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Normal cells burn glucose efficiently with oxygen. Cancer cells largely ferment it — even when oxygen is present. Otto Warburg noticed this in 1924 and won a Nobel Prize. A century later, we're finally understanding why cancer cells prefer this wasteful strategy, and how to use it against them.

Your cells don't repair damaged mitochondria — they eat them. Mitophagy is a selective autophagy pathway that tags dysfunctional mitochondria for destruction, and its failure is implicated in Parkinson's, aging, and metabolic disease.

David Sinclair's bet is straightforward: aging is an information problem, NAD+ is part of the repair machinery, and replenishing it might reverse the epigenetic damage that accumulates with age. The mouse data is compelling. The human data is still being gathered. The debate is genuinely unsettled.

What happens when you treat DNA like code and cells like hardware? Synthetic biology lets scientists — and now undergrads — build living systems from scratch, reprogramming organisms to do things evolution never imagined.

Synthetic biology treats genetic circuits like transistors — composable, programmable parts. Researchers have built bacterial sensors for landmines, yeast producing antimalarial drugs, and cells that compute logical operations. The design-build-test cycle is accelerating.

The mitochondria story connects endosymbiosis, maternal inheritance, oxidative stress, and the evolution of multicellular life. Here's how those threads weave into a single, stranger picture of what you are.

Mitochondrial diseases can be devastating and untreatable. MRT offers a way to break the maternal inheritance chain — but doing so requires making an embryo with genetic material from three individuals, which is where the ethics get complicated.