1/11 If you went to a doctor with a broken leg and he started putting a cast on your arm, you’d question it immediately. Yet something similar is happening in how we approach heart disease. /2
2/11 Statins block the mevalonate pathway, a fundamental biological process involved in more than just cholesterol production. This pathway is essential for cellular energy, hormone synthesis, and repair mechanisms. /3
3/11 Disrupting it isn’t a neutral act. It has wide-ranging effects across the body.
Heart disease is not a “cholesterol problem.” It’s a complex, multifactorial condition driven by metabolic dysfunction and chronic stress on the body. /4
4/11 Insulin resistance sits at the center of this. When the body loses the ability to handle glucose properly, it triggers a cascade of damage - higher blood sugar, increased triglycerides, lower HDL, and a pro-inflammatory state that damages blood vessels. /5
5/11 Chronic inflammation is another key driver. Arterial plaques don’t just appear. They form in response to injury and inflammation in the vessel walls. Without addressing the source of that inflammation, we’re only treating symptoms.
/6
6/11 Infections also play a role. Research suggests certain pathogens can contribute to vascular inflammation and plaque instability, adding another layer to the disease process.
High blood pressure places mechanical stress on artery walls, making them more vulnerable /7
7/11 to damage and plaque formation. It’s not just a number, it’s part of the disease mechanism.
Obesity, particularly visceral fat, acts like an endocrine organ. It releases inflammatory signals, worsens insulin resistance, and accelerates cardiovascular risk.
/8
8/11 When we focus narrowly on lowering cholesterol, we risk missing the bigger picture. The real opportunity lies in addressing root causes: metabolic health, diet quality, physical activity, sleep, and stress. /9
9/11 If the root causes remain - insulin resistance, chronic inflammation, metabolic dysfunction, the disease process continues quietly beneath the surface.
The real question isn’t whether a drug can shift a biomarker.
10/11 It’s whether we’re willing to confront what’s actually driving the disease in the first place.
Until we do that, we’re not treating heart disease, we’re managing its shadow. In nearly two decades of looking closely at statins, I’ve yet to see a single case of CVD
/11
11/11 that was truly reversed through drugs.
What I see, time and again, are people reclaiming their health when they address root causes: improving their diet, restoring metabolic balance, moving more, sleeping better, & reducing chronic stress.
That’s where real change happens.
• • •
Missing some Tweet in this thread? You can try to
force a refresh
1/8 What the LDL is going on ? "Because the presence of coronary artery disease can be associated with the proportion of small, dense LDL, we analysed the effect of statins on small, dense LDL subfractions in people without coronary artery disease. /2
2/8 Unexpectedly, in the analysis, the proportion of small, dense LDL was significantly higher in patients treated with statins. Moreover, there were no differences in CRP, plasma fibrinogen, HOMA–IR,BMI, or metabolic syndrome between the statin and control groups. /3
3/8 Therefore, we concluded that the increase in small, dense LDL proportion was influenced by statins but not by the other variables."
Well spotted👏. Upregulation of LDL receptor activity by statins decreases large, buoyant LDL more than small, dense LDL because statins /4
1/13 We live in a post-truth era where single biomarkers are taken out of context and used to construct incomplete, and often misleading, narratives. ApoB is one of the clearest examples of this. /2
2/13 Measuring ApoB in isolation is fundamentally misleading, because while it reflects the number of atherogenic particles, it tells us nothing about the protective role of ApoA1-containing lipoproteins. It is the ApoB/ApoA1 ratio that truly matters, as it captures /3
3/13 The balance between atherogenic and protective forces, and has consistently been shown to be a stronger predictor of cardiovascular risk than ApoB alone.
So why are we continuing to vilify ApoB ? In reality, ApoB becomes problematic primarily when it has been modified by /4
1/6 This comes from the statin toxicity document (). Its real purpose ? To steer patients away from cheap, generic statins toward newer, more expensive cholesterol-lowering drugs./2ahajournals.org/doi/10.1161/CI…
2/6 Ironically, in trying to downplay generic statins, they shot themselves in the foot by laying out in meticulous detail how statins harm every cell and organ in the body.
Statins inhibit HMG-CoA reductase, blocking the mevalonate pathway. /3
3/6 This isn’t just about cholesterol, it reduces isoprenoids, coenzyme Q10, and other molecules essential for cell energy, signaling, and repair.
Muscles: mitochondrial dysfunction, myopathy, weakness, rhabdomyolysis. /4
1/7 LDL is not just a cargo carrier. In its native form, it’s protective, carrying essential lipids and antioxidants like CoQ10, helping cells function and supporting vascular health. The danger doesn’t come from LDL itself. /2
2/7 It comes from how we damage LDL, and what happens to it in the body. High blood sugar, processed fats, seed oils, and chronic oxidative stress can modify LDL, making it more prone to damage. But infection is another potent trigger. /3
3/7 When pathogens enter the body, immune cells release reactive oxygen species (ROS) as part of the defense. This can oxidize LDL, turning it into a pro-inflammatory particle. Oxidized LDL is taken up by macrophages, forming foam cells, which accumulate in the artery wall /4
1/13 Statins don’t “lower cholesterol.” They cripple the mevalonate pathway, the body’s core engine for energy, repair, and longevity.
What follows is the science Big Pharma left out:
/2
2/13 The pathway
The enzyme HMG‑CoA reductase doesn’t merely make cholesterol; it governs the entire mevalonate‑isoprenoid cascade, the pipeline that produces:
Cholesterol (for membranes & hormones),
CoQ10 (mitochondrial respiration),
Dolichols (cell‑surface signalling),
/3
3/13 Prenylated proteins (cell growth),
Isopentenyl adenine (tRNA integrity).
Block that enzyme, and you choke every branch.
What happens in the liver
Most statins accumulate in the liver. Mevalonate synthesis collapses -cholesterol & isoprenoids fall. /4
1/8 A study from the Essen group in Germany compared normal-dose Atorvastatin (10 mg/day) with high-dose Atorvastatin (80 mg/day)
Over one year, patients were followed for the progression of coronary artery calcification using electron-beam computed tomography. /2
2/8 Despite lowering LDL from 109 mg/dL to 87 mg/dL, there was no difference in the progression of calcified coronary atherosclerosis. Reductions in hsCRP and fibrinogen were similar between the low- and high-dose groups, indicating that 80 mg provided no measurable /3
3/8 advantage over 10 mg. These results suggest that Atorvastatin offers little or no meaningful anti-inflammatory benefit, and any modest effects may be offset by pro-inflammatory mechanisms.
/4