al. 2005).

Probiotics have not been shown in controlled trials to be effective for constipation in adults
(Ouwenhand, Lagstrom et al. 2002) or children (Banaszkiewicz and Szajewska 2005).

One study of Lactobacillus plantarum for the treatment of IBS showed an improvement in abdominal pain
and flatulence compared to placebo (Nobaek, Johansson et al. 2000).

Another study of 72 patients with IBS who got either the probiotics Lactobacillus salivarius or
Bifidobacterium infantis or a placebo drink for 8 weeks showed a greater reduction of IBS symptoms
with probiotics (O'Mahony, McCarthy et al. 2005).

A small study of 23 IBS patients who got either Lactobacillus GG or placebo showed no differences
between the groups in pain, urgency or bloating between groups (O'Sullivan and O'Morain 2000).

Probiotics have been shown in some trials to reduce antibiotic induced diarrhea when given in conjunction
with antibiotics (D'Souza, Rajkumar et al. 2002; Szajewska, Ruszcynski et al. 2006). For IBS, food elimination diets have been attempted with varying success (Spanier, Howden et al. 2003)
with elimination of wheat, eggs, dairy products, and fresh fruits and vegetables, depending on
the sensitivity of the individual patient.

Some foods may mediate an immune response in certain people, characterized by the release of
immune mediators like IgeE and IgG4. In a subgroup of IBS patients these types of reactions
may contribute to their symptoms (Park and Camilleri 2006).

Studies have shown that obese people have more gastric reflux than people of normal weight (Nandurkar, Locke et al. 2004).

Moderate exercise directly reduces symptoms of IBS and dyspepsia apart from its role in weight
loss and promotes the movement of food out of the stomach and into the intestine (Bi and Triadafilopoulos 2003).

Chapter 10. Antibiotics & Vaccines

Half of all antibiotics are prescribed for viral illnesses or other disorders for which they have no use (2007).

Over the last past half century there has been a dramatic increase in the production of antibiotics,
from 2 million pounds per year in 1954 to over 50 million pounds per year today in the US ((2007).

Most of those antibiotics are being given to farm animals. With the shift of agriculture in
the US from pasture grazing of animals to feed lots there has been a need to provide massive
amounts of antibiotics to farm animals to prevent epidemics of disease ((Pollan 2006).

Another advantage of giving antibiotics to farm animals is that it promotes growth. Although
it is not know why antibiotics promote growth some ideas include the possibility that
antibiotics eliminate bacteria that consume nutrients in the gut, thus allowing for more
uptake of nutrients by the host (i.e. the farm animals) ((Gaskins, Collier et al. 2002).

The massive exposure to antibiotics in the meat that we eat, in runoff from farms into the
drinking water, in addition to the antibiotics we are given for a variety of disorders
(which may or may not be responsive to antibiotics) may have contributed to the current epidemic of obesity (Ternak 2005).

In the past 20 years, there has been over a 13-fold increase in the number of bacteria
resistant to methicillin ((Wolfe, Sasich et al. 2005).

The second and third generation antibiotics, including cefuroxime, cefotaxime, ceftazidime,
and ceftriaxone, are more commonly associated with Clostridium difficile (2006).

Other antibiotics that commonly cause this infection are ampicillin and amoxicillin. It is
an especially drug-resistant bacteria and is responsible for 3 million cases of diarrhea
and inflammation of the colon and 5000-20000 deaths each year (Brody 2006).

The newer strains of this bacteria are becoming more toxic and more deadly, and are
now resistant to antibiotics like the fluoroquinolones to which they were previously susceptible (Brody 2006).

For years doctors in Holland have been using the “wait and see” approach with much
success. In years of treating children this way there have been no adverse outcomes
(Del Mar, Glasziou et al. 1997; (Damoiseaux, (van Balen et al. 2000; (Little, Gould et al. 2001; Little, Gould et al. 2002; Spiro, Tay et al. 2006).

A meta analysis of all studies showed that 60% of children treated with a placebo
have no pain after 24 hours. Early use of antibiotics reduced pain by 41% compared
to placebo at 2-7 days. Antibiotics doubled the risk of vomiting, diarrhea, or rash.
Seventeen children had to be treated to reduce pain in one child ((Del Mar, Glasziou et al. 1997).

A recent study showed that 81% of patients prescribed fluoroquinolones were not prescribed
these drugs appropriately ((Lautenbach, Larosa et al. 2003).

For example, amongst women with a new onset bladder infection, only 37% were given the
preferred treatment, which is Septra, while 32% were given Cipro ((McEwen, Farjo et al. 2003).

The most common side effects of fluoroquinolones are nausea, vomiting, and diarrhea,
which occur in 3-6% of patients ((King, Malone et al. 2000).

The first generation of quinolones included nalidixic acid (NegGram) and cinoxacin (Cinobac).
These drugs are used for uncomplicated urinary tract infections (King, Malone et al. 2000).

At most there are less than 2000 cases of influenza related deaths per year (Doshi 2005).

Pending legislation in the form of the Flu Protection Act will revamp US flu vaccine policy.
The legislation will require CDC to pay makers for vaccines unsold "through routine market mechanisms."
The bill will also require CDC to conduct a "public awareness campaign" emphasizing "the safety a
nd benefit of recommended vaccines for the public good " (Doshi 2005).

Mefloquine has a number of neurological side effects including dizziness (96%), nausea (82%),
and headache (73%) (Rendi-Wagner, Noedl et al. 2002).

[Mefloquine] has also been associated with an increase in psychiatric symptoms in 11-35% of
patients (Rendi-Wagner, Noedl et al. 2002; van Riemsdijk, Ditters et al. 2002; van Riemsdijk, Sturkenboom et al. 2002).

Mefloquine users have a number of other symptoms, including vertigo in 96%, nausea in 82%,
and headache in 73% (Rendi-Wagner, Noedl et al. 2002).

Dihydroartemisinin-piperaquine (Artekin) was shown to be as effective as artesunate-mefloquine
in the treatment of malaria-infected children (Smithius et al. 2006).

Efficacy of lindane has been decreasing over the past few decades to lindane due to the
emergence of treatment resistant lice (Burkhart 2004).

Lindane acts on lice by stimulating their central nervous system similar to DDT. Those
with lesions on their head can develop central nervous system toxicity if they apply the
lotion on the head. This is an obvious concern for the many little children who are applying
this lotion on top of their head for the elimination of head lice, which they may have to do twice (Burkhart 2004).

Malathion is not absorbed into the body in significant quantities. The product label says
to leave on for 8 hours, although this is overkill and may lead to lice resistance and
should not be followed. It should not be used in pregnancy or breast feeding (Burkhart 2004).

However these three studies were either authored by Ranjit Chandra, MD (one of them in
The Lancet) or were published in his journal by a mysterious “Dr. A.L. Jain”. It later was
determined that the studies probably never took place (Meguid 2005; O'Neill-Yates 2006).

At $300 million in annual US sales Echinacea is the most popular herbal remedy for the common cold (Canedy 1998).

Yet despite promotions for prevention, Echinacea has not been shown to be useful in the prevention of colds (Kligler 2003).

Based on some small earlier trials that were performed primarily in Germany with variable
quality of methodology, echinacea was initially claimed to reduce the length of colds (Dorn, Knick et al. 1997; Kligler 2003).

Results of more recent randomized, double blind trials, conducted in the U.S. with appropriate
methods (Caruso and Gwaltney 2005) however, have not been consistent with this.

In another study 399 volunteers were given either Echinacea or placebo and then were exposed
to the cold virus. There were no differences in the percent of volunteers who became
infected in the Echinacea group (81%) versus the placebo group (85%) or in other laboratory
measures of infection (Turner, Bauer et al. 2005).

These studies and others caused Dr. Vernon Wright of Baylor School of Medicine to write
“echinacea does not have a significant antiviral or therapeutic effect for patients
with the common cold. It follows that the considerable expense of its widespread use
in the treatment of the common cold is not justified.”((Knight 2005).

Probiotics are live microbial supplements taken to improve the microbial balance of the colon.
Probiotics are used more commonly in Europe than the US, with the highest usage in France
(32 doses per day amongst 1000 people) ((Goossens, Ferech et al. 2005).

Probiotics for which there is some evidence of efficacy include the bacteria
Lactobacillus GG and the yeast Saccharomyces boulardii (S. boulardii). Strains of
Lactobacillus include L. rhamnosus GG, L. acidophilus NCFM, L. casei Shirota,
L. reuteri MM53, L. casei CRL431, L. rhamnosus GR-1, and L. fermentum RC-14 (Reid 1999).

They can be taken by mouth as a supplement and are added to various yoghurts and
food products. Probiotics compete in the gut with pathological bacteria like
Clostridium difficile and Escherichia Coli (E. Coli), which can become more prominent
after antibiotic treatment, leading to antibiotic associated diarrhea (AAD). Probiotics
including Lactobacillus and S. boulardii have been shown to prevent diarrhea when given
in conjunction with antibiotic treatments in children (Szajewska, Ruszcynski et al. 2006)
and adults (D'Souza, Rajkumar et al. 2002).

Probiotics have also been advocated for recurrent urinary tract infections and yeast
infections in women. Intravaginal placement of Lactobacillus casei had been shown in
uncontrolled studies to restore normal urogenital flora in women and prevent UTIs and yeast infections (Reid 1999).

Chapter 11. Osteoporosis Drugs

In another study Karpf and colleagues analyzed data on postmenopausal women with osteoporosis randomized
to treatment with alendronate (N=1012) or placebo (N=590) collected by the manufacturer (Merck) as well as pooled data
from several published studies. They found a 9.0% rate of non-vertebral fractures in the alendronate group versus 12.6%,
a difference that was marginally statistically significant. 6/1012 women (0.6%) on alendronate versus 7/590 (1.2%)
on placebo had a hip fracture, a difference of .6% that was not statistically significant (Karpf et al 1997).

Susan Ott, M.D., Associate Professor in the department of medicine at the
University of Washington, and a specialist in the area of bone physiology and
osteoporosis, wrote a letter to the Journal of Clinical Endocrinology & Metabolism
in which she said that, “there is no doubt that alendronate increases bone strength
and decreases fracture rate during the first 4 years of use, but after that the
profound suppression of the bone formation rate may begin to have a negative effect.”(Ott 2001).

Animals treated with bisphosphonates have a decrease in bone turnover (Li, Mashiba et al. 2001).

Women on alendronate were found to take up to two years to heal after a fracture,
and had markedly suppressed bone formation on biopsy (Odvina, Zerwekh et al. 2005).

Dr. Cesar Migliatori (Migliatori 2003) of NOVA Southeastern University in Ft. Lauderdale,
Florida, reported 5 cases of patients treated intravenous zoledronic acid or pamidronate
for treatment of cancer who developed osteonecrosis of the jaw after a tooth extraction
(related to the impaired bone healing caused by decreased bone turnover with
bisphosphonate treatment). All patients developed infections of the bone that
would not respond to antibiotics or surgery. They had chronic pain and problems with eating, speaking, and dental hygiene.

In another review 10% of patients treated for cancer with zoledronic acid and
4% treated with pamidronate developed osteonecrosis of the jaw after three years of treatment (Durie, Katz et al. 2005).

Although most of the cases of osteonecrosis of the jaw have been reported in
patients with bone metastases or myeloma treated with intravenous bisphosphonates,
(Durie, Katz et al. 2005; Woo, Hellstein et al. 2006) there are now emerging cases
in patients who took the medication only for the “prevention of osteoporosis.”

A total of 15 cases of osteonecrosis have been reported with oral alendronate,
one with oral risedronate and one with ibandronate, taken for the treatment of
osteoporosis or Paget’s Disease (a disease of bone formation)
(Migliatori 2003; (Pogrel 2004; Marx, Sawatari et al. 2005; Purcell and Boyd 2005; Woo, Hellstein et al. 2006).

Of the 368 cases of osteonecrosis associated with bisphosphonates reported
worldwide as of 2006, 94% were in patients treated intravenously for cancer
and 60% were after a dental procedure (Woo, Hellstein et al. 2006).

Teriparatide (Forteo) is a form of parathyroid hormone, the hormone that
regulates calcium and phosphate metabolism in the bone and kidney. It is
given by daily injection and is approved for women with new vertebral fractures;
it was approved with restrictions because it causes bone cancer in laboratory animals.
At best it can reduce the risk from 0 7% to 0.2% (Wolfe, Sasich et al. 2005).

Other studies in individuals outside nursing homes found no beneficial effects
from Vitamin D and calcium supplementation in terms of hip fracture prevention
(Flynn 2004; (Shea, Wells et al. 2004; (Porthouse, Cockaynes et al. 2005; Winzenberg, Shaw et al. 2006).

Studies have shown that the simple act of aging is ten times more important in
terms of fracture risk than bone mineral density (Aitken 1984).

Osteoporotic fractures of the hip are inversely related to exercise (Aitken 1984).

Chapter 12. Oral Contraceptive Pills and Hormone Replacement Therapy

Theoretical failure rate of OCPs is 0.1%, and true failure rate is 3% due to incorrect use (Batur, Kiran et al. 2003).

The injectable long acting contraceptive medroxyprogesterone (Depo-provera) is
given by a physician or nurse by intramuscular injection and provides three months
of contraceptive protection. This compound, however, has been associated with an
increase in bone mineral loss when given to teenagers (Busen 2004).

For smokers there is an increased risk with OCPs that gets worse with age.
For instance, the risk of death is 1 in 200,000 per year in non-smoking women
under the age of 35. However risk increases with age and smoking to 1 in 700 per year for smokers over age 35 (Hatcher 2004).

The risk of cervical cancer doubles after 10 years of oral contraceptive therapy
in women with a history of human papilloma virus infection (HPV) (Smith, Green et al. 2003).

There was some early evidence from the Nurses’ Health Study published in 1995 that
showed a 32% increase in breast cancer with HRT (Colditz, Hankinson et al. 1995).

Other studies of estrogen replacement have shown increased rates of uterine
(Zeil and Finkle 1975) and ovarian cancer (Rodriguez, Patel et al. 2001).

HRT doubles the risk of blood clots that can lead to deadly pulmonary emboli
(Cushman, Kuller et al. 2004) (blood clots that travel to the lung and have up to a 50% mortality rate).

HRT also increases the risk of gall bladder disease and of getting your gall bladder removed by 60% (Cirillo, Wallace et al. 2005).

Another study showed that HRT actually accelerated the progression of thickening
of the coronary arteries, and doubled this risk of dying of heart disease (Rapola and Virtamo 1997; Waters, Alderman et al. 2002).

A recent metaanalysis showed a 29% increase in risk of stroke (Bath and Gray 2005).

Estrogen alone (Premarin), given to women with a hysterectomy, like estrogen and
progesterone, was shown to increase the risk of stroke, decrease the risk of bone
fracture, and have no effect on cardiovascular disease (WHISC. 2004).

Estrogen affects brain areas involved in memory like the hippocampus (Woolley and McEwen 1992)
which has led to the idea that the decline in estrogen after menopause is associated with a decline in memory function.

Based on observational studies, it was originally believed that HRT prevented the development of Alzheimer’s Disease and other dementias,
(Baldereschi, Di Carlo et al. 1999; LeBlanc, Janowsky et al. 2001) and improved memory
function or delayed the normal decline of memory with aging in women without dementia (Jacobs, Tang et al. 1998).

A number of studies have looked at more subtle and specific memory functions.
Studies in women without depression or dementia found no change in a variety of
specific memory tests, including ability to learn word pairs, find words, remember
a paragraph, or connect numbered dots (Barrett and Kritz-Silverstein 1993;
Polo-Kanola, Portin et al. 1998; Binder, Schechtman et al. 2001; LeBlanc, Janowsky et al. 2001).

Most importantly, the studies that used random assignment to HRT or placebo for
postmenopausal women, eliminating the kind of self-selection of educated women to
take HRT which can influence results of these studies, showed no effect of HRT
on memory ((Polo-Kanola, Portin et al. 1998; (Binder, Schechtman et al. 2001).

What about women with surgically induced menopause? Studies of women with
hysterectomy and bilateral oopherectomy (removal of ovaries and uterus)
have shown an improvement in memory function with HRT, although these
studies were uncontrolled ((Sherwin 1988; (Phillips and Sherwin 1992).

In terms of benefits, HRT does reduce the loss of bone mineral density
that occurs with normal aging, and reduces the risk of osteoporotic fracture (Cauley, Robbins et al. 2003).

HRT leads to an 80% reduction in symptoms with an associated improvement
in quality of life (Wiklund, Karlberg et al. 1993).

HRT also improves memory and cognition in women with highly symptomatic
hot flashes (Yaffe, Sawaya et al. 1998; LeBlanc, Janowsky et al. 2001).

HRT has been shown to be better than a placebo in the treatment of depression
in women who develop depression around the time of menopause (Schmidt, Nieman et al. 2000; Soares, Almeida et al. 2001).

Stressed post-menopausal women who were caring for a spouse with depression
reported lower hostility when compared to placebo (Steffen, Thompson et al. 1999).

Replacement of estrogen and testosterone in women who had their uterus and
ovaries removed also resulted in an improvement in mood (Sherwin and Gelfand 1985).

Dierdre Hill PhD and colleagues at the University of Washington in Seattle
conducted a phone interview study in 204 women one year after they had received
a prescription for HRT. They found that 40% of women were no longer taking HRT as originally prescribed ((Hill, Weiss et al. 2000).

An initial study of 104 postmenopausal women randomized to 40 g daily of
soy or a placebo showed a statistically significant reduction in number of hot flashes
that was greater for soy (45%) that was greater than the reduction obtained with placebo (30%) (lbertazzi, Pansini et al. 1998).

Other placebo controlled trials did not find any efficacy of soy extract for hot flashes ((Nelson, Vesco et al. 2006).

Heidi Nelson, M.D., a Professor of Medicine at Oregon Health Sciences
University in Portland, Oregon, and colleagues recently reviewed the literature
for nonhormonal therapies for hot flashes, looking at the reduction in the number
of hot flashes per day with different treatments (Nelson, Vesco et al. 2006).

Studies have shown that women who exercise develop hot flashes one third as often
as women who do not during menopause (Ivarsson, Spetz et al. 1998).

Chapter 13. Diabetes Drugs

Women who have had gestational diabetes also have a 20 to 50 percent chance of
developing type-2 diabetes within 5 to 10 years (2007).

From 2000 to 2010 the prevalence of type-2 diabetes is projected to increase by
46%, from 151 million to 221 million world-wide (Zimmet, Alberti et al. 2001).

The growing prevalence of type-2 diabetes over the last 20 years has led to terms
such as “diabesity” (obesity plus diabetes) and “metabolic syndrome”
(abdominal fat, insulin resistance, increased lipids, and hypertension).
Once again, we see a modern disease caused by modern living, in this case, a bad diet (Schlosser 2001; Critser 2003).

The prevalence of diabetes in Chinese ranges from 2% in China to 15% to
ethnic Chinese in Mauritius, showing how when ethnic Chinese move from their
native country to other cultures they have a corresponding increase in diabetes (Zimmet, Alberti et al. 2001)

Psatients who have diabetes and heart failure should not take glitazones or
metformin, as recommended by the FDA. In spite of this, 24% of patients with
diabetes and heart failure are prescribed these medications (Masoudi, Wang et al. 2003).

This was described as due to “the power of marketing over evidence based
medicine in guiding treatment practices.”(Yki-Jarvinen 2005).

Overall there is an 8 pound weight gain with glitazones (Scheen 2004).

Glitazones actually create fat cells, which may represent part of the way
they increase weight (Spiegelman 1998).

Glitazones also cause fluid build up, a side effect that is at least twice as
common when given with insulin, which has led the insulin-glitazone combination to be banned in Europe (Scheen 2004).

Ten million Americans spend $150 million a year for chromium supplements, making
it the best selling mineral supplement after calcium (Hellerstein 1998).

One uncontrolled study showed improvement on a test that is a marker of the stages
leading up to diabetes (called the glucose tolerance test) in three out of six
diabetics given 1000 micrograms of chromium, with no effect on non-diabetics (Glinsmann and Mertz 1966).

Another study compared placebo to trivalent chromium at 200 microgram per day for
six weeks followed by a cross over (placebo patients then took chromium). There was
no effect on the glucose tolerance test (Uusitupa, Kumpulainen et al. 1983).

Another study randomized 76 patients with atherosclerotic disease to 250 micrograms
of chromium chloride or placebo for 7-16 months. In the patients with diabetes, there
were no differences between the chromium treated patients and the placebo group (Abraham, Brooks et al. 1992).

One study randomly assigned 180 Chinese subjects with Type-2 diabetes to two doses of
chromium picolinate or placebo for four months. Glucose control was improved with the
higher dose of 1000 micrograms per day of chromium as well as on measures of blood glucose and insulin levels (Anderson, Cheng et al. 1997).

A three-week German study of 328 patients with type-2 diabetes and diabetic neuropathy
received either intravenous alpha lipoic acid (ALA) or a placebo. The study results found
a statically significant improvement in symptoms pain, tingling, and disability related
to neuropathy in those who got the ALA (Ziegler, Hanefeld et al. 1995).

The study also looked at 73 patients with type-2 diabetes and cardiac neuropathy who
had taken either oral ALA or placebo – there was an improvement in measures of cardiac
heart rate conductance in those who took ALA (Ziegler, Conrad et al. 1997).

In an attempt to replicate these promising results, another multi-center study of 509
patients with diabetic neuropathy received three weeks of intravenous ALA followed by
six months of oral ALA or placebo. This time there were no statistically significant
differences in ALA versus placebo in changes in the total symptoms (Ziegler, Hanefeld et al. 1999).

The same group also looked at 120 patients after three weeks of intravenous ALA or
placebo use, and they showed a statistically significant change in symptoms (Ametov, Barinov et al. 2003).

One important study looked at patients in an intermediate between health and diabetes
who had what is called impaired glucose tolerance, a condition that often progresses to
full diabetes. At-risk individuals who met with a nutritionist who helped them change
their diet and lifestyle (more exercise, less fat and saturated fat, more fiber) cut
their risk of developing diabetes by 58%, even though they only lost 8 pounds on average (Tuomilehto, Lindstrom et al. 2001).

Chapter 14. Dementia Drugs

Alzheimer’s Disease (AD) affects 4 million people in this country (Bachman, Wolf et al. 1993).

Before the age of 65 1 in 1000 people will develop Alzheimer’s. After 65, it affects 1 in 50, and after age 80 the risk is 1 on 5 (2007).

Nursing home care is necessary at some point, often at the 6-year mark. Risk factors for AD are family history, age, and Down’s syndrome (Sloane 1998).

The condition is caused by the development of plaques in the brain that are filled with
something called amyloid. These plaques are concentrated in parts of the brain involved
in learning and memory, including the hippocampus, frontal lobe, cingulate, temporal and
parietal cortex. On a chemical level, there is damage to the acetylcholine system, which
plays a role in memory, i.e., a loss of receptors for this chemical in the hippocampus and other areas (Blokland 1996).

Diagnosing Alzheimer’s in the early stages of the illness is often difficult (Callahan, Hendrie et al. 1995).

One of the factors weighing most heavily on families dealing with a loved one who
suffers from Alzheimer’s is its cost: $16,000 per year for the care of affected patients,
including the costs of nursing homes, doctors, and medications (2006).

Memory loss is one of the most, if not the most, devastating results of Alzheimer’s.
Scientists have been able to pinpoint one of the causes, a loss of acetylcholine function
or the neurotransmitter involved in learning and memory, and this has led the rush to
develop drugs that would counter its decline (Delagarza 2003).

For many years estrogen and progesterone were thought to prevent the development of
Alzheimer’s Disease, to be beneficial for the cognitive dysfunction of AD patients
(Baldereschi, Di Carlo et al. 1999; LeBlanc, Janowsky et al. 2001).

Hormones were thought for many years to improve memory function in normal people or
delay the normal decline of memory with aging (Jacobs, Tang et al. 1998).

In spite of the fact that antipsychotics should not be used to treat dementia in
the absence of a psychotic disorder, only one quarter of elderly patients on
antipsychotics actually have a psychotic disorder (Wang, Schneeweiss et al. 2005).

Atypical antipsychotic medications can interfere with glucose metabolism,
increasing the tendency to develop adult onset (Type 2) diabetes, and rarely
ketoacidosis (Nasrallah 2003; Nasrallah and Newcomer 2004; Newcomer 2004).

Increased diabetes has been seen with olanzepine (Hedenmalm, Hagg et al. 2002;
Koro, Fedder et al. 2002; Newcomer, Haupt et al. 2002; Sernyak, Leslie et al. 2002;
Gianfrancesco, White et al. 2003; Leslie and Rosenheck 2004) and clozepine
(Hedenmalm, Hagg et al. 2002; Koro, Fedder et al. 2002; Newcomer, Haupt et al. 2002;
Sernyak, Leslie et al. 2002; Leslie and Rosenheck 2004) with less risk with risperidone
(Koro, Fedder et al. 2002; Sernyak, Leslie et al. 2002; Lindenmayer, Czobor et al. 2003;
Leslie and Rosenheck 2004) and the typical antipsychotics (Koro, Fedder et al. 2002; Lindenmayer, Czobor et al. 2003).

There are conflicting results for quetiapine (Sernyak, Leslie et al. 2002;
Gianfrancesco, White et al. 2003; Leslie and Rosenheck 2004).

The risk of death when using typical antipsychotics was even higher than the risk
of death with atypical antipsychotics (Wang, Schneeweiss et al. 2005).

Risperidone and quetiapine were associated with a two-fold increase in stroke
in patients with dementia. Moreover, neither quetiapine and rivastigmine were effective
for treatment of agitation in elderly demented patients, and quetiapine was associated
with a more rapid cognitive decline over time compared to placebo (Ballard, Margallo-Lana et al. 2005).

An antidepressant drug in the monoamine oxidase inhibitor (MAOI) class that is often
used for AD patients is called selegiline (Eldepryl). Overall, studies have not shown
this medication to be effective for mood or cognitive problems in AD (Delagarza 2003).

Amitriptyline and doxepin are designated as not to be prescribed to the elderly.
In spite of this these two medications make up the most commonly inappropriately
prescribed medications for the elderly, making up 23% of all such medications
(21% of medications prescribed for the elderly are felt to be inappropriate) (Paton and Ferrier 2005).

Neither folate nor Vitamin B supplementation resulted in an improvement in scores
of cognition after two years (McMahon, Green et al. 2006).

Ginkgo is felt to be a neuroprotective agent and antioxidant (Sierpina, Wollschlaeger et al. 2003).

Studies have shown some benefit with gingko in patients with dementia, although the
effects on cognitive tests were not greater than the modest effects of anticholinesterase
inhibitors, and were not associated with subjective impression of improvement by
families and doctors (LeBars, Katz et al. 1997; Oken, Storzbach et al. 1998).

Chapter 15. Antidepressants

“I was never trained to view a human body like a physician does,” she said.
“I personally found sitting in on an exam embarrassing ”(Mulligan 2003).

The pharmaceutical industry has wiggled its way into psychiatrists’ offices in more ways than one. Steve Sharfstein MD,
(Sharfstein 2005) the President of the American Psychiatric Association, now bemoans
the fact that the “bio-psycho-social” model had given way to the “bio-bio-bio” model,
where there is a total focus on medication, to the exclusion of other treatments, like
various forms of talking therapy, exercise, which works for depression, as I describe
later, or working with families (Kravitz, Epstein et al. 2005).

Interestingly, by making consumers more likely to talk to their doctors about going
on a medication, when patients ask for an antidepressant they get it 76% of the time
compared to patients with the same symptoms who don’t ask to go on antidepressants.
They are given antidepressant prescriptions only 31% of the time (Curtis, Ostbye et al. 2004).

Twenty one percent of medications given to the elderly are felt to be inappropriate,
and one out of every four of these inappropriate medications is amitriptyline or doxepin (Paton and Ferrier 2005).

The SSRI medications have not been shown to work better than the older tricyclics (Healy 2004).

In fact, they actually have less efficacy than is commonly believed (DUAG 1990).

The Danish Study Group found that the older tricyclic medication clomipramine
worked better for severe depression than paroxetine, although it had more side effects (Greenburg, Bornstein et al. 1994).

A more recent meta analysis from data submitted to the FDA also showed that 80%
of the improvement with antidepressants come from the placebo response (Thase 2002).

When the data of all studies performed on venlafaxine (Effexor), fluoxetine (Prozac),
and nefazodone (Serzone), was lumped together, there was only about a 2-point
improvement on a 62 item scale (the 21 item Hamilton Depression Scale) above
and beyond the placebo response. The response to this was that the effects of
antidepressants are modest, even if real, and that it is not ethical to give placebo (Brugha, Bebbington et al. 1992; Ronalds, Creed et al. 1997).

Some have questioned whether a 2 point increase on a 62 item scale that may not
be sustainable is a clinically meaningful improvement (Geddes and Cipriani 2004).

Worry about the efficacy of SSRIs prompted a re-examination of the efficacy of
antidepressants in general, and a look at how placebos may work just as well (Walsh, Seidman et al. 2002).

A meta-analysis showed that there was a highly variable response to placebos, up
to 50%, and that the placebo response rate in studies of depression seemed to be growing over the years (Linde, Berner et al. 2005).

SSRI treatment is also associated with about a three-fold increase in risk of
gastrointestinal bleeding. Although for the average patient there typically is
not an increased risk of bleeding, if you are taking aspirin or an NSAID you
should be on another medication for protection of your stomach, like prilosec (Chambers, Johnson et al. 1996).

The risk of suicidal thinking and suicide appears to be much higher for conditions
other than isolated major depression,(Thase 1998) so it is important to not use these medications lightly.

One study looked at 228 pregnant women who had been exposed to fluoxetine and compared
them to matched controls. There was no difference in pregnancy loss or major
birth anomalies. There was an increase in minor birth anomalies in the fluoxetine
treated women (16% v 7%). However, exposure to fluoxetine in the 3rd trimester was
associated with a 9-fold increase in jitteriness (tremors, irritability, agitation,
and respiratory distress), as well as increase in premature delivery (Chambers, Hernandez-Diaz et al. 2006).

Another study looked at 377 mothers who had a baby with primary pulmonary hypertension
(PPH) compared to women with non-PPH babies. Women with PPH babies had a six- fold
increase in use of SSRI antidepressants after the 20th week of pregnancy compared
to controls. SSRIs (which included paroxetine, fluoxetine, sertraline and citalopram)
most associated were paroxetine and sertraline (fluoxetine did not show an effect) (Cohen, Altshuler et al. 2006).

One study looked at data from a number of randomized, placebo controlled trials of
Effexor, tricyclic antidepressants and SSRIs for the treatment of depression
(Thase, Entsuah et al. 2001). Overall, venlafaxine had a success rate of 74%
that was statistically significantly better than SSRIs, which only had a 61% success
rate, and tricyclics, which only had a 58% success rate. The difference in the efficacy
of tricyclics and SSRIs was not statistically significant.

Other studies have shown better responses for venlafaxine (Lieberman, Greenhouse et al. 2005)
and duloxetine (Williams and Holsinger 2005) than tricyclics and SSRIs.

Venlafaxine has been associated with a dose dependent increase in blood pressure (Einarson, Arikian et al. 1999).

St. John’s wort has been shown to be better than placebo in some earlier controlled
studies and equally effective as tricyclic antidepressants in the treatment of depression (Linde, Ramirez et al. 1996).

A meta-analysis of St. John’s wort for both major and minor depression was consistent
with greater efficacy, about a 60% increase over placebo (Bressa 1994).

S-Adenosylmethionine (SAMe) is a molecule found in all human cells that is also promoted
as a supplement for the treatment of depression. A meta-analysis from Italy that pooled data
from several small studies concluded that SAMe was better then placebo and equivalent
to tricyclic antidepressants in efficacy with fewer side effects (Morelli and Zoorob 2000).
However there was considerable variability in the studies conducted.

Kava (or Kava-kava) is an extract of the roots of the Polynesian plant Piper
methysticum used in the South Pacific for its sedative, aphrodisiac, and stimulatory effects (Wheatley 2001).

Several controlled trials have shown that Kava reduces anxiety in patients with
anxiety disorders (Witte, Loew et al. 2005).

There is one study I know of that has looked at the effects of omega-3 fatty acids
on symptoms of bipolar disorder (Stoll, Severus et al. 1999).

A number of studies, dating from the mid 1990s to more recently, show that cardio
vascular and resistance or weight training combat mild to severe depression (Martinsen 1987).

It turns out that exercise results in a surge of serotonin, the neurotransmitter
which make us feel good right after working out, as well as a long-term mood shift
once you’ve started exercising regularly. These effects may be related in part to an
increased growth in brain cells (Karacabey, Saygin et al. 2005).

Regular exercise has favorable effects on the immune system as well (Schnohr, Kristensen et al. 2005).

A study of 12,028 randomly selected individuals age 20-79 showed that increasing
physical activity was associated with a 70% reduction in self-reported stress as
well as decreased life dissatisfaction. Even 2-4 hours of walking per week was
associated with significant gains (Atlantis, Chow et al. 2004).

Another study of a group of employees showed reductions in stress levels and depression,
and improvements in feelings of health and vitality, after a 24 week program of aerobic
exercise compared to a control group (Greist, Klein et al. 1979; Martinsen 1987; Singh and Singh 2000).

A 1985 study looked at 43 patients with depression; about half were treated for the
condition with antidepressants. Patients were randomized to receive 9 weeks of
exercise training (aerobic for one hour, three times a week at 50-70% maximum
aerobic capacity) or occupational therapy. Exercise was associated with statistically
significantly greater decreases in depression as measured by the Beck Depression Inventory
(a measure of symptoms of depression) (Martinsen, Medhus et al. 1985).

In another study 86 patients with depression who were treated with antidepressants
but did not have a therapeutic response were randomized to exercise or health education
classes. Exercise involved weight bearing exercise for 45 minutes twice a week for ten weeks.
More patients treated with exercise had an improvement as measured by a 30% improvement on a
scale for the measurement of depression called the Hamilton Depression Scale (55% got better
with exercise versus 33% without, a difference that was statistically significant) (Mather, Rodriguez et al. 2002).

In another study 83 patients with major depression underwent aerobic exercise training
versus not changing what they were doing before. Exercise training was associated with
better symptom improvement in terms of anxiety and general symptoms but not depression (Veale, Le Fevre et al. 1992).

Researchers at Freie University in Berlin also found that thirty minutes of exercise
a day significantly improved the moods of patients who had been suffering from depression
for nine months. In a report published in the British Journal of Sports Medicine,
12 patients with depression underwent 10 weeks of training on a treadmill at
30 minutes a day. There was a statistically significant 6-point drop in depressive
symptoms as measured with the Hamilton Depression Sale (Dimeo, Bauer et al. 2001).

A recent report in 2005, explained the results of a 3-year long study in 80 patients
designed to test whether exercise is an efficacious treatment for mild to moderate
major depressive disorder and what amount would be needed to see a positive difference
in depressed people. The report, published in The Journal of Preventive Medicine
(January 2005) found that a half-hour a day of exercise six days a week is the
ideal “dosage” to improve the mood of people who have mild to severe depression (Dunn, Madhukar et al. 2005)

One study added exercise to antidepressant treatment in 17 patients who did not
have a complete response to antidepressant medication (Trivedi, Greer et al. 2006).

Studies have shown that high fat foods lead to changes in mood (Lacasse and Leo 2005).

Experimental studies have shown that intake of fats leads to feelings of sleepiness that
are not related to the food alone (Wells, Read et al. 1997; Wells, Read et al. 1998).

Diets deficient in folate and Vitamins B6 and B12 are also associated with depression (Reynolds, Carney et al. 1984).

Chapter 16. Insomnia Treatments

Recent studies have shown that insomnia has an important effect on promoting a
variety of poor physical health outcomes including a link between being overweight and lack of sleep (Taheri 2006).

Though many of these medications do in fact help people sleep more, people who
take sleeping pills say that they feel more satisfied about the extra sleep they
get, but the gains they get from extra sleep on their ability to think and function
the next day is offset by the long lasting side effects of the drugs such as impairments
in memory and cognition (Holbrook, Crowther et al. 2000).

Serax has the least effects on memory and as a result is recommended as the best
benzodiazepine to use for a sleeping pill, although to be used for less than four
weeks (all medications for insomnia are not recommended for long term use) (Wolfe, Sasich et al. 2005).

On average, benzodiazepines increase the user’s sleep time by about one hour more
sleep per night (Holbrook, Crowther et al. 2000).

Use of benzodiazepine medications is associated with a 60% increase in road traffic
accidents. This increased safety risk is not seen with other psychotropics, including
antidepressants. Risk was increased with concurrent alcohol usage and age. An increased
risk was also seen with zopiclone, one of the newer generation insomnia mediations (see below) (Barbone, McMahon et al. 1998).

Some argue that the new Z drugs have less potential for abuse than the benzodiazepines (Hajak, Muller et al. 2003).

However, systematic studies have not shown them to be more effective or safe than the
benzodiazepines, although they cost several times more (Holbrook 2004).

For instance, pooling of data from three trials with a total of 96 patients showed no
difference between benzodiazepines and zopiclone for time to fall asleep, although
benzodiazepine treated patients slept 23 minutes longer There were no differences
between benzodiazepines and zopiclone in major side effects (adverse events) (Holbrook, Crowther et al. 2000).

And no difference between the different Z drugs for safety or efficacy has been established (Holbrook 2004).

A recent review by the UK National Institute for Clinical Evidence (NICE) showed
no difference between the different Z drugs (Sonate, Lunesta, Ambien, or Imovane)
in efficacy, next day impairment, or risk of withdrawal or dependence (NICE 2004).

Ambien increases slow wave sleep, which has been associated with sleepwalking,
Cases of people getting up, walking around the house, cooking, and even driving,
have been reported. There are cases of people who got out of bed after taking
ambien (sometimes with a glass of wine), driving, and getting into car accidents,
with absolutely no memory of what happened. Some people got up in the middle of
the night and crashed their cars into parked cars, and then tried to drive away,
later having no memory of what happened (Saul 2006).

One recent incident that made headlines involved a man on a trans-Atlantic flight who took
Ambien with two glasses of wine. In his sleep, he tore off his clothes and threatened to
kill himself and others. As a result, the plane had to make an emergency landing. He had no memory of the incident (Saul 2006).

Tricyclics make up 23% of all prescribed medications for the elderly (Curtis, Ostbye et al. 2004).

Amitriptyline is the most common inappropriately prescribed psychotropic medicine for the elderly (Mort and Aparasu 2000).

Some plants are known to have psychoactive properties, like poppy seed and Indian hemp.
These include almonds, chamomile, catmint, fennel, hops, lettuce, lime, marjolaine,
mullein, oats, orange flower, passion flower, may blossom, rosemary, and willow (Leathwood, Chauffard et al. 1982).

Valerian is an extract of the Valerian root (Valeriana officinalis) and is widely
prescribed in Europe for the treatment of insomnia (Hadley and Petry 2003).

Valerian is available as a supplement in the US. In an early study, 166 volunteers
were given Valerian, a Valerian containing commercial product, or placebo. After
three doses, Valerian was associated with a significant decrease in the time it
takes to fall asleep and improvement in sleep quality. Sleep was better in the
pure Valerian extract than in the proprietary product Hova®, which contains Valerian extract (Leathwood, Chauffard et al. 1982).

An uncontrolled study of 54 subjects showed a reduction in heart rate, blood pressure,
and subjective distress to a stressful task after receiving Valerian (Cropley, Cave et al. 2002).

Another study of 16 patients with sleep disorders randomly assigned patients to
two doses of Valerian or a placebo nightly and measured EEG measures of sleep
as well as subjective reporting of sleep quality while patients were sleeping
in a sleep laboratory. Side effects include vivid dreams in as many as 16% of
cases,(Wheatley 2001) and less commonly drowsiness, depression, dizziness, headaches or blurred vision.

When the patients were given a single dose of Valerian, the lower does had no
effects on subjective or EEG measures of sleep (Diaper and Hindmarch 2004).

Kava (or Kava-kava) is an extract of the roots of the Polynesian plant Piper
methysticum used in the South Pacific for its sedative, aphrodisiac, and stimulatory effects (Wheatley 2001).

Active compounds include the kava pyrones, which may have effects on the brain.
Several controlled trials have shown that Kava reduces anxiety in patients with anxiety disorders (Witte, Loew et al. 2005).

One study looked at 24 subjects with stress induced insomnia treated for six
weeks with 120 mg of kava daily followed by two weeks off treatment and then
Valerian for another six weeks. Both Kava and Valerian improved sleep
(decreased onset, longer sleep time) and reduced stress severity. Side
effects of Kava include dizziness (12%), dry mouth, gastric disturbance,
diarrhea, dizziness, drowsiness, depression (Wheatley 2001) and more rarely
liver failure, which has caused it to be banned in some countries.

Chapter 17. Drugs for Sexual Dysfunction

Pfizer spokeswoman Janice Lipsky told Times reporter Gardiner Harris that
Levitra had benefited from, “false claims and public relations in which they
inaccurately state that Levitra works faster and is better, neither of which is true.”(Harris 2003).

Viagra works because it inhibits the cyclic guanosine monophosphate (cGMP)
phosphodiesterase type 5 (PDE5) enzyme, which results in an increase in blood
flow in the corpus callosum of the penis, resulting in erection (Viera, Clenney et al. 1999).

Viagra has been shown to be highly effective for ED. Men complaining of ED
had a four fold improvement in their ability to achieve and maintain an erection,
which was significantly better than placebo (Goldstein, Lue et al. 1998)

Viagra should not be taken more than once a day and should not be used with
other drugs for ED (Viera, Clenney et al. 1999).

Studies have shown that obese men with ED who underwent a diet and exercise program
lost 14 pounds and had an improvement of 14 to 19 on the International Index of
Erectile Function. These gains were statistically significant, although not of the same magnitude of Viagra (Esposito, Giugiliano et al. 2004).

Chapter 18. Vitamins and Supplements

If you followed the advice of one company (Life Extension), as many do, you would spend a
minimum of $7,248 per year on vitamins.
*$7,248 spent per year on vitamins from Life Extension, include Cognitex ($74),
Life Extension Mix ($104), Super Booster Softgels ($42), Super –Absorbable CoQ10 ($164),
Mitochondrial Energy Optimizer with SODzyme ($82), Bone Restore ($21), Super EPA/DHA with
Sesame Lignans and Olive Fruit Extract ($32), Enhanced Natural Prostate Formula ($38),
Keto DHEA ($40), Super Mira Forte ($56), S-Adenosyl-methionine (SAMe) ($35), Healthprin ($15).
source: website of Life Extension.

Most patients who use alternative medicines never tell their doctors (Elder, Gillcrist et al. 1997; Del Mundo, Shepherd et al. 2002).

In fact, the people in the scientific community are now calling on researchers to
stop spending money on vitamin supplement trials because we know these products are
either useless or harmful in terms of health (Morris and Carson 2003).

The most important fact to remember about the beneficial effects of vitamins: they are
related to the nutritional content of the foods they are found in (Lichtenstein and Russell 2005).

The Danes were puzzled by the fact that they had an increase in osteoporosis in their
women. They analyzed a number of factors, and found that excessive intake of vitamins,
whether through fortified foods or other sources, was associated with an increased risk
for osteoporosis in their county. They found a link with excessive intake of vitamins
through American fortified foods, such as breakfast cereals (Melhus, Michaelsson et al. 1998).

A spokesperson for Denmark said that “the Danish population already has a high intake
of calcium, iron, B6 and folic acid…the knowledge on toxicity of vitamins and minerals
is very limited and practically nonexistent for children…[vitamin deficiencies exist]
only in small groups like immigrants who aren’t getting enough vitamin D or pregnant
women who need folic acid. We need to take care of all of the groups in our population.”(2004).

The RDA determined how many vitamins and minerals we need to take in daily in our diets (Silverman, Romano et al. 1999).

Vitamin E has been shown in animal studies to reduce free radicals that cause oxidative
stress are associated in animal models with atherosclerosis (Prasad and Kalra 1993).

The Life Extension Foundation (affiliated with the vitamin and supplement manufacturer
Life Extension), reported that the number of vitamins in fruits and vegetables farmed
in the US has been declining over the past 50 years. They stated that “for those who
find the new, unregulated world of genetically manipulated vitamin less vegetables
unpalatable—or find that they don’t want to eat vegetables that have absorbed…
pesticides in the soil…high quality standardized supplements are one way of incorporating
a standard amount of known nutrients in the diet…” (Mitchell 2005).

There never really was good evidence that vitamin pills provided helpful anti-oxidants in the first place (Greenberg and Sporn 1996).

Another study showed that for every 1 mg increase in retinol (a form of Vitamin A).
There was a 68% increase in risk of hip fracture (Melhus, Michaelsson et al. 1998).

In fact, a national epidemic of osteoporosis in Swedish women was traced to a supplementation
of Vitamin A in food in that country (Melhus, Michaelsson et al. 1998).

Denmark has recently banned Kellogg’s fortified cereals because of concerns about the effects
of excess amounts of vitamins and minerals in the cereal, including Vitamin A (2004).

Mega doses of Vitamin A can also cause dry skin, swelling of the brain, psychosis, depression,
headache, ulceration of the colon, and a range of other toxic effects
(Gerber, Raab et al. 1954; Marie and See 1954; Oliver and Havener 1958; Bass 1959;
Restak 1972; Pasquariello, Schut et al. 1977; Bendich and Langseth 1989; McCance-Katz and Price 1992; Cocco, Diaz et al. 2002).

This has been known since explorers of the North Pole in the 19th Century became
psychotic after eating polar bear liver, which has high concentrations of Vitamin A (Rodahl and Moore 1943; Selhorst, Waybright et al. 1984).

One study showed that taking high doses of Vitamin A during pregnancy was associated
with an increase in birth defects, primarily deformations of nervous tissue and the heart (Rothman, Moore et al. 1995).

The average woman already gets 120% of required Vitamin A from diet alone, so there is no need for supplementation (Hunt 1996).

Chapter 19. Medications in Children

Prescriptions for Ritalin, the popular drug for Attention Deficit Hyperactivity Disorder
(ADHD), rose three-fold from in a four year period from 1991 to 1995 (Zito, Safer et al. 2000).

Ritalin can interact with a number of antidepressant and antihypertensive medications by
decreasing elimination of these drugs and therefore increasing their concentrations in the
blood and causing toxic side effects (Bralow 2003; Rybacki 2004).

All of the amphetamine like stimulants, including Ritalin and Adderall, have been linked to
approximately a doubling of heart related deaths in children (Nissen 2006).

The Medicines and Healthcare products Regulatory Agency (MHRA) of the United Kingdom (UK),
after reviewing the evidence, quickly decided that all SSRIs, with the exception of fluoxetine,
did not have efficacy for the treatment of childhood depression, and were associated with a doubling of suicidal thoughts (2004).

None of these medications were associated with a clinically meaningful improvement in
depression for children, which led to the conclusion that their risks outweighed their benefits (Newman 2004).

Only Prozac was shown to have efficacy without the risk of increased suicidal ideation.
A recent meta-analysis showed overall a 59% increase in suicidal thoughts in children prescribed SSRIs compared to tricyclic (Martinez, Rietbrock et al. 2005).

In the US, doctor visits for antipsychotic treatment increased from 201,000 in 1993 to 1,224,000 in 2002 (Olfson, Blanco et al. 2006).

A study of children in Tennessee’s Managed Care program for Medicare showed that the
number of prescriptions for antipsychotics doubled in a five-year period ending in 2001 (Cooper, Hickson et al. 2004).

Chapter 20

The increase in obesity is predicted to lead to a blunting or decline in life expectancy
in the 21st century (Olshansky, Passaro et al. 2005).

The American Medical Association, and other medical organizations worldwide, including the
Canadian Medical Association, recommended against getting annual physical and blood work unless you have a disease (Prochazka, Lundahl et al. 2005).

This is based on scientific evidence that screening normal people with annual laboratory
tests and physical exams does not add to health care outcomes (Canadian Task Force on the Periodic Health Examination 1979).

PAP screens for cervical cancer in women can be done every three years if they have had
two consecutive negative tests; after the age of 35 they can be done every five years (Canadian Task Force on the Periodic Health Examination 1979).

Women age 50-59 are recommended to have annual breast exam and mammography (Canadian Task Force on the Periodic Health Examination 1979).

Negative publicity about drug safety and the FDA led to an Institute of Medicine Report
in 2006, with a number of recommendations for the future, including increased monitoring of
drugs after approval, increased regulatory powers for the FDA, and increased transparency for studies performed by drug companies (Psaty and Burke 2006).





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