In the 1960s zinc was identified as an essential trace metal for humans. Zinc has a lot of jobs in the body, namely as a catalyst component of over 300 different enzymes including growth, immune defense, cognitive function, and bone health. Advances in technology and measuring capabilities have advanced us from a single zinc enzyme found in 1939, to a prediction that the human genome project would find 3% of genes encode zinc proteins, to a total of 3207 known zinc proteins. Deficiencies of zinc can happen due to low intake, inadequate zinc absorption, increased zinc excretion or an increased need of zinc, as in children and pregnant women. The purpose of this paper is to briefly discuss a few of the roles zinc plays in the human body. These include zinc deficiency and impaired calcium entry into cells and its effects (decreased appetite and immune dysfunction), zinc and male infertility, as well as zinc and diabetes.

In closing part II of this series I left you with some very compelling data from the study “Tryptophan metabolism via the kynurenine pathway in patients with the eosinophilia-myalgia syndrome” by Silver et al which suggests that the eosinophilia-myalgia syndrome (EMS) crisis in the late ‘80s was more than just an issue of isolated batches of contaminated L-tryptophan supplements. In fact, it may be that EMS patients presented with major pre-existing alterations in tryptophan metabolism that created a susceptibility that made them more prone to adverse reactions to both contaminated and uncontaminated L-tryptophan supplements. Now I would like to present selected quotes from the discussion section of that paper which offer the authors’ interpretation of a data set that flies squarely in the face of the generally accepted conclusion derived over 20 years ago that elimination of the contaminant in L-tryptophan supplements totally eliminated the risk of developing EMS in all populations when these supplements are ingested.

THERE ARE MANY BIOLOGICAL CO-CONSPIRATORS INVOLVED IN THE AGING PROCESS and the development and perpetuation of degenerative diseases. Advanced glycation end products (AGEs) are prime culprits that have not received the attention they deserve. AGEs act in multiple ways to impair human function and damage tissues. There are also multiple ways we can intervene to minimize the damage produced by AGEs.

“We worry about what a child will become tomorrow, yet we forget that he is someone today.” Stacia Tauscher Who are today’s children? Are they the healthy little bundles of unexpressed potential we think they are or are they a time bomb waiting to go off. Recent literature and research seems to point in the direction of the time bomb. Diseases and conditions that were reserved for the adult population are now starting to surface in children. Why? Because, as Pearl Buck said “If our American way of life fails the child, it fails us all,” and today’s children have been failed.

Based on the Belongia et al1 paper from 1992 that I reviewed in part I of this series, there is, in fact, no controversy in the so-called tryptophan – eosinophilia-myalgia syndrome (EMS) controversy. Contaminated batches of supplemental tryptophan were involved in the vast majority of EMS cases, which ceased to appear after the FDA banned all further sales of supplemental tryptophan. Therefore, the contaminant must have been the sole causative factor.

What you are about to read is the first in a series of newsletters I wrote in 2013 and 2014 about an interesting and strange set of experiences. These experiences led me to completely re-evaluate my stance on whether supplemental L-tryptophan might pose a significant health threat to a small but notable portion of the population.

What you are about to read is the first in a series of newsletters I wrote in 2013 and 2014 about an interesting and strange set of experiences. These experiences led me to completely re-evaluate my stance on whether supplemental L-tryptophan might pose a significant health threat to a small but notable portion of the population.

THERE IS SOMETHING FRUSTRATING about talking to patients who take pain medications and believe in their heart that the drugs are doing them good. We see the advertisement for Alleve that show a woman with arthritis taking Alleve so she can have a better work out. Doctors, when prescribing NSAIDs, impart the idea that the drugs actually help the condition. Too often people in pain are given drugs to mask their symptoms, but are given the idea that healing is somehow being facilitated. The purpose of this paper is to give the practitioner a tool to teach patients.

For thousands of years, humankind has rhapsodized about wheat. “Breaking bread” with those whom you love is one of the greatest joys of life, isn’t it? We work hard to be successful “breadwinners” for our families, working hard to “place bread on the table” and “saving dough for a rainy day.” Memories of freshly baked bread are embedded within our minds, and olfactory organs, as well as our hearts. You have the idea. What is the issue, then, with wheat and its brother grains that graced our tables for millennia? The answer is that for a lot of people, a slight allergy to gluten and similar proteins found in wheat, rye or even barley can lead to autoimmune problematic diseases.

Disease is thought to be a pathological process, such as schizophrenia, throat infection, etc. The degree of deviation from a biological norm is the factor used to quantify a disease. Another similar term, illness, is thought to be an unhealthy feeling that is internally rooted in a patient. Sickness is the external expression of a state of unhealthiness. It can be chronic or acute – the latter being more serious. It is considered to be a societal recognition of an illness. If your illness is recognized by the society you live in, it will be considered sufficiently important for sickness benefits, such as excusing absenteeism, reimbursement for treatment expenses, etc.

Vitamin D, also known as calciferol, is technically not a vitamin, but really a fat-soluble prohormone (hormone precursor with little hormonal activity itself). The two major forms of vitamin D are D2 (ergocalciferol) and D3 (cholecalciferol). Vitamin D3 is photosynthesized in the skin when it is exposed to ultraviolet radiation (UVB radiation), and vitamin D2 is made naturally in plants when they are exposed to ultraviolet radiation. The main function of Vitamin D was previously believed to be in the prevention of diseases such as, rickets and osteomalacia. However, there has been recent discoveries that vitamin D may also help prevent a variety of diseases such as: cancer, cardiovascular disease, multiple sclerosis, rheumatoid arthritis, congestive heart failure, stroke, type 1 diabetes, chronic pain, high blood pressure, and may help defend the body against microbial invasion.

Alarming statistics have been emphasized through research findings and the media concerning a global crisis of vitamin D deficiency. Severe vitamin D deficiency is clinically defined as 25(OH)D <30 nmol/L (or 12 ng/mL). Prevalence rates in the United States of a severe vitamin D deficiency have been reported as 5.9%, 7.4% in Canada, and 13% in Europe. Prevalence of 25(OH)D levels <50 nmol/L (or 20 ng/mL) have been estimated to be 24% in the United States, 37% in Canada, and 40% in Europe. These numbers could be a reflection of the dramatic increase in vitamin D testing, large variability in mean serum 25(OH)D which can vary up to 300%, analytic procedures utilized to determine 25(OH)D, or even variable among the available assays. For example, there was more than a 50-fold increase in the incidence of testing for vitamin D deficiency in UK primary care between 2005 and 2015.12 Other countries have also demonstrated a substantial increase in vitamin D testing. In light of this, The Endocrine Society has published clinical guidelines on testing for vitamin D deficiency. Only those at risk for developing a vitamin D deficiency are recommended to be tested, and population screening or screening those not at risk is contraindicated. Regardless of which factors might be contributing to a vitamin D deficiency, most of the population is in fact, not deficient in vitamin D. Current data indicates that serum 25(OH)D levels in the general United States population have increased over the last decade (2007-2017). Public health campaigns increasing awareness, expanded testing, association with diseases, and roles beyond bone health have played important roles in reversing this trend. This presents an important opportunity to revisit vitamin D.