Lipidmaxxing

What to test

• ApoB above range. This is the single most important number, it counts the total atherogenic particles in your blood. Below 90 mg/dL is fine for most people, below 80 for anyone actively optimising, below 60 for anyone with cardiovascular risk factors or family history. Above those thresholds is the clearest signal to act.

• Triglycerides above 100 mg/dL. Reflects metabolic health and how your liver is handling fat. Elevated triglycerides reshape your whole profile toward more small dense LDL, lower HDL, and more remnant particles.

• HDL-C above 50 mg/dL for men, above 60 for women. Below that is the flag. Low HDL doesn't cause damage directly the way high LDL does, but it means your protective systems, cholesterol removal from artery walls, antioxidant protection of LDL, endothelial protection, are all running weak.

• LDL-C under 100 mg/dL for most people, under 70 if you have cardiovascular risk factors or family history. Always read it alongside ApoB. They usually track together but diverge in metabolic syndrome, insulin resistance, and high triglycerides, and when the two disagree, ApoB is the number that matters.

• Lp(a) under 50 mg/dL (or under about 75 nmol/L). Test it once, it's genetically set and barely moves. If it's high you can't lower it much through lifestyle or most drugs, but knowing shifts the whole risk picture toward more aggressive control of everything you can modify.

• Family history or known risk factors. Early heart disease in close relatives, existing metabolic dysfunction, or high visceral fat all move you up the ladder faster, regardless of where today's numbers sit.

The

Bloodwork Panel covers each marker in depth.

0- Lifestyle

• Get lean. If you're carrying excess fat, getting lean is the single most impactful thing you can do for your lipid profile. Visceral fat drives insulin resistance, which makes the liver overproduce VLDL, that means higher triglycerides, more small dense LDL, lower HDL, plus inflammatory signalling that damages artery walls. Below 15% body fat is where most men see their best metabolic markers, below 22-25% is where most women do.

• Eliminate trans fats completely. No biological function, harmful at any intake. Raises LDL, lowers HDL, promotes inflammation. Zero, not "less."

• Reduce saturated fat. Saturated fat lowers LDL receptor expression on liver cells, which slows LDL clearance and raises circulating LDL. Keep it to 15-20g per day, replace with monounsaturated fat (olive oil, avocado) and omega-3 sources (fatty fish). White fish > chicken > red meat for protein.

• Increase soluble fibre to 10-15g per day. Soluble fibre binds bile acids in the gut and blocks their reabsorption, so the liver has to pull cholesterol out of the blood to make replacements, which lowers LDL. Practical sources:
  
  Psyllium Husk, oats and oat bran, ground flaxseed (grinding is mandatory). Roughly 10g psyllium husk plus 20g ground flaxseed plus 80g oats gets you to 12-14g. Ramp up slowly if you get bloating or gas.

• Cardio, 5 x 20 minutes of zone 2-3 per week. Conversational pace, 60-70% max heart rate, 30 minutes daily is the easiest and most beneficial version. Cardio makes arteries more resilient to the particles that are there: faster blood flow creates friction on the endothelium, which stimulates eNOS and raises nitric oxide production, and over time trains the endothelium to produce more of it chronically. That improves endothelial function, lowers blood pressure, and makes the vessel lining less permeable to LDL. It also raises HDL, lowers triglycerides, and improves insulin sensitivity.

• Keep estrogen in the upper-normal range. Estrogen increases LDL receptor expression on liver cells (faster clearance, lower LDL), stimulates HDL production, and is anti-inflammatory on the vessel wall.

• Do not smoke. Smoking worsens every lipid marker through multiple mechanisms, smokers run significantly higher LDL than non-smokers.

• Manage stress. Sustained stress is part of what drives LDL to oxidise in the artery wall in the first place, which is the step that actually triggers plaque formation.

1- OTC supplements

• 
  Citrus Bergamot, 500-1500 mg per day of a standardised extract. A polyphenol extract that has shown LDL-lowering and triglyceride-lowering effects across several studies. Reasonable first-line OTC option.

• 
  Omega-3 (fish oil), 3-4g EPA+DHA per day. The main lipid effect is lowering triglycerides, with added anti-inflammatory benefit in the artery wall and improved endothelial function. Most off-the-shelf fish oils are underdosed, a capsule labelled "1000mg fish oil" often holds only 300mg of actual EPA+DHA, so check the EPA and DHA content per serving, not the total weight. Make sure it’s not oxidised or you’ll do more harm than good.

• 
  Berberine, 500mg two to three times daily with meals. A plant alkaloid that lowers LDL by roughly 20-25% by suppressing PCSK9 and activating AMPK, also lowers triglycerides and fasting glucose. Major caveat: it inhibits several liver enzymes (CYP3A4, CYP2D6, CYP2C9), so it changes how your body processes statins and other medications. If you combine it with a statin, use a lower statin dose and monitor liver enzymes.

• 
  Red Yeast Rice, 1,200-2,400 mg daily in divided doses with meals. Contains monacolin K, which is chemically identical to lovastatin and works through the same reductase inhibition. The catch is that monacolin K content varies dramatically between products, so dosing is unpredictable, the goal is 5-10mg monacolin K per day. If you're going to use a statin mechanism, a pharmaceutical statin with a known dose is more reliable. If you go this route, co-supplement
  
  CoQ10 (ubiquinol) (100-200mg daily) to offset the downstream depletion that comes with HMG-CoA reductase inhibition.

• 
  Psyllium Husk, 5-10g per day mixed into water, taken before meals. The most concentrated practical source of soluble fibre, it binds bile acids in the gut so the liver pulls cholesterol from the blood to replace them, lowering LDL. Cheap, well tolerated, and the most reliable way to hit the soluble-fibre target if food alone isn't getting you there. Ramp up slowly and take it with plenty of water.

2- Prescription lipid drugs

• 
  Statins (atorvastatin, rosuvastatin). The most widely prescribed lipid drugs. They inhibit HMG-CoA reductase, the enzyme the liver uses to make cholesterol, so the liver upregulates LDL receptors to pull more LDL from the blood, the main mechanism is increased clearance. They reduce ApoB by roughly 30-50% depending on dose and compound, with rosuvastatin and atorvastatin the most potent. A subset of users get dose-dependent muscle pain, and liver enzymes should be monitored.

• 
  Ezetimibe, 5-10 mg once daily. Blocks cholesterol absorption in the intestine, so the liver upregulates LDL receptors to compensate. Usually added to a statin when the statin alone isn't hitting the ApoB target, the combination beats doubling the statin dose and is generally better tolerated. Well tolerated with very few side effects. No dedicated page yet, worth adding.

• PCSK9 inhibitors (
  
  Evolocumab,
  
  Alirocumab). PCSK9 is a protein that tags LDL receptors for destruction, block it and the receptors survive longer, dramatically increasing clearance. They cut LDL by 50-60% on top of statins, and also lower Lp(a) by about 20-30%, which is notable because almost nothing else does. Subcutaneous injection every 2-4 weeks, expensive but increasingly accessible. Well-tolerated.

• 
  Bempedoic acid. Inhibits an enzyme upstream of HMG-CoA reductase, but only activates in the liver, not muscle, which is why it avoids the muscle-related side effects some people get on statins. A genuine alternative for the statin-intolerant.

• 
  Fibrates (fenofibrate) . Primarily lower triglycerides by activating PPAR-alpha, which raises fatty acid oxidation in the liver and cuts VLDL production. Most useful in the high-triglyceride, low-HDL metabolic pattern where triglycerides are the main driver.

• Prescription omega-3 (
  
  Icosapent Ethyl). Purified EPA at 4g/day, has shown cardiovascular benefit in trials beyond what dietary omega-3 provides, with a significant triglyceride-lowering effect plus an anti-inflammatory contribution through the resolvin and protectin pathways.

3- Experimental and adjacent compounds

• 
  Retatrutide, A GLP-1/GIP/glucagon triple agonist that, beyond fat loss, meaningfully improves the lipid profile, phase 2 trial showed reductions in triglycerides and improvements across the panel. Much of the benefit likely runs through body composition (less visceral fat, better insulin sensitivity), though there may be direct hepatic effects too.

• 
  SR9009 (Stenabolic). A Rev-Erbα/β agonist that has shown lipid improvements in preclinical research alongside anti-inflammatory effects, modest fat loss, and improved mitochondrial function. The evidence base is essentially all preclinical, with very little human data.

• 
  Tadalafil (Cialis), low-dose daily 2.5-5 mg. PDE5 inhibition improves endothelial function and blood flow through better nitric oxide signalling and lower blood pressure. The direct effect on the lipid panel itself is modest, this is more relevant for vascular health broadly.

• 
  GW501516 (Cardarine) improves lipids through PPAR-delta agonism, but caused cancer development in animal studies at higher doses and longer durations. The risk-benefit does not justify it.