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Snapshot: Type 2 diabetes, along with other chronic diseases, is now thought to be caused in part by an overactive normal process in the body called inflammation. All drugs developed to reduce inflammation have side effects, and it seems that the more powerful the drug, the more dangerous the side effects. Over the past decade, our research has shown that nutritional ketosis is surprisingly effective at reducing chronic inflammation. This observation helps explain the rapid and dramatic benefits seen in type 2 diabetes and may also demonstrate the potential to improve several other chronic diseases.
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Inflammation is a complex of cellular signals and responses from our immune system that allows our body to recognize and respond to infection and injury. If our inflammatory response is very weak, we run the risk of infection or poor healing. However, if the response is too great or hyperactive for too long, we risk suffering chronic damage from type 2 diabetes, coronary heart disease, many common cancers and Alzheimer’s disease.
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This balance between too little and too much inflammation is extremely delicate and controlled by many factors, including our genetics, environmental toxins and many aspects of our diet. One of the first purified drugs for human use was an anti-inflammatory compound, aspirin. Currently, we have several classes of drugs designed to control inflammation, but safe handling of their doses and timing requires professional vigilance to avoid dangerous side effects.
Over the past decade, nutritional ketosis has emerged as a powerful modulator of inflammation. Unlike drugs that usually only target one aspect of the body’s immune response, ketone immune modulation (KIM) appears to be equally effective at balancing anti-inflammatory effects in a safe, sustainable and very powerful way. Using various blood tests that monitor various markers of inflammation, nutritional ketosis has been shown to reduce these markers to levels comparable to the most powerful drugs currently available. Importantly, it appears to do so without the serious side effects that are typical of most medications. Here we present some of the evidence behind KIM as a breakthrough treatment that could allow us to prevent and reverse what is now considered a chronic progressive disease.
Physicians have studied inflammation since Greek times, but these initial observations were for more severe forms that cause noticeable symptoms such as redness, heat, pain and swelling.
With the invention of the microscope, scientists discovered white blood cells and observed that they rise during fever and injury, only to come back down when the disease is over. From this information, they identified a “normal range” within which most apparently healthy people have white blood cell counts (WBC).
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Beginning in the mid-1980s, however, pioneering researchers began a process to define new normal ranges for white blood cell counts. Early reports linked chronic levels in the upper half of the “old normal” range to an increased risk of heart attack, even in people with normal cholesterol levels²,³. In other words, inflammatory biomarkers that are in the range predictive of future disease cannot be considered normal.
But this is just the beginning. Since then, these high normal levels of white blood cells, along with another test that reflects inflammation in the body, called C-reactive protein (CRP), have also been shown to predict the development of type 2 diabetes⁴, many common types of cancer⁵, ⁶ and possible Alzheimer’s⁷.
In addition to white blood cell count and CRP, many different cell types, proteins and lipid-derived molecules are involved in regulating inflammation and immune function. These belong to various class names such as cytokines, chemokines, eicosanoids and isoprostanes. While the details of these compounds—origin, function, and interactions—are too complex for this overview, we need to understand the breadth and finesse of this network of interacting bioactive factors. Perhaps most importantly, its “up” or “down” regulation is a delicate process that maintains the body’s basic immune and repair functions.
The processes in the body that regulate growth, repair, defense against infection and recovery from injury are some of the most fundamental processes for survival. Considering that they have evolved over a billion years, it is understandable that the interrelated functions of immunity and inflammation are multilayered and extremely complex. Every organ in the body, from the skin to the gut, has its own unique defense mechanisms that kick in when it senses a threat. When an organ is damaged, it sends signals into the blood to alert the rest of the body. Thus, a localized infection of the legs or lungs can lead to a generalized fever.
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So whether it’s an acute local infection causing severe inflammation and fever, or something more subtle like a food allergen irritating the gut, these general immune and inflammatory markers can be measured in the blood. Some of these measurable markers are cell types called white blood cells, some are proteins produced in different organs such as muscle, liver or fat tissue, and some are peroxidized fats released from cell membranes. Through these circuit signals, the various systems of the body communicate, and the entire process is elegantly coordinated to preserve life and function without overreacting (for example, reaching too high a temperature or producing too many white blood cells).
In some cases, however, this delicate balance becomes overstimulated and a class of disorders known as autoimmune diseases can develop. In this case, the body’s activated defense system attacks some of its own organs and causes diseases such as rheumatoid arthritis, lupus, psoriasis, and type 1 diabetes. These immune disorders, in turn, increase the amount of inflammatory markers in the blood, which affects more organs over time. For example, people with chronic rheumatoid arthritis have a higher risk of heart disease, as do people with type 2 diabetes.
Modulation of inflammation and the immune response have been popular targets for drug development since aspirin. In general, older, better-known drugs tend to have a more common mode of action and a wider range of side effects. Recent drug research has focused on specific enzymes, bioactive molecules or types of white blood cells involved in inflammation in an attempt to reduce side effects, but this has proven to be a double-edged sword. By focusing on only one step in the complex cascade of the inflammatory/immune system, it is likely to distort the system rather than reduce the effects of inflammation in a balanced manner.
The risks associated with long-term use of various anti-inflammatory drugs are well known and often outweigh the expected benefits. One example is long-term use of aspirin, which has been shown to reduce heart attacks in people already diagnosed with coronary heart disease. When used in this setting (as “secondary prevention”), it was associated with lower long-term mortality. However, when aspirin was regularly used in people without known heart disease (primary prevention), overall mortality (mainly fatal bleeding) was significantly increased⁸.
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In another example, a monoclonal antibody targeting the cytokine IL-1beta and its C-reactive protein (CRP) was retrospectively administered to people with known heart disease and elevated CRP levels in their blood. The purpose of this study was to see if a drug that lowers CRP without lowering LDL cholesterol could prevent heart attacks. After a study of 10,000 people over 4 years, there was a significant 15% reduction in heart disease mortality; however, all-cause mortality did not differ between the active drug group and the placebo group. Why: Monoclonal antibodies reduce immune function, leading to increased deaths from infection⁹.
These two examples are typical of a series of studies suggesting that the long-term side effects of current anti-inflammatory drugs may eventually outweigh their beneficial effects. Therefore, this type of long-term treatment is reserved for patients whose underlying inflammation puts them at high risk — for example, rheumatoid arthritis, severe asthma, or organ transplantation.
There are many refined foods or nutrients that claim to have anti-inflammatory properties, but most of these claims are based on inconsistent, limited or non-existent human research data. Fish oil¹⁰ and green tea¹¹ are some of the most popular anti-inflammatory nutrients that have yet to stand up to scrutiny when offered as supplements.
Another popular antioxidant with anti-inflammatory properties is vitamin E (especially in the alpha-tocopherol form). It has been used in hundreds of studies with mixed results. At very high doses (1200 mg/day), vitamin E appears to lower CRP in people with type 2 diabetes12, but it may have other risks13. Another natural form of vitamin E—gamma-tocopherol—has even more potent anti-inflammatory and stress-stressing antioxidant properties¹⁴, ¹⁵, ¹⁶, ¹⁷ alone or in combination with the omega-3 fatty acid DHA¹⁸. This latest study shows that by combining moderate doses of