Cancer: How We Did Ourselves In

01 · Framing

Cancer as rogue evolution, not a moral verdict

Cancer is an insidious genetic disease, more visible with age, and an evolutionary trait that turned rogue. Genetic abnormalities accumulate until a cell gains a growth advantage over surrounding tissue.

That survival instinct sits at the genetic level across generations. Most mutations are harmless and help the host adapt. Those that grow too fast harbour destructive tendencies. That is the essence of cancer.

Living cells still translate the outside world. Our working window is no longer geological time. From hunter-gatherer life through agrarian society, industry, and the digital epoch, the span is roughly 5,000 years. Lifestyle shifts that drive DNA damage are often gradual, not dramatic enough to force conspicuous morphology.

Damage arrives through hereditary, replicative, and environmental paths. They may act alone or together. In Singapore and similar equatorial, shift-heavy, food-rich cities, environmental load is often the part people can still move: UV year-round, night work, tobacco, alcohol, processed and pickled foods, and everyday chemical habits.

This opinion sits in a short series: mutations and evolution · modifiable risk · contemporary treatment options · TCM alongside cancer care.

02 · Map

Seven modifiable risk clusters

Risk is cumulative. The more factors stack, the higher the probability of disease. Discretionary pleasures under kind conditions can become occupational hazards when choice is thin.

1. UV and tanning

Unprotected sun, indoor beds, and altitude flying raise UVA and skin-cancer risk. Open the UV cluster.

2. Tobacco in every form

Active smoke, second-hand smoke, residual toxins on soft surfaces, and smokeless tobacco all carry carcinogens. Open the tobacco cluster.

3. Sleep and circadian disruption

Very short or very long sleep, and chronic night-shift work (IARC Group 2A), link to higher cancer risk in studied settings. Open the sleep cluster.

4. Obesity and inflammation

Insulin as a growth signal plus chronic IL-6 / TNF-α inflammation creates a friendlier microenvironment for tumour growth. Open the weight cluster.

5. Alcohol, stillness, and diet

Regular alcohol, sedentary hours, processed and high-heat red meat, and heavy pickled foods each add documented load. Open the diet cluster.

6. Everyday chemical habits

Very hot drinks, microwaving polystyrene, forced petrol topping-off, and diesel exhaust are quieter, repeatable exposures. Open the habits cluster.

7. Oncoviruses and H. pylori

Named viruses and Helicobacter pylori are risk factors for specific cancers; vaccination still matters where available. Open the infection cluster.

03 · UV

UV, tanning, and altitude load

Takeaway. Limit unprotected sun to about half your burn time; skip tanning beds; remember cabin UV rises at cruise altitude.

Cats love sunbathing, and so do humans who share about 90% of their DNA with cats. Strong sunlight year-round is a perk of living near the equator, yet it is less kind to fair skin. A practical sun rule limits exposure to about half the duration that would burn a given skin type. That window still supplies vitamin D many people seek.

Ignoring that limit lets UVA damage DNA. Consequences include skin discolouration and both precancerous and cancerous skin lesions.

Indoor tanning is no safer, and may be more harmful than ordinary sun exposure. Tanning beds emit mainly UVA and promote squamous cell carcinoma and basal cell carcinoma. Indoor tanning before age 20 increases melanoma risk by nearly 50% in cited data, with risk rising with each use. Golfers also face higher melanoma and non-melanoma skin-cancer rates from cumulative UV.

Frequent flyers may add unnoticed load. At a common cruising altitude of about 10,000 metres, UV intensity roughly doubles sea-level exposure. Reflection from surrounding clouds can fill the cabin with ambient UV before counting cosmic ionising radiation.

04 · Tobacco

Tobacco in every form

Takeaway. There is no safe tobacco exposure. Cessation still cuts risk sharply, including years after quitting.

Tobacco smoking was a status symbol in its heyday. For men it signalled modernity and strength. For women it was sold as rebellious independence and glamour. For children it offered a fleeting sense of adulthood. Collective smoking still buys transient camaraderie.

Each inhalation introduces some 4,800 toxins, including about 70 identified carcinogens, and raises risk across many cancers. Life expectancy for smokers is at least ten years shorter than for non-smokers. That setback may reverse if the habit ends before age 40. Even for older smokers, risk of stomach, mouth, throat, lung, or oesophageal cancer is halved five years after cessation.

Involuntary smoking carries comparable cancer risk. There is no defined safe level of second-hand smoke. Passive exposure is not limited to breathing another person’s exhalation. Chemicals that linger in furniture, wallpaper, carpets, and fabric can permeate a room long after the cigarette is gone.

Smokeless tobacco is not a safe alternative. Besides higher nicotine content, oral tobacco contains at least 28 chemical carcinogens linked to mouth, stomach, oesophageal, and other cancers.

Active and passive smokers are advised to avoid ACE or Vitamin A (beta-carotene) and Vitamin E (alpha-tocopherol) antioxidant combinations in this context.

05 · Sleep

Sleep, shifts, and circadian load

Takeaway. Aim for a stable night length (not under 6 hours or over 10 as a habit); treat chronic night-shift work as a named occupational risk.

The sleep-cancer link is still being mapped, yet studies show a positive correlation between poor sleep and elevated cancer risk.

Duration is not a simple “more is better” story. A 2022 article in Cancer Epidemiology observed that sleeping more than 10 hours daily elevates risk of many cancers, including colon, liver, breast, and lung cancer in both sexes. Short sleep under 6 hours is specifically associated with higher risk of colon polyps and stomach cancer.

The International Agency for Research on Cancer (WHO) classifies night-shift work as Group 2A (probable carcinogen). Nurses, cabin crew, and people on overnight or graveyard shifts who live with circadian disruption may show higher rates of hormone-dependent cancers such as breast and prostate cancer. Anyone with long-term sleep-cycle disruption shares that peril.

Circadian rhythms help regulate cell proliferation, apoptosis, and DNA repair during sleep. They are powered in part by melatonin from the pineal gland. People with displaced or disrupted rhythms often show low melatonin or its metabolites. Melatonin has immuno-enhancing actions and is recognised for oncostatic properties that can interfere with tumour growth across initiation, progression, and metastasis phases in studied settings.

06 · Weight

Obesity and inflammation

Takeaway. Excess weight raises cancer risk through insulin growth signalling and chronic inflammation, not only through “metabolic disease” labels.

Most people link overweight and obesity with insulin resistance, not cancer. When cell insulin receptors become less sensitive, the pancreas secretes more insulin and serum levels rise. As a growth factor, high insulin can trigger rapid cell proliferation, reduce apoptosis, and push DNA regulator genes out of control. That means more opportunity for replicative error and cancer development in liver, pancreas, kidney, breast, and other sites.

Another harmful feature is sustained inflammation. Acute inflammation is a short-term defence. Chronic inflammation, with lymphocytes, macrophages, and proliferation of vessels and connective tissue, is a long-term disorder and a favourable microenvironment for tumour growth.

Obesity predisposes to a pro-inflammatory state through mediators such as IL-6 and TNF-α. TNF-α tends to be overexpressed in overweight states; IL-6, linked with obesity, influences the liver to synthesise C-reactive protein, a marker of systemic inflammation. Inactive lifestyle and poor dietary habits often travel with the same picture.

07 · Moderation

Alcohol, stillness, and what we eat

Takeaway. Cap alcohol and red meat, stay moving, and treat processed meat and heavy pickles as occasional, not daily defaults.

Alcohol

Advocates sometimes suggest a daily glass for the heart. Whatever the cardiovascular debate, much research links regular alcohol with roughly doubled incidence of cancers including breast, liver, stomach, pancreatic, mouth, and oesophageal cancers in both sexes. The liver metabolises alcohol into acetaldehyde, a toxic known carcinogen that damages DNA and impairs repair, opening a path to mutation.

Alcohol’s half-life is about five hours, so full clearance after a drink can take around 25 hours. At an average metabolic rate near 7 g per hour, the Centres for Disease Control and Prevention advise against more than two alcoholic drinks a day or ten drinks a week as a practical ceiling. Each gram of alcohol yields about 7 calories (fat is about 9), so regular drinking also feeds weight and cholesterol load, themselves cancer risk factors.

Sedentary life

Physical activity has declined across civilisation. Desk-bound work and leisure spent gaming or on the sofa keep many people still. Physically active people show lower rates of many cancers and better outcomes after diagnosis. The National Cancer Institute links exercise with lower serum hormones (for example oestrogen) and growth factors such as insulin, reduced inflammation, improved immunity, faster gut transit that shortens bowel contact with potential carcinogens, and prevention of obesity.

Processed food, red meat, and pickles

Modern marketing fuels craving for processed food, especially processed meat. Eating any processed meat raises risk of stomach and colorectal cancers. Salting, curing, fermenting, and smoking rely on nitrates and nitrites that can become N-nitroso compounds when ingested and nitrosamines when heated. Nitrosamines are strong carcinogens implicated across lung, brain, liver, kidney, bladder, stomach, oesophagus, and nasal sinus tissues. Processed meat also poses a greater bowel-cancer risk than red meat alone.

Heme iron in red meat catalyses endogenous formation of cancer-causing N-nitroso chemicals. Grilling, barbecuing, or cooking red meat at high temperatures releases heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) that can damage bowel cells. A practical ceiling often cited is 450 grams of red meat per week to avoid raising colorectal cancer risk.

Pickled foods can support gut probiotics and still raise concern for nasopharyngeal carcinoma when nitrate and nitrite loads are high and form nitrosamines with dietary protein. Sauerkraut and kimchi belong in moderation, not daily excess.

08 · Habits

Everyday habits that add load

Takeaway. Cool hot drinks, never microwave polystyrene, stop topping off petrol after the click, and treat diesel exhaust as a serious airborne carcinogen.

Some detrimental habits look innocuous. Many people favour soups piping hot for aroma, or start the day with very hot coffee or tea. Observational studies show that drinks above about 60°C can scald the tongue and irritate the oesophagus; repeated exposure elevates oesophageal cancer risk. Let liquids cool.

Takeout containers are meant to ferry food home. Reheating food in polystyrene is a different act. IARC has upgraded styrene from possibly carcinogenic to probably carcinogenic for humans. Microwaving in polystyrene lets styrene leach into food; repeated exposure is linked with higher risk of leukaemia, lymphoma, pancreatic, and oesophageal cancers. Prefer your own container, or disposables made from polypropylene.

At the petrol pump, do not force more fuel after the nozzle clicks off. That topping-off releases vapour and carcinogens such as benzene. Even at air levels around 0.5 mg/m³, forced filling is linked with higher kidney and nose cancer risk in cited exposures.

For diesel vehicles, diesel exhaust is more carcinogenic than second-hand cigarette smoke in comparative framing, is linked to lung cancer, and may raise risk for oesophageal, stomach, and other cancers.

09 · Infection

Oncoviruses and infection risk

Takeaway. Named viruses and H. pylori raise specific cancer risks; vaccination and behaviour change still cut incidence where tools exist.

Viral infection is one step in a longer cancer process. Long delays between infection and malignancy make causal links hard to prove for any single person. Infection is necessary for some cancers, yet most infected people never develop cancer. Oncoviruses are therefore risk factors for named malignancies.

Viruses promote cancer in several ways. Immune killing of infected cells raises turnover and mutation opportunity. Persistent infection drives chronic inflammation and oxidative stress that can accumulate mutations and remodel pathways. Some viruses corrupt host DNA and deregulate cell cycle, DNA repair, and apoptosis. A long-weakened immune system is also less able to suppress growth and mobilisation of cancer cells.

Vaccination and personal behaviour change reduce infection incidence where tools exist. Beyond viruses, the bacterium Helicobacter pylori is associated with stomach cancer.

The list above is not exhaustive and keeps evolving. Conceptually these factors can often be controlled or substituted at the individual’s discretion, so they are called modifiable. Risk remains a numbers game: the more factors one amasses, the greater the probability of disease.

Many risk factors sit in lifestyle. That does not mean choice is always free. When life is kind, risk factors look like discretionary pleasures. Under harsher conditions they can be immutable occupational hazards.

I still remember a documentary that followed a high-rise construction worker in Hong Kong. Sole breadwinner, diagnosed with a skin malignancy, he kept working in hot weather to provide for his family. He ate cheap processed food to save money. As the building rose, solar load intensified, and he succumbed under aggravated conditions. Even knowing the risks, his place in the food chain left little room to change them.

Is it then relevant to ask cancer patients how they did themselves in? As physicians we do not judge, and we would never ask. We focus on the treatment regime at hand.