The Rising Cancer Threat: How Modern Lifestyles and Treatments Contribute to the Growing Epidemic

After half a century of extensive (and wildly expensive) research, and vast numbers of clinical trials – ClinicalTrials.gov currently lists 433,955 studies – cancer remains the second-leading cause of death in the United States, after heart disease. It is first or second in all developed countries, and it’s getting worse; over the last few decades, the incidence of cancer in adults under 50 years of age has steadily increased in those countries (source). We currently experience a 50% and rising lifetime risk (source).

The risk is increasing with each generation. People born in 1960 experienced higher cancer risk before they turn 50 than people born in 1950, and we predict that this risk level will continue to climb.

Shuji Ogino, a professor at Harvard Chan School and Harvard Medical School, and a physician-scientist in the Department of Pathology at the Brigham and Women’s Hospital

It is not just a matter of a single cancer, which might possibly be attributed to a specific stressor. This is a very general problem, involving cancers of the breast, colorectum, endometrium, oesophagus, extrahepatic bile duct, gallbladder, head and neck, kidney, liver, bone marrow, pancreas, prostate, stomach, and thyroid. Cervical cancer, which is significantly prevented by the HPV vaccine, is a notable exception.

Colorectal cancer is a particular concern; diagnoses in young adults doubled from 11% in 1995 to 20% in 2019 (source).

The fact that so many cancers are increasing in young adults tells us that causative factors are in play from a very early age. The trend also implies that our many defences against cancer, which we share with most multicellular organisms, are being progressively eroded. It is obviously our diet and lifestyle that are doing the damage, but public health today is effectively owned by the pharmaceutical industry. This is why prevention lags behind cancer treatments, which are far more profitable.

This is unfortunate. Despite significant and ongoing advances in cancer survival and treatment success rates, chemotherapeutic drugs generally reach a point of failure.

In some cases, they fail in the short to medium term, because the patient dies with overwhelming infection enabled by immunosuppression or from some acute iatrogenic effect. Mostly, however, this approach fails in the longer term because it induces resistance. Initially positive results are generally followed by resurgence, and very often increased malignancy (source). Currently, 90% of chemotherapy failure is due to the growth and metastasis of cancers related to drug resistance (source).

Solid cancers contain many different types of cancer cells, which function in a coordinated and collective manner. In this sense, a tumor is very like an organ, or perhaps even an organism. These different cells are genetically diverse with differing functions, genomes, and epigenomes, and hence different susceptibilities (source).

Due to this genetic diversity, some cancer cells are better able to avoid, sequester, metabolise, or excrete drugs, have enhanced repair/increased tolerance to DNA damage or higher antiapoptotic potential.

The cancer collective responds and attempts to adapt to its microenvironment, as all living entities do. Apply chemo, and standard Darwinian rules apply. Vulnerable cells die, cells more able to withstand the drug survive, and the cancer mass eventually becomes drug-resistant.

This is like antibiotic resistance, but worse. When treating infection, antibiotics do not kill all the pathogenic bacteria but reduce their numbers to the point where the immune system can take over. Chemo degrades immune function and makes it less able to complete the process, so now the balance of power shifts further to the cancer.

A recent review put it like this: ‘A brief review of the history of cancer research makes one wonder if modern strategies for treating patients with solid tumours may sometimes cause more harm than benefit’ (source).

And it gets more complicated.

In common with all life forms, cancer is driven to survive by a sort of imperative to live, an impulse to grow, continue, and breed. This not only occurs at the cellular level but also at the level of the whole cancer. There is a bewildering interplay of information within the cancer, with multiple mediators exchanging information between different populations of cancer cells and between cancer cells and host cells, including connective and immune cells (source).

If (when) treatment doesn’t kill all cancer cells outright but leaves a few at the verge of death, some of those cells co-opt intracellular machinery normally involved in physiological healing, and rebound into life. This is termed anastasis, Greek for ‘rising to life.’

Those cells that do come back are more invasive than before, and they drive other cancer cells towards compensatory proliferation. They do so via activation of Caspase-3, a protein normally linked to apoptosis in damaged cells but which can take on an opposite role, promoting carcinogenesis, metastasis, and therapy resistance (source).

These proliferation-stimulating and pro-survival pathways have been referred to as ‘Phoenix Rising,’ with cancer rising from the ashes of the tumor that was targeted by chemo or radiotherapy. The cancer emerges more ‘determined’ than ever to succeed. This is an important cause of treatment failure.

Prevention Is Better Than A Cure

All the above makes cancer prevention an attractive option. If we could optimise it and standardise it, we could theoretically reduce the numbers of cancer patients who eventually require treatment. If, perhaps, we could learn the lessons of the past.

In mid-Victorian England, cancer was recorded as a relatively minor cause of death in a population with an average life expectancy (after age 5) comparable to today’s social classes C and D, which most closely resemble the mid-Victorian population .

This situation is reasonably similar to what prevails in contemporary vestigial groups, such as the Tsimane of Bolivia. Among this group, endometrial, ovarian, breast, prostate, lung, and colorectal cancers appear to be rare; however, cancers with a more infectious etiology, such as cervical cancer, are more common .

It is worth reviewing the factors that might have protected our ancestors and are now leaving us vulnerable. The Victorian exposome was very different from ours, as represented in the following, far from comprehensive, table :

In summary, the mid-Victorian metabolism was very unlike ours and was cancer-hostile, whereas ours is cancer-permissive. Cancer cells were likely being formed in the bodies of Victorians at the same rate as today, but they emerged in a well-defended environment. The cancer statistics of the period , while imperfect, suggest that relatively few of those cancers achieved clinical significance.

The Victorian diet consisted almost exclusively of basic produce with low caloric/high phytonutrient density and contained none of the ultra-processed foods that dominate today’s diet and are increasingly linked to cancer . Their cooking techniques were generally low temperature (i.e., below 100°C), spirits were seldom consumed, and tobacco was rarely smoked, although it was taken as snuff .

In an age before IT and the internal combustion engine, people were also physically very active . Type 2 diabetes, a leading cause of cancer deaths today, was rare, as was obesity.

Due to the mid-Victorian exposome, the milieu intérieur was anti-inflammatory, euglycemic, and eubiotic. It was more immune-competent than ours, with β-glucan-mediated up-regulated innate immunity and an enhanced TH1/TH2 ratio . It was replete with polyphenols, carotenoids, and a range of other phytonutrients that promoted cancer cell redifferentiation, cell-cycle arrest, apoptosis, ferroptosis, cell contact inhibition, enhanced innate immune functions, and ECM stabilization .

Cancer cells emerging in this terrain were confronted with multiple barriers to survival and growth.

In contrast, the modern milieu tends to be pro-inflammatory, immune-compromised, hyperglycaemic, dysbiosis, and depleted of chemo-preventive phytonutrients. It is exposed to higher intakes of cooked meat and similar carcinogens, and the industrial diet’s reduced content of phase 2-inducing phytochemicals likely extends their half-life.

Our lower intakes of prebiotic fibre create an unhealthier colonic microbiota , with shifts in oestrogen and oestrogen metabolites linked to an increased risk of breast cancer . Prostate cancer risk may also be affected, although the data are diverse. Our lower levels of physical activity lead, in part, to increased obesity, Type 2 diabetes, and mTOR signalling .

The multiple lines of defence that eukaryotes like ourselves had to develop in order to win the prisoners’ dilemma posed by our single-cell prokaryote ancestors have been degraded by the modern lifestyle. The evidence that these changes have made our bodies more cancer-friendly can be clearly seen in current public health trends.

It will be objected that many micro- and phytonutrients have been tried as single agents in cancer models and found wanting. This is entirely unsurprising and is more of a reflection of today’s mono-therapeutic/pharmaceutical mindset than of the way in which a pre-transitional diet and lifestyle operate to provide many obstacles to cancer progression. This resembles antimicrobial or chemotherapeutic polypharmacy, where multiple agents are co-administered to make it more difficult for the target to acquire resistance.

This cancer-hobbling is hinted at in mid-Victorian cancer statistics .

Daniel McLachlan, Principal Medical Officer of the Royal Chelsea Hospital in London between 1840 and 1863, with ongoing responsibility for over 500 patients, published his magnum opus, A Practical Treatise on the Diseases and Infirmities of Advanced Life in 1863. It was a leading geriatric medicine textbook of the time.

In 800 pages of detailed clinical observations, he makes only a few references to cancer (primarily of the GI tract) and describes a series of 854 death records, which included only 47 cases of cancer .

At a 5.5% incidence, mid-Victorian overall cancer rates were approximately 10% of ours, if McLachlan’s figures are accurate. Given the technology of the time, how much weight can we put on them?

While his and his colleagues’ ability to detect cancer at an early stage was considerably less advanced than ours, the data noted here are based on autopsies conducted by physicians who recorded cancer without prejudice, and who were certainly able to identify gross tumours post mortem. Leukaemia, too, were already well-characterized by that time .

The mid-Victorian autopsy data may therefore reflect, however imperfectly, the 10% of cancer subjects in whom a genetic risk factor can be identified. McLachlan alludes to this, noting a strong familial disposition to stomach cancer . He could see a link that is today largely obscured by the larger numbers of cancers occurring in individuals without genetic risk, but who are subject to a cancer-promoting exposome.

There is another apparent key point of difference between ourselves and the mid-Victorians.

We expect the incidence of cancer to rise exponentially with age, in line with the declining ability of our many checkpoint systems. I believe that this pattern may, in fact, be an artifact, due to the extensive disrepair of our multiple cancer defenses. Cancer cells arriving at any age are likely to survive and, over time, present as clinical disease. Given a similar number of cancer cells being added to the total per unit of time, the rate of clinical emergence will undoubtedly increase as we age and our immune systems decline.

In a mid-Victorian, cancer cells emerging at any age were subject to multiple barriers to progress and generally failed to thrive. Among the mid-Victorians, this reportedly produced a different temporal frequency of clinical cancers, with an average age of presentation of circa 40 , compared to 60 today.

This suggests that a significant number of these cases may have been genetically susceptible, as suggested above. If this is indeed the case, it would follow that mid-Victorians without genetic risk factors were substantially less at risk than their counterparts today.

Finally, and for comparative purposes, it is interesting to consider cancer rates in other animals. Among 42 species of primates kept in controlled and optimized conditions (i.e., without predation and minimal risk of trauma), the cancer mortality rate is circa 5% . This more closely resembles vestigial and reported mid-Victorian rates than our own, and appears to make contemporary Homo sapiens an outlier.

A strategy to reduce exposure to carcinogenic factors, up-regulate all of our many anti-cancer defences, and perhaps restore or at least move towards mid-Victorian rates of cancer begins with abstention from tobacco and alcoholic spirits, and the minimization or avoidance of ultra-processed foods.

The second step involves maintaining a healthy weight and engaging in at least an hour of physical activity a day .

A third step may eventually involve nutritional enhancement via functional foods and supplements designed specifically to recreate a pre-transitional metabolome. This could be achieved by combining an omega-3 HUFA/amphiphile polyphenol combination, a blend of different-length prebiotic fibres, and a comprehensive micro- and phytonutrient support program designed to reproduce the mid-Victorian profile.

This strategy may not only help reduce the number of patients requiring cancer treatment, but also provide support to those who have been treated and are now in remission—a group for whom we currently have no substantive recommendations. Its efficacy will theoretically be highest when used as part of a holistic approach that includes both lifestyle and medical support.