CONNECT | GROW | TRANSFORM

Every decision you make — what to eat, whether to snack, how much to serve — draws on this limited pool of cognitive energy. Psychologists call this decision fatigue: the more choices you face, the weaker your self-control becomes. This is why dieting is so hard. You’re not only fighting hunger hormones and cravings, you’re draining a limited mental resource dozens of times a day. And when it runs out, biology takes over.

If a calorie is not a calorie — if we can’t reliably know how much of it is absorbed, how much is lost in digestion, and what its metabolic fate will be — then how would anyone know how many calories to cut?

And if a calorie is not a calorie — if we can’t reliably know how much of it is absorbed, how much is lost in digestion, and what its metabolic fate will be — then how would anyone know how many calories to cut? Are people expected to constantly battle with calorie math, obsess over every bite, track every number on an app, and then feel guilty for “going over” — even though the body never sees those calories the way the food label does?

So while calories tell us how much potential energy a food contains, they tell us nothing about how your body will respond to that food. Two foods with identical calorie counts can have dramatically different effects on hunger, hormones, and fat storage.

Progesterone and estrogen repeatedly stimulate breast tissue and the uterine lining. Without the “breaks” of pregnancy and lactation, this repeated turnover is thought to increase the risk of fibroids, endometriosis, and possibly breast and endometrial cancers.

Your hormones aren’t the enemy. They’re the original biohack — refined over millions of years to help you survive and thrive. When you learn to work with their rhythm, you unlock a level of ease and effectiveness that no one-size-fits-all diet can match.

Seed oils rich in linoleic acid (LA), such as soybean, corn, sunflower, safflower, and canola oil, provide the exact substrate (PUFAs) that enzymes like lipoxygenase (LOX) and myeloperoxidase (MPO) use to oxidise LDL particles.

What’s actually most prone to oxidation in LDL is the fatty acid tail of the cholesteryl ester in the “oil barrel” (and the PUFA in the phospholipid shell). Cholesterol itself — the rigid steroid ring — is remarkably stable. Pure cholesterol won’t just oxidise easily in the body.

When the metabolic environment is calm — low inflammation, low oxidative stress, good insulin sensitivity — LDL particles circulate, deliver nutrients, and return to the liver without incident. But in an inflamed environment, those same particles can get trapped, oxidised, and turned into plaque.

The simple claim “saturated fat raises LDL, therefore causes heart attacks” is outdated. A more accurate view must consider biochemistry, particle quality, metabolic health, and dietary context.