To The End!
Fighting for what science shows can harm your reputation, make you lose your job, and… who know how far they will go! This the story of Maryanne Demasi, Ph.D., an investigative science journalists:
“I became the subject of attacks by those with vested interests. Secret documents revealed food industry giants initiated ‘active defence’ against me (and others) for challenging their marketing messages.
It manifested in social media attacks, industry-sponsored propaganda by so-called ‘experts’ paid to undermine my credibility, critics’ calls for my sacking, and vexatious complaints about my scientific integrity.
Eventually, our entire team was axed from the ABC. The TV executives who promised to support us, the same people who approved and applauded our programs, were now the ones walking us all out the door.”
As always, things must be understood in context. The context here is revealing that statins don’t save lives. As we all know, many doctors are just too happy to prescribe statins. The pressure is on them by the pharmaceuticals as well as their pockets. Check if your doctor’s name is listed here, and if so, check how much money, lunches, dinners, “research funds” (clinical doctors don’t do research), etc., they have earned for the past 3 years. This database works for US doctors only–and be careful how you enter the name of your doctor. Enter only last name and state!!! Doctors have funny ways for evading discovery…!!
The Truth About Statins
If you only read one paper about statins, this is the one you should read in the BMJ (British Medical Journal). This academic paper reviewed all published statins clinical trials. Only 11 statin clinical trials included mortality information, so they only used those 11. Note: doctors are making “life-saving” or “life-destroying” decisions based on 11 small-scale clinical trials, and the world is go-gaga over statins, but do they have a reason to celebrate? This research paper presents an unbiased and professional research, comparing all findings available.
The goal of the research:
The researchers wanted to see the magnitude of the statistical significance in terms of long-term outcome to see if statins saved lives, and if so, by how much.
The findings:
“Death was postponed between −5 and 19 days in primary prevention trials and between −10 and 27 days in secondary prevention trials. The median postponement of death for primary and secondary prevention trials were 3.2 and 4.1 days, respectively.”
When you see a negative number, as in -10, that actually means the those people died 10 days sooner than those not on statins. The average lifetime increase (after several years of statins use) is 3-4 days. not much to celebrate there after years of side effects!
What Is At Stake?
Millions and billions of dollars to the pharmaceutical companies and thousands (in some cases hundreds of thousands) of dollars in the pockets of statins prescribing doctors are at stake. At least, that how statin-supporter-doctors and big pharma see it, and why Dr. Demasi was fired. However, the real loser is YOU dear reader. Why? Because you pay however amount as your copay, you lose muscles, fracture bones, end up with cancer, lose your memory, get dementia and Alzheimer’s, Parkinson’s and a host of other diseases., lose your libido, end up with Viagra or similar to have sex, and in some cases, even destroy your heart–the very thing you want to save–by taking statins.
Most Common Adverse Effects
The most common adverse effects are headache, difficulty sleeping, flushing of the skin, tenderness, or weakness (myalgia), drowsiness, dizziness, nausea or vomiting, abdominal cramping or pain, bloating and gas, diarrhea, constipation, rash, muscle pain and damage, increased risk of diabetes mellitus, and liver damage. In a study over 5 years of statin treatments resulted in 75 cases of diabetes, 7.5 cases of bleeding stroke, and 5 cases of muscle damage per 10,000 people treated. Other adverse effects include neuropathy, pancreatic, liver, and sexual dysfunction.
Adverse events are more common in clinical practice than in randomized clinical trials. A systematic review concluded that clinical trial meta-analyses underestimate the rate of muscle pain associated with statin use. In some studies the rate of rhabdomyolysis is low. Rhabdomyolysis can result in life-threatening kidney injury. The risk of statin-induced rhabdomyolysis increases with age, use of other medications such as fibrates, and hypothyroidism.
There are some genetic variants that make this condition much more likely–though find a doctor who checks for your genetics before they prescribe statins. The gene SLCO1B1 (Solute carrier organic anion transporter family member 1B1) codes for an organic anion-transporting polypeptide that is involved in the regulation of the absorption of statins. A rather common variant in this gene can significantly increase the risk of myopathy and rhabdomyolysis.
I find it interesting that of the number of people I know who are on statins, two are cases of rhabdomyolysis–so it cannot be that rare… food for thought.
Coenzyme Q10 (ubiquinone) production is blocked by statin use.
Cognitive effects
There are many reports of cognitive impairment with statins but their reporting is mixed. The FDA package insert on statins includes a warning about the potential for possibly reversible cognitive effects. While some research show minimal cognitive effects, some show confused effects, others, particularly case studies, show major cognitive effects.
My personal experience with those taking statins, is a general consistency with the case studies: cognitive decline for all people I know who take statins. In fact, other than muscle aches and pains, memory loss is the most frequently heard complaint. There is also an inverse relationship between LDL and ageing. Meaning, as we get older, a higher LDL is actually to our benefit, so reduced LDL is to our detriment, and causes shorter lives.
Diabetes
Use of statins is associated with an increased risk in developing type 2 diabetes. In fact, it may double the risks. Statins reduce glycemic control. Statins are thought to decrease the cells’ uptake of glucose from the bloodstream. One way this is thought to occur is by interfering with cholesterol synthesis (duh moment) which is necessary for the production of proteins responsible for glucose uptake into cells, such as GLUT1.
Cancer
There are many studies that find connection between statins use and cancer, such as breast cancer. In general, it is likely not statins themselves that cause cancer but rather their lowering of LDL. There appears to be an inverse correlation between LDL and cancer risk. And that is because LDL has a beneficial role in helping our immune system to remove pathogens and harmful cells–meaning it is part of our immune system we reduce when we reduce LDL. In addition, LDL is the carrier of all fat-soluble vitamins and minerals. By blocking all these essential vitamins and minerals, our cancer-prevention-power is reduced, and our general health is compromised. So statins may be indirectly associated with increased cancer rates, weakened immune system, weakened body and mind, and vitamin and mineral deficiencies.
Concluding Thoughts
So what is really at stake? Your health! Your life! Your money! Your future! Pay attention! Don’t let yourself be trapped. Understand the possible outcome–3-4 days of increase in lifespan–and match that with the possible negative experiences–as listed in the long list of side effects.
As for Dr. Maryanne Demasi: being fired for a job so well done that a company’s livelihood became at stake, and this revealed their corruption, is a testament of your success and achievement. You have become a power to recon with. Congratulations!
Your comments are welcome, as always, and are moderated for appropriateness.
Angela
Clueless Doctors & Scientists 
When you say “Only 11 statin clinical trials included mortality information” it actually should be more specific about and state “survival curves” instead. Moreover, as I pointed out to Dr. Kendrick, Dr. Demasi and Dr. Harcombe before, Kristensen et alter only estimate the average survival gain achieved by everybody on the treatment arm (dead or alive) within the trial’s running time. Yes, that means all survivors to placebo are contributing with the value ZERO to that average bringing it down. I explain it thoroughly here.
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I totally agree Andrés. There are a lot of mistakes in that article–and all articles that come up showing any benefit to statins with respect to health improvement and/or increase of lifespan, for that matter. As you pointed out in your explanation, and a statement by Dr. Malcolm Kendrick, no one is coming out of this alive, so lives are not saved, they are merely extended.
I also have a quibble with such “life extension” because it needs to be relative to the full life-length of a person and also whether that extension is a worthy one, which is yet another question. Personally, I would rather die in a heart attack than endure and die after years of torture fighting cancer… So add individual choice into the mix as well, and statins will soon start adding negative benefit and we should rather pay big pharma for not having to take them.
You have elegant but complicated statistics (I knew there was a reason for me to leave the doctoral program in statistics, which I started by the way, and get my doctorate in neuroeconomics instead) on your page. 😉
Thanks for your comment.
Angela
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That will take more careful reading, thanks!
Back in the day some researchers used to plot separate graphs for each subject. That would be enlightening, I suspect you might find a few subjects will life significantly extended,which would be the ones statins are good for, while the rest cluster around the few days mark.
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But even those for whom the statin is good for gain no life extension much… you can see the max on their summary. I think the max is like 10 days or something.
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Malcolm Kendrick (among others) has pointed out that CVD peaked and then declined again, and statins made not an impact on the graph. Then there’s the NNT site where they also list NNH (Number Needed to Harm) which also puts them in perspective.
I was lucky not to get any side effects but stopped taking them anyway when I realised they shut down the entire mevalonate pathway just to reduce “cholesterol” which is nothing to do with heart disease anyway. Well I suspect a lipid panel, especially trigs and HDL, serves as an indicator for metabolic mayhem such as insulin resistance. And on that subject high carb low fat diets which supposedly prevent heart disease actually cause it through other mechanisms like diabetes and obesity so another own goal.
As I wrote on the previous blog they tell you to eat the wrong diet so they can prescribe the antidotes. Thinking further, they also tell you to do the wrong kind of exercise which destroys your joints, and keep out of the sun, which prevents synthesis of vitamin D and nitric oxide.Did they get ANYTHING right?
The Anointed vs. the Wisdom of the Crowds
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Lol, totally correct. I wrote an article or two on NNT and NNH, read the latest one here: https://www.hormonesmatter.com/statins-who-needs-them/
One important caveat you didn’t mention. And that is: one can be on the sun 24/7 and will not have an ounce of D3 unless one also has a bunch of cholesterol and fats, because D3 is converted from cholesterol via the sun by the use of fat… Thus unless we eat a healthy diet rich in cholesterol and fat, nothing we can do about D3. So diet remains essential to contain a bunch of animal fats and cholesterol. 🙂
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Indeed, I had my D3 tested at 95, without supplementing. You should have seen my doctor’s face when I said
“That’ll be all the grass-fed butter and cheese then!”
Bless her, she’s starting to come around after I’ve been low carb for fourteen years.
Excellent article. I am persuaded by Malcolm Kendrick among others that LDL does not actually penetrate the endothelium. When the endothelium is damaged by any of a number of factors, a new layer rapidly grows over the damage sealing all kinds of crud beneath it, LDL included. The LDL is part of the repaid crew but doesn’t work properly when it’s damaged – oxidised, glycated etc. doesn’t properly engage with its receptors and the macrophages attempt to eat it along with the other trapped debris.
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I agree with you. There are others who disagree with the endothelium-penetration theory, including me. It comes in from the other end and stops beneath the endothelium. I have not spent time on looking at it further, only noted that “jeez, we don;t even know what we are talking about at it’s basics” so why are we (by we I mean the experts who are clearly not experts) even considering explaining the situation if even the entry-point is questionable.
Congrats on your D3. I would have loved to see her face! 😉
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awesome video Chris! Thanks!!
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