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Endoplasmic reticulum stress is somewhat analogous to a "traffic jam" inside the ER, and the unfolded protein response is a pro-inflammatory "traffic alert" in response; another more creative analogy would be that of an origami artist forced to fold and produce more than possible, with the resultant emotional breakdown/outrage analogous to the inflammatory UPR. Without the metabolic insults of excess glucose and excess saturated fatty acids—both of which are overpresent in Americanized/Westernized diets but which would have been absent for the vast majority of human history—the main expected stressors for induction of ERS would have been of microbial origin, and thus the resultant "alarms" and amplification of immune responses would have clearly been a positive and meaningful response; now that industrialized societies have essentially codified hyperglycemia and higher intakes of saturated fat, this ERS-UPR pathway is maintained in a higher state (quantitatively more) of sustained activation (longer duration). Saturated long-chain fatty acids activate TLR4 and induce NFkB-mediated inflammation via ERS-UPR and routes that are independent from ERS-UPR. While the ERS-UPR pathway effects elaboration of pro-inflammatory cytokines in an NFkB-dependent manner, the opposite is also true: NFkB activation causes ERS-UPR. Therefore, one would reasonably expect that inhibitors/modulators of the NFkB pathway (detailed elsewhere in this chapter) would be of therapeutic value in conditions of ERS-UPR; however, the clinical focus should always remain on identifying and eliminating the origin of the ERS-UPR/NFkB activation.
Conveniently and consistently overlooked social causes and medical consequences of obesity, insulin resistance, and medical management thereof: I wish to make an extra effort to point out a few items here to underscore their importance; in this paragraph, I will restate and reframe a few ideas to ensure that readers fully grasp the realization I am trying to impart. Readers, of course, have the option to bypass these particular perspectives, but let's at least consider them before making that decision. Œ The medical-pharmaceutical goal of using drugs to "enhance insulin sensitivity" is simple-minded, noncurative, and self-serving: Pharmacologic enhancement of insulin sensitivity in lieu of actually correcting the causes (mostly dietary, microbial, xenobiotic, and lifestyle) of insulin resistance increasingly occurs to me as a stupid idea (i.e., a forced pharmacologic override of normal physiology), leveraged by drug companies via drug-promotional journal articles and advertisements upon uninformed doctors and patients, who are purposefully kept ignorant by medical school and public education, respectively. The drug treatments for long-term management of insulin resistance offer no chance for curing the disease and simply keep patients in a state of perpetual drug dependency while medical doctors have basically become enslaved to the pharmaceutical industry. Many of these facts also apply to the long-term management of so-called chronic hypertension, which is likewise nearly always readily curable (not merely treatable) with nonpharmacologic means; some of this data was reviewed in my earlier books and articles covering diabetes and hypertension and will be revisited and expanded in Volume 2 of the Inflammation Mastery series.   Insulin resistance is cytoprotective: The idea that the human body could be an infinite repository for glucose and other high-energy fuel substrates—storing these reactive molecules endlessly and without consequence—is among the feeblest ideas to permeate and be absorbed into the clinical practice of medicine in general and the treatment of diabetes mellitus type-2 in particular. Fuel overload—caused solely by an excess of glucose+fructose with variable amounts of lipid and sodium and an insufficiency of nutrients and physical exercise—causes numerous consequential intracellular and organism-damaging events including oxidative damage, immune impairment, antioxidant depletion, mitochondrial dysfunction, endoplasmic reticulum dysfunction, and systemic inflammation; faced with an excess intake of glucose+fructose and fatty acids sourced from processed and nutrient-depleted foods, the body's only way of blocking these intracellular events is by blocking cellular uptake of fuel in general and glucose in particular, and by this innate self-protective wisdom of the body do we have "insulin resistance" formerly called by a more accurate name of "glucose intolerance." Very importantly, note that the term "glucose intolerance" implies a problem with glucose (consumption) and therefore suggests a low-cost low-carbohydrate dietary remedy, while the term "insulin resistance" is much more ambiguous and suggests a problem with insulin and the "need" for "insulin-sensitizing drugs", or simply more insulin (pharmaceutical grade, via injection). Ž Insulin resistance is the predictable outcome of an unnatural diet and physically-constrained lifestyle: The overconsumption of processed foods is the primary cause of insulin resistance via nutrient deficiencies (e.g., chromium, cholecalciferol, magnesium, fiber and phytonutrients), substrate overload (e.g., glucose, n6 fatty acids, fructose, and pro-inflammatory sodium), and accumulation of dysmetabolic intermediates such as palmitate and ceramide; adding dysbiotic microbial exposures (natural) and xenobiotic exposures (artifactual from corporate-government irresponsibility) synergizes with modern malnutrition (fuel overload with nutrient deficiency) to create the perfect storm for insulin resistance, obesity, metabolic syndrome and hypertension.  Insulin resistance and related inflammatory and cardiometabolic consequences can be produced on a population-wide basis: Making nutrient-poor fuel-rich foods less expensive than health-promoting foods, excising nutrition education and physical education (formerly "P.E." from when I was a grade-school student) from public and private schools, allowing xenobiotics to be distributed among the population at levels severe enough to cause endocrinologic (e.g., metabolic and reproductive) impairment, limiting opportunities and incentives for public recreation and exercise (e.g., making car-ownership mandatory in many communities while blocking access to parks, bikeways, etc) is a perfect way to make an entire population obese and diabetic—witness the trends in the United States (images below).  Obesity and related inflammatory and cardiometabolic consequences are expensive (to the benefit of pharmaceutical-medical interests) and are unequally distributed among social/racial/economic groups: According to the US CDC[1] in 2014, "More than one-third of U.S. adults (34.9%) are obese and obesity-related conditions include heart disease, stroke, type 2 diabetes and certain types of cancer, some of the leading causes of preventable death. The estimated annual medical cost of obesity in the U.S. was $147 billion in 2008 U.S. dollars; the medical costs for people who are obese were $1,429 higher than those of normal weight. Obesity affects some groups more than others: Non-Hispanic blacks have the highest age-adjusted rates of obesity (47.8%) followed by Hispanics (42.5%), non-Hispanic whites (32.6%), and non-Hispanic Asians." ‘ Obesity trends (in America) follow very clear changes in governmental, social and economic policy—when people are insecure/scared about their personal finances and the stability of their society, they eat more: In a brilliant Op-Ed article titled "The Political Roots of American Obesity", Kihn describes what he calls "the American syndrome" as having started most clearly with changes in America's political climate in 1980; before this time, obesity trends had been both low and consistent for decades. Starting in 1980, economic insecurity started to skyrocket in the United States, and the obesity epidemic was initiated on a population-wide level. According to Kihn, starting in 1980, new government policies acted quickly to dismantle unionized worker protections and thus quality of work life—where people spend much or most of their adult lives, job security, worker safety, and quality pay with living wages; the most obvious single event (which had a ripple effect throughout the country and clearly indicated the change in America's social contract) was the President-authorized firing of more than 11,000 unionized air traffic controllers which was followed by nation-wide "union busting", the marked declines in job/income security, and the now famous processes of "out-sourcing" jobs to temporary and part-time workers and "off-shoring" jobs to low-paying countries with no worker protections and no sustainable environmental policies. Kihn argues very cogently that while obesity may result from overeating fats and sugars, the drive to overeat has an emotional basis in survival and resource insecurity; this trend of society-wide insecurity and anxiety has its origins in national policies that make people fearful for their survival—namely, job and income insecurity.

§  "American Syndrome" and "The Political Roots of American Obesity" (Truthout 2013 May[2]): "When we [look at the trends and causes of obesity], we will discover that the obesity epidemic in America is essentially a mental health problem, whose underlying causes are economic and political. ... As more and more Americans have seen their standard of living sink and their stress factors increase, they have taken to the all-purpose, all-American sedative—food—in a big way."

§  Obesity, diets, and social inequalities (Nutr Rev 2009 May[3]): "Obesity and type-2 diabetes follow a socioeconomic gradient. Highest rates are observed among groups with the lowest levels of education and income and in the most deprived areas. … This article discusses obesity as an economic phenomenon. Obesity is the toxic consequence of economic insecurity and a failing economic environment."

§  Poverty is obesogenic (Nutr Hosp 2013 Sep[4]): "Many studies have shown an overall socio-economic gradient in obesity in modern industrialized societies. Rates tend to decrease progressively with increasing socio-economic status."

§  Economic security and "scientifically educated individualism" are protective against obesity (BMJ Open 2014 May[5]): "This might suggest that economically secure, scientifically educated individualism may therefore be protective against obesity."