Nutrition on noema

Intermittent fasting: what actually works

Mon, 04 May 2026 00:00:00 +0000

Abstract. “Intermittent fasting” has entered public discourse as a single category, but very different practices live under the same label — from daily 16:8 to the five-days-a-month fasting-mimicking diet. On the daily protocols the literature is by now clear: at equal calories, they don’t drive more weight loss than a classic diet, and the “extra” metabolic benefits are small or extrapolated from mice. The case that holds up clinically is the FMD: five days a month of heavily reduced intake, with replicated human data on insulin sensitivity, inflammatory markers, and cardiometabolic profile. The molecular rationale runs through mTOR — the amino-acid and insulin sensor that periodic fasting modulates over a long enough stretch, while sixteen hours of daily fasting modulates only briefly. A disproportionate enthusiasm remains: 16:8 autophagy, white-fat browning, “demonstrated” longevity are still mostly rodent stories. Here I try to separate the solid case (FMD, early time-restricted eating for specific profiles) from the noise.

When an idea actually works in medicine and nutrition, it usually doesn’t need evangelists. When it does, it’s worth looking carefully.

Intermittent fasting reached the general public around 2012-2013 with Michael Mosley’s The Fast Diet and the 5:2 protocol, and from there it never stopped: 16:8, 18:6, 20:4, OMAD, alternate-day fasting, fasting-mimicking diet, prolonged fasts of three, five, seven days. Every variant has its book, its influencer, its biological rationale told as if it were the answer.

Yet if you go back to the basic question — which intermittent fasting does something unique that a good normal diet doesn’t? — the answer that emerges from the better literature of the last ten years is one and specific: the protocol with the most convincing clinical data isn’t 16:8, but the fasting-mimicking diet developed by Valter Longo’s lab at USC. Five days a month, not sixteen hours a day. It’s a different thing, and it has to be told as such.

Living Forever

Wed, 22 Apr 2026 00:00:00 +0000

Abstract. Two parallel literatures circulate on longevity: the one from laboratories — slow, full of caveats — and the one from the market, which sells certainties where research offers well-characterised uncertainties. Here I lay out where solid data exist (caloric restriction, sleep, exercise, rapamycin in mice), where there is much marketing with little evidence (peptides, NAD+, premium clinics), and why the promise of an indefinitely upgradable body confuses mechanistic plausibility with biological control. The most dangerous thing is not ignorance: it is certainty.

The longevity industry thrives on a simple promise: that the body, like software, can be upgraded indefinitely. Biology, unfortunately, has other plans.

I have worked with data long enough to know that the most dangerous thing is not ignorance. It is certainty.

Years spent in the lab studying how genetics, epigenetics, and maternal care shape behaviour, stress resilience, and neuropsychiatric vulnerability in animal models teach you one fundamental thing: biological systems cannot be controlled, they have to be negotiated with. You touch one variable and all the others move — often in ways you had not anticipated, sometimes in ways you cannot even measure correctly. Then you step out of the lab, navigate the healthcare system from the other side — as a mother, as a patient, as someone trying to build an overall picture while the system hands you back fragments — and you realise that this complexity does not disappear just because someone has built a two-million-dollar protocol on top of it.

This article is not a defence of the healthcare status quo, which has its own enormous and well-documented failings. It is an invitation to look more honestly at what we actually know — and at what is being sold to us as if we knew it.

Honest medicine

Tue, 21 Apr 2026 00:00:00 +0000

Abstract. I’m Sara Lo Russo, a biologist and behavioural neuroscientist. I’ve spent a decade between the lab, clinical nutrition practice and science writing, and this site exists because I wanted an Italian voice on longevity, neuroscience and nutrition that stays anchored to the literature — not to marketing. Articles are structured the way a good study is: a plain-language introduction anyone can follow, then progressively more technical sections for readers who want the mechanisms and the citations.

Where I come from¶

Master’s degree in Evolutionary Biology from the University of Rome Tor Vergata, with a thesis in behavioural neuroscience on the role of genetic background in maternal behaviour and stress resilience. Co-author of five peer-reviewed publications in international journals — Biomedicines, Neuroscience, Developmental Psychobiology and two in Frontiers in Behavioral Neuroscience (one, the other) — on how genetics, epigenetics and maternal care shape behaviour and neuropsychiatric vulnerability in murine models (laboratory mice and rats).

Preclinical research at the Istituto Superiore di Sanità in Rome and at the FutureNeuro Centre of the Royal College of Surgeons in Ireland in Dublin. Years of clinical nutrition consulting with adult patients, including complex contexts: chronic disease, eating disorders, ketogenic diet therapy for epilepsy. Italian secondary-school teaching qualification in Mathematics and Science.

The full picture — publications, roles, training — lives in my curriculum.

What I want to do here¶

I want an integrated, honest medicine, grounded in research rather than in marketing. That means writing about longevity, neuroscience, nutrition and brain health while taking the time to cite the studies, to separate what we know from what we tell ourselves, and to openly state what we don’t yet know.