Another disease that may provide a temporary benefit is cancer. Research noticed many decades ago that cancer cells frequently had altered energy production, favoring anaerobic glycolysis, and the very rapid consumption of glucose despite having functional mitochondria (1). More recent researchers found an association between higher fasting blood glucose and increased incidence of multiple types of cancer (2). Also, diabetes and hyperglycemia are “associated with an elevated risk of developing pancreatic, liver, colon breast, and endometrial cancer (3).” A study found hyperglycemia to be a predictor of reduced chances of surviving various cancers (4).

Leukemia, a type of blood cancer, can even cause serotonin loss and incretin inactivation to limit insulin secretion, which could further suppress glucose entry into normal cells (5). Research found elevated expression of a glucose transporter and sensitivity to a glycolysis inhibitor in childhood acute lymphoblastic leukemia cells (6). Also, a risk score based on a distinct glucose metabolism signature correlated to the poor survival of individuals with acute myeloid leukemia (7).

Amazingly, out of “26,743 total cancer deaths in men and women, 848 were estimated as attributable to having a fasting serum glucose level of less than 90 mg/dl (8).” That means that less than 4% of cancer deaths associate with a low fasting blood glucose level. Therefore, cancer has an important relationship with glucose that requires further investigation.

The temporary benefit of most cancers is they rapidly remove excess glucose from the bloodstream. Cancer cells accomplish this removal by depending on glycolysis, even in aerobic conditions. Usually, normal cells only depend on glycolysis when there is not enough oxygen to use the aerobic energy production ability of the mitochondria.

By depending on glycolysis for energy production, even in aerobic conditions, cancer cells need about 19 times “more glucose uptake to obtain equivalent amounts of energy as normal cells (9).” This removes more glucose from the bloodstream at a quicker rate. Researchers note that “a near-universal property of primary and metastatic cancers is upregulation of glycolysis, resulting in increased glucose consumption, which can be observed with clinical tumour imaging (10).”

Amazingly, most cancer cells consume glucose at such a high rate that doctors use specific trackable glucose and positron emission tomography (PET) scans to locate the tumors by following where the glucose is going.

This removal of glucose by cancer cells is useful because too much glucose in the blood can cause a lot of damage. For example, excessive glucose in the blood can glycate LDL cholesterol, making the LDL much more vulnerable to oxidation (11). Both oxidized and glycated LDL can contribute to atherosclerosis, the buildup of plaque in the arteries (12).

Increased plasma levels of oxidized LDL were found to be one of the strongest predictors of acute coronary heart disease (13). Other researchers found inflammation raised heart disease risk (14). There is also an association between multiple glucose-related factors and an elevated risk of heart disease (15). The impact of glucose on heart disease is also important because heart disease increases the risk of having heart attacks.

As an important side note, some types of contraceptives raised glucose levels following a glucose tolerance test (16). Research found an association between high estrogen levels and more insulin resistance in vitro (17). Therefore, be cautious when selecting contraceptives.

Glucose in the bloodstream also leads to the formation of advanced glycation end-products (18). These activate AGE receptors (RAGE), further increasing inflammation (19) (20).

Multiple researchers also note the association between diabetes, a condition of excess blood glucose, and heart disease risk (21) (22) (23). Diabetes also increases the risk of stroke (24).

These examples are but a small representation of the link between excess glucose in the blood and serious health problems. By removing large quantities of glucose from the bloodstream, many cancers are providing additional time to correct problems with inflammation, metabolism, and nutrition. 

Whereas most cancers provide this extra time, high blood glucose levels can cause immediate critical damage, like strokes or heart attacks, resulting in sudden death.

In the evolutionary history of humans, continual sources of foods that spiked blood glucose levels were uncommon. There were periods of higher glucose availability, such as the periodic fruiting of wild plants and occasional heavy dependence on roots. However, most of the time, there were no foods that skyrocketed blood glucose levels. In that situation, cancer may have simply come and gone in vulnerable individuals, as glucose availability naturally shifted with the seasons. In the past, most cancers were rare anyways because of the active lifestyles and food quality available to ancient humans.

Unfortunately, in modern society there is constant access to refined foods that rapidly increase blood glucose levels. This raises insulin levels, which limits fat metabolism, causing cells to excessively metabolize glucose. This increases reactive oxygen species generation, damaging the mitochondria and worsening inflammation. Cancer is not designed to manage the modern-day continual access to refined carbohydrates. Therefore, many cancers are now deadly, which is especially influenced by the higher levels of chronic psychological stress in the modern world.

Interestingly, cancers tend to appear where there was a past injury or infection. This is because both conditions increase inflammation and damage normal cell function in a specific area of the body. The damaged cells cannot metabolize efficiently, leading to higher levels of glucose around the area of damage. This damaged area also has increased inflammation, which affects cancer by slowing the methylation cycle, activating cancer-promoting genes already built into the DNA.

Even in a situation of injury or infection, cancer may be simply stepping in to help reduce the excess glucose until metabolism improves and inflammation drops. Once the original problem heals, then cancer may slowly disappear as the healed regular cells take the glucose away and the methylation patterns shift due to reduced inflammation.

If many cancers thrive on glucose, then a ketogenic diet, which is low in glucose, might have anti-cancer effects. A review noted that 72% of animal studies found evidence for an anti-tumor effect on ketogenic meal plans (25). Other researchers also note that keto diets may reduce tumor growth (26). In contrast, increased intake of high glycemic foods that spike blood glucose associate with a higher risk of multiple cancers (27).

Ketogenic diet applications for cancer need to be aware of both protein and phytochemical intake. Some ketogenic followers eat excess protein rather than eating more fat. Research, which did not look at the ketogenic diet, found low protein intake associated with a lower risk of cancer if the individual was under 65 years of age (28). The same research found protein did not have that effect in people over 65 years old (28).

This difference could relate to higher insulin-like growth factor 1 (IGF-1) levels at a younger age. Increased protein intake amplifies IGF-1 activity and increases cell growth, which can cause cancerous cells to grow. Therefore, not eating too much protein may help lower cancer risk.

IGF-1 also negatively affects autophagy, which is a self-eating process performed by the cells. Autophagy often improves metabolic efficiency because cells eat the most inefficient and damaged parts of themselves. Autophagy is critical because inefficient cell components, especially inefficient mitochondria, increase inflammation and the risk of many health problems. There is further discussion of autophagy later.

The other consideration on a ketogenic diet is consuming plenty of phytochemical-rich foods. Inexperienced people begin the high-fat food plan and remove many plants that have beneficial phytochemicals. Vegetables, such as the dark green leafy types, are the most critical part of any food plan because of their impressive phytochemical and mineral content.

In general, the ketogenic approach may be most helpful when protein consumption is moderate, and dark green leafy vegetable intake is high. Adding various spices may also benefit health because of their phytochemical content.

Unfortunately, because of the technology-driven trend to focus on genetics, the view of many people is that genetic mutations cause cancer. They think most types of cancers are primarily because of genetic inheritance. People often declare they simply have the wrong genes and suspect an inherited cancer is only a matter of time. However, “the vast majority of human cancers show no obvious familial inheritance (29).”

Many people that excessively focus on genetics may also believe the increased glucose uptake of cancer is a side effect of these genetic changes. However, research has found a “direct role of increased aerobic glycolysis in inducing the cancer phenotype (30).” The increased uptake of glucose occurs before many cancers start to grow. 

Despite frequently still having functional mitochondria that can create much more energy than glycolysis, many cancers will over activate glycolysis to rapidly metabolize glucose for energy. As mentioned, the rapid metabolism of glycolysis allows cancer cells to quickly remove glucose from the blood, which may help protect the body from an immediately worse health problem.

Rather than the old paradigm of most cancers occurring due to accidental genetic mutations, this new paradigm sees most cancers, not all cancers, as having a purposeful and temporarily helpful function. This function is the removal of glucose from the blood when there is too much inflammation and inefficient metabolism.

Typically, the metabolic problems occur because of excess reactive oxygen species caused by many different factors, such as injury, infection, pollution, psychological stress, and consuming too many refined carbohydrates. These problems are usually present for a long-time for cancer to develop to the point of symptoms and seeing cancer on medical scans.

However, the purposeful design of cancer is not meant for an environment that has continual access to foods that spike blood glucose levels. Stopping refined carbohydrate and processed food consumption is critical for reducing inflammation and cancer risk.

In addition, psychological stress, even if hidden from the conscious mind, also needs healing. This is because stress powerfully affects inflammation. Unfortunately, stress if often ignored since stress can hide from awareness and involve confronting intense energy and emotions. Do not overlook the importance of reducing psychological stress.

As mentioned, inflammation and reactive oxygen species can lead to mitochondria inefficiency, which often causes insulin resistance and higher blood glucose. If inflammation raises blood glucose levels, and glucose feeds most cancers, then inflammation increases cancer risk.

If there is a link between cancer and inflammation, then males will have an increased risk of cancer because the male immune system is more pro-inflammatory than the female immune system, which has more self-regulation. Unsurprisingly, males have a higher rate of cancer than females (31).

Another critical indication of the link between cancer and inflammation is many localized infection-based cancers may start due to inflammation caused by the infection (32) (33) (34) (35) (36) (37). Also, serum high-sensitivity C-reactive protein (hs-CRP), a marker of inflammation, correlated with cancer risk (38). In addition, “in most cancers, chronic inflammation precedes tumorigenesis (37).” 

Amazingly, researchers report “only 5-10% of all cancer cases can be attributed to genetic defects, whereas the remaining 90-95% have their roots in the environment and lifestyle (37).” This is critical because an individual can change multiple environmental and lifestyle factors that reduce inflammation and cancer risk.

Inflammation can also increase cancer risk via epigenetic modifications. As mentioned in Chapter 3, inflammation slows down the methylation cycle in multiple ways, such as disabling enzymes and redirecting cysteine to produce glutathione, which is a powerful antioxidant.

The methylation inefficiency can limit the methylation of genes that control cancer. The reduced methylation of genes is known as hypomethylation. Researchers note a hypomethylation of genes that promote cancer (39). Also, reduced methylation is present in almost all types of human tumors (40).

Importantly, cancer severity correlated to the amount of hypomethylation (41). This means cancer was more severe when there was less methylation. Other researchers also report global DNA hypomethylation in association with cancer, remarking that “unlike genetic alterations, DNA methylation is reversible (42).”

Interestingly, amongst global hypomethylation, there is usually also hypermethylation of specific DNA sections. Research found hypermethylation of tumor suppressor genes (43) (44). Currently, many cancer researchers focus on this limited and specific hypermethylation.

However, this hypermethylation potentially happens as an indirect consequence of the initial, and more common, hypomethylation (41). Research notes “there is often more hypomethylation than hypermethylation of DNA during carcinogenesis, leading to a net decrease in the genomic 5-methylcytosine content (45).” There is also the likelihood something still unknown about tumor suppressor genes makes these areas more susceptible to hypermethylation amongst the more common hypomethylation pattern.

Perhaps CpG islands affect the specific hypermethylation seen amongst the more common global hypomethylation. CpG islands have a unique DNA arrangement that might attract superoxide, a reactive oxygen species, which has nucleophilic properties. Superoxide, acting as a signaling molecule, may affect DNA in a manner that encourages methylation (46). This may occur in specific areas of DNA and lead to site-specific hypermethylation.

Importantly, other reactive oxygen species can also cause specific hypermethylation (46). Therefore, reactive oxygen species explain both cancer features; the frequent global hypomethylation and the limited but targeted hypermethylation of tumor suppressors.

The ability of inflammation to cause hypomethylation is an elegant design. There are unmutated genes built into DNA that promote the growth of cancer, but an efficient methylation cycle usually keeps these genes turned off. Chronic inflammation can cause the hypomethylation of these cancer-promoting genes, which turns these genes on. This prepares the body to create cancer around the time that normal cells have become resistant to glucose because of the same chronic inflammation.

As discussed, excess reactive oxygen species can damage the ability to metabolize glucose, leading to insulin resistance and higher blood glucose levels. Excess reactive oxygen species also disable methylation cycle enzymes, causing the methylation cycle to slow down and become inefficient. Therefore, too many reactive oxygen species first cause chronic inflammation, antioxidant depletion, and sustained methylation cycle inefficiency before many cancers start to grow.

Chronic inflammation also limits immunity. This affects cancer because many cancer cells are normally found by a well-functioning immune system and destroyed. If the immune system is limited, then cancer cells grow more easily and can hide from the weakened immune system.

If inflammation causes most cancers, then reducing the inflammation using many nutrition and life changes may stop most cancers.

For example, eating low-glycemic plants that have many nutrients and phytochemicals may reduce inflammation and increase methylation cycle efficiency. Also, eating more healthy fats gives cells an energy source that makes fewer reactive oxygen species than glucose.

Also, making sure to fulfill all daily nutrient requirements by tracking food intake supports enzyme essential for antioxidant defenses and detoxification. These steps and many others reverse overall DNA hypomethylation and reduce blood glucose levels.

Regular exercise, improving sleep, periodic fasting, and caloric restriction also reduce inflammation and help stop cancer.

However, psychological stress is one of the most critical problems that needs improvement to reduce cancer. This is difficult, as cancer is a stressful condition because of pain and confrontation with mortality. There is further discussion about psychological stress later.

As this book hopefully makes clear, reducing chronic inflammation and getting quality nutrition may be the key to improving not only cancer, but also many other health conditions, including difficult ASD symptoms.

Unfortunately, many modern societies have multiple risk factors that increase inflammation. A few of these factors are excess refined carbohydrate consumption, not enough dark leafy green vegetables, eating throughout the day, not exercising, too much psychological stress, using lights late at night, and not sleeping enough.

All these risk factors were not a consistent problem for our ancient ancestors. As simply part of natural living, they consumed low glycemic load whole food, periodically fasted, frequently exercised, and ate plenty of animal fat. Critically, they also ate many fresh, phytochemical-rich vegetables. This ancient lifestyle balances inflammation and maintains mitochondria efficiency.