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Health news:
 
June 2010 - Dec 2013

Minimizing breast cancer risk

May 2010

Time to move beyond salt ?

Salt hypothesis vs. reality

Is sodium bad?

April 2010

Salt studies: the latest score

From Dahl to INTERSALT

Salt hypothesis' story

March 2010

Salt war

Do bone drugs work?

Diabetes vs. drugs, 3:0?

February 2010

The MMR vaccine war: Wakefield vs. ?

Wakefield proceedings: an exception?

Who's afraid of a littl' 1998 study?
 

January 2010

Antibiotic children

Physical activity benefits late-life health

Healthier life for New Year's resolution

 

December 2009

Autism epidemic worsening: CDC report

Rosuvastatin indication broadened

High-protein diet effects

 

November 2009

Folic acid cancer risk

Folic acid studies: message in a bottle?

Sweet, short life on a sugary diet

 

October 2009

Smoking health hazards: no dose-response

C. difficile warning

Asthma risk and waist size in women

 

September 2009

Antioxidants' melanoma risk: 4-fold or none?

Murky waters of vitamin D status

Is vitamin D deficiency hurting you?

 

August 2009

Pill-crushing children

New gut test for children and adults

Unhealthy habits - whistling past the graveyard?

 

July 2009

Asthma solution - between two opposites that don't attract

Light wave therapy - how does it actually work?

Hodgkin's lymphoma in children: better alternatives

 

June 2009

Hodgkin's, kids, and the abuse of power

Efficacy and safety of the conventional treatment for Hodgkin's:
behind the hype

Long-term mortality and morbidity after conventional treatments for pediatric Hodgkin's

 

May 2009

Late health effects of the toxicity of the conventional treatment for Hodgkin's

Daniel's true 5-year chances with the conventional treatment for Hodgkin's

Daniel Hauser Hodgkin's case: child protection or medical oppression?

April 2009

Protection from EMF: you're on your own

EMF pollution battle: same old...

EMF health threat and the politics of status quo
 

March 2009

Electromagnetic danger? No such thing, in our view...

EMF safety standards: are they safe?

Power-frequency field exposure
 

February 2009

Electricity and health

Electromagnetic spectrum: health connection

Is power pollution making you sick?

January 2009

Pneumococcal vaccine for adults useless?

DHA in brain development study - why not boys?

HRT shrinks brains

NEWS ARCHIVE
2009
2008
2007

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August 2007

Statins side effects

Statins - Benefits - }Side effects - Real problem - Alternatives

The benefit of statin-reduced cholesterol production - less of arterial build-up and insomuch lower risk of cardiovascular complications - is accompanied by some major drawbacks. One is that the main cause of all evil, inflammation-causing free radicals, toxin and pathogen inflicted damage to your blood vessels (and other tissues), is left out.

In other words, your more immediate risk - cardiovascular problem - may be lessened, but you are being left on a longer-term downhill, with the damage to your blood vessel lining and cell membranes worsening. That causes accelerated aging and increases your risk of developing other degenerative diseases. While statins do exert certain anti-inflammatory action, they are certainly not a substitute for healthy diet and lifestyle.

Secondly, by interfering with liver function, statins can destabilize and damage this vital organ. Even if there is no clear signs of liver dysfunction or damage, long-term effects are unpredictable.

Thirdly, by a forced, arbitraty reduction of body's cholesterol production, statins may disrupt its cholesterol supply for other vital needs, such as cellular membrane consistency, synthesis of vitamin D, or production of adrenal and steroid hormones. This, combined with the above two negative effects, is likely causing most of statins' standard adverse effects.

Furthermore, the liver enzyme blocked by statins is also needed for synthesis of coenzyme Q10, a very important nutrient for energy production at the cellular level. Among other functions, it is, ironically, needed for heart health.

According to published incidence frequency (%) for the most common pravastatin side effects (it is dosage related, so these numbers will vary with deviations from the usual, average dose) are as follows:

 • 2%-7% incidence, each: nausea and vomiting, common cold, headache, diarrhea, skin rash, constipation, fatigue, gas, indigestion or heartburn, muscle pain (myalgia) and flu

• 1%-2% incidence, each: pain (including stomach, joint and chest), dizziness, liver dysfunction, peripheral neuropathy, muscle cramps and vision problems 

• below 1% each: allergic reactions, depression, irritability, insomnia, muscle tissue breakdown (rhabdomyolysis) , memory loss, and impotence

Other possible statins' adverse health effects include swelling, shortness of breath, disturbances in body temperature regulation, weight change, hunger, breast enlargement, blood sugar changes, dry skin, blood pressure changes, nausea, bleeding, and ringing in ears or other noises.

Statin drugs cause nerve damage (polyneuropathy, nerve malfunction in the legs and, sometimes, arms) in one in every 2200 patients (CNN, August 2002). For people over 50 that were on the drug for over two years, the chances of nerve damage were 26 times higher than for the general population. The brain is not spared either: another study (Muldoon) found out that after only 6 months on statin therapy,

100% of the participants had measurable decline in cognition.

List of all possible statins' side effects is much longer. For instance, reference for atorvastatin (Lipitor) given to physicians -

                    http://www.lipitor.com/content/LipitorPI.pdf

(p23-24) lists well over a hundred of them.

Statins don't seem to be "very, very safe" anymore, do they? One of the most dreaded possible side effects, breakdown of the muscle tissue (rhabdomyolysis), which can result in life-long disability, or even death from renal failure, has come to focus due to the events surrounding withdrawal from the market of cerivastatin (Baycol) in 2001. The post-marketing analysis confirmed 52 deaths from rhabdomyolysis it caused, and 385 non-fatal cases.

Studies - Graham D.J. et al., Andrejak et al. - have found that the incidence of rhabdomyolysis with cerivastatin was 6-12 times higher than with other statins which, according to the cerivastatin figures can be approximated at 1 in 20,000 in a year period.

However, the Graham study has found that the risk increases significantly when statins are combined with another popular lipid-lowering agent, fibrates (approx. 1 in 3500 incidence when used alone), to approx. 1 in 1600. It gets even worse for older patients with diabetes, where the odds of suffering rhabdomyolysis are about 1 in 500, on the combined statin/fibrate therapy. Other factors that can significantly increase your risk from statin/fibrate therapy induced rhabdomyolysis include old age, female gender, renal or liver disease, hypothyroidism, debilitated status, surgery, trauma, excessive alcohol intake, and heavy exercise (Shek, Ferrill).

When projected to 5-year period, in order to make it comparable to the figures given earlier (NNT table), it comes to the approximate average incidence rate of 0.025% for statins alone, 0.14% for fibrates alone, 0.3% for statin/fibrate combination, and 1% for older patients with diabetes on the combined statin/fibrate therapy.

Since the incidence w/o therapy is statistically zero, this translates into the NNT (rounded off) of 4000, 700, 300 and 100, respectively.

While the risk with statin-alone therapy is statistically negligible (at ~20 million U.S. users, it still comes to

about 1,000 rhabdomyolysis cases a year),

and very low with fibrate-alone therapy, it becomes significant with the combined statin/fibrate therapy, especially if you have one or more of the extra risk factors listed above. Thus, for the primary cardiovascular prevention, other alternatives are very advisable. Keep in mind that the risk of other serious side effects, listed above, adds up to a significantly greater overall risk.

And we can add to that list the long-lingering suspicion that statins can make it easier for cancer cells to proliferate.

It is no secret that both, statins and fibrates cause cancer in rodents. It has been disclosed in their product information since early 1990's. For lovastatin, the cancer causing concentration in rodents is three to four times that in humans (for the  maximum recommended dose), while for gemfibrozil (fibrate-type cholesterol lowering medication sold as Lopid) it is 1.3 the human dose. If you wonder

how a drug with rodent carcinogenicity at concentrations so close
to those in human patients could have been approved for
long-term preventive use,

the answer is that the FDA decision-makers simply ignored its Metabolic Drug Advisory Committee's recommendation not to.

Rodent carcinogenicity doesn't necessarily translate into human carcinogenicity, but certainly commands caution. More so considering that these drugs are intended for long-term use, and that their primary purpose - lowering body's cholesterol production - can itself have cancer promoting effect.

No one disputes that cellular membranes need sufficient supply of cholesterol for proper functioning. A recent study (Anderson et al.) has thrown more light on how cholesterol deficiency within cellular membranes negatively affect signaling pathways within the cell, increasing the chances for abnormal cellular division, that is, cancer.

More specifically, cholesterol is needed to hold together a group of enzymes deactivating extra cellular signal-related kinase (ERK). Kinases, or regulatory proteins (enzymes), are the key controllers of cellular activity. If cholesterol is in short supply, the ERK becomes overactive, and overactive ERK is being

linked to multiple forms of cancer.

Another recent study (Karas et al.), on over 41,000 patients, was set to explore ways to minimize statins' negative effect on liver and muscle tissue, but unexpectedly stumbled over the numbers indicating that folks with low "bad" (LDL) cholesterol had

one extra cancer on every 1,000 patients,

compared with a group with high "bed" cholesterol levels. The study is not conclusive, since it doesn't establish whether these extra cancers are produced by too little of "bad" cholesterol (very unlikely, but can't be entirely ruled out), or by statins directly. However, it is just the latest addition in the long-term pattern of indications of the statins-cancer connection.

The official response is, as expected, that benefits of statin are still greater, and justify its use. The same old phrase that seems to be assuming that statins are equally beneficial for all,

and that there is no other viable alternative available.

Let's take a closer look at these two assumptions.

According to the major studies - funded by manufacturers and, for that reason, likely to be biased to some extent - statins offer relatively significant benefits

only in secondary prevention treatments.

That is, for those with existing cardiovascular disease. At present, they count only for about 1/4 of all statin users.

For the rest of them, those without existing cardiovascular disease, the benefits are either marginal or non-existing. They limit to somewhat reduced incidence of major cardiovascular events - about a single event for every 50 patients in a 5-year treatment on the average - but with no reduction in mortality. Moreover, as it is known for a long time, and confirmed again in the recent (2005) study by Abramson and Wright,

for woman and those older than 69 years of age,
statins didn't even do that much (or little).

Oddly enough, Abramson and Wright analyzed those very studies that the government cited as the basis for including woman and those over 65 years old among the official beneficiaries of statin therapy, in its major 2001 revision of the U.S. guidelines. Expanding the category of those who officially benefit from statins to those at moderately high risk of developing cardiovascular disease, the government increased the number of Americans to whom statins are recommended from 13 to 36 million.

No objections from the statin manufacturers were noted.

The question is, how much the potential benefits from statin therapy measure up against their potential dangers for those at low-to-moderate risk of developing cardiovascular disease. In other words, for 3 out of 4 statin users. The answer is: not favorably. The benefits range from none to low, while the possible side effects are many, some of them very serious. So let's turn to what statin manufacturers pretend doesn't exist: viable alternatives to statins for lowering the risk of cardiovascular disease.

Interestingly, the National Guideline Clearinghouse (NGC, a government agency), lists as the primary therapy for elevated LDL ("bad") cholesterol the following:

• weight loss,
• physical activity,
• TLC (therapeutic lifestyle change) and
• quitting smoking.

Only as secondary therapy, for those with existing cardiovascular disease, it lists statins, fibrates, niacin, bile acid sequestrant and Ezetimibe (medication inhibiting absorption of dietary cholesterol).

This is in contrast to the prevailing current practice, where statins are widely prescribed to those without existing cardiovascular disease.

Indirectly, and probably unintentionally, the NGC primary therapy recommendations flirt a little with the nutritional factor, by advocating weight loss and quitting smoking. Weight loss usually includes dietary changes. Nicotine, among others, depletes body's reserves of C vitamin (which are in most people insufficient to begin with), one of the nutrients crucial for cardiovascular health.

Otherwise, the NGC primary therapy recommendations are fairly confused, because all its primary therapy recommendations can fit under a single category, the therapeutic lifestyle change. On the other hand, it doesn't even mention directly nutritional aspect, the single most powerful therapy for the potential problems caused by elevated cholesterol levels.

CONTINUES: Hypertension - the real problem
 

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