Cancer Screening
Questions from the Clinic:
How effective is cancer screening? What is the best overall way to avoid cancer?
How Effective is Cancer Screening?
A recent study on the overall effectiveness of cancer screening grabbed headlines across the globe, shocking many and calling into question the value of cancer screening in general. The headline: "Only 14% of diagnosed cancers in the U.S. are detected by screening.”(1)
One reason for the low number is because only four types of cancer – breast, cervical, colorectal, and lung – have recommended screening tests, while controversial tests (PSA) or no tests exist for many cancer types.
On top of this, the report only referred to the percentage of cancers detected; it did not provide the metric that matters the most to people. Notably, of the 14% of people that had cancer detected by screening, how often did this detection result in a cure?
This is where it gets murky. The confusion is due to the way a “success” is recorded in the statistics. Specifically, a “success” is often reported as 5-year survival – not overall survival, or the metric that matters to most people. In other words, just because a screening diagnoses a cancer doesn't mean it always translates into a life saved.
One of the main issues is something called lead-time bias. Lead-time bias can distort the ultimate value of cancer screening: total lives saved. Below is an example of lead-time bias.
In this example, the lives of the people screened have not been extended at all. Here's the rub: in the people screened, because the diagnosis date is recorded earlier, the statistics record a 5-year survival of 100%. The data for screening then looks excellent, yet in the only metric that matters, overall survival, it is entirely an illusion.(2)
Clinical trials have shown that screening saves lives for common cancer types, such as cervical, colorectal, lung, and breast cancer; however, the benefit amount is misunderstood. For example, in mammography in women aged 50 to 59, more than 1,300 women must be screened to save one life. Additionally, such calculations do not consider the potential harms of screening, such as unnecessary and invasive follow-up screening tests or anxiety caused by false-positive results.(2)
If you need clarification, you’re not alone. A questionnaire designed to test doctors' knowledge of cancer statistics showed widespread misunderstanding among physicians; 76% of those surveyed incorrectly believed that an improvement in 5-year survival demonstrates that a test saves lives.(2)
The only way to eliminate all the bias in cancer screening statistics is through a randomized trial comparing people assigned to screening with those assigned to a control group. The control group follows routine care without screening, and the study counts the total deaths in each group at a lengthy follow-up.
One such trial compared the lung cancer screening value of C.T. scans to traditional chest x-rays in smokers. The trial found a 0.4% reduction in lung cancer mortality, going from 1.7% in the chest x-ray group to 1.3% in the C.T. scan group. This was a statistically significant outcome that helped determine best practices, but in absolute numbers it reduced death from lung cancer by less than one out 200 compared to chest x-ray screening.(3)
Last year, the first randomized trial was published to determine colonoscopy's overall benefit. The trial compared a group screened by colonoscopy to a group not receiving a colonoscopy – a landmark, gold-standard study. The report's results shocked the cancer community and stirred up controversy. The results: colonoscopy only cut colon cancer risk by roughly a fifth, far below past estimates of the screening’s efficacy, yet, stunningly, it didn’t provide any significant reduction in colon cancer mortality.(4)
When all the biases are accounted for, the reported value of cancer screening may be overstated. "Everyone has been led to believe that screening is better than it actually is," said Dr. Otis Brawley, an oncology professor at Johns Hopkins University.(5)
Amidst all this confusion, how should someone objectively evaluate cancer screening? For one, it helps to understand the way the data is reported. You may see pamphlets in your doctor’s office that show 5-year survival changes from 10% to 90% if you're screened for a specific type of cancer. These statistics don’t account for lead-time bias and ignore the only value that genuinely matters – overall survival.
When evaluating any cancer screening, ask your doctor the one question that cuts through all the noise:
“What's my chance of dying from this if I'm screened or if I'm not screened?”
I am not suggesting you abandon these screening programs but rather better understand their impact. Don't settle into complacency that cancer is not a worry, given your standard screening schedule. There are no guarantees to avoid or significantly delay any disorder, but “banking” only on our established guidelines on screening to safeguard you and your family is false hope.
What is the Best Way to Prevent Cancer?
The above survey on cancer screening begs the following question: If only 14% of cancer is detected through cancer screening -- and the value of early detection is not absolute -- what can I do to prevent cancer from occurring in the first place?
The idea of “chemoprevention” (the use of certain substances to help lower a person's risk of developing cancer or keep it from coming back) has captivated cancer researchers for decades. Initially, researchers took a reductionist approach, searching for the nutritional “magic bullets” that might reduce the risk of cancer. The NIH has spent enormous amounts of time and money looking at antioxidants like beta-carotene, selenium, and vitamin E, and vitamins like folate, vitamin D, and others. When the dust settled, the results were often counterintuitive. For example, researchers initiated a randomized, double-blind, placebo-controlled primary-prevention trial in the 1980s to test the ability of beta-carotene to prevent cancer in smokers. Surprisingly, the study found an 18% increased risk of lung cancer in over 29,000 male smokers taking 20 mg of beta-carotene daily.(6) A second research effort found the same for vitamin E, once suspected to reduce the risk of prostate cancer. A 2001 study of 35,000 men demonstrated that the men who took 400 international units (I.U.) of vitamin E daily had more prostate cancers than men who took a placebo.(7)
The Effect of Overall Lifestyle on Cancer Prevention
Even though single nutrients failed to deliver the hoped-for results in cancer prevention, epidemiologists studying the effect of overall lifestyle arrived at a far different conclusion.
A 2017 American Institute of Cancer Research report examined these studies and estimated that 50% of all cancers are preventable through better diet, physical activity, weight reduction, and other modifiable risk factors.(8)
Studies like these suggest that it is not any single nutrient or phytochemical that reduces cancer risk. Rather, it is a “biological action package” – or, in other words, the totality of nutritional and lifestyle influences that combine in a “network effect” to reduce cancer risk.(9)
Cancer Prevention, Diet, and Insulin Resistance
Let’s start with diet; many Americans have a condition called insulin resistance – the most recent study shows that it affects up to 88% of Americans to some degree.(10) Insulin resistance leads to weight gain and vice versa – a vicious cycle. Two leading causes of insulin resistance are overconsumption of processed carbohydrates and lack of physical activity.
The connection between insulin resistance and cancer begins with the hormone insulin. Insulin resistance can slowly develop over decades, causing the pancreas to release more and more insulin to compensate for the cell’s increasing “resistance” to insulin’s signal – a condition called hyperinsulinemia.
The connection to cancer then centers on a hormone that is a close cousin of insulin, an anabolic hormone called insulin-like growth factor 1 (IGF-1). IGF-1 typically promotes normal growth during childhood and replaces damaged cells with new ones as we age. A healthy, fit adult has small amounts of circulating insulin and IGF-1.
Our cells have independent receptors for insulin and IGF-1 and a hybrid receptor that can bind both insulin and IGF-1 – because their molecular structures are very similar. The hybrid receptor is where the connection between diet and cancer collides. When someone has increasing insulin levels due to insulin resistance, the IGF-1 signal is amplified through the hybrid receptor to a pathological degree, setting the stage for cancer.
Real-world evidence of this cancer/diet connection comes from a village high in the mountains of Ecuador where a small population of people with a condition called Laron Syndrome live. People with Laron Syndrome have passed a genetic mutation in the IGF-1 receptor from one generation to the next. A consequence of this mutation is dwarfism because the cells don’t receive the growth signal from IGF-1 during childhood. But another significance of Laron Syndrome surprised the researchers studying this community: people with Laron syndrome are essentially immune from cancer. Without the IFG-1 signal, cancer rarely develops.(11)
Other studies also show this striking relationship within the average population, demonstrating that insulin resistance increases the risk for many types of cancer.(12)
Chronic Inflammation and Cancer
Like insulin resistance, chronic inflammation is causative in developing cancer and chronic disease. Like IGF-1 and insulin, the pro-inflammatory cytokines (cell messengers proteins) that cause inflammation are potent growth factors that set the stage for cancer to develop.
A simple experiment performed by two brothers in the 1950's demonstrated the potent connection between inflammation and cancer. The brothers performed a straightforward experiment designed to test the hypotheses that inflammation promotes cancer growth. To do this, they injected cancer cells into the portal vein that leads directly to the liver in two groups of mice. In one group of mice, they did nothing more than inject the cancer cells. In the other group, they injected the cancer cells and then performed a series of incisions across the bellies of the mice to induce the release of inflammatory cytokines to see if the cytokines influenced cancer development. Then they waited to see how many mice in each group developed cancer. The results were striking. While none of the mice in the first group developed cancer, many mice in the incision group developed cancer.(13)
Chronic inflammation is primarily lifestyle-driven – it occurs when we "decouple” the lifestyle patterns that best match our physiology. Our bodies are finely tuned to respond to environmental inputs from whole foods, physical activity, a natural circadian rhythm (sleep/wake cycle), and social connections. Industrial food processing and modern conveniences that reduce our activity level, artificial light, and societal trends that have led to isolation and loneliness have broken this fragile relationship – the result is chronic inflammation.
Evidence for this comes from studying traditional cultures that have yet to adopt modern lifestyles. These cultures have high levels of physical activity, eat unprocessed food, lack circadian rhythm disruptions from artificial light exposure at night, and tend to have strong social connections. Multiple studies have shown that people living in these traditional environments rarely demonstrate the elevated markers of chronic inflammation that have become common in individuals living in modern societies. (14, 15, 16, 17, 18, 19, 20)
Conclusion
Traditionally, cancer screening strives to detect cancer early and save lives. Yet, a sober look at the statistics reveals that it does not prevent most deaths due to cancer. To meaningfully reduce the risk of dying from cancer, studies guide us toward a holistic lifestyle approach that explicitly addresses the most significant public health problems in the developed world: insulin resistance and chronic inflammation. Unfortunately, the prevailing care pattern of our healthcare system ignores these early signals and jumps in when a definitive later-stage diagnosis arrives. Once again, treating disease and not promoting health and prevention.
Fortuitously, “re-coupling” your lifestyle to a more “ancestral” pattern can significantly reduce one’s chances of developing insulin resistance and chronic inflammation – the two conditions strongly linked to cancer risk. Ancestral living means addressing the entire “biological action package” by eating whole, unprocessed foods, avoiding excessive amounts of carbohydrates and sugars, staying active, avoiding circadian rhythm disruptions, and maintaining close and meaningful relationships.
We have organized a simple yet novel proactive solution with a panel of 12 blood draw combinations called the Predict Panel, coupled with an input survey on lifestyle, body measurements, and functionality to measure your current state of insulin resistance, inflammation, and more. We then consider five possible supplements and a few prescription medications, if needed, that all have long-term data on reduction in all-cause mortality. We then follow you like a friendly coach to modify required lifestyle changes to the point of steady-state and new labs that verify success. This “upstream” approach is low cost and can be done from your living room or office (except for a visit to your local Quest Lab Drawing Site). Details of the program are found below at MeakinMetabolicCare.com / Metabolic Optimization Protocol (MOP) and check out the parallel program for existing cancer patients (C-MOP).
Your Health is Your First Wealth,
Remember, Stay the Course, Strong and Curious,
And promise me- to be your own best doctor,
- Chuck and Travis
Travis Christofferson MS Travis Christofferson: books and biography
Questions from the Clinic (rationally researched for you) from CoachItForwardChuck.com
Chronic Disease Prevention Program- Metabolic Optimization Protocol (MOP) Metabolic Optimization Protocol - Meakin Metabolic Care .
Cancer Patient- Metabolic Optimization Protocol (C-MOP) Cancer Metabolic Optimization Protocol - Meakin Metabolic Care
Meakin Metabolic Care Website - Meakin Metabolic Care
Heal Navigator (care partner) Oncology Nurse Navigators
Disclaimer: This information is not meant as direct medical advice. Readers should always review options with their local medical team. This is the sole opinion of Dr. Meakin based on a literature review at the time of the blog and may change as new evidence evolves.
1 https://www.norc.org/PDFs/GRAIL/State-Specific%20PCDSs%20chart%201213.pdf
2 https://www.cancer.gov/about-cancer/screening/research/what-screening-statistics-mean
3 https://www.cancer.gov/types/lung/research/nlst
4 Bretthauer M, Løberg M, Wieszczy P, Kalager M, Emilsson L, Garborg K, Rupinski M, Dekker E, Spaander M, Bugajski M, Holme Ø, Zauber AG, Pilonis ND, Mroz A, Kuipers EJ, Shi J, Hernán MA, Adami HO, Regula J, Hoff G, Kaminski MF; NordICC Study Group. Effect of Colonoscopy Screening on Risks of Colorectal Cancer and Related Death. N Engl J Med. 2022 Oct 27;387(17):1547-1556. doi: 10.1056/NEJMoa2208375. Epub 2022 Oct 9. PMID: 36214590.
5 https://www.cnn.com/2022/12/14/health/cancers-detected-by-screening-report/index.html
6 Albanes D, Heinonen OP, Huttunen JK, Taylor PR, Virtamo J, Edwards BK, Haapakoski J, Rautalahti M, Hartman AM, Palmgren J. Effects of alpha-tocopherol and beta-carotene supplements on cancer incidence in the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study. Am J Clin Nutr. 1995 Dec;62(6 Suppl):1427S-1430S. doi: 10.1093/ajcn/62.6.1427S. PMID: 7495243.
7 https://www.nih.gov/news-events/nih-research-matters/prostate-cancer-risk-vitamin-e-supplements
9 http://www.alternative-therapies.com/at/web_pdfs/boyd.pdf
12 Tabák AG, Jokela M, Akbaraly TN, Brunner EJ, Kivimäki M, Witte DR. Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study. Lancet. 2009 Jun 27;373(9682):2215-21. doi: 10.1016/S0140-6736(09)60619-X. Epub 2009 Jun 8. PMID: 19515410; PMCID: PMC2726723.
13 https://www.youtube.com/watch?v=H8zVrYEW8vE
14 McDade, T. W. Early environments and the ecology of inflammation. Proc. Natl Acad. Sci. USA 109, 17281–17288 (2012).
15 Carrera-Bastos, P., Fontes-Villalba, M., O’Keefe, J. H., Lindeberg, S. & Cordain, L. The western diet and lifestyle and diseases of civilization. Res. Rep. Clin. Cardiol. 2, 15–35 (2011).
16 Raichlen, D. A. et al. Physical activity patterns and biomarkers of cardiovascular disease risk in hunter-gatherers. Am. J. Hum. Biol. 29, e22919 (2017).
17 Kaplan, H. et al. Coronary atherosclerosis in indigenous South American Tsimane: a cross-sectional cohort study. Lancet 389, 1730–1739 (2017).
18 Lindeberg, S. & Lundh, B. Apparent absence of stroke and ischemic heart disease in a traditional Melanesian Island: a clinical study in Kitava. J. Intern. Med. 233, 269–275 (1993).
19 Lindeberg, S., Berntorp, E., Nilsson-Ehle, P., Terént, A. & Vessby, B. Age relations of cardiovascular risk factors in a traditional Melanesian society: the Kitava Study. Am. J. Clin. Nutr. 66, 845–852 (1997).
20 Lindeberg, S., Eliasson, M., Lindahl, B. & Ahrén, B. Low serum insulin in traditional Pacific Islanders—the Kitava Study. Metabolism 48, 1216–1219 (1999).