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For 74,000 years, one ancient killer quietly dictated where early humans could survive across Africa

Increasing evidence suggests that our species emerged through interactions between populations living in different parts of Africa, rather than from a single birthplace. Until now, however, most explanations for how those populations were distributed across the continent have focused on climate alone. The new research shows that disease—specifically malaria—also played a crucial role.

In a paper published in Science Advances, researchers from the Max Planck Institute of Geoanthropology, the University of Cambridge, and colleagues have investigated whether Plasmodium falciparum-induced malaria shaped human habitat choice between 74,000 and 5,000 years ago, the critical period before humans dispersed widely beyond Africa and before agriculture dramatically altered malaria transmission.

The study shows that malaria, one of humanity’s oldest and most persistent pathogens, influenced habitat choice by pushing human groups away from high-risk environments and separating populations across the landscape. Over tens of thousands of years, this fragmentation shaped how populations met, mixed, and exchanged genes, helping create the population structure seen in humans today. The findings suggest that infectious disease was not simply a challenge early humans faced: it was a fundamental factor shaping the deep history of our species.

Circadian Timekeeping Through Nutritional and Metabolic Sensory Networks

Circadian rhythms are predictable biological patterns that recur about every 24 h and, in mammals such as humans, are entrained to daylight by the hypothalamic suprachiasmatic nucleus (SCN). Although light is a potent zeitgeber for the SCN, cells outside of the SCN can synchronize to daily nutrient and metabolic cues. In these tissues, nutrient metabolic processes are regulated by the molecular clock in anticipation of food availability or scarcity. Furthermore, nutrients and metabolic processes themselves may act upon members of the molecular clock to regulate their expression and activity. These interactions maintain synchrony between the SCN and food-entrainable clocks when activity and nutrient intake align.

A generative AI framework unifies human multi-omics to model aging, metabolic health, and intervention response

Circadian rhythms are predictable biological patterns that recur about every 24 h and, in mammals such as humans, are entrained to daylight by the hypothalamic suprachiasmatic nucleus (SCN). Although light is a potent zeitgeber for the SCN, cells outside of the SCN can synchronize to daily nutrient and metabolic cues. In these tissues, nutrient metabolic processes are regulated by the molecular clock in anticipation of food availability or scarcity. Furthermore, nutrients and metabolic processes themselves may act upon members of the molecular clock to regulate their expression and activity. These interactions maintain synchrony between the SCN and food-entrainable clocks when activity and nutrient intake align. However, the light-entrainable SCN and food-entrainable clocks can become desynchronized, particularly in modern society where humans are commonly exposed to shift work and jet lag. Therefore, the mechanisms for sensing nutrients at specific times of day are critical components of circadian timekeeping and organismal homeostasis. In the following narrative review, we aim to synthesize current evidence on time-of-day-dependent nutrient sensing in mammalian systems, examine how nutrient-derived signals and metabolic processes interact with molecular clock mechanisms across cellular and tissue levels, and evaluate the integration of central and peripheral clocks in regulating gene expression, energy utilization, and organismal homeostasis, including the impacts of feeding cycles and circadian disruption. While previous reviews have discussed circadian nutrient metabolism, this review provides conceptual support for the role of nutrients as time-of-day signaling mechanisms.

When pomegranates meet the artery wall: How gut-derived metabolites may stabilize atherosclerotic plaques

For years, pomegranates have enjoyed a reputation as a “heart-healthy” fruit. As a cardiovascular researcher, I have often been asked a seemingly simple question: If pomegranates are so good for us, how exactly do they work? Our recent study, published in Antioxidants, set out to answer that question—not by focusing on the fruit itself, but by following what happens after the body and, crucially, the gut microbiome gets involved.

Atherosclerosis—an inflammatory disease that underlies heart attacks and strokes—develops slowly. It begins when low-density lipoprotein (LDL) particles become trapped and oxidized in artery walls, triggering immune cell recruitment, chronic inflammation, and eventually plaque formation. Drugs such as statins are effective but not perfect; many patients continue to carry significant “residual risk.” This has driven interest in other preventative and therapeutic agents. These include nutraceuticals—bioactive food components that may potentially complement existing therapies.

Among these, pomegranate polyphenols, especially a compound called punicalagin, have stood out. But there is a catch. Punicalagin itself is poorly absorbed. What actually enters the bloodstream in meaningful amounts are urolithins: small molecules made when the gut bacteria metabolize punicalagin and its breakdown product, ellagic acid.

#Polymath

This is one of my favourite comparisons: polymathy is cognitive biodiversity.

Monoculture farming depletes soil, invites disease, collapses under pressure. One blight, one drought and the whole field dies.

Why do we accept the same fragility in how we think?

The specialist mind is similar to a monoculture. Trained to the depth in one domain and optimized for known conditions. When the paradigm breaks, it can only do what it has always done.

People who consume ultra-processed foods have worse muscle health, study suggests

Researchers found that a diet high in ultra-processed foods is associated with higher amounts of fat stored inside thigh muscles, regardless of calorie or fat intake, physical activity or sociodemographic factors in a population at risk for knee osteoarthritis. Results of the study were published in Radiology. Higher amounts of intramuscular fat in the thigh could potentially increase the risk for knee osteoarthritis.

Ultra-processed foods usually have longer shelf lives and can be highly appealing and convenient. They contain a combination of sugar, fat, salt and carbohydrates which affect the brain’s reward system, making it hard to stop eating.

These foods include breakfast cereals, margarines/spreads, packaged snacks, hot dogs, soft drinks and energy drinks, candies and desserts, frozen pizzas, ready-to-eat meals, mass-produced packaged breads and buns, which all include synthesized ingredients.

Scientists Reveal Why Bread Can Cause Weight Gain Without Overeating

New research in mice shows how eating bread can cause body weight and fat mass to increase, even though caloric intake stays at a similar level.

The research, led by a team from Osaka Metropolitan University in Japan, highlights how carbohydrates can contribute to weight gain as well as excessive fat intake – which is what dietary advice tends to focus on.

This isn’t the first time nutritionists have talked about bread and carbohydrates and their contribution to weight gain, but there hasn’t been much detailed research into the relationship – especially wheat flour – or into what might be happening at a metabolic level.

Fields as Formal Causes, with David Bentley Hart

In this conversation, Rupert Sheldrake and David Bentley Hart delve into the concept of fields in physics, discussing their nature as non-material formative causes and their historical context in scientific thought. They explore the idea that fields, such as gravitational and electromagnetic, act as top-down causes, aligning with Aristotle’s formal and final causes, and argue for a re-evaluation of these ancient concepts in modern science.

Chapter List:

00:00 — Introduction.
01:14 — Exploring Fields as Causes in Nature.
02:08 — Magnetic Fields and Formative Processes.
04:19 — Gravitational Fields and Formative Effects.
06:10 — Aristotle’s Formal and Final Causes.
07:32 — Challenges in Understanding Fields.
09:09 — Fields as Top-Down Causes.
10:34 — Morphic Fields and Formative Causation.
12:23 — Information Theory vs. Form.
14:15 — Fields and Order in Physics.
17:15 — Semantic and Syntactic Information.
18:18 — Universal Gravitational Field.
19:44 — Strong and Weak Nuclear Fields.
21:18 — History of Field Theory and Ether.
23:14 — Gilbert’s Magnetic Theory.
24:46 — Mind-like Structure in Nature.
25:39 — Combination of Top-Down and Bottom-Up Theories.
27:07 — Mechanistic Models and Their Limitations.
28:52 — Recovering Aristotelian Causality.
31:39 — Conclusion and Reflection on Fields as Modern Souls.


Dr Rupert Sheldrake, PhD, is a biologist and author best known for his hypothesis of morphic resonance. At Cambridge University, as a Fellow of Clare College, he was Director of Studies in biochemistry and cell biology. As the Rosenheim Research Fellow of the Royal Society, he carried out research on the development of plants and the ageing of cells, and together with Philip Rubery discovered the mechanism of polar auxin transport. In India, he was Principal Plant Physiologist at the International Crops Research Institute for the Semi-Arid Tropics, where he helped develop new cropping systems now widely used by farmers. He is the author of more than 100 papers in peer-reviewed journals and his research contributions have been widely recognized by the academic community, earning him a notable h-index for numerous citations. On ResearchGate his Research Interest Score puts him among the top 4% of scientists.

https://www.sheldrake.org

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