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Long read: Cancer risk and metabolism – the case for policies that support lifestyle change

The profound impact of a cancer diagnosis, whether personal or affecting a loved one, is undeniable. The term "cancer" frequently evokes negative emotions due to its pervasive presence within our communities and personal experiences.

By Dr Ben Noble, MBSS, MRCGP, PhD

The profound impact of a cancer diagnosis, whether personal or affecting a loved one, is undeniable. The term “cancer” frequently evokes negative emotions due to its pervasive presence within our communities and personal experiences.

Data from Cancer Research UK highlights the significant burden of this disease, with an estimated three million individuals currently living with cancer in the UK, projected to rise to four million by 2030.

Tragically, cancer claims the lives of approximately 167,000 individuals annually, an average of 460 deaths each day, impacting families across generations, grandparents, parents, spouses, siblings, and children.


 

Tune in to public health messaging and you’ll notice that the vast majority of resources are directed to detecting the signs and symptoms of cancer as early as possible. This is certainly true in primary care, where initiatives around health professional education, increased access to diagnostics and targeted screening aim to increase the proportion of cancer patients diagnosed in the early stages. Early stage refers to before the cancer has had chance to spread, when the disease is generally much easier to treat.

There is no doubting the link between cancer and metabolism. Metabolism is derived from the Greek word “metabole” which means change and refers to the countless chemical processes necessary to sustain life. In metabolism, some substances, e.g. food, are broken down to yield energy while others are created within the body.

Public health messaging from NHS England

Metabolism is influenced by:

  • Age
  • Gender
  • Muscle-to-fat ratio
  • Nutrition
  • Physical activity
  • Hormone function

It may be considered logical, then, that the processes that govern energy production and cell synthesis are also linked with the uncontrolled cell growth seen with cancer.


 

How can we think about cancer differently?

In the main, cancer, as well as heart disease and dementia, is an “acute” presentation of chronic changes that have been ongoing within the body over the course of decades.

We readily accept that our joints are subject to wear and tear as we reach middle age but are not as aware that our organs also undergo repeated traumas leading to suboptimal performance, and potentially cancer, as we age.

Visceral fat compared with subcutaneous fat

For example, years of repeated overeating causes excess energy to be stored as fat, to a point when our stores (primarily under our skin, or subcutaneous) are full. At this point, fat is increasingly deposited and stored around our organs, leading to insulin resistance and inflammatory changes.

This is compounded by physical inactivity, such that we don’t burn off the excess energy we’re storing as fat or maintain healthy bones and muscles.

In these conditions, even our individual cells show signs of weathering. Mitochondria, our crucial, energy-producing organelles, our cell batteries in other words, become dysfunctional when exposed to the persistent inflammation associated with poor metabolic health.

Mitochondrial degeneration in turn causes tissue damage and hinders regeneration.
Now add some toxic substances to this environment of wear and tear, such as tobacco smoke, alcohol, certain processed foods and polluted air and we’ve created a cocktail of cellular damage, persistent inflammation and suppressed repair mechanisms.

Cancer occurs when abnormal, or damaged cells divide in an uncontrolled way. If we create the right environment for this to happen, over many years our risk of the disease increases.

Conversely, if we maintain good metabolic health and resist lifestyle choices which lead to persistent cell damage, we significantly reduce our risk for cancer, even if we are genetically predisposed to cancer in the first place.

Rather than focus our efforts on diagnosing cancer as early as possible, could we look upstream and prevent cancer occurring in the first place, or at least significantly delay its onset?


 

How do we know that cancer and metabolic health are so closely linked?

 

Poor metabolic health is characterised by high blood sugar, obesity, or excess body fat around the waist, high blood pressure (hypertension) and unhealthy levels of blood lipids. This creates the fertile soil in which cancer cells can grow.

Cancer growth is driven by metabolism. Cancer cells consume glucose at a much higher rate than normal cells, which produces the cellular environment for further growth and division.

Insulin enables the fast influx of glucose in cancer cells and there is already some evidence in laboratory animals that calorie restriction reduces cancer mortality.1

Repeated stress to our metabolism has been linked with many cancers. For example, type II diabetes is associated with oesophageal, colorectal, pancreatic, breast, endometrial, brain and renal cancers. It is estimated that 20 per cent of cancer patients have diabetes – indeed, cancer is the leading cause of death among diabetics.2

The National Cancer Diagnosis Audit revealed that 76 per cent of newly diagnosed cancer patients in England had at least one co-morbidity, hypertension being the most common, followed by cardiovascular disease and then diabetes joint 3rd.3

With poor metabolic health being so closely linked with hypertension and cardiovascular disease, we can conclude that the metabolic decline leading to diabetes is the real risk factor for cancer, rather than simply having diabetes itself.

This trend is seen with other markers of poor metabolic health. For example, the link between obesity and cancer is well-established, prompting Cancer Research UK to launch an awareness campaign in 2019.4

The Health Survey for England 2021 estimates that 63.8 per cent of adults are overweight (BMI 25-30), including 25.9 per cent who are obese (BMI ≥ 30).

An International Agency for Research on Cancer (IARC) Working Group concluded that there is consistent evidence that increased body fat is associated with an increased risk of many different cancers.4 Table 1 (below) shows the risks reported in representative studies.

Table 1. Cancer relative risk and obesity. Adapted from IARC working group 2016.4

Despite obesity being a cancer risk factor by itself, research has shown that the more metabolically unhealthy an obese person is, the higher the risk of cancer.5

Finally, a study in 2022 concluded that metabolic dysfunction alone is a key risk factor for obesity-related cancer.6


 

What might an altered approach to cancer look like?

The future of cancer diagnoses may well involve sophisticated, DNA-based blood tests and other, non-invasive tests to screen and diagnose at the earliest possible point. But the future for public health must surely be to facilitate the deferral or complete avoidance of a cancer diagnosis in the first place.

We already know enough about cancer incidence to say that improving the metabolic health of the nation would drastically reduce the rate of cancer diagnoses alongside other significant benefits for the nation’s health.

Research tells us there are three lifestyle areas that, if left unhoned, will set in motion a wide array of physiological and biochemical processes resulting in inevitable poor health and disease.

1. Physical activity

Physical activity is defined as any movement that uses skeletal muscles and requires more energy than being sedentary.

From the available evidence, there can be little doubt that exercise, or physical activity, has the potential to exert the greatest influence over how long we live and how well we live. Even minimal exercise, done regularly, can lengthen our lives by several years, help us to retain our independence in older age and defer or delay the onset of chronic diseases, including cancer.

The suggestion that physical activity reduces the risk of cancer was made in the early 20th century by two studies which looked at the effects of active occupations on cancer mortality rates in men.7,8 Since then, there has been substantial evidence that increased physical activity reduces the risk of many cancers.

Breast cancer:A meta-analysis in 2016 showed that the most physically active women had a 12-21 per cent lower risk of breast cancer compared to the least physically active.9 This effect was seen in both pre- and post-menopausal women.9,10

Colorectal cancer: A meta-analysis in 2019 examining the associative risk of colon and rectal cancer and physical activity of varying intensity levels showed that increased physical activity considerably decreases cancer risk.11 A 2016 meta-analysis observed that those who were most physically active had a 19 per cent lower risk of colon cancer than the least active.12

Lung cancer: Evidence linking increased physical activity with lower risk of lung cancer is subject to bias from the effects of smoking but is still compelling.13 For smokers and ex-smokers, a meta-analysis from 2016 showed that physical activity was associated with a reduced risk of lung cancer.

Renal cancer: A 2013 meta-analysis demonstrated a 12 per cent reduced risk of renal cancer in the most active compared to the least active individuals.14

Bladder cancer: A 2014 meta-analysis looking at leisure and occupational physical activity demonstrated a 15 per cent lower risk for bladder cancer at the highest activity level compared to the most sedentary.15

Endometrial cancer: Highly physically active women had a 20 per cent lower risk of endometrial cancer in a 2015 meta-analysis.16 This may be biased by the fact that obesity, which is strongly linked with endometrial cancer, is less likely in women with increased physical activity.

Oesophageal cancer: A 2014 review found a 21 per cent reduced risk of oesophageal cancer in the most, compared with the least physically active.17

Stomach cancer: A meta-analysis in 2016 found a 19 per cent lower risk of stomach cancer in the most physically active compared with the least active.18

For many other cancers, there is more limited associative evidence with physical activity. However, with the link between poor metabolic health and cancer being so strong, it’s likely that further research will clarify the association with healthy lifestyle choices, like physical activity, and a widespread reduction in cancer risk.

The mechanisms by which poor physical fitness and sedentary behaviour increase cancer risk are varied, reflecting the wide-ranging effects throughout the body.

  • Systemic inflammation: Sedentary lifestyles and poor fitness promote a pro-inflammatory state. Adipose (fatty) tissue dysfunction in these individuals leads to elevated levels of pro-inflammatory cytokines like IL-6 and TNF-α, which can damage DNA and impede immune function, facilitating cancer incidence.19
  • Altered immune function: Chronic inflammation disrupts the delicate balance of the immune system. Suppressed immune cell activity and reduced immune surveillance hinders the body’s ability to detect and eliminate pre-cancerous cells.20
  • Elevated insulin in the blood (hyperinsulinaemia) and insulin resistance: Chronic sedentary behaviour and poor fitness contribute to insulin resistance (through reduced muscle activity, impaired glucose uptake, increased visceral fat accumulation, and impaired mitochondrial function), a hallmark of metabolic syndrome. Elevated insulin levels can stimulate growth factor pathways, promoting cancer cell proliferation.21
  • Bile acids and gut microbiome: Sedentary lifestyles are associated with alterations in gut microbiome composition (through reduced microbial diversity, impaired gut motility, increased intestinal permeability, altered lipid metabolism and increased stress hormones). Dysbiosis can lead to increased production of bile acids, some of which possess mutagenic properties, potentially contributing to carcinogenesis.22,23,24
  • Altered sex hormone levels: Obesity, often linked to sedentary behaviours, is associated with altered sex hormone levels, particularly increased oestrogen in postmenopausal women. These hormonal imbalances promote the growth of hormone-sensitive cancers like breast and endometrial cancers.25

In order to achieve optimum metabolic health through physical activity, a balanced approach is required, incorporating aerobic, strength and flexibility/balance training. In line with recommendations from Cancer Research UK and the NHS, adults should aim for at least 150 minutes of moderate intensity aerobic exercise, or 75 minutes of vigorous intensity aerobic exercise per week.26,27

Examples of moderate intensity activities include:

  • Brisk walking
  • Riding a bike at an easy pace
  • Pushing a lawnmower
  • Hiking

Vigorous activities include:

  • Running
  • Swimming
  • Cycling fast or on hills
  • Walking upstairs
  • Sports, e.g. football, rugby, netball, hockey
  • Skipping
  • Aerobics
  • Gymnastics
  • Martial arts

Very vigorous activities include:

  • Lifting heavy weights (depending on how this is done, lifting weights is not necessarily an aerobic activity. Although strength training should be undertaken as part of a well-rounded programme of exercise, it wouldn’t count against the recommended 75-150 minutes of aerobic exercise).
  • Circuit training
  • Sprinting up hills
  • Running upstairs
  • Spinning classes
  • Interval running

Examples of muscle strengthening activities include:

  • Carrying heavy shopping bags
  • Lifting weights
  • Working with resistance bands
  • Heavy gardening, e.g. digging
  • Wheeling a wheelchair
  • Lifting and carrying children

Examples of flexibility/balance activities include:

  • Yoga
  • Pilates
  • Tai chi

Scientific studies have consistently demonstrated the importance of the intensity, duration and frequency of physical activity in cancer prevention.28

Aerobic exercise has been shown to reduce systemic inflammation, enhance immune function and help maintain a healthy body weight. The evidence for the associated health benefits of physical activity, including reduction of cancer risk, is overwhelming.28,29,30,31,32,33

Strength training is beneficial for preserving muscle mass, improving insulin sensitivity and reducing hyperinsulinaemia, providing protection against cancer risk factors in addition to aerobic exercise.34

Flexibility exercises not only reduce risk of injury but are effective for stress reduction, promoting relaxation, and may indirectly lower cancer risk by improving mental health and hormone balance.35

While meeting the recommended guidance for physical activity is important for reducing cancer risk, it’s important to note that even small amounts of activity can be beneficial, especially if done on a regular basis.

It is also likely that exceeding recommended activity levels will give further health benefits. People who undertake low intensity exercise (an intensity which causes slight breathlessness but allows conversation, often referred to as zone 1 or zone 2 training) will increase their overall cardiovascular fitness more so with longer periods of exercise.32

Ultimately, there is no doubt that incorporating enjoyable forms of physical activity into the daily routine can lead to long term health benefits additional to cancer risk reduction.


2. Nutrition

It has been suggested that diet and nutrition could account for 20-25 per cent of the worldwide cancer burden.36,37

The evidence for cancer risk and diet is most reliably based around 3 main areas:

  • Obesity
  • Processed food
  • Alcohol

Obesity

Obesity alone is responsible for 4-8 per cent of all cancer cases. Table 1 quantifies the relative cancer risk by organ according to current evidence.38

Furthermore, metabolically unhealthy obese people (those with abnormal blood glucose and lipid parameters) have an even higher cancer risk, implying that the processes leading to metabolic dysfunction are potentially carcinogenic.5 Hence, a diet which contributes to metabolic dysfunction is also contributing to processes which promote the likelihood of cancer.

Processed food

There is a growing body of evidence linking ultra-processed food (UPF) not only with poor health outcomes but increased risk of cancer. This is especially concerning as UPF accounts for 56.8 per cent of the total UK diet.39

UPFs are industrially manufactured products containing significant amounts of added sugars, fats, artificial flavours and other additives. They often undergo significant processing from their constituent parts and contain little or no whole foods.40 Examples include packaged snacks, sugary drinks, breakfast cereals and reconstituted meats.

A large, multinational, European study found a link between UPF consumption and an increased risk of various cancers.41 Each 10 per cent increase in UPF consumption corresponded to a 6 per cent increase in overall cancer mortality, with a particularly strong association for ovarian and breast cancers (16 per cent and 30 per cent increase, respectively).

A further, large, European study investigated the link between UPF consumption and overall mortality, showing a significant association with risk of death from cancer specifically.42

The exact mechanisms by which UPFs might influence cancer risk are still under investigation. Current theories include:

  • Nutritional imbalance: UPFs tend to be low in fibre, vitamins and minerals, while being high in unhealthy fats, sugars and sodium. This nutritional imbalance is likely to alter the gut microbiome, promote inflammation and disrupt healthy metabolic processes, leading to a cell-damaging, or cytotoxic environment.43
  • Additives and contaminants: Certain additives and processing techniques used in UPFs may introduce potentially harmful, carcinogenic compounds such as nitrosamines or advanced glycation end products (AGEs).44

Alcohol

It has previously been widely reported that moderate alcohol intake is associated with improved health outcomes.45,46 However, the relevant studies are almost universally tainted by healthy user bias, i.e. the people who are still drinking in older age are doing so because they are healthy, not the other way round. Additionally, people who do not drink alcohol are often avoiding it for a health- or addiction-related reason. And such studies exclude those who have already died from the consequences of alcoholism.

A study in 2017 found that once confounding factors that may accompany moderate alcohol consumption are removed (low BMI, affluence, and not smoking), there is no intake of alcohol that can be considered healthy.47

Numerous studies have established a clear association between alcohol consumption and an increased risk of several cancers. The World Cancer Research Fund highlights strong evidence linking alcohol intake to cancers of the mouth, pharynx, larynx, oesophagus (gullet), bowel (colon and rectum), liver, and female breast.48

  • Mouth, Pharynx, and Larynx Cancers: A 2020 meta-analysis involving over 800,000 participants found a positive dose-response relationship between alcohol consumption and these cancers, with a particularly strong association observed for those who also smoke.49
  • Oesophageal Cancer: Alcohol consumption at any level is associated with a risk of oesophageal squamous cell carcinoma, ranging from 1.3x to 5x increased risk for light to heavy drinking respectively.50,51
  • Bowel Cancer: Moderate to heavy alcohol consumption is associated with 1.2x to 1.5x increased risk of colorectal cancers compared with no alcohol consumption.50,51
  • Liver Cancer: Heavy alcohol consumption is associated with approximately 2x increased risk of hepatocellular carcinoma.50,51
  • Breast Cancer: Epidemiological studies have consistently found a dose-dependent increase in breast cancer risk with alcohol consumption. Compared with non-drinkers, light drinkers have a small increased risk (1.04x), moderate drinkers had a 1.23x, and heavy drinkers a 1.6x increased risk.50,51

Evidence is emerging that alcohol consumption may also be linked to melanoma, prostate and pancreatic cancers.50,52

The exact mechanisms by which alcohol promotes cancer are still being investigated. However, some potential explanations include:

  • Acetaldehyde toxicity: alcohol metabolism produces acetaldehyde, a highly reactive and carcinogenic compound that can bind to DNA and proteins, leading to cellular damage and genetic mutations.
  • Oxidative stress and inflammation: alcohol consumption induces oxidative stress and inflammation, which can promote DNA damage, cell proliferation, and tumour growth.
  • Disruption of hormone balance: alcohol consumption can disrupt hormone levels, including oestrogen and insulin-like growth factor 1 (IGF-1), which are implicated in cancer development and progression.
  • Enhanced carcinogen activation: alcohol consumption may enhance the activation of carcinogens present in tobacco smoke or dietary sources, increasing the risk of cancer in exposed tissues.
  • Calorie density: alcohol is highly calorific and provides no nutritional benefit to the body. It is thus an important contributor to obesity in many people.

In summary, there is no “recommended” level of alcohol consumption, in that studies have shown no beneficial effects. There is overwhelming evidence that alcohol is a risk factor for cancer, causing cell damage and promoting metabolic dysfunction.

A significant trend in recent years is the decline in binge drinking and heavy alcohol consumption among younger age groups. However, it is essential to note that alcohol consumption patterns vary across different demographic groups and regions within the UK, tending to be higher in those who already have significant risk factors for cancer.

The consumption of UPFs has been increasing globally. In UK adults, 57 per cent of daily energy intake is derived from UPF, with an even higher proportion seen in adolescents (66 per cent).39,53

Reducing alcohol and UPF intake are important lifestyle interventions for anyone looking to improve their overall health and reduce their risk of cancer.

Other nutritional considerations

While the evidence regarding the impact of dietary fibre on cancer risk remains inconclusive, high fibre intake is associated with numerous health benefits, including improved digestive health, as well as reduced risk of obesity and chronic diseases. While it seems likely that fibre influences cancer risk through its effects on digestive health and metabolism, further research is needed to establish a definitive link.54

Excessive sugar consumption, particularly from added sugars in processed foods and sugary beverages, has been linked to various adverse health outcomes, including obesity, type 2 diabetes, and cardiovascular disease. While the direct relationship between sugar intake and cancer risk is still under investigation, high sugar diets may indirectly contribute to cancer development through their association with obesity and metabolic dysfunction. Additionally, elevated insulin levels (insulin “spikes”) resulting from frequent sugar consumption can stimulate cell proliferation, potentially promoting the growth of cancer cells. Although studies provide insights into the potential effect of sugar on cancer development, further research is required to clarify the extent of that effect.55

Observational studies have shown an inverse relationship between diets high in plant-based foods, rich in phytochemicals (the compounds which often give fruits, vegetables, grains and herbs their colours, flavours and aromatic qualities), and cancer incidence. It is thought that they modulate chemical signalling pathways through their anti-oxidant effects, protecting cells from undergoing molecular changes that trigger carcinogenesis.56 However, this is an emerging area of research, and the role of phytochemicals and cancer risk reduction remains undetermined.

Recent evidence suggests that the composition of the gut microbiota, the community of microorganisms living in the digestive tract, may influence cancer risk. Certain dietary patterns, including those rich in fibre, probiotics, and prebiotics, can positively affect the balance of gut bacteria, whereas others, including those predominated by UPF, have negative affects which may have implications for cancer prevention. This represents an intriguing area of investigation, with at least one study having already suggested a causal relationship between the gut microbiota and cancer.57


 

3. Emotional health

A range of psychosocial factors are associated with long-term conditions, health and life expectancy. In terms of cancer risk, it’s less helpful to look for associations between cancer incidence and emotional health, more to understand how poor emotional health and lack of sleep can contribute to metabolic dysfunction.

Emotional health

I use emotional health here to refer to our day-to-day psychological wellbeing, as opposed to mental health, which often refers to clinical disorders requiring health professional input.

Stress and poor emotional health can exert profound effects on metabolism, just as lack of exercise and poor nutrition can.

Research indicates a number of mechanisms through which poor emotional health impacts metabolic processes which contribute to cancer risk:

  • Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS): Chronic stress activates the HPA axis and the SNS, resulting in increased production of stress hormones such as cortisol and adrenaline. Persistent elevation of stress hormones can disrupt glucose metabolism, promote insulin resistance and contribute to adipose tissue accumulation.58
  • Disruption of hormone balance: Chronic stress can disrupt the balance of key hormones involved in metabolism, including cortisol, insulin and leptin (a hormone associated with appetite suppression, released by adipose cells). This in turn increases the risk of insulin resistance and obesity.59
  • Systemic inflammation: Stress and poor emotional health are associated with systemic inflammation, characterised by elevated levels of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α). Persistent inflammation disrupts insulin signalling, promoting insulin resistance.60
  • Immune suppression: Disruption of immune signalling pathways is mediated primarily through activation of the HPA axis during times of stress. Suppression of immune mediators, such as cytokines and chemokines, causes impairment of immune cell recruitment, activation, and function.61,62 The impairment of immune cells, such as T cells, B cells and NK (natural killer) cells, compromises their ability to recognise and eliminate pathogens and abnormal cells, increasing vulnerability to infections and cancer.62
  • Altered eating patterns: Unhealthy eating patterns, such as emotional, binge, or disordered eating, are a feature of poor emotional health. These eating patterns disrupt energy balance and promote weight gain.63
  • Epigenetic modifications: Gene expression patterns are altered in the environment of chronic stress. This can lead to altered adipose tissue metabolism, thereby contributing to endocrine changes that further disrupt energy balance.64
  • Physical inactivity: Poor emotional health and stress promote feelings of fatigue and apathy. Studies have shown that individuals experiencing high levels of psychological distress are more likely to engage in sedentary behaviours such as prolonged sitting, watching TV, or using electronic devices excessively.65

Sleep

Quality sleep is more important to our health than most people appreciate, and chronic sleep disturbances are inextricably linked with metabolic dysregulation, including type II diabetes.

Sleep disturbances fall into three broad categories, each one linked with adverse health outcomes, including increased risk of cancer through metabolic dysfunction.

  • Insufficient sleep duration: Chronic sleep deprivation, characterised by consistently obtaining less sleep than recommended (usually less than 7-8 hours per night for adults), can disrupt metabolic processes. Insufficient sleep duration has been linked to alterations in glucose metabolism, insulin sensitivity, and appetite regulation, leading to increased hunger, cravings for high-calorie foods, and weight gain.66 Studies have shown that short sleep duration is associated with elevated levels of ghrelin (a hormone linked with hunger and reduced satiety) and decreased levels of leptin (a hormone linked with appetite suppression), which can dysregulate satiety and promote overeating.67
  • Poor sleep quality: Poor sleep quality, characterised by frequent awakenings, difficulty falling asleep or staying asleep, and non-restorative sleep, can impair metabolic function. It does this through dysregulated cortisol levels, altered sympathetic nervous system activity, and disrupted circadian rhythms.68 Furthermore, inadequate or disrupted deep sleep and rapid eye movement (REM) sleep stages, may further exacerbate metabolic abnormalities.69
  • Irregular sleep patterns: Irregular sleep patterns, such as shift work, jet lag, or irregular sleep-wake schedules, can disrupt the body’s circadian rhythm and lead to metabolic disruption. Circadian rhythms affect the timing of metabolic processes, including metabolism of glucose and lipids, and energy expenditure.70 Shift workers in particular are at higher risk of obesity, insulin resistance, and metabolic syndrome due to the malalignment of their sleep-wake cycle and natural circadian rhythms.71

In summary, the psychological equilibrium associated with good emotional health and quality sleep is essential to our physical health too. Indeed, physical activity, nutrition, emotional health and sleep are fundamentally linked and must be considered on equal terms if optimal health and resistance to chronic disease and cancer are to be achieved.


 

Conclusion

The burden of poor metabolic dysfunction on the health system is significant, but more importantly, the impact on quality of life is greater.

By making lifestyle choices that predispose to chronic disease and life-threatening illness we are also reducing our chances of living the lives we would like to lead as we age. The majority of people would hope they could play with their grandchildren, go on holidays abroad, enjoy a walk in nature, do their own shopping and generally live life with energy, focus and mental clarity into middle and old age.

As a nation, we stand at a crossroads in our approach to healthcare—a juncture where prevention takes precedence over intervention, and proactive measures supplant reactive responses. Embracing a holistic paradigm that prioritises upstream interventions aimed at reducing the risk of chronic diseases, particularly cancer, is not only prudent but imperative in safeguarding the health and well-being of our communities.

By allocating resources to bolster access to physical activity, healthy nutrition, and positive emotional health, we might embark on a transformative journey towards a future where disease prevention is paramount. Investing in initiatives that promote regular exercise, whether through community fitness programs, accessible recreational facilities, or active transportation infrastructure, empowers individuals to embrace movement as a cornerstone of wellness.

Similarly, enhancing access to nutritious foods lays the foundation for metabolic health and cancer prevention. By dismantling barriers to healthy eating, such as fresh food deserts and socioeconomic disparities, we foster an environment where nutritious choices are not only available but accessible to all.

Moreover, nurturing positive mental outlooks and emotional resilience is essential in mitigating the detrimental effects of chronic stress and sleep disturbances on metabolic function. From mindfulness practices to social support networks, investing in mental health resources and education equips individuals with the tools to navigate life’s challenges with fortitude.

Those in positions of leadership have a collective responsibility to champion a holistic approach to health engagement. By cultivating partnerships across sectors—healthcare, education, government, and community organisations—we can amplify the impact and effect meaningful change on a societal scale.

In embracing this upstream model of metabolic health, we transcend the confines of traditional healthcare delivery models, which wait for people to become sick or sufficiently at risk of significant disease. If prevention could take precedence over treatment, and empowerment supersede dependency, health would not merely be the absence of disease but the presence, through purposeful choices, of vitality and resilience.


 

References

All references and links can be accessed here.

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