Mother of the No-Seed-Oil Movement | NY Times Bestselling Author | Standing Up to the Sickness Industry
Dear fellow family medicine doctors: If you want to know how statins really affect your patients you have to learn to read between the lines. I just had to take a test on a statin research paper to keep my board certification. The paper is called “Treat-to-Target or High-Intensity Statin in Patients With Coronary Artery Disease” [link below] and it’s a great example of the kind of unethical data presentation I see all too often. The study compares the effects of two levels of statin drug dosages. One called “high intensity” meaning patients got maximum doses of their statin (20 of Crestor or 40 of lovastatin), and one called “treat to target” meaning people were given the amount of statin required to get their LDL between 50 and 70 mg/dl. People in the treat-to-target group generally took lower doses of statins and their LDL levels were a little higher. People in the high-intensity group generally took higher doses and had slightly lower LDL levels. What did that slight difference in LDL do to their health? The people with lower LDL levels (in the “high intensity” statin group) did worse. They died significantly more often than the people with higher LDL levels in the less aggressive treatment group. This difference had a p-value of <0.001 meaning it was statistically significant. This suggests having a lower LDL is WORSE than having a higher LDL. It also suggests more drug equals more death. So how do they report this finding that goes counter to everything we hear about how dangerous cholesterol is and how safe statin drugs are? The study authors don’t tell you what I just told you. They don’t want you to know the truth. So they use doublespeak. They say the “treating to target strategy is “noninferior” to treating with “high intensity” statin doses.” They spin a negative into a neutral. That’s fraud. But unless you have your cynical hat on, you will be fooled. This is just one example of how doctors get fooled. I’ve covered others in previous posts, most notably here: However, a much bigger fraud centers on the very notion that saturated fat is bad for us. I just spent 4 years writing a book called Dark Calories, which I hope will open eyes to how a medical organization pulled off the deadliest deception ever perpetrated on humanity. JAMA article here: https://lnkd.in/eE7Wz7mP To learn about Dark Calories visit https://lnkd.in/eRnWG-q7 #cholesterol #preventativemedicine #familymedicine #hearthealth #statins Ken Berry, MD Jeffry Gerber, MD, FAAFP The Florida Academy of Family Physicians (FAFP) Laurence Bauer Joseph Scherger
Garry Welch
7mo
Thanks Cate Shanahan MD for your important work and public education efforts to help fellow Docs and Patients - So, you essentially found a Relative Risk (RR) of 7.3% MORE (13/177=7.3) CVD events/death with the high dosage statin - that was played down in the paper summary- RR is the pharma industry's preferred statistical marketing language but only when they are looking to overstate small clinical benefits of CVD drugs. In those cases they avoid using Absolute Risk Reduction (ARR) or Number Needed to Treat (NNT) stats that will be the more honest insights for doctors and patients to consider. Many statisticians and researchers have written about this" RR vs ARR/NNT" issue and the misleading use of RR statistics. We have better CVD markers than LDL: including oxLDL for atherosclerosis being the amount of LDL damaged by modern lifestyles including glycation and oxidation of circulating LDL. Also, we have more focus on ApoB (# particles) and insulin resistance that better reflect underlying disease and metabolic syndrome. I hope others stumble onto the use of high potency statins to treat "Bad LDL" in CVD and instead zero in on modern seed oils, sugars, refined grains, & food chemicals damaging our lipid transport system.
Tom Rifai
7mo
Dr, so cherry pick a study and forget about all of the other randomized controlled and Mendelian trial data? We should assume that it’s good to have familial hypercholesterolemia? You are doing just the unethical fear mongering cherry picking that you are criticizing. And to not even differentiate LDL-C from LDL-P/ApoB nor mention any control for Lp(a) and on and on? Then pushing the saturated fat is good for you narrative despite evidence as wide as the Finland experience? You also failed to mention that in the strand of truth of statin toxicity virtually all true lipidologist and Cardiometabolic Health Congress Cardiometabolic Health Congress certified experts like myself, Thomas Dayspring, MD FACP, FNLA and William Cromwell, MD, FAHA, FNLA no longer often use high dose statin therapy (and certainly not lovastatin) - we combine ezetimibe with low-dose atorva or rosuva therapy. Notably, no drug for me as I’ve learned to enhance my hepatic clearance of LDL particles by increasing my saturated to PUFA ratio with TLC. ApoB 70mg/dL. Coronary artery calcium score zero. Fully clean triphasic peripheral arterial dopplers. Everyone reading this post, please talk to your doctor before stopping statin therapy if you’re on one.
Jessica Talbot
7mo
What are your thoughts on the recent adding of LDL cholesterol as a dementia risk factor? (In their words a 'compelling risk' when the actual study said modest for mid age only? correlation not causation). The study also looked to me like some statistical shenanigans went on the get the results they wanted. They also excluded lots of people and those on statins (wouldn't it have been worthy to see the data on those people too... reduced risk of dementia? To better support their premise). Then I see videos with Dr's saying 'we need to treat more aggressively, earlier and longer' to prevent dementia? I can't help but wonder if they are losing ground with cardiovascular disease (patients and Drs questioning statin use more) so want to shift the focus to dementia.
Bill Fabrey
7mo
Sounds suspiciously like marketing by big pharma. I never did well on any statins and my cardiologist gave up trying. I am sceptical that they help anyone.
Execellant Cate thanks so much! The Choesterol scam has been going on for too long, since Ancel keys sold us false information the Farmington study hidden from us & Proctor Gamble funding AHA with $1.3 million to get this racket going,still going strong. Doctors have been trying to prescribe statins to me for 25 years, I have refused. What happened to the days when 300 mg/dl was OK? The average LDL in Switzerland is 265 mg/dl, they have lower cardiovascular illnesses & deaths per capita than us! With global revenue of $1 trillion it is going to take a while. Will not happen soon!Now, we have the GLP1 scam proliferating .Can you fathom that Ozepic alone enhanced the GDP of Denmark (via Novo NordisK). As someone said “medicine advances one funeral at a time”. However, the Lifestyle Medicine, Functional Medicine, Medicne 3.0 has left the station.Thanks to doctors like you & many others who are tirelessly working writing books & using social media etc to educate us who are not doctors. Regularly, I see doctors getting certified in Lifestyle Medicine.We owe muvh gratitude to all of you.In the meantime, we can hope to contribute a minute fraction amount of towards making the likes of Novo Nordisk & Eli Lilly towards bankruptcy 🤣🤣
Huh, I guess I never knew that noninferior is a synonym for BETTER. I have never been a fan of statins but I knew when the statin fans started saying there is no such thing as “too low”for LDL that they had sold their souls to the devil. We need cholesterol for cell membranes! Even a first year med student knows this.
Firstly cholesterol is not the primary problem. It is a late stage component of atherosclerosis. Further it is not a LIPID, it is a STEROID, it just happens to have the chemical characteristics of being soluble in lipids. So there is no BAD or GOOD Cholesterol, it is simply a single molecule. The problem with vascular disease is that lipids that are being transported are OXIDIZED, the lay term for that is RANCID. When deposited into the vascular wall they attract macrophages whose job is to "eat the dysfunctional rancid lipids". Histologically this is the source of the FOAM cells (macrophages full of oxidized lipids) that is the start of atherosclerosis. If you want to truly abrogate this process the focus should be on the health of the lipids i.e. not oxidized, rather than lowering cholesterol (again a steroid not a lipid and so it does not form foam cells). We have done an enormous disservice to the public with good/bad cholesterol and developed a multi-billion $ industry that is off target. Lowering cholesterol can affect levels of all steroids, as they ALL stem from cholesterol, as well reducing CoQ10, which is also derived from cholesterol, an important mitochondrial nutrient.
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7moCurrently reading a book called “Drug Muggers” where the author describes the health impacts of depleting CoQ10 with statins - Leg cramps, high blood sugar, impotence, fatigue, depression, LFT abnormalities and even cardiac arrhythmias/ palpitations are all possible effects of low CoQ10. What’s worse, providers sometimes then treat those symptoms with more medication. Statins are a gateway to SE and polypharmacy it seems!