Carnivore diet myths: saturated fat, fiber, and LDL

About a third of people who start carnivore see their LDL cholesterol rise, yet markers like fasting insulin, triglycerides, and hs-CRP staying in normal range matter more for heart risk than that single number, and fiber turns out to be unnecessary since a meal of meat and eggs is fully digested within about two hours.

  • What to do: Cover vitamin gaps with two to four ounces of liver a week, or a liver supplement, and track A1C, fasting insulin, triglycerides, HDL, and hs-CRP alongside LDL instead of watching LDL alone.
  • Why it matters: The clogged-artery fear comes from a decades-old ad campaign, not physiology, since arteries sit at body temperature and dietary fat never solidifies inside them, and pre-diabetes, obesity, and smoking carry more established heart risk than elevated LDL.
  • How to apply it: Treat carnivore as a genuine elimination diet by removing seed oils, grains, and legumes, keep the rendered fat instead of pouring it out, and mix it with a zero-sugar condiment like mustard.
  • Metrics: Roughly a third of people see LDL drop, a third stay the same, a third rise, and about 1% spike sharply; meat clears the stomach in around two hours.
  • Tools: An organ-based seasoning blend with beef liver and garlic adds about half an ounce of liver to a meal without changing the taste.
  • Exceptions: People managing severe autoimmune or inflammatory conditions may skip spices and seasonings for the first 90 to 180 days to rule out triggers.

Why two huge anti-inflammatory heart trials failed

ZEUS suppressed CRP by the largest margin any anti-inflammatory heart trial has achieved, yet its hazard ratio for cardiovascular events landed at 0.99, a near-exact null result that shows lowering a blood marker doesn't guarantee lowering actual heart attack risk.

  • What to do: Don't treat a single CRP reading as proof of high or low cardiovascular inflammation risk on its own; ask your doctor how it fits with your LDL, Lp(a) and overall risk profile instead of reacting to that number in isolation.
  • Why it matters: Mendelian randomization studies show genetic variants that change CRP levels don't change cardiovascular disease risk, while variants that change LDL or Lp(a) do, so CRP is a correlated marker of inflammation, not a proven causal driver of heart disease.
  • How to apply it: If you have a high Lp(a) on a blood test, know that current Lp(a)-lowering drugs still haven't proven a cardiovascular benefit in a completed phase 3 trial; aggressive LDL management remains the well-proven lever available today.
  • Metrics: ZEUS enrolled over 6,300 patients with kidney disease and CRP above 2 mg/L; HORIZON enrolled about 8,300 patients with Lp(a) above 70 mg/dL and lowered Lp(a) by 70 to 80%, likely short of the roughly 100 mg/dL reduction modeling suggested was needed.
  • Tools: Newer research is shifting from blood-based markers like CRP toward direct imaging of coronary artery inflammation, such as PET-MRI and CT-based fat attenuation index scans, to select patients more precisely for future anti-inflammatory drug trials.

Nine fitness tests you can run on yourself, with numbers

A grip strength under 40 kg for men or 35 kg for women, or a VO2 max under 35 and 30 ml/kg/min, flags a specific weak point that can quietly cap overall fitness even when strength training and cardio otherwise look fine.

  • What to do: Test all nine fitness adaptations once a year, spread across about three days, rather than assuming a single workout or the way you look reflects your overall fitness.
  • Why it matters: Each adaptation, from grip strength to VO2 max, can become a hidden performance ceiling on its own, so a single weak category can limit progress even when everything else is trained well.
  • How to apply it: Start with non-fatiguing tests like body composition and movement screening after 48 hours of rest, then do power and strength testing while fresh, and save anaerobic capacity and VO2 max for separate days since they're demanding.
  • Metrics: Target grip strength above 40 kg (men) or 35 kg (women), a 30-plus second dead hang, a broad jump equal to your height, an FFMI of 20-plus (men) or 18-plus (women), 25-plus push-ups (men) or 15-plus (women), and a VO2 max above 35 ml/kg/min (men) or 30 (women), with 50-plus considered genuinely fit.
  • Tools: A hand-dynamometer (about $25), a pull-up bar, a stopwatch or heart rate monitor, and free online one-rep-max and VO2 max calculators cover nearly every test without a lab.

ApoB, plaque, and when to start treating heart disease

Without an ApoB particle depositing cholesterol in the artery wall there is no atherosclerosis: it is the necessary substrate, and the single worst gene variant raises cardiovascular risk by under 50 percent while high blood pressure, smoking, or diabetes each multiply it by two to four.

  • What to do: Get an Lp(a) once in a lifetime and add an ApoB to your standard lipid panel, along with blood pressure and waist size. If you have high ApoB with a bad family history, consider a low dose statin plus ezetimibe even if imaging shows no plaque.
  • Why it matters: Lowering ApoB and LDL cuts events in every trial, and kept cutting them going from 70 to 15 mg/dL. Lower for longer is better, and treatment intensity should match plaque burden.
  • How to apply it: Use the PREVENT calculator, which now covers ages 30 to 79 and gives a 30 year risk. A calcium score only sees calcified plaque and coronary CT angiography detects more; a clean coronary does not rule out plaque elsewhere. Re-evaluate yearly and repeat imaging in three to seven years.
  • Metrics: physiologic ApoB below 40 to 50 mg/dL, the level we are born with; a threshold of about 5,000 mg/dL years of accumulated LDL cholesterol; example of taking ApoB from 90 to 60 with a low dose statin and ezetimibe; hazard ratio of the worst gene below 1.5.
  • Tools: standard lipid panel, ApoB, Lp(a), PREVENT calculator, coronary calcium score, coronary CT angiography, Life's Essential 8, statins, ezetimibe, PCSK9 inhibitors, bempedoic acid.
  • Exceptions: you can live to 120 with an untreated LDL of 300 mg/dL and never have an event; the isolated number predicts mainly at the extremes, not in the middle range where most people sit.

Fatty liver disease is silent in nearly a third of adults

Nearly a third of the world's population carries excess fat in the liver, and the disease stays silent until scarring already limits how the organ functions, according to hepatologist Aleksander Krag.

  • What to do: Ask your doctor for a FIB-4 test if you have type 2 diabetes, obesity, or elevated liver enzymes, and track your abdominal circumference at home as a simple risk signal.
  • Why it matters: Fat in the liver alone is dynamic and often harmless, but fibrosis, the scarring, is what predicts real disease, and it advances roughly one stage every 7 years, or every 3 years if heavy alcohol is involved.
  • How to apply it: Cut back on daily drinking, since even a few alcohol-free days a week reduces calories and gives the liver a break, moderate fruit intake because fructose converts directly to liver fat, and keep drinking coffee, which is consistently linked to better liver outcomes.
  • Metrics: Steatosis threshold is more than 5% liver fat by weight. Up to 38% of people believed to have purely metabolic liver disease actually drink enough alcohol to reclassify, based on blood alcohol metabolite testing.
  • Tools: FIB-4 index (age, liver enzymes, platelets) for first-line screening, and fibroscan or elastography for confirmatory liver stiffness measurement.
  • Risks: Smoking independently raises fibrosis risk, and women face a steeper alcohol-risk curve than men for liver damage.

Can you build muscle in a calorie deficit? The data

Above roughly 20% body fat, lifters in an 8-week study gained about a kilogram of lean mass whether they sat in a 150-calorie or a 350-calorie deficit, with the bigger deficit simply burning more fat, evidence that body fat, not the scale, decides whether a calorie deficit blocks muscle growth.

  • What to do: If you're above about 20% body fat, train hard, eat around 1.6 g of protein per kilogram of body weight, and hold your deficit under 400 calories a day instead of eating at maintenance or in a surplus.
  • Why it matters: Your body treats fat stores as spendable energy until you approach a lower body fat threshold, so a moderate deficit above that threshold doesn't compete with muscle growth the way older "eat big to get big" advice assumes.
  • How to apply it: Below about 12% body fat, switch strategy: add a small surplus and raise protein toward 2.5 g/kg, since the body starts guarding fat stores and looking at muscle as a fuel source instead.
  • Metrics: Add roughly 8 percentage points of body fat to every threshold above if you're a woman; muscle loss in a deficit becomes common around a 500-calorie shortfall on average, per the underlying meta-regression.
  • Exceptions: Weight-class athletes who keep cutting to stay lean often plateau, then add muscle quickly once they move up a class and stop restricting energy, a real-world version of the same body fat effect.

Laser or skincare: what red, brown, and texture need

Every laser in the country targets only red, brown, or water, so before paying thousands for a package the question is which of the three it treats, and for pigment and mild redness a well built routine often does the same job for the price of a dinner.

  • What to do: Identify your lane: brown (spots), red (redness and vessels), or water (texture). For brown, use actives that block pigment production such as arbutin, licorice root, niacinamide, and tranexamic acid, plus chemical exfoliation at night. For an inflamed barrier, cut the routine to one or two calming products.
  • Why it matters: Skincare is like the diet and the laser is like liposuction: without a supporting routine the laser result is lost. For texture a laser does in three months what skincare takes two or three years to match, and no cream collapses a broken capillary.
  • How to apply it: Do not exfoliate in the morning, keep glycolic acids for the night. With melasma, choose a picosecond laser and expect more than 10 to 12 sessions. Hydroquinone is used two months on and two months off. With retinoids, prioritize consistency over intensity.
  • Tools: kojic acid, arbutin, licorice root, niacinamide, tranexamic acid, Major Fade Hyper Serum, Murad dark spot serum, SkinCeuticals CE Ferulic, Paula's Choice C15, Flash Mask, hydroquinone, Skin Rocks HPR, Shani Darden Retinol Reform, Combat Cream, Aveeno Calm + Restore, Left Un-Red Reducer Serum; VBeam, Fraxel 1927 and 1550, picosecond lasers, microneedling with and without radiofrequency, erbium and CO2 lasers.
  • Exceptions: with an inflamed barrier do not laser, repair first; with broken capillaries skincare does not work and you need the VBeam; with active acne do not laser texture until breakouts are controlled.
  • Risks: hydroquinone is not for long term use; retinoid prescriptions are poorly tolerated if overused; a product sold as a topical 10 percent azelaic acid was not what the label said.

Peter Attia on hormone therapy, testosterone and toxins

Women on hormone replacement therapy who also take testosterone report better sleep, mood and bone density, yet most doctors never raise the option, decades after the Women's Health Initiative wrongly scared a generation away from estrogen and progesterone.

  • What to do: If you're perimenopausal or menopausal and your doctor hasn't discussed testosterone or progesterone dosing with you, ask directly or find a new doctor.
  • Why it matters: The Women's Health Initiative data were misread decades ago, and that mistake cost a generation of women access to hormone therapy and pushed researchers out of the field.
  • How to apply it: Track symptoms like sleep disruption, mood changes and low libido, then bring a specific list to your provider instead of waiting for them to raise hormones first.
  • Risks: Metformin is a reasonable diabetes drug but has little rationale for people without diabetes or prediabetes; an SGLT2 inhibitor may be a better metabolic option before metformin is used off-label.
  • Exceptions: Skip intermittent fasting if you have a history of disordered eating, since it can quietly reinforce restrictive patterns.

Chronic illness treatment order: mold, Lyme and EMF

Patients with mold toxicity, Lyme disease and long COVID often get worse, not better, when doctors treat downstream problems like methylation or mitochondrial dysfunction before calming an overloaded nervous system, because a body stuck in cell danger response won't respond to treatment until it registers that it's safe.

  • What to do: If you have chemical or sensory sensitivities alongside chronic fatigue, address the limbic and vagal nervous systems first, before starting binders, detox protocols or mitochondrial support.
  • Why it matters: The cell danger response shifts the body into a defensive, shut-down state during infection or toxic exposure, and treatments aimed at deeper repair simply won't get a response until that state resolves.
  • How to apply it: Ask for a urine mycotoxin test if you suspect mold, since a positive result is unambiguous, and match any binders to the specific toxins that test reveals rather than using a generic detox protocol.
  • Tools: Limbic retraining programs like the Dynamic Neural Retraining System, the Gupta Program and Primal Trust, plus gentle vagal stimulation with devices like Apollo Neuro, are the entry point for patients too sensitive to tolerate mold or Lyme treatment directly.
  • Risks: Staying in a moldy home while trying to treat mold toxicity, even with a strong protocol, tends to keep patients sick because ongoing exposure outpaces healing.

What mitochondria really do beyond powering your cells

Mitochondria do not only make ATP: they decide how a cell splits its fuel between staying itself and making more of itself, and when a heart cell tips that balance toward growth it enlarges and fails.

  • What to do: Treat your body as a constellation of cellular metabolisms, not a single metabolism. Avoid chronic excess calories, which overpower mitochondria, and use exercise to raise energy demand rather than leaving the system overloaded at rest.
  • Why it matters: An overpowered mitochondrion generates reactive oxygen species that damage the genome and proteins and contribute to mutations, disease, and aging. When cells devote too much energy to growing rather than functioning, you get the enlarged heart that will not pump, cancer, and inflammatory disease.
  • How to apply it: Remember that mitochondria are inherited only from the mother and carry their own genome; local ATP production is why exercise and the use of each tissue shape their function. The mitochondrial pyruvate carrier, MPC1 and MPC2, is a key decision point for the fate of glucose.
  • Metrics: neurons with projections up to a meter long that mitochondria travel along; the IGF-1 growth pathway links larger size to shorter lifespan within a species; sprinters and gymnasts outlive very large athletes by about 3 to 6 years on average.
  • Risks: excess energy at the front end, the energy toxicity described by Layne Norton, does harm beyond stored fat; mutations accumulate with age, and by 50 each person is a mosaic of their original genome and mutated cells.