Think of a house in winter.  The thermostat is set to 21°C and the central heating works to hold it constant.  Open a window and heat escapes, the thermostat senses the drop in temperature and the central heating kicks in again until the temperature is restored.  The temperature is defended: whatever pushes it off target, the system works to bring it back.

Nobody would think the temperature is controlled by the boiler, because they understand it is the setting on the thermostat that regulates the temperature in the house.

The body regulates fat mass in a similar way.  Energy balance and calories in versus calories out is arithmetically true, but it describes the room temperature rather than the regulation of the thermostat.  The more useful question is what sets the dial and what happens biologically when we try to force weight down.

The Body Defends Fat Mass, Not Body Weight

Physiological pathways regulating fat mass resemble those governing core body temperature, blood glucose and blood pressure.  All sense the internal and external environment and respond homeostatically to keep the regulated variable within a narrow range^1,2.

In steady state, fat mass is typically held within roughly 1-3% of its defended level¹.  The defended level is the amount of fat mass the body works to maintain, resisting sustained loss or gain.  Importantly, the body appears to regulate fat mass rather than body weight itself.  This becomes evident when astronauts enter microgravity and they do not change their bodyweight because weight is not defended but fat mass is.

How the Brain Senses Calories, Not Just Volume: The Gut-Brain Axis

When nutrients reach the intestine, enteroendocrine cells (i.e. specialised hormone-secreting cells within the gastrointestinal tract) release a co-ordinated pattern of hormones including GLP-1, PYY, oxyntomodulin, cholecystokinin and amylin, while ghrelin (i.e. an appetite stimulanting hormone) secretion from the stomach and duodenum is suppressed^1,2.

These signals reach the subcortical areas of the brain through the circulation and vagal pathways and their magnitude is influenced by the calories contained in the meal¹.  They contribute to satiation, which brings a meal to an end and to satiety that determines the period between meals².

Much of this happens without conscious involvement.  Calories rather than volume of food appears to be important because far more satiety is achieved with two litres of full fat milk versus two litres of water.

How the Brain Senses Fat Mass: Leptin

The second input is the size of the body fat store itself.  The circulating signal that communicates the size of fat mass to the brain is leptin, which was identified in the early 1990s^3,4.

Leptin acts on hypothalamic pathways including the melanocortin system and interacts with melanocortin signalling to influence food intake and energy expenditure¹.

The importance of this circuitry is illustrated most clearly in rare genetic forms of obesity.  Children with rare genetic variants affecting this pathway (for example, in LEP, LEPR, POMC or MC4R ) can develop severe early-onset obesity accompanied by profound hunger and impaired satiety⁵.

Many genetic variants linked to obesity affect how the brain and nervous system regulate hunger, fullness and eating behaviour^6,7.

Obesity can therefore be understood as a disease characterised by dysregulation of brain-based systems interacting with the gut, adipose tissue, genetics and the environment.

Leptin appears to be the most impactful signal that can activate or deactivate the fat mass defence mechanisms of the subcortical areas of the brain unless the disease of obesity is controlled.

Leptin links the size of the adipocyte mass to the brain systems that regulate appetite and energy expenditure and falling leptin levels during fat loss help activate the biological responses that oppose further loss.

Unwanted Weight Gain Reflects a Rising Fat Mass that the Body Tries to Defend

The pathophysiology of obesity can be understood as involving impaired leptin signalling, similar to insulin resistance in type 2 diabetes^2,8.  When central leptin signalling is impaired, the counter-regulatory responses that would normally limit further fat accumulation become less effective.

Fat mass expands until sufficient signalling is restored, at which point a new higher fat mass becomes biologically defended^1,2.  Increased food intake during this process is thus a consequence of the underlying disease biology.  Once a higher fat mass is established, the body defends it against calorie restriction in much the same way it defended the previous lower level^1,2.

Why “Eat Less, Move More” Does Not Tell the Full Story

When calorie intake falls and fat mass is reduced, leptin levels decrease substantially, triggering a co-ordinated and durable biological response until the fat mass is restored to the defended homeostatic position.

Energy

Studies spanning four decades have shown that after weight loss the body becomes more energy-efficient, with total daily energy expenditure falling approximately 15–20% below what would be expected for the person’s new body size and composition^2,9.

This metabolic adaptation makes weight loss more difficult to maintain, because the body defends against further weight loss.  The adaptation persists for as long as the reduced fat mass is maintained and may diminish as fat mass is regained^1,10.

Hormones

Following substantial weight loss, thyroid hormone concentrations fall without the expected compensatory rise in Thyroid-Stimulating Hormone (TSH)^2,11.  Satiety-related gut hormone responses weaken while ghrelin increases and some of these adaptations persist for at least a year^2,12,13.

Appetitive Behaviour

Appetitive behaviour refers to the behaviours and the motivations underlying them that lead people to seek out, choose and consume food.

After weight loss, people often feel less satisfied by the same portion and become hungry sooner and this is frequently accompanied by greater preoccupation with food, increasingly described as “food noise”^2,14.

This can result in a stronger drive to obtain food, which may also be accompanied by an increased preference for energy-dense foods.

What the Diabetes Prevention Program Showed

The Diabetes Prevention Program^15,16 illustrates both the effectiveness of intensive lifestyle intervention and the difficulty of maintaining the initial weight loss over time.

Participants in the lifestyle group lost an average of approximately 7kg in one year.  Over subsequent years, some of the lost weight returned and after 10 years of effort the group was only 2kg below their baseline weight^15,16.

The pattern of initial weight loss followed by partial weight recurrence is consistent with the metabolic adaptations that oppose sustained fat mass reduction^2,16.  People who experience weight recurrence after diet-induced weight loss should therefore not be viewed as non-adherent or insufficiently motivated.

Understanding their biology may be far more productive².

Where does Food and Diet Quality Fit

None of this diminishes the role of good quality nutrition.  It places nutrition within the biology of appetite regulation.

An instructive example comes from an inpatient randomised trial comparing highly-processed and unprocessed diets designed to be matched for presented calories, energy density, macronutrients, sugar, sodium and fibre.  Participants consumed approximately 500kcal per day more during the highly-processed diet and gained weight over two weeks¹⁷.

Food texture has been shown to influence eating rate and post-meal satiety, with harder-textured highly-processed meals consumed more slowly and associated with greater fullness and lower subsequent snack intake, compared with soft textured highly-processed meals¹⁸.  The findings illustrate how food’s composition and texture can influence spontaneous energy intake without deliberate calorie counting.

Higher-protein dietary patterns can likewise improve satiety and reduce overall calorie intake in some settings¹⁹.  Some aspects of eating including hunger, meal size, meal frequency and satiation are strongly physiologically driven and may respond to nutritional therapies, pharmacotherapies and/or surgical therapies.

Others including food choice, meal structure, culture and the household food environment remain important targets for nutritional and behavioural intervention², albeit the target is not weight loss but health gains, especially in quality of life gains that may occur without weight loss .  The two are complementary rather than competing.

Obesity Medicines Change Adipocyte Mass Regulation

With the exception of orlistat, current obesity medicines are understood to act through subcortical brain pathways involved in fat mass regulation².  Improvement in appetitive behaviour often occurs before substantial weight loss becomes apparent²⁰.

This may be explained by considering the obesity medications as putting the disease of obesity under control, thus creating a lower fat mass that needs to be defended.  Therefore, the only way for the subcortex of the brain to achieve the new defended fat mass is to make the person less hungry, feel fuller and reduce portion sizes.

Consequently the person may experience a reduction in appetitive behaviour, often interpreted as a reduction in “food noise”².  Discontinuation of effective obesity treatment commonly leads to relapse of the disease of obesity and a higher fat mass that is defended.  This results in renewed hunger and weight recurrence, supporting the concept that obesity often requires long-term treatment^2,21,22.

Surgery Works Through Similar Biology

Metabolic-bariatric surgery was once viewed primarily as a mechanical treatment.  We now understand it acts through changing the homeostatic regulatory mechanisms similar to those targeted by pharmacotherapy.

Gastric bypass and sleeve gastrectomy alter gut-derived signals including GLP-1, PYY and ghrelin, improving appetite control and reducing the biological drive that would otherwise promote weight recurrence^1,2.

Some return of hunger as weight loss reaches a plateau does not necessarily represent treatment failure; it may reflect a new homeostatic balance being reached².

Table 1. Biological Responses to Fat Mass Reduction by Treatment Approach

What This Means for Nutrition Practice

Obesity should be viewed as a chronic disease not simply because excess adiposity causes complications, which alone would make it a risk factor, but because the system that defends fat mass itself becomes dysregulated¹.

Framing obesity primarily as a failure of restraint overlooks this biology and only serves to reinforce stigma²⁴.

Nutritional quality, physical activity and behavioural support remain important for every person with obesity and are sufficient for some when it corrects the dysregulated biological system.

But for many people with obesity, medications or metabolic-bariatric surgery are necessary components to control the disease of obesity rather than optional additions once lifestyle has “failed”².

At the same time, food quality, protein adequacy, food structure, nutrient composition, sensory properties, dietary patterns and the wider food environment remain central to good nutrition practice that may increase health gains independent of weight loss.  Their importance does not diminish if these approaches cannot effectively treat the disease of obesity, because the impact of quality of life is often weight loss independent.

Improved biological appetite control may create more favourable physiological conditions in which good nutritional interventions can be sustained.

The thermostat in the house is set too high.  What we put into the room still matters a great deal, but it is not a substitute for resetting the dial.

The study, presented at NUTRITION 2026 by Dr Xiaowen Wang, investigated whether the health effects of plant-based diets differed according to their level of processing.

Dr Wang and team analysed dietary and health data from three long-running US cohort studies:

• Nurses’ Health Study (1984-2018)
• Nurses’ Health Study II (1991-2021)
• Health Professionals Follow-Up Study (1986-2020)

The analysis included 203,275 adults (160,690 women and 42,585 men) who were free from cancer, cardiovascular disease (CVD), and type 2 diabetes (T2D) at baseline.

Researchers developed six plant-based diet indices that differentiated between healthy and unhealthy plant foods while also accounting for whether foods were ultra-processed (UPF) or non-ultra-processed.

Over the follow-up period, researchers documented:

• 26,209 cases of cardiovascular disease
• 21,006 cases of type 2 diabetes
• 55,493 deaths

Researchers found that overall diet quality was strongly associated with the risk of cardiovascular disease, type 2 diabetes and mortality.  Individuals following healthier dietary patterns – regardless of level of processing – experienced better health outcomes, while those consuming poorer-quality diets had higher cardiometabolic disease risks.

Notably, only the unhealthy ultra-processed plant-based diet pattern showed a statistically significant association with increased mortality risk.  Importantly, within healthy and unhealthy categories, the health risks were almost identical regardless of processing classification.

This study challenges the assumption that highly processed foods are inherently detrimental within plant-based eating patterns.  The findings suggest that the health benefits of a plant-based diet depend more on the nutritional quality of the foods chosen than on how processed they are.

This large prospective study indicates that healthy plant-based foods can support cardiometabolic health regardless of their level of processing, whereas poor-quality plant-based diets are associated with less favourable outcomes.

Hosted by the KHNI and moderated by Mary Shelman, founder of the Shelman Group, this session brought together Wolfram Schlenker, the Ray A. Goldberg Professor of the Global Food System at Harvard University, and Juan Aguiriano, Group Head of Marketing and Sustainability at Kerry.

The discussion examined how climate shocks, environmental pressures, and geopolitical volatility are exposing real fragility – driving all-round disruption leading to unpredictability, supply instability, and price variability.

The panel explored the growing complexity shaping food and agriculture and why resilience must sit at the centre of every decision.  Embedding sustainable resilience into risk management was identified as strengthening a company’s ability to forecast and anticipate disruption and ultimately generate long‑term value.

Speakers highlighted the complexities around trade-offs between sustainability, affordability, resilience, and nutrition – while at the same time meeting consumer expectations.  They pointed to the expanding role of data and AI in enabling more resilient production systems, smarter and more adaptive supply chains, and better-informed consumer decision-making.

The message is clear: sustainable resilience is no longer a cost – it’s core to risk management and long-term growth.  Food’s future lies not in producing more, but in producing better — driven by partnership, innovation, and a mindset built for resilience.

So, while it may sound obvious, a varied and balanced diet that provides adequate nutrients is the foundation of a healthy immune system.  However, some nutrients receive particular attention for their role in immune health, including vitamins A, C and D, as well as the minerals such as zinc and selenium¹.

There is also evidence for the immune benefits of other nutrients and ingredients, such as long-chain omega-3 fatty acids, probiotics and beta-glucans².

Immunonutrition

Read how each of the nutrients listed below support the immune system.  It is important to bear in mind that micronutrients have additional health benefits to immune health.  Click on each nutrient/non-nutrient below to learn more:

• Vitamin A
• Vitamin C
• Vitamin D
• Selenium
• Zinc
• Probiotics
• Beta Glucans

How the Immune System Works?

The immune system is the body’s way of protecting itself from infection by foreign invaders like bacteria and viruses.  It helps the body stay healthy and recover when illness does occur and is made up of the innate (general) and adaptive (specialised) immune system³.

The innate immune system is the body’s first line of defence.  When pathogens like infectious bacteria or viruses get into the respiratory tract or gastrointestinal system, the innate immune system responds by sending cells like neutrophils or macrophages to remove the threat.  These cells try to engulf the invading pathogen or create enzymes to destroy it.

The adaptive immune system specifically targets the pathogen and takes over from the innate immune system.  It is often described as the ‘memory’ of the immune system.  Once exposed to a pathogen, the immune system can remember the identity of that pathogen for the future and quickly mount a defence specific to that pathogen.

Impact of Age and Physical Activity on Immune Health

Immune health becomes especially important in vulnerable age groups like infants and the elderly. Both physical and psychological stress can also compromise the immune system.  Examples include over-exercising, emotional stress and surgery.

This article was published in March 2022 and updated on June 15, 2026.

On 30 April 2026, the Kerry Health & Nutrition Institute (KHNI) hosted an expert scientific webinar on Megatrends Shaping Tomorrow’s Food.  The panel featured the KHNI Scientific Advisory Council: Professor Imed Gallouzi, Dr Lisa Ryan and Professor Martin Bloem.

A central theme was longevity—defined not simply as living longer, but as enabling people to remain cognitively sharp, physically active and independent throughout extended lifespans.

The panel highlighted key nutrients that contribute to healthy aging, and that approaches to longevity differ significantly across socio‑economic groups, influencing both affordability and access to nutritious foods.  Therefore, equitable longevity solutions must consider these disparities.

With the rapid rise of GLP‑1 medications, the panel discussed both their benefits and emerging concerns.  The panel outlined nutrients and food formats that may be particularly supportive for GLP‑1 users.  This led to a broader conversation about food processing.

While often viewed negatively, processed foods remain a practical necessity and an essential source of nutrition for many populations.

The panel also examined how AI and emerging technologies—such as wearables and smart health systems—are reshaping personalised nutrition.  These tools may help individuals monitor stress, understand their nutritional needs and tailor dietary choices to their lifestyles.

However, the speakers stressed that the value of these tools depends entirely on the quality, accuracy and representativeness of the data that underpins them.  As technology accelerates, ensuring robust, high‑quality data will be critical for delivering meaningful health outcomes.

To close the webinar, just before the Q&A session, each member of the Scientific Advisory Council shared a final take‑home message for the audience.

Professor Martin Bloem emphasised the importance of simplicity—whether in health or nutrition, consumers need straightforward practical solutions to help them stay healthy.

Dr Lisa Ryan highlighted that optimal health relies on both good nutrition and regular physical activity.

Professor Imed Gallouzi underscored the potential of technology, noting that emerging tools can support better eating habits, healthier routines and improved overall lifestyle.

Zinc is a popular nutrient in winter supplements.  It is an essential nutrient and the second most abundant trace element in the body, after iron¹.

It is found in every cell in the body and involved in many bodily processes.  It is required by cells from both the innate (general) and adaptive (specialised) immune system².

The innate immune system is the body’s first line of defence.  When pathogens like infectious bacteria or viruses get into the respiratory tract or gastrointestinal system, the innate immune system responds by sending cells like neutrophils or macrophages to remove the threat.  These cells try to engulf the invading pathogen or create enzymes to destroy it.

The adaptive immune system specifically targets the pathogen and takes over from the innate immune system.  It is often described as the ‘memory’ of our immune system.  Once exposed to a pathogen, the immune system can remember the identity of that pathogen for the future and quickly mount a defence specific to that pathogen.

The role of Zinc in the immune system includes:

• • helping to maintain the integrity of the skin and muscular membranes, preventing pathogen entry into the body.
  • supporting the growth and differentiation of immune cells.
  • supporting the phagocytic activity of monocytes and help regulate cytokine release.
  • antibody production, particularly IgG and helping the immune system distinguish between “self” and “non-self”³.

This role has been recognised in an approved European Union health claim for zinc stating that it “contributes to the normal function of the immune system” and is available to foods that meet defined criteria within the EU⁴.

Are there Recommended Intakes for Zinc?

Zinc recommendations range from 5 to 11mg per day for adults, varying by each global region⁵.  In the US, the Institute of Medicine (IOM) recommendations are 11mg per day for men and 8mg per day for women⁶.

Similarly, the Chinese Nutrition Society Reference intake (RNI) is 12mg per day for adult men and 8.5 mg per day for women⁸.  In Europe, the European Food Safety Authority has established a Population Reference Intake of 9.4 to 16.3mg per day for men with low to higher intakes of dietary phytate and 7.5 to 12.7mg per day for adults women with low to higher intakes of phytate⁷.

Most people in developed countries get enough zinc through their diet, meaning their immune system isn’t missing the zinc it needs.  For example, in the US around 18% of people do not meet the Estimated Average Requirement (EAR) of zinc per day.

This means most people are not zinc deficient, but  certain people may still benefit from eating more zinc in their diet.

Where can Zinc be Sourced in Dietary Sources

Zinc is mostly found in seafood, beef, poultry, beans, nuts or fortified cereal.  Phytic acid, found in cereals, legumes and nuts, is known to decrease zinc bioavailability¹.  Evidence shows that the biofortification of varieties of staple crops may be useful in improving the zinc status of an individual⁵.

Table 1. Zinc content of common foods in the diet⁹

What Happens with a Zinc Deficiency?

Zinc deficiency is a widespread global health issue, particularly prevalent in low- and middle-income countries.  About 17.3% of the world’s population¹⁰ is at risk of inadequate zinc intake.  When the body doesn’t have enough zinc, it does not develop a strong immune response.

Zinc deficiency affects many different organs and tissues in the body with signs and symptoms varying by age⁹.  For example, zinc deficiency can delay growth and cause diarrhoea and alopecia in children and it can alter cognitive and psychological function in older adults.

Most people in developed countries get enough zinc through their diet but it can affect more vulnerable groups.  For example, the percentage of people in the US that do not meet the  Estimated Average Requirement (EAR) of zinc varies from 16% in households with full food security to 27% in those with very low food security¹¹.

In Europe, the average intake of zinc is above the recommended amount.  However, certain vulnerable populations may benefit from including more zinc rich foods or supplements in their diet e.g. those on plant-based diets with little animal foods and the elderly⁵.

Are there Health Risk of Excess Intakes?

Excessive amounts of zinc can cause nausea, dizziness, headaches, gastric distress, vomiting and loss of appetite and chronic large doses of 50mg of zinc or more can inhibit copper absorption and reduce immune function⁹.

Excessive intakes from food sources are unlikely but may occur with excessive supplementation.  The IOM Tolerable Upper Intake Level for zinc is 40mg per day for adults.  EFSA has set the Tolerable Upper Intake Level (UL) for total daily zinc intake from all sources (diet and supplements) at 25mg per day for adults.

This level is based on the reduction of copper status¹².  Lower limits are recommended for younger groups.

Is Zinc Supplementation Effective?

A 2024 Cochrane review ¹³ based on 34 randomised controlled trials in children and adults (15 prevention, 19 treatment) showed that compared with placebo, taking zinc preventatively may make little to no difference to whether a person catches a cold or to the duration or severity of the cold.

Taking zinc for treatment of an existing cold may reduce the duration but the authors were not confident of the quality of the result which they describe as low to very low.

The most common negative sides effects were irregularities in taste and stomach upset.  A recent review however supports a preventive role of zinc supplementation in reducing the incidence and burden of respiratory infections, particularly in children with recurrent disease and in zinc-deficient populations¹⁴.

This article was published in March 2020 and updated on March 31, 2026.

Vitamin D, sometimes known as ‘the sunshine vitamin’, is a fat-soluble vitamin important for bone health, muscle function and the immune system^1-4.  Vitamin D is also being investigated for its role in protecting against some chronic diseases including cardiovascular disease and type-2 diabetes¹.

Vitamin D exists in two primary forms:

1. vitamin D2 (ergocalciferol) which is obtained from plant and fungi sources that have been exposed to UV light.
2. vitamin D3 (cholecalciferol), found in animal-based products such as fatty fish, eggs and liver³.

Both forms of vitamin D are biologically inactive when ingested and are absorbed in the small intestine.  They are transported to the liver and converted into 25-hydroxyvitamin D (25(OH)D), also known as calcifediol or calcidiol, followed by conversion in the kidneys into 1,25-dihydroxyvitamin D (1, 25(OH)2D), or calcitriol, which is the biologically active form used by the body (Figure 1)³.

Studies have shown that vitamin D3 leads to a greater increase of serum 25(OH)D than vitamin D2⁵.

The ‘sunshine vitamin’ gets its name from the fact that it is also produced in human skin from 7-dehydrocholesterol when exposed to sunlight, or more specifically, UVB rays.

Functions

Research shows that vitamin D plays a significant role in bone health, muscle health and the immune system:

1. 1. Bone health: Vitamin D is a critical regulator of calcium absorption.  In its active form, 1,25(OH)2D, it interacts with the vitamin D receptor (VDR) in the small intestine resulting in an increase in calcium and phosphate absorption².  However, calcium homeostasis is primarily regulated to maintain serum calcium within a narrow range for metabolic reasons with the parathyroid gland, bone, intestine and the kidney working together in this role⁴.  Chronic vitamin D deficiency that results in an increase in parathyroid hormone leads to increased bone resorption, compromising the structure of the skeleton and increasing the risk of fracture thus vitamin D sufficiency is important to optimise skeletal health⁴.
   2. Immune health: Vitamin D plays a crucial role in regulating both the innate and adaptive immune responses.  The expression of VDR in many different immune cells has been well demonstrated⁶.  It modulates the activity of immune cells such as B cells, T cells and antigen-presenting cells and promotes a balanced immune response.  Vitamin D deficiency is associated with an increased risk of hospitalisation for respiratory tract infections⁷ and supplementation has been shown to boost antigen-specific immunity in older adults with sub-optimal vitamin D status⁸.  Genetic variation in the VDR genes has also been linked to Vitamin D deficiency and the development of autoimmune disease⁶.
   3. Muscle function: The identification of a VDR in skeletal muscle cells, along with the strong association between vitamin D deficiency, muscle atrophy and sarcopenia, suggests an important role in muscle function⁹.  Proposed mechanisms include modulation of protein synthesis, mitochondrial metabolism and energy production, which may influence performance.  However, the effects of vitamin D3 supplementation on muscle mass, strength and physical performance remain debated, with conflicting findings.  Meta-analyses of randomised controlled trials in athletes have not shown conclusive benefits, highlighting the need for further research^10,11.  In contrast, supplementation has been associated with improved muscle strength in postmenopausal women¹².  Interpretation of trial results should consider whether populations have insufficient or sufficient vitamin D status and whether any supplementation used has increased 25(OH)D levels sufficiently as these factors may influence outcomes¹³.
   4. Mental health: Emerging evidence suggests a link between vitamin D and mental health – its neuroprotective properties may contribute to its role in mental wellbeing, reducing neuroinflammation, supporting serotonin synthesis and improving brain plasticity¹⁴.  Recent meta-analysis suggests no benefit of supplementation in healthy individuals¹⁵ but potential effects on depressive symptoms in those with major depressive disorder or with milder, clinically significant depressive symptoms¹⁴.  However, more high-quality research trials are needed.
   5. Other Potential Roles: Vitamin D has other roles in the body, including modulation of cell growth, neuromuscular function and glucose metabolism¹⁶.  Ongoing research is also exploring the potential benefits on other health conditions including heart disease, diabetes and musculoskeletal diseases like multiple sclerosis¹⁷.

In European Union countries, approved health claims are available for the role of Vitamin D in supporting a wide range of functions including maintaining normal bones and teeth, muscle and immune function as well as supporting absorption of calcium and phosphorous subject to conditions.

In China, claims relating to the health of bones and teeth and the absorption and utilisation of calcium and phosphorus are also available for vitamin D containing foods subject to conditions.

Recommended Intakes

In some countries, national dietary reference tables can lag behind updated clinical practice or more recent Vitamin D supplementation policies.

• • United States:  The Institute of Medicine (IOM) Recommended Dietary Allowance (RDA) for vitamin D is 600 IU (15 micrograms) daily for adults aged 19–70 and 800 IU (20 micrograms) daily for adults over 70 years, assuming minimal sun exposure¹⁸.
  • Europe:  The European Food Safety Authority (EFSA) has set an adequate intake at 15 micrograms per day for healthy individuals over one year of age including pregnant and lactating women to ensure the majority of the population will achieve a serum 25(OH)D concentration near or above the target of 50 nmol/L¹⁹.
  • China: The Chinese Nutrition Society have set a daily Reference Nutrient intake of 400 IU (10 micrograms) for adults aged 18-50 and 600 IU (20 micrograms) for adults over 50 years²⁰.

Dietary Sources

Foods rich in vitamin D include oily fish (e.g., salmon, mackerel and sardines), egg yolks and offal.  However, sources are limited and there are high levels of inadequacy of vitamin D intake globally²¹.

In some countries, fortification of staple food (e.g., milk, margarine, cereals) is used to increase vitamin D intake but these policies differ by region and are often voluntary, leading to variable dietary contributions.

For this reason, local food composition data and values should be used when estimating intakes.  For example, milk is frequently quoted as a source of vitamin D but only when vitamin D fortified milk is available.

Liver is a source of vitamin D but is not widely consumed and is not recommended during pregnancy because of its high vitamin A content²².

Among plant-based options, mushrooms exposed to sunlight or UV radiation can supply vitamin D2.

Vitamin D – Beyond Food

The level of 25(OH)D in populations varies geographically due to latitude, skin pigmentation, sun exposure, diet and supplement use.

While endogenous production of vitamin D from sun exposure is also a potential source, recommendations to limit sun exposure to prevent skin cancer and limited sunlight in higher latitudes during winter mean that it cannot be relied upon as a source.

In many countries, vitamin D supplementation is recommended either during winter or throughout the year for more vulnerable populations (e.g. pregnant women, elderly, those with darker skin)^23-25.

The Endocrine Society also recommend supplementation for children aged 1 to 18 years and those aged 75 years and older as well as pregnant women and those with high-risk prediabetes²⁶.

Vitamin D Deficiency

The concentration of 25(OH)D in blood serum is currently the main indicator of vitamin D status as it reflects vitamin D produced through both sunlight and from the diet.  There is no universal agreement on the threshold for vitamin D ‘deficiency’.

However, there is widespread acknowledgement of vitamin D deficiency using the most conservative 25(OH)D threshold of < 25/30 nmol/L, in both low- and high-income countries¹.  Depending on the world region, the prevalence of serum 25(OH)D below this threshold  ranges from ~5 to 18% and 24 to 49% for levels below 50 nmol/L²¹.

Vitamin D deficiency in toddlers and young adults can cause rickets and slow brain development.  Deficiency in adults causes osteomalacia (brittle bones) increasing susceptibility to fractures.

Confirmed vitamin D deficiency is typically treated with high-dose supplements for a limited number of weeks followed by a maintenance dose²⁸.

Excess Intakes

It is important to remember that as a fat-soluble vitamin, vitamin D can be stored in the liver and excessive amounts should be avoided.

An upper daily limit of 100 micrograms from all sources has been set in the US by the IOM for those 9+ years¹⁸ while an upper daily limit of 50 micrograms for children and 100 micrograms for adults has been recommended by the EFSA²⁷.

In Closing

Ongoing research continues to explore vitamin D’s potential benefits further refining our understanding of its role in human health.  While vitamin D is essential, further research is needed to fully understand its role in various health conditions and to establish clear guidelines for supplementation.

This article was originally published on March 18, 2025 and updated on March 3, 2026.

Therefore, nutrition science research is essential for advancing our understanding of human health and supporting evidence based decision making.

Research in this space aims to clarify how nutrients, bioactives and other food components influence health, inform dietary guidance and policy and support strategies to prevent disease.

A wide range of study designs are used in nutrition research and no single study design can answer every question².  Understanding the purpose, strengths and limitations of each approach helps distinguish between stronger and weaker evidence, so the hierarchy of research methods is key to evaluating the quality of evidence.

Visualising study designs as a pyramid (Figure 1) highlights how evidence strength varies.  Studies at the lower levels of the pyramid tend to offer limited, less practical insights, while those at the top delivering stronger evidence with greater relevance to real world nutrition choices^3,4.

Figure 1.  The hierarchy of evidence ranks different types of research according to the strength of the conclusions ³.  (Licensed under CC BY 4.0)

Systematic reviews and meta analyses sit at the top of this hierarchy because they provide data across multiple studies to provide more comprehensive conclusions.

Randomised controlled trials and prospective cohort studies typically provide the most robust evidence when examining relationships between dietary exposures and health outcomes.

However, the rapid growth of the field — and the diversity of methods used — can make it challenging for practitioners and consumers to interpret findings and translate them into practice.

Foundational Research: Non-Human Studies

Foundational research — including in vitro studies in cells or tissues and in vivo studies in animal models — plays a critical role in uncovering the biological mechanisms that underpin how nutrients, ingredients and other food components behave in controlled settings.

These early stage studies provide directional evidence that helps shape hypotheses and supports the rationale for human research.

It is important to note that isolated cells and tissues and animals do not replicate the complexity of human physiology.

Differences in metabolism, exposure levels and biological responses mean that findings cannot be directly translated to human outcomes.  For instance, a compound that influences cellular metabolism in vitro, for example, may behave very differently within the interconnected systems of the human body.

However, the value of foundational research becomes clear when it is integrated with human data.  For example, while observational research links smoking with cancer, cell studies identify the carcinogenic compounds responsible.

So, when mechanistic evidence aligns with human outcomes, confidence in the overall conclusion(s) is strengthened.

Observational Studies

These studies track large groups of people over time, in real-world settings, to understand how lifestyle behaviours — including dietary patterns — relate to health outcomes.

These studies identify population level patterns and provide potential associations that warrant further investigation in more controlled study designs.

Observational studies cannot determine cause and effect relationships and, hence, the impact of a single dietary or lifestyle factor.

Common observational designs include prospective cohort studies, case–control studies and cross sectional studies, each offering different strengths for understanding how diet and lifestyle influence long term health.

Case Control Studies

Case control studies compare people who already have a specific health condition (the cases) with similar individuals who do not (the controls).

Researchers then look back in time to assess whether past exposures — such as dietary habits — differ between the two groups.  For example, comparing fruit and vegetable intake in people with and without heart disease may help identify potential associations with disease risk.

These studies are relatively quick and cost effective, making them especially useful for investigating rare conditions or outcomes that would be difficult to study prospectively.

They can also examine multiple potential risk factors at once and often serve as an important first step in identifying associations that warrant further research.

However, case control studies face several methodological challenges.  Because exposure information is collected retrospectively, they are highly susceptible to recall bias — particularly when individuals with a disease remember past behaviours differently from those without it.

Selection bias, confounding and reverse causation can also limit the strength of conclusions.  For instance, if higher consumption of non sugar sweeteners is observed among people with obesity, it may reflect dietary changes made after weight gain rather than a causal effect of sweeteners.

Cohort Studies

Cohort studies are observational studies that are either prospective or retrospective, depending on when the data were collected. In a prospective cohort, participants complete questionnaires and undergo measurements at the start of the study.  On the other hand, with retrospective cohort studies, researchers “look back” to analyse the relationship.

Prospective cohort studies follow large groups of people in real world conditions over many years — sometimes decades — to explore how dietary and lifestyle exposures relate to the development of diseases.  Participants provide information at baseline and at regular intervals on factors such as diet, physical activity and health status.  Dietary intake is usually self reported, which introduces challenges such as misreporting, difficulty estimating portion sizes and changes in behaviour over time.

By tracking outcomes over time, researchers can examine patterns and test hypotheses.  Collectively, prospective cohort studies have shaped much of our understanding of how diet and lifestyle influence chronic disease risk, such as cardiovascular disease or osteoporosis.

However, their long duration means they are time and resource intensive.  As with all observational research, these studies can identify associations but cannot establish cause and effect relationships.

Cross Sectional Studies

This type of research provides a snapshot of health behaviours, exposures and outcomes in a population at a single point in time.

They are typically conducted through surveys or brief assessments that collect information on both potential risk factors and health indicators simultaneously.

However, cross sectional research has important limitations.  Because exposure and outcome are measured at the same moment, it is not possible to determine which came first.

This raises the issue of reverse causality — for example, whether a dietary behaviour contributes to a health outcome or whether the health outcome influences how participants report their diet.

Cross sectional studies can also be affected by selection bias and recall bias, particularly when participants’ awareness of their health status shapes how they report past behaviours.

Despite these constraints, cross sectional studies are cost effective, relatively quick to conduct and useful for estimating the prevalence of dietary habits, lifestyle behaviours, or health conditions in a population.  They can also highlight potential associations worth exploring in more rigorous study designs.

A typical cross sectional study might compare dietary patterns across countries to explore whether differences in diet align with variations in cardiovascular disease prevalence.

Randomised Controlled Trials (RCTs)

Randomised controlled trials (RCTs) are considered the gold standard for determining cause and effect relationships^1,2,5.

Participants are recruited and randomly assigned to a control (placebo) group or an intervention group, ensuring the groups are comparable at baseline.  For example, in an RCT examining the Mediterranean diet and cardiovascular risk, the control group might follow a standard low fat diet while the intervention group adopts a Mediterranean pattern³.

After a defined study period, researchers compare outcomes such as heart attacks or strokes between groups.

Because randomisation minimises confounding factors, differences in outcomes can be attributed to the intervention itself.

This is why RCTs provide the strongest evidence for causation rather than correlation. When conducted as double blind trials, neither participants nor researchers know who receives the treatment, further reducing bias and mitigating placebo effects.

Despite their strengths, RCTs come with practical and ethical constraints.  They are expensive, often involve small sample sizes and may struggle with long term adherence, especially when testing complex dietary patterns.

Ethical considerations limit the ability to test harmful exposures or withhold beneficial treatments.

Systematic Reviews and Meta Analyses

Systematic reviews and meta analyses sit at the top of the evidence hierarchy because they provide a comprehensive overview of existing evidence and can reveal whether findings are consistent across different populations and settings.

However, these methods are only as strong as the quality and consistency of the studies they include and rely on thorough, unbiased inclusion of all relevant evidence.

A systematic review uses a structured, transparent process to identify, evaluate and summarise all relevant research on a specific question.

When the included studies are sufficiently similar in design, population and outcomes, researchers may conduct a meta analysis, which statistically pools results to generate a single, weighted estimate of effect. Larger, well designed studies contribute more heavily to this estimate than smaller or lower quality studies.

Systematic reviews and meta analyses help determine whether scientific findings are consistent, generalisable and reliable and they often guide policy decisions, clinical recommendations and future research priorities.

In Summary

Science is a continuous process.  It can move slowly and often involves uncertainty, yet it remains the most reliable way to build understanding about the world and human health.  Many types of studies contribute to this evidence base, each with its own strengths and limitations and no single study provides a definitive answer.  Progress happens because researchers continually evaluate and refine one another’s work, identifying opportunities to improve methods and explore new questions.

The KHNI Health and Nutrition Megatrends, now in its eighth edition, highlights the scientific, technological, and consumer-driven changes redefining global food systems.

Sleep supports our brain function, our the circulatory system, our metabolism and our long-term memory retention¹.  Lack of sufficient sleep over time can lead to long-term complications, such as increased blood pressure and a weakened immune system².

What does a Good Night’s Sleep Consist of?

The amount of sleep needed will depend on the stage of life and other factors such as activity level and certain co-morbidities.  Babies initially sleep as much as 16 to 18 hours per day, which may boost growth and development (especially of the brain).

School-age children and teens on average need about 9.5 hours of sleep per night.  Most adults need 7-9 hours of sleep a night, but after age 60, night time sleep tends to be shorter.

Phases of Sleep

During sleep, our brains progress from two different sleep states: REM (rapid-eye movement) sleep and non-REM sleep.  

• REM sleep occurs in the first 90 minutes after falling asleep.  The body’s systems are more active compared to deeper states of sleep.  This state almost mimics wakefulness as breathing is fast and irregular, heart rate and blood pressure are near waking levels.  During REM sleep emotional experiences are processed and memories are consolidated.  In addition to memory consolidation and emotional regulation, REM sleep also supports other cognitive functions such as mood stability, restorative brain activity, and brain development, especially in infants and children where neural pathways are growing and refining.  Interestingly, REM sleep increases in duration in the latter half of the night, which is why we often wake up from a dream in the morning hours.
• Non-REM sleep follows as the brain gently drifts from a state of alertness to sleep, body temperature decreases and eye movements slow down.  Brain activity occurs in small bursts and heartbeat and muscles relax further.  The final stage of non-REM sleep is the deep sleep period.  All systems slow even further, including brain waves.  It can be difficult to rouse a person awake during this intense deep state of sleep³.  Non-REM sleep contributes to physical repair and recovery, growth & development, supports immunity, regulates hormones and enhances memory consolidation.

Nutritional Interventions for Sleep Quality

Diet can significantly influence circadian rhythms and sleep quality. Nutrients that support the production of key sleep-related hormones, such as melatonin and serotonin, are particularly beneficial.

Foods rich in tryptophan, an amino acid precursor to serotonin and melatonin, include turkey, chicken, nuts (especially almonds and walnuts) and seeds.  These foods help regulate sleep-wake cycles by enhancing melatonin synthesis, which aligns with the body’s natural sleep rhythm.

Complex carbohydrates found in whole grains, oats, and legumes can improve tryptophan’s availability to the brain, promoting a restful sleep.

Magnesium and potassium, present in foods like leafy greens, bananas, and sweet potatoes, also play a role in relaxing muscles and calming the nervous system, which is essential for preparing the body for sleep.

Omega-3 fatty acids, found in fatty fish, like salmon and sardines, have been shown to support circadian alignment by influencing serotonin levels, which can improve sleep quality.

Vitamin B6 (in foods like bananas, chickpeas and fortified cereals) and vitamin D (in eggs, fish and fortified products) are essential for the synthesis of serotonin, helping to regulate mood and improve sleep quality.

Additionally, antioxidant-rich fruits like cherries and berries contain natural melatonin, which may aid in promoting earlier sleep onset.  Caffeine-free herbal teas such as chamomile and valerian root also have calming effects that can help with falling asleep and maintaining restful sleep.

Botanical extracts have been increasingly studied for their potential to support sleep quality.

One such extract is Withania somnifera, commonly known as ashwagandha.  Ashwagandha is considered an adaptogen, helping the body adapt to stress and balance the body’s physiological processes.

While more research is needed, early studies have shown that ashwagandha may improve sleep onset, duration, and quality, especially in those experiencing stress-related sleep issues.

Both alcohol and caffeine can significantly disrupt sleep quality.  Caffeine stimulates the nervous system and acts as an adenosine receptor antagonist, blocking adenosine which promotes sleep.  This causes an increase in alertness and delaying the onset of sleep.

Consuming caffeine, especially in the afternoon or evening, can reduce the total sleep time and impair normal sleep¹⁴.

Alcohol, while initially sedating, can lead to fragmented sleep and a reduction in REM sleep.  It also disrupts the body’s natural temperature regulation and increases night time awakenings. Limiting both of these can help achieve more restorative and uninterrupted sleep¹⁵.

Sleep and Disease Risk

Insufficient or poor-quality sleep is increasingly recognised as risk factors for a range of chronic diseases.  Studies have linked chronic sleep deprivation to elevated risks of cardiovascular disease, type 2 diabetes, obesity, and some neurodegenerative conditions.

Disrupted sleep also impairs metabolic function, especially glucose metabolism and insulin sensitivity.  Inadequate sleep has also been associated with increases in system inflammation and elevated blood pressure, both of which can contribute to cardiovascular risk.

Poor sleep may also impact immune function, which increases the risk of infectious disease.  Finally, lack of adequate sleep also contributes to increase in mental health risk such as stress, anxiety, and depression.

Emerging research continues to explore the significant role that diet plays in sleep quality.

As we advance in understanding these connections, there is a growing opportunity for industries to implement evidence-based nutritional guidance and develop innovations, such as tailored meal plans and/or supplements, that support better sleep and overall health.