Recent headlines have had a lot of people eyeing their frying pans with suspicion. Clickbait titles claimed seed oils like canola and sunflower might be causing colon cancer. Even some of the more reputable publications fell prey to the frenzy.

This came not long after Robert F. Kennedy Jr. announced Americans are being unknowingly poisoned by seed oils. He suggested "It’s time to make frying oil tallow again" and cut seed oils subsidies, apparently to make McDonald’s healthy.

Influencers, media outlets, and politicians have all jumped on the bandwagon, spinning tales of toxic oils lurking in our pantries. But is there any truth to these claims? Let’s break it down with some solid science.

TL;DR – Seed oils don’t cause colon cancer

The argument against seed oils is that the linoleic acid they contain increases inflammation, which is linked to cancer. However, a substantial body of evidence exonerates linoleic acid:

• A study which followed 2,480 people for 22 years found that those with higher levels of linoleic acid were 43% less likely to die from any cause, and that higher linoleic acid levels were not associated with cancer deaths, meaning they did not increase or decrease cancer mortality risk.1

• Another large meta-analysis, which included 68,659 people in 13 different countries who were followed for up to 32 years, found that people with higher levels of linoleic acid had a 7% lower risk of cardiovascular disease and a 22% lower risk of death from cardiovascular events.2

• A meta-analysis of 30 different studies, involving 1,377 participants, found that eating more linoleic acid did not change levels of inflammatory markers in the body.3

The study that sparked the recent seed oil hysteria

It started last month when a study by Soundararajan et al. was published in Gut (by the British Medical Journal).4 Researchers analysed tumour samples from 81 colorectal cancer patients, and compared these to biopsies of non-cancerous tissue taken from a nearby site within the same individuals.

This type of research is classified as a ‘hypothesis-generating study’. These studies are designed to gather observations and form initial hypotheses, which can be tested in follow-up experimental studies in order to draw reliable conclusions. In the case of Soundararajan et al.'s study, its observational nature (and the reliance on data from a single point in time) make it impossible to determine how the observations occurred, allowing only for hypothesis generation at this stage.

What did the study show?

Key findings from the comparison of tumour and non-tumour biopsies:

• Tumour cells and their surrounding tissue showed higher levels of certain inflammatory lipids (fats). This is where some people have implicated seed oils, as some of those lipids are derived from linoleic acid.

• The tumour cells exhibited lower levels of compounds that reduce inflammation.

• Tumour cells and nearby immune cells showed a dysregulation in the expression of genes related to lipid metabolism, preventing these cells from transitioning from an inflammatory state to an inflammation-resolving state.

These observations hint at unresolved inflammation in the tumour microenvironment, but this is not exactly groundbreaking news given that chronic inflammation is a known hallmark of cancer development.

The figures below, direct from Soundararajan et al.’s study, show a difference between the lipid profiles of tumour cells and normal cells. While we can hypothesise that these altered lipid profiles may have supported tumour growth and survival, these findings certainly don’t link linoleic acid consumption to colorectal cancer.

The media misstep

Here’s where it falls apart: finding inflammatory lipids in tumour cells doesn’t mean those lipids caused the cancer. The study’s authors never made that claim. And even if inflammatory lipids were indeed a culprit, they could have come from any dietary source of linoleic acid — including meat fats, eggs, soy, nuts, avocados, or processed foods. Crucially, Soundararajan et al. didn’t review the participants’ diets in any way.

Just a note here to say that Soundararajan et al.’s work is a solid exploratory investigation. The problem lies not with the research but with how it’s been misinterpreted and sensationalised in the media.

Journalists appear to have latched onto a hypothesis by Soundararajan et al. that Western diets — low in fibre and high in linoleic acid — might have contributed to the inflammation they observed in the tumour environments. However, this hypothesis needs to be weighed against all the evidence we’ve just looked at, which shows that moderate to high (but not excessive) linoleic acid intake is actually very good for us.

So are seed oils good or bad?

Seed oils have a rich nutritional profile. They’re a good source of omega-6 fats, which are essential for life, and are rich in vitamin E.

There has been much debate about linoleic acid, the main omega-6 fat found in seed oils. Because linoleic acid is linked to inflammation, some people worry that it might increase the risk of cancer and heart disease. Linoleic acid is an ‘essential fatty acid,’ meaning it is vital for life but can’t be synthesised by the body — it must be obtained through our diets.

Linoleic acid metabolises into arachidonic acid, which plays many critical roles in the body. It supports development, helps fight infections, and assists wound healing. Additionally, it’s a critical component of our cellular membranes, which provide structure to every single cell in the body.

A look at the evidence

With all the fuss around linoleic acid, researchers have been studying it for decades — there is no shortage of quality data. Here are some of the strongest studies:

1. Reduced death rates

Researchers in Finland followed 2,480 people for an average of 22 years. They took regular blood samples to measure levels of omega-6 fats, including linoleic acid and arachidonic acid. They also tracked deaths.5

The results show that:

• Those with higher levels of linoleic acid were 43% less likely to die from any cause.

• Those with higher levels of linoleic acid had a 46% lower risk of dying from heart disease.

• Those with higher levels of linoleic acid had a 52% lower risk of dying from non-heart disease and non-cancer causes (e.g., respiratory diseases or infections).

• Higher linoleic acid levels were not associated with cancer deaths, meaning they did not increase or decrease cancer mortality risk.

• The protective effect of linoleic acid (against death) was similar whether or not participants had a history of chronic diseases like heart disease, cancer, or diabetes.

Takeaway: Higher levels of linoleic acid in the blood are associated with a lower risk of death. Importantly, the study found no evidence that higher omega-6 fat levels increase cancer-related deaths. Seed oils appear to be protective rather than harmful.

2. No change in inflammation

A meta-analysis of 30 different studies, involving 1,377 participants, analysed what happened to inflammation markers when people increased the amount of linoleic acid in their diets.6

The results show that eating more linoleic acid did not change levels of inflammatory markers in the body (including cytokines, TNF, IL-6, or adiponectin).

The one caveat was that, in some cases when people made an extreme increase in linoleic acid intake, there was a slight increase in CRP levels (an inflammatory marker in the bloodstream) — though this effect wasn’t consistent across studies.

Takeaway: Adding moderately more linoleic acid to your diet, such as from seed oils, doesn’t increase inflammatory markers. However, extreme increases in linoleic acid intake might have small effects on CRP in some people.

3. Reduced cardiovascular disease

Another large meta-analysis compiled 30 long-term studies conducted in 13 different countries. The analysis included 68,659 people who were followed for up to 32 years.7

Researchers looked at levels of linoleic acid in the blood and tissues, and compared this to rates of heart attack, stroke, or death from cardiovascular causes. They also checked whether factors like age, sex, diabetes, or use of medications affected the results.

The results show that people with higher levels of linoleic acid in their bodies had a 7% lower risk of cardiovascular disease and a 22% lower risk of death from cardiovascular events. Arachidonic acid was also found to lower the overall risk of cardiovascular events.

Takeaway: Eating foods rich in linoleic acid, like seed oils, may help prevent heart disease and lower death from cardiovascular causes.

4. Improved physical function

Researchers in the States analysed data from a group of older adults (average age of 74 years) who had participated in a larger study about ageing, health, and energy use. The participants’ diets had been tracked, and those eating a suboptimal amount of linoleic acid were classified as having "low LA intake."8

The results show that people with low linoleic acid intake were 2.5 times more likely to have trouble climbing stairs compared to those who consumed more linoleic acid. Results were adjusted to account for other factors that might affect physical ability, such as age, weight, and other health conditions.

Takeaway: Eating enough linoleic acid may help maintain physical function in older adults. Linoleic acid is essential for our cells to produce energy.

The case against seed oils

Alright, we get it — the linoleic acid in seed oils saves lives. So why has it stirred up so much debate?

• Some research in animals has linked high linoleic acid intake to increased inflammation and tumour growth. For instance, studies have found that mice on diets rich in linoleic acid showed enhanced tumour growth.9

• In laboratory cell-based studies, linoleic acid has shown pathways leading to inflammation. One example is a study of trophoblast cells, where exposure to linoleic acid led to an increase in prostaglandin, a pro-inflammatory mediator.10 However, large human studies (like those already discussed) have failed to confirm this.

• A few human studies (discussed above) have suggested extreme linoleic acid intake could slightly raise CRP levels, an inflammatory marker. However, this effect is inconsistent across studies and minimal at best.

It’s important to remember that, while lab studies and animal models can raise theoretical concerns, they don’t always translate to real-world human outcomes. The overwhelming body of large-scale human research shows that linoleic acid is good for our health when consumed at normal to high (but not excessive) dietary levels.

High heat can make seed oils harmful

One thing to keep in mind when cooking tonight’s dinner is that harmful byproducts, known as reactive metabolites, can form when seed oils are heated to very high temperatures — such as during deep frying. Polyunsaturated fats (like those found in seed oils) are particularly prone to oxidation at high heat, leading to the production of toxins such as aldehydes and ketones. These can increase oxidative stress in the body, which may contribute to health issues over time.

However, it’s important to distinguish between different cooking methods. The general use of seed oils in everyday cooking — such as sautéing or baking at moderate temperatures — is unlikely to produce harmful byproducts. Proper storage and avoiding excessive reheating can further minimise the risk. When used appropriately, seed oils are a safe and nutritious part of a balanced diet.

The real culprit: Ultra-processed foods

If you’re looking for dietary villains, ultra-processed foods are the real culprits. These foods are typically low in fibre, high in refined carbohydrates, and loaded with salt, sugar, and – yes – seed oils. However, it’s the overall nutritional profile of these foods, not just the oils, that’s a problem. Overconsumption of ultra-processed foods has been linked to chronic inflammation, weight gain, and an increased risk of lifestyle-related diseases. Shifting to a balanced diet rich in whole, minimally processed foods is far more effective for health than fixating on the type of oil in your frying pan.

Takeaways for your kitchen

Should you ditch seed oils entirely? Not necessarily. Here are some practical tips to keep your meals healthy while avoiding the media scaremongering:

• Incorporate a variety of oils, such as olive oil, avocado oil, and flaxseed oil, to diversify your fat sources – but don’t shy away from seed oils.

• When you’re cooking at high temperatures, choose oils with high smoke points and stable fatty acid profiles, such as avocado oil or refined olive oil (extra virgin is less stable at high temperatures). Seeing smoke is a clear indicator that an oil is breaking down into harmful compounds.

• Prioritise high-fibre foods to help reduce inflammation and support gut health. Think whole grains, beans, and leafy greens.

• Limit ultra-processed foods. This simple step is one of the most effective ways to manage your intake of less-than-ideal ingredients, and prevent excessive seed oil consumption.

Seed oils aren’t the enemy. Misinformation is. The notion that seed oils are driving a colon cancer epidemic is a textbook case of oversimplification and media hype. While it’s wise to be mindful of your omega-6 intake, demonising a single ingredient without understanding the broader dietary context does more harm than good. So, go ahead and stir-fry those veggies. Your colon – and your common sense – will thank you.

As we step into the new year, many of us are setting ambitious resolutions for better health. But what if I told you that small, manageable changes have a bigger effect on well-being? Science increasingly shows that small, sustainable habits, rather than drastic overhauls, are the key to long-term health.

Let’s take a look at the research. As always, individual studies must be interpreted in the context of wider evidence - all of the studies below are well supported.

Slight diet adjustments yield big results

Takeaway: Replacing just 10% of daily calories from processed foods with whole food alternatives adds an additional 48 minutes of healthy lifespan per day.

Dietary adjustments don’t have to be extreme to make a difference. A study published in Nature Food analysed the epidemiological evidence for over 5,800 foods, and revealed that even small changes to dietary composition significantly impact our quality of life. The title of the study says it all: Small targeted dietary changes can yield substantial gains for human health and the environment.1

Key Results

• Replacing 10% of our daily intake (around 190 calories) from processed foods with whole food alternatives resulted in a 48-minute gain in healthy lifespan per day, and a 14% reduction in mortality from all causes.

• This same 10% dietary change led to a 33% reduction in the dietary carbon footprint.

• Foods like fresh fish with tomatoes add up to 82 minutes of healthy lifespan per serving, while frankfurter sandwiches and hotdogs cost 36 minutes per serving.

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Moderate exercise goals are enough

Takeaway: Just 150 minutes of moderate exercise each week (such as brisk walking) gains almost maximal results, and reduces the risk of premature death by up to 25%. Doing additional exercise doesn’t add much extra benefit, though it isn’t harmful either.

Consistent physical activity is one of the most effective ways to increase quality of life. In a recent study published in Circulation, Lee et al. analysed data collected from 116,221 adults over 30 years. Participants regularly reported their leisure-time activities, and researchers looked at how these activities affected the risk of dying (from any cause), heart-related problems, and other health issues.2

It’s worth noting that certain forms of exercise, such as strength training, have been shown to offer specific health benefits beyond the scope of this particular study.

The analysis used the 2018 Physical Activity Guidelines for Americans, which recommend:

1. 150 to 300 minutes of moderate activity per week (brisk walking, gardening); or

2. 75 to 150 minutes of vigorous activity per week (running, aerobics); or

3. A mix of both, where one minute of vigorous activity is equivalent to two minutes of moderate activity.

Key Results

• Meeting the activity guidelines: Doing the recommended amount of moderate activity reduced the risk of mortality by 19–25%, while the recommended amount of vigorous activity reduced this risk by 15–31%, with even stronger protection against heart-related mortality.

• Exceeding the activity guidelines: Doing additional moderate activity only lowered the risk of mortality by another 3%, and additional vigorous activity added a 2–4% risk reduction.

• Greatly exceeding the guidelines: Exceeding twice the amount of recommended activity didn’t provide any extra benefit, but wasn’t harmful either.

• Moderate vs vigorous activity: For those who met the moderate activity recommendation, adding vigorous activity didn’t provide extra benefits. For those who didn’t do enough moderate activity per week, adding vigorous activity reduced their mortality risk.

Sleep: The underrated resolution

Takeaway: Poor sleep is overwhelmingly associated with the new onset of a plethora of chronic health conditions, including high blood pressure, depression, anxiety, obesity, and heart failure.

If there’s one resolution you shouldn’t overlook, it’s sleep. Nature Medicine published a fantastic study this year which used Fitbit to track the real-world sleep data of 67,850 people for up to 6.5 years. Researchers also tracked participants’ health metrics.3

Key Results

Sleeping too little (<6 hours) or too much (>10 hours) is strongly associated with an increased likelihood of developing certain conditions:

• High blood pressure: Sleeping 5 hours per night was linked to a 29% increased risk of developing hypertension, while sleeping 10 hours was linked to a 61% increase.

• Depression: Sleeping 5 hours was linked to a 64% increased risk of new onset depression, and 10 hours to a 163% increase.

• Anxiety: Sleeping 5 hours was linked to a 46% increased risk of developing anxiety, and 10 hours to a 130% increase.

• Heart failure: Increased REM sleep was linked to a 49% reduced risk of heart failure, whereas increased light sleep was linked to a 130% higher risk.

Going to bed at the same time each night matters. Irregular sleep patterns were strongly associated with:

• 75% higher likelihood of developing major depressive disorder;

• 55% higher likelihood of developing generalised anxiety disorder;

• 49% higher likelihood of developing obesity;

• 39% higher likelihood of high cholesterol;

• 127% higher likelihood of bipolar disorder;

• 60% higher likelihood of migraines.

Small mindfulness goals go a long way

Takeaway: Even short mindfulness sessions, ranging from just 5-20 minutes in length, can improve our mental and physical well-being.

Mental health often takes a backseat in New Year’s resolutions, but brief mindfulness interventions are a practical, low-commitment way to improve well-being. A large systematic review analysed data from 85 smaller studies involving 7,837 participants, most of whom were healthy adults under 30 years old, to understand whether short mindfulness sessions affect health. Participants completed a diverse range of general mindfulness practices, such as breathing exercises and body scans.4

Key Results

• Improved attention & focus: Participants showed a 20–25% increase in sustained attention after a brief mindfulness exercise.

• Improved emotional regulation: A single mindfulness session reduced negative affect (e.g., feelings of sadness or anger) by up to 15%, depending on the task.

• Reduced cravings: Brief mindfulness exercises like ‘urge-surfing’ reduced the intensity of cravings, such as nicotine cravings, by around 20%.

• Reduced anxiety: Researchers found a 14% reduction in self-reported anxiety after a single 10 minute session.

• Improved stress resilience: Brief mindfulness sessions reduced cortisol levels (a stress hormone) and improved self-reported stress scores. Heart rate and blood pressure during stress-inducing tasks were also reduced.

A healthier 2025

This new year, remember: meaningful health changes don’t require monumental effort. Small, science-backed shifts in our daily routines can have a major effect on overall health.

Instead of vowing to do intense exercise every day, walking for 30 minutes five times per week gives 97% of the same benefits as going beyond the activity guidelines. This goal is realistic, trackable, and far more likely to stick.

What are your 2025 resolutions? Let me know in the comments, and let’s go on this health journey together. Here’s to a happy, healthy new year!

Before diving in, I want to highlight a post from Evolution and Psychiatry featuring Anne-Laure Le Cunff’s insightful work on ADHD. It offers a strengths-based perspective, reframing ADHD as an evolutionarily adaptive trait. This approach invites us to move beyond a deficit-focused lens and embrace the unique abilities that individuals with ADHD bring to our modern world.

Evolution and Psychiatry

The Hypercuriosity Theory of ADHD

It is an absolute pleasure to introduce to our readers Anne-Laure Le Cunff who recently published a paper in Evolutionary Psychological Science titled…

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a year ago · 34 likes · 5 comments · Evolution and Psychiatry

Why the word 'miscarriage' is misleading

This is a topic close to my heart. Like so many other women, I've experienced pregnancy loss — for me, it came during an IVF journey that had already felt long and challenging. As I journeyed through the weeks that followed, women all around me shared their own stories of loss. I was struck by just how common the experience is, but also by the prevalence of guilt and self-doubt. To echo the words of Taylor Swift: "Did some force take you because I didn't pray?" Or was it because I was stressed last week, ate that salmon, didn’t exercise enough, or perhaps exercised too much?

Self-blame is a common response, but a closer look at the science absolves us of personal responsibility and is, ultimately, freeing. Most pregnancy losses aren’t caused by anything the person carrying the pregnancy did or didn’t do. Instead, they’re overwhelmingly the result of chromosomal abnormalities — issues that prevented the embryo from developing because it didn’t have the correct ‘instruction manual’ needed to grow into a healthy baby.

This reframing matters. Even the term ‘miscarriage’ implies fault, as though the womb-holder ‘mis-carried’ the pregnancy. But when we look at the biology, it becomes clear that this term is misleading. Let’s explore why, and understand how the science of pregnancy loss can lead to a kinder and more accurate narrative.

Causes of pregnancy loss

Recent studies show that up to 68% of pregnancy losses are caused by chromosomal abnormalities.1 These are random errors in the embryo's DNA that occur during conception or early cell division, and are entirely unpreventable. The remaining 32% of pregnancy losses result from a diverse range of factors. While the vast majority of these other factors are also unpreventable, our focus today is on chromosomal abnormalities, as these are by far the most common cause of pregnancy loss.

Chromosomal abnormalities

Pregnancy begins with the combination of genetic material from the sperm and egg to form an embryo. Each contributes 23 chromosomes, creating a full set of 46. These chromosomes act as the embryo’s instruction manual, containing all the information needed for development. When the genetic material combines correctly, the embryo is considered 'euploid' — it has the right number and structure of chromosomes. Euploidy is essential for the embryo to grow and thrive.

Errors can occur before or during fertilisation or during early cell division, which lead to an embryo that has too many or too few chromosomes, or structural defects within the chromosomes. This is called ‘aneuploidy’. In most cases, these abnormalities happen randomly and are not influenced by the actions of the person carrying the pregnancy. The same biological processes that create our unique individuality, through the random assortment of chromosomes from Mum and Dad, also lead to aneuploidy in some embryos.

How chromosomal abnormalities cause pregnancy loss

An embryo containing the correct number and structure of chromosomes has a complete instruction manual for the complex process of cell division, organ formation, and overall growth. However when an embryo is aneuploid — having too many or too few chromosomes — these instructions are incomplete or contradictory. This prevents the embryo from progressing through critical developmental milestones.

Unlike some biological processes that can be corrected by the body, an aneuploid embryo cannot develop into a healthy baby, even in the most supportive environment. Even in a 'perfect womb', if there were such a thing, these embryos would not be viable.

The stage at which an aneuploid pregnancy will end depends on which section of the embryo's DNA is abnormal. If a critical section is missing, the pregnancy might end very early (or the embryo might not even implant). However, if the chromosomal abnormality affects a gene that's not needed until later in embryonic development, the pregnancy might continue for the first few months.

How common are chromosomal abnormalities?

Research shows that approximately 47-52% of all human embryos are aneuploid (chromosomally abnormal), though most of these don't make it to implantation.2 Individual rates of aneuploidy vary with maternal age – but even young parents still have aneuploidy rates of about 30%. This high rate of chromosomal abnormalities reflects the inherent variability and randomness of reproduction, which is necessary to create the incredible genetic diversity we see around us. But the same variability and randomness that have given birth to the remarkable diversity of life on Earth also occasionally lead to outcomes incompatible with life. Such is the beauty and fragility of genetic variation.

Fortunately, most aneuploid embryos don’t make it to implantation. Studies suggest that the majority either arrest in development during early cell division stages (prior to implantation) or fail to establish the biochemical communication required for implantation.3

A compassionate reframing

When we understand that most pregnancy losses are due to factors beyond anyone’s control, it becomes clear that in most cases the womb-holder did not ‘mis-carry’ anything. They gave their body to provide the best environment possible for the pregnancy to thrive. If the embryo couldn’t survive, it’s most likely because genetic variation processes resulted in an incomplete set of instructions, or one of several other equally unavoidable causes.

‘Miscarriage’ is a medical term, defined as the spontaneous loss of a foetus before the 20th week of pregnancy. While it remains important to have universal medical definitions, it can be helpful to shift our language when appropriate. By referring to miscarriage in terms like ‘pregnancy loss’ or ‘embryo loss’ we provide a more compassionate framing, remove the implied blame, and create space for understanding and healing. This also opens the door to greater awareness of the biological complexity behind pregnancy loss. This reframing matters.

Healing after pregnancy loss

For those who have experienced pregnancy loss, understanding the biology can be a powerful step toward healing. Here are three key points to remember:

1. Most pregnancy losses are unpreventable. Chromosomal abnormalities are random and beyond anyone’s control, as are almost all other causes of pregnancy loss.

2. Pregnancy loss is common. About 15% of known pregnancies end in loss,4 making it a shared experience for many. You’re not alone.

3. It’s okay to grieve. Whether the loss occurred at seven weeks or seventeen, it’s a significant loss and grief is a valid response.

If you’ve experienced pregnancy loss, I see you, and I honour your story. It’s not your fault, and you’re not alone. By understanding the biology and shifting our language, we can build a culture of informed compassion.

Support resources for families experiencing pregnancy loss.

If you found this article meaningful, I invite you to share it with someone who might need these words. Together, we can foster a better understanding of pregnancy loss and support one another with compassion and care.

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We’ve all pulled the occasional late night, buoyed by caffeine and the promise of a Sunday sleep-in. But what if that lost sleep isn’t as benign as we’d like to believe? Mounting evidence reveals a stark and unsettling truth about the impact of our modern lifestyles: sleep deprivation is linked to heart disease, cognitive decline, Alzheimer’s disease, autoimmune disorders, diabetes, depression, cancer, and countless other conditions. Sleep — or the lack thereof — might just be one of the most underrated health threats of the modern age.

What happens when we sleep

At first glance, sleep might seem like an inefficient biological trait, leaving animals vulnerable to predators and cutting into time that could be spent on essential survival activities. Yet, despite these apparent drawbacks, evolution has consistently preserved sleep across the animal kingdom, with some species sleeping for up to 20 hours a day (looking at you, Little Brown Bat). This begs a fascinating question: what makes sleep so indispensable that evolution has not only retained it, but seemingly prioritised its role?

Sleep is the body’s nightly pit stop: a chance to undertake critical repair and recalibration.1 While many mysteries of slumber remain unsolved, we do know that during sleep:

• Nerve cells communicate, reorganise, and repair.

• The brain flushes out toxic waste products like amyloid, which is linked to Alzheimer’s disease.

• The pituitary gland releases hormones critical for tissue repair, muscle growth, and cellular regeneration.

• The body’s core temperature drops, providing the optimal environment for cellular repair processes.

• Blood pressure drops, allowing vascular repair and reducing strain on the heart.

• Organs like the liver ramp up detoxification processes, flushing out the day’s toxins to keep the body running clean.

• The immune system steps into overdrive, churning out cells vital for defence and repair.

• Key hormones regulating appetite, metabolism, and stress are rebalanced.

• The hippocampus consolidates memories and optimises problem-solving processes.

• Natural killer cells patrol the body, destroying cancer and virus-infected cells.

When sleep falters, this finely tuned system collapses. Instead of renewal, the body is left with chronic inflammation, diseased cells, heightened stress, and accelerated wear and tear.

Sleep loss breeds chronic inflammation

Research by Irwin and colleagues shows that even a single night of poor sleep floods the bloodstream with inflammatory molecules, like interleukin-6 and tumour necrosis factor-alpha.2 These molecules raise inflammation across the body, and are ominously linked to chronic conditions such as arthritis, cardiovascular disease, and depression. Their presence after just one restless night highlights the toxicity of our modern sleep-deprived lifestyles. Missing sleep isn’t just an inconvenience; it’s a biochemical grenade, releasing harmful agents that wreak havoc on the body.34

A large meta-analysis paints an even darker picture: people who routinely clock fewer than six hours of sleep experience persistently high levels of these inflammatory molecules compared to those enjoying a restorative seven to eight hours.5 This low-grade inflammation quietly erodes tissues and organs, setting the stage for chronic conditions like cardiovascular disease, insulin resistance, and cognitive decline. The cumulative damage of sleep deprivation undermines nearly every vital body system.

Hypertension and cardiovascular disease

One of the most well-documented casualties of poor sleep is our cardiovascular health, and the evidence is striking. Chronic sleep loss has been linked to elevated rates of hypertension, arrhythmias, and even heart attacks. A massive study that analysed data from 470,000 participants revealed that those who routinely slept less than six hours per night had a 48% increase in rates of coronary heart disease, compared to those who enjoyed the recommended 6-8 hours’ sleep.6 Another extensive study, involving over 1.3 million participants, found those who averaged less than six hours’ sleep were 12% more likely to experience premature death from any cause.7

One of the key mechanisms underlying this is chronic inflammation. Inflammatory molecules, which are elevated in the bloodstream when we’re sleep deprived, directly damage the delicate lining of blood vessels. This damage impairs the ability of our arteries to relax and maintain proper blood flow and pressure. Over time, this damage accumulates, paving the way for hypertension and a cascade of other cardiovascular complications.

Brain fog, mood swings, and Alzheimer’s disease

The effects of sleep deprivation on the brain are profound and far-reaching. In the short term, missing sleep leaves us grappling with impaired attention, memory lapses, and poor decision-making. Long-term consequences, however, are significantly more troubling. Research led by Cedernaes shows that sleep loss accelerates the buildup of amyloid plaques in the brain — a hallmark of Alzheimer’s disease.8

When we sleep, the glymphatic system — a network of fluid channels in the brain — circulates fluid to flush out toxic waste products, including amyloid. This system is highly active during sleep but largely inactive when we’re awake. Research has shown that amyloid starts accumulating in the brain after just one night of sleep deprivation.9 Some researchers believe that the universal need for sleep across species partly reflects the requirement for the brain to enter a state of deep rest in order to flush out toxic waste products.

Emotionally, the impact of poor sleep is equally devastating. A meta-analysis of 21 studies by Baglioni et al. identified a strong relationship between sleep deprivation and the exacerbation of depressive symptoms.10 Once again, the chronic low-grade inflammation caused by sleep loss is believed to underlie this finding. (Check out my article The Hidden Culprit Behind Depression for a deep dive into the research linking inflammation to our mental health.)

The diabetes connection

Sleep deprivation and diabetes are a destructive duo. Insufficient sleep directly increases insulin resistance and disrupts glucose metabolism, sending blood sugar regulation into turmoil. Spiegel et al. demonstrated that just six nights of restricted sleep (limited to four hours per night) led to a staggering 30% reduction in insulin sensitivity — a level comparable to early diabetes.11 Once again, the disease process is mediated by those inflammatory molecules that are elevated during times of sleep loss. Inflammatory cytokines impair the body’s ability to efficiently process glucose, exacerbating metabolic dysfunction.

The hidden cost of sleep loss

Sleep deprivation has far-reaching consequences for almost all aspects of physical and mental health. Beyond the conditions already discussed, sleep loss is also linked to:

• Weakened immune function and prolonged recovery from infections.

• Increased risk of neurodegenerative conditions like Parkinson’s disease.

• Higher stroke risks and worsened outcomes for existing heart conditions.

• Disruption of hunger-regulating hormones, driving appetite and weight gain.

• Gastrointestinal disorders, including irritable bowel syndrome and altered gut microbiota.

• Heightened sensitivity to pain and reduced effectiveness of pain relief.

• Disrupted thyroid and adrenal gland function, leading to hormonal imbalances.

• Abnormal reproductive hormone levels, with reduced fertility and pregnancy outcomes.

• Accelerated skin ageing due to impaired cellular repair processes and reduced collagen production.

• Higher rates of breast, prostate, and colorectal cancers.

• Dry eyes, blurred vision, and other ocular issues.

• Weakened vaccine efficacy.

• Increased likelihood of accidents, including fatal car crashes.

Why aren’t we sleeping?

Sleep deprivation has become alarmingly common, but why? Some blame it on the pervasive trifecta of technology, stress, and 24/7 culture. Blue light from screens suppresses melatonin, the hormone that signals the body to sleep. Late-night scrolling, midnight emails, and endless to-do lists keep our brains on high alert.

Even our diets conspire against us; processed and sugary foods disrupt sleep. The good news is that a Mediterranean diet rich in whole grains, fruits, and healthy fats has been shown to improve all features of sleep — including quality, duration, and reduced daytime sleepiness.12

What can we do about it?

Understanding the consequences of sleep deprivation can motivate us to push back against those late-night demands, though that’s easier said than done in today’s world! As with most aspects of health, lifestyle adjustments remain the most accessible and effective strategies: sticking to a consistent sleep schedule, limiting screen time before bed, dimming artificial lights, incorporating relaxation techniques like mindfulness or meditation, regular physical activity, and a balanced diet have all been shown to support restorative sleep.

When lifestyle adjustments don’t fit the bill, sleep specialists offer a range of interventions, including melatonin supplementation, pharmacological treatments, blue-light therapy, cognitive-behavioural therapy for insomnia (CBT-I), positive airway pressure therapy, and even surgical intervention.

The science is clear: sleep is a necessity. Chronic sleep deprivation erodes both mental and physical health, one night at a time, leaving us vulnerable to a cascade of illnesses. By reclaiming our sleep, we can disarm the silent epidemic and wake up to better health.

References

For years, we’ve considered depression to be a wiring issue — a misfire of brain chemistry with a bit of serotonin shortage here and too much stress there. But a growing body of research is flipping that notion on its head, suggesting that inflammation — the same process that fights off colds, heals sprained ankles, and causes us to regret last night’s questionable takeout — might also be pulling the strings behind our mood swings. The idea that depression could be part brain, part immune system may sound bizarre, but there’s a lot of research supporting this theory. So, what exactly is going on beneath the surface?

Inflammation: Friend or Frenemy?

Inflammation is the body’s emergency response team — like an army of highly trained soldiers rushing in to defend against infection or heal injury. But what happens when this army overstays its welcome? Picture them not just fighting invaders but also ransacking the city. That’s chronic inflammation, and it could be culpable for our mood changes.

A meta-analysis of 82 studies found notable differences in levels of inflammatory molecules between people with depression and those without.1 With names that could be plucked from a sci-fi novel - Interleukin-6, tumour necrosis factor-alpha, and C-Reactive Protein — these inflammatory molecules were consistently elevated in those battling depression. Research has even found that higher levels of these molecules are associated with increased severity of depression and suicidality.2 These molecules are our bodies’ prime defenders, but when they hang around too long they can cause all sorts of problems, mental health included.

How Inflammation Toys with Our Moods

So, how does inflammation mess with our minds? Some inflammatory molecules, like cytokines, can sneak past the blood-brain barrier. Once inside the brain, these molecules activate specialised immune cells called microglia. Microglia are the brain’s tidy housekeepers, keeping things in order. But when inflammation ramps up they can go rogue, remodelling neural connections, and disrupting the delicate balance of neurotransmitters like serotonin and dopamine.3

Perhaps some of the most compelling evidence linking inflammation to depression comes from the autopsies of suicide victims. Numerous pathologists have found higher levels of activated microglia in the brains of suicide victims, implicating these neural housekeeper cells in exacerbating depressive symptoms.4

Think of it like a botched home renovation — with microglia tearing down walls that should have stayed up, and disrupting the electricity so the lights won’t stay on. That’s what chronic inflammation does to our brains, disrupting essential connections and leading to the emotional numbness and brain fog we associate with depression.

So Where’s All This Inflammation Coming From?

Enter Michael Berk and his team, who did a deep dive into the origins of this inflammation, and guess what? The evidence points straight to our modern lifestyles. A poor diet, lack of exercise, obesity, smoking, stress, and even gut issues can all send our immune systems into a frenzy.5

If our diet is packed with processed foods or we’ve been enjoying a bit too much sedentary bliss, we could be laying the groundwork for chronic inflammation. Stress, in particular, is a prime offender. Research shows that prolonged stress cranks up levels of pro-inflammatory molecules called cytokines, in both humans and animals. ⁵ The longer the stress drags on, the higher the inflammation, and the greater the risk of slipping into depression.

An Evolutionary Quirk?

But why would evolution saddle us with a system that can mess with our moods so dramatically? There’s a theory: during times of illness or injury, feeling low-energy and disinterested in life may have been a survival advantage. Running around and socialising while unwell wouldn’t have helped our early ancestors heal. Instead, “sickness behaviour” — that desire to shut down and withdraw — might have been nature’s way of ensuring we conserved energy and didn’t spread our germs to the tribe. It’s biology’s way of saying, “Stay in your cave; let your body recover.”

What Does This Mean for Treatment?

So, should we all start gobbling anti-inflammatories like candy? Not so fast. It turns out that common antidepressants, particularly SSRIs, have anti-neuroinflammatory effects of their own, which could explain why they work so well for some people.6 However, they’re far from a universal fix.

Emerging research suggests that people with elevated inflammatory molecules — like CRP or cytokines — might benefit from treatments specifically targeting inflammation, though more research is needed. ³ There’s also real potential for new, personalised treatments, where we custom-tailor immunotherapies based on individual immune profiles (especially with cutting-edge biologic drugs on the horizon). There’s a future where we’ll be spared the horrible trial-and-error approach of current antidepressant prescribing.

In the meantime, there are everyday ways to cool down the inflammatory fire. Regular exercise, a Mediterranean-style diet, and improved sleep habits have all been shown to reduce inflammation. ⁵ They’re not a magic bullet, but getting out for a brisk walk or trading that processed snack for some leafy greens can go a long way in improving both our mental and physical health. It turns out that modulating our own immune systems is within reach for most people.

Viewing depression through the lens of inflammation adds another piece to an intricate and incomplete puzzle, fitting alongside what we already know about brain chemistry. The complex interplay between the immune system, lifestyle, and mental health reminds us that we are, quite literally, a product of both mind and body. These 21^st century medical advancements are incredibly exciting, and new immunotherapies are going to change medicine as we know it. Watch this space.

In our modern capitalist world, we’re often told that success lies in more — more money, more status, more stuff. But an extraordinary 80-year-long study conducted by Harvard researchers turns that assumption on its head. The Harvard Study of Adult Development,1 which followed 724 people over eight decades, has revealed that social relationships — not fame, money, or even career success — are the true key to a happy and healthy life.

So, what did they find? It turns out that the quality of a person’s relationships at age 50 was the best predictor of their health and happiness at age 80. Those with strong, fulfilling relationships lived longer, happier lives, regardless of wealth or social status​. People with close social ties had lower levels of stress, less mental decline, and fewer chronic illnesses​. In contrast, loneliness proved to be as harmful to health as smoking or alcoholism.2 Let that sink in for a moment.

Interestingly, the relationships didn’t need to be smooth sailing. Couples who bickered but felt they could count on each other in tough times still experienced the same health benefits as those in more harmonious relationships​. It turns out that feeling supported and connected matters far more than always seeing eye-to-eye.

The Dunedin Study in New Zealand, which has followed over 1,000 people since birth, echoes similar findings.3 Those with better social and emotional connections, not the most affluent, reported the highest satisfaction across their lives. Like the Harvard study, Dunedin researchers found that material wealth had little impact on long-term well-being. Once basic needs were met, more money didn’t increase health or happiness​.

On a personal level, this resonates with me deeply. I come from a family of ambitious visionaries — always striving to grow and build. Yet, despite their outward success, I’ve seen firsthand that there’s never quite ‘enough.’ The satisfaction of a new venture quickly fades, and the next pursuit begins — an endless cycle of wanting more. Meanwhile, it’s the small, shared moments, like laughter over dinner or leaning on each other in tough times, that create lasting joy.

In a world that often pushes us to chase the next promotion or bigger pay cheque, the Harvard study reminds us of what truly matters. By investing in our relationships, whether with family, friends, or even acquaintances, we can find the secret to a long and fulfilling life.

Relationships, it turns out, are the ultimate investment.

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