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GGT - Iron and your Cell Membrane Health

HOW DOES OMEGA-3 OIL DEFICIENCY CAUSE IRON OVERLOAD? 

AND CAN RESULT IN: 

  • Metabolic Syndrome
  • Heart diseases
  • Sudden Cardiac Death
  • Diabetes
  • and much more! 

THE INFORMATION ON THIS PAGE WILL TELL THAT STORY


Welcome to Health-e-Iron newest page. I am Health-e-Iron's founder and CEO, Gerald "Gerry" Koenig. I only discovered the connections between impaired iron metabolism and what's commonly referred to as "Omega-3" deficiency about a year ago. I was researching the scientific literature for a review article entitled "Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk," which was published in the journal "Disease Markers" in October (2015). The article was co-authored by Dr. Stephanie Seneff, a Senior Research Scientist from MIT.

Iron overload in the U.S. Navy's captive bottlenose dolphins

I had been studying iron overload in captive animals (i.e., those fed my man) for about ten years, of course, along with my human disease research. Iron overload among wild animal species is very rare; it generally doesn't occur unless the animals are exposed to environmental toxins (persistent or acute), or confronted with the absence of key components of their traditional diet in their native habitat. Unfortunately, iron overload occurs frequently when wild animals are fed by man! The animals most affected appear to be bottle-nose dolphins, black rhinos, South American tapirs, some lemur species, and several species of birds, mainly soft-billed varieties.

We first provide two studies that recently alerted us to the connection of an unhealthy mixture of dietary fats to iron overload in captive bottlenose dolphins. Together, these studies demonstrate how iron-overload disease can occur as a result of an unhealthy diet, leading to a sub-optimal ratio of the fatty acids and a poor, phospholipid ratio. The first study shows how proper diet can correct this in the first case, basically by "changing the oil" in the cell membranes. The second study details how iron reduction by phlebotomy treatment reversed iron overload and significantly reduced liver enzymes including GGT levels. Thus demonstrating a process in dolphins that has been effectively used in humans for well over 100 years. This small group of captive dolphins had been suffering from various metabolic disorders approximately 17 years. 

Dr. Seneff's and my 2015 GGT review is the third paper below. Further below that we provide literature that connects  "Omega-3 deficiency" to impaired iron homeostasis in humans. This situation has been demonstrated to lead to a multitude of diseases and adverse health conditions in humans. The good news is that many or most of these ills can be correctly by simply "changing the oil."  


Increased dietary intake of saturated fatty acid heptadecanoic acid (C17:0) associated with decreasing ferritin and alleviated metabolic syndrome in dolphins   Free full text

AbstractSimilar to humans, bottlenose dolphins (Tursiops truncatus) can develop metabolic syndrome and associated high ferritin. While fish and fish-based fatty acids may protect against metabolic syndrome in humans, findings have been inconsistent. To assess potential protective factors against metabolic syndrome related to fish diets, fatty acids were compared between two dolphin populations with higher (n = 30, Group A)and lower (n = 19, Group B) mean insulin (11 ± 12 and 2 ± 5 μIU/ml,respectively; P < 0.0001) and their dietary fish.In addition to higher insulintriglycerides, and ferritin, Group A had lower percent serum heptadecanoic acid (C17:0) compared to Group B (0.3 ± 0.1 and 1.3 ± 0.4%, respectively; P < 0.0001). Using multivariate stepwise regression, higher percent serum C17:0, a saturated fat found in dairy fatrye, and some fish, was an independent predictor of lower insulin in dolphins. Capelin, a common dietary fish for Group A, had no detectable C17:0, while pinfish and mullet, common in Group B's diet, had C17:0 (41 and 67 mg/100g, respectively). When a modified diet adding 25% pinfish and/or mullet was fed to six Group A dolphins over 24 weeks (increasing the average daily dietary C17:0 intake from 400 to 1700 mg), C17:0 serum levels increased, high ferritin decreased, and blood-based metabolic syndrome indices normalized toward reference levels. These effects were not found in four reference dolphins. Further,higher total serum C17:0 was an independent and linear predictor of lower ferritin in dolphins in Group B dolphins. Among off the shelf dairy products tested,butter had the highest C17:0(423mg/100g); nonfat dairy products had no detectable C17:0. We hypothesize that humans' movement away from diets with potentially beneficial saturated fatty acid C17:0, including whole fat dairy products,could be a contributor to widespread low C17:0 levels, higher ferritin,and metabolic syndrome. [Health-e-Iron Note: clearly, this information triggered our interest in this important area. We cited the next article in our paper as well, because it highlights the connection of elevated levels of GGT in bottlenose dolphins similarly affected by the metabolic dysfunction caused by iron overload

Use of phlebotomy treatment in Atlantic bottlenose dolphins with iron overload Free full text

CASE DESCRIPTION: 3 adult (24- to 43-year-old) Atlantic bottlenose dolphins (Tursiops truncatus) with chronic episodic malaise and inappetence associated with high serum aminotransferase (ALT and AST) activities, high serum iron concentration, and serum transferrin saturation > 80% were evaluated. CLINICAL FINDINGS: Results of histologic examination of liver biopsy specimens revealed hemosiderosis in all 3 dolphins. Except for chronic lymphocytosis in 1 dolphin, results of extensive diagnostic testing revealed no other abnormalities. For each dolphin, a diagnosis of iron overload of unknown origin was made. TREATMENT AND OUTCOME: Phlebotomy treatment was implemented to reduce body stores of iron. Each phlebotomy procedure removed 7% to 17% (1 to 3 L) of estimated blood volume.Treatment consisted of an induction phase of weekly phlebotomy procedures for 22 to 30 weeks, which was complete when serum iron concentration and aminotransferase activities were within reference ranges and serum transferrin saturation was < or = 20% or Hct was < or = 30%. Total amount of iron removed from each dolphin was 53 to 111 mg/kg (24.1 to 50.5 mg/lb) of body weight. One dolphin required maintenance procedures at 8- to 12-week intervals when high serum iron concentration was detected. CLINICAL RELEVANCE: Although the cause of the iron overload and high serum aminotransferase activities remained unknown, phlebotomy treatment successfully resolved the clinicopathologic abnormalities, supporting a role of iron overload in the hepatopathy of the 3 dolphins. [Health-e-Iron Note: The full paper describes how this intervention also reduced serum GGT levels to within the normal range for dolphins. In two of the dolphins, phlebotomy reduced GGT levels by several hundred U/L. Here is a quote from the body of this text: "During 13 to 19 years of observation, the 3 dolphins had episodes of nonspecific clinical illness ...(as noted above). Attempted treatments included administration of antimicrobials with or without corticosteroids. Despite short-term resolution of clinical signs, episodic increases in serum ALT and AST activities and iron concentration continued over time in all 3 dolphins." We make note here of a comparison to human "standard medical care.". What's reported here aptly mirrors the case of such "standard treatment" for humans. Whenonly"clinical signs or symptoms" are treated,these conditions can linger for many years without resolution!]

Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk Free full text

Gamma-glutamyltransferase (GGT) is a well-established serum marker for alcohol-related liver disease.However, GGT’s predictive utility applies well beyond liver disease: elevated GGT is linked to increased risk to a multitude of diseases and conditions, including cardiovascular disease, diabetes, metabolic syndrome (MetS), and all-cause mortality. The literature from multiple population
groups worldwide consistently shows strong predictive power for GGT, even across different gender and ethnic categories. Here, we examine the relationship of GGT to other serum markers such as serum ferritin (SF) levels, and we suggest a link to exposure to environmental and endogenous toxins, resulting in oxidative and nitrosative stress. We observe a general upward trend in population levels of GGT over time, particularly in the US and Korea. Since the late 1970s, both GGT and incident MetS and its related disorders have risen in virtual lockstep. GGT is an early predictive marker for atherosclerosis, heart failure, arterial stiffness and plaque, gestational diabetes, and various liver diseases, including viral hepatitis, other infectious diseases, and several life-threatening cancers.We review literature both from the medical sciences and from life insurance industries demonstrating that serum GGT is a superior marker for future disease risk, when compared against multiple other known mortality risk factors. [Health-e-Iron Note: on page 5 of the our full text article, we discussed the findings of the dolphin studies in a broader context including human diseases, and introduce a discussion of how both GGT and serum ferritin, which have consistently been measured at higher levels among African American populations, compared to age- and gender-matched American white populations, and how these differences are directly proportional to observed health and mortality differences between these populations, as well as differences observed between these populations and Hispanic Americans. The topic of racial disparities is discussed on our full text page 10, paragraph 7. GGT: Ethnic Differences in Oxidative Stress and Iron Measures. This topic will be expanded through additional research and other publications provided below: We have added three papers directly below. We used the first one to help document how, (from review page 1,Aberkane et al.), "when GGT levels are elevated, damage to red blood cell membranes can occur causing the release of these potentially toxic transition metals, which can further result in chain, prooxidant reactions."  We used Aberkane et al. again to introduce the topic of iron overload in bottlenose dolphin (page 5.)

Erythrocytes as targets for gamma-glutamyltranspeptidase initiated pro-oxidant reaction  Free full text

Abstract: Gamma-glutamyltranspeptidase (GGT) is a well known cell plasma membrane and serum circulating enzyme. In clinical chemistry, GGT is used as a marker of alcohol consumption and drug uptake. Serum GGT activity varies in hepatobiliary diseases and cancer. This enzyme is involved in glutathione (GSH) metabolism, which is generally associated with antioxidant properties. However, in recent years, findings from our group and from others showed that GGT-catalysed extracellular metabolism of GSH leads, in the presence of iron, to the generation of reactive oxygen species (ROS). It was demonstrated that those highly reactive species oxidise lipids, cell surface protein thiols or activate transcriptional factors such as Nuclear Factor κB (NFκB). The objective of the present work is to determine whether the red blood cells are targets for plasma GGT-initiated pro-oxidant reaction. The results obtained demonstrate that the GGT/GSH/iron system oxidises isolated erythrocyte membranes. A significant release of haemoglobin and a decrease of erythrocyte deformability are also observed. In addition, in vivo studies showed a relationship between plasma GGT activity and erythrocyte deformability in 20 studied subjects. In conclusion, GGT-mediated ROS production is able to oxidise erythrocytes and thus disturbs their functions. [Health-e-Iron NoteThe following 2016 paper was authored by two senior scientists from the Environmental Protection Agency (EPA). Several other similar papers have been published since the beginning of 2015. These will be provided further below, space permitting.]

Effects of Environmental Pollutants on Cellular Iron Homeostasis and Ultimate Links to Human Disease  Free full text

Abstract: Chronic disease has increased in the past several decades, and environmental pollutants have been implicated. The magnitude and variety of diseases may indicate the malfunctioning of some basic mechanisms underlying human health. Environmental pollutants demonstrate a capability to complex iron through electronegative functional groups containing oxygen, nitrogen, or sulfur. Cellular exposure to the chemical or its metabolite may cause a loss of requisite functional iron from intracellular sites. The cell is compelled to acquire further iron critical to its survival by activation of iron-responsive proteins and increasing iron import. Iron homeostasis in the exposed cells is altered due to a new equilibrium being established between iron-requiring cells and the inappropriate chelator (the pollutant or its catabolite). Following exposure to environmental pollutants, the perturbation of functional iron homeostasis may be the mechanism leading to adverse biological effects. Understanding the mechanism may lead to intervention methods for this major public health concern. [Health-e-Iron Note: In the full text, the authors support their hypotheses using numerous citations to cover the purported effects of several of the most commonly deployed pollutants (e.g., glyphosate and 2,4-D) still in widespread use, as well as the disease conditions and poor outcomes associated with high levels of serum ferritin. The authors cover most of the same disease conditions we have covered throughout this web site, for example, see their comments on neurodegenerative diseases and our Iron and GGT in the Brain page. We will point to a new study, further down on this page that during the period from 1999 to 2010, the U.S. experienced a 52.4% increase in the age-adjusted Alzheimer's disease death rateThe following paper is the third in the series we promised above. The authors discuss the evidence supporting their observation that serum ferritin functions as an intracellular iron storage molecule while inside the cell, and also as an inflammatory disease marker when it is measured in the serum, and is generally absent its former iron content.]

Serum ferritin is an important inflammatory disease marker, as it is mainly a leakage product from damaged cells Free full text

"Serum ferritin" presents a paradox, as the iron storage protein ferritin is not synthesised in serum yet is to be found there. Serum ferritin is also a well known inflammatory marker, but it is unclear whether serum ferritin reflects or causes inflammation, or whether it is involved in an inflammatory cycle. We argue here that serum ferritin arises from damaged cells, and is thus a marker of cellular damage. The protein in serum ferritin is considered benign, but it has lost (i.e. dumped) most of its normal complement of iron which when unliganded is highly toxic. The facts that serum ferritin levels can correlate with both disease and with body iron stores are thus expected on simple chemical kinetic grounds. Serum ferritin levels also correlate with other phenotypic readouts such as erythrocyte morphology. Overall, this systems approach serves to explain a number of apparent paradoxes of serum ferritin, including (i) why it correlates with biomarkers of cell damage, (ii) why it correlates with biomarkers of hydroxyl radical formation (and oxidative stress) and (iii) therefore why it correlates with the presence and/or severity of numerous diseases. This leads to suggestions for how one might exploit the corollaries of the recognition that serum ferritin levels mainly represent a consequence of cell stress and damage. [Health-e-Iron Note: next, we provide a couple of studies showing that Sudden Cardiac Death, certainly an ominous concern for most people, particularly when they are still young, is a serious among men. The first case is a study of 20,551 male physicians.]   

Fish Consumption and Risk of Sudden Cardiac Death Free full text

 Context.—Dietary fish intake has been associated with a reduced risk of fatal cardiac end points, but not with nonfatal end points. Dietary fish intake may have a selective benefit on fatal arrhythmias and therefore sudden cardiac death. Objective.—To investigate prospectively the association between fish consumption and the risk of sudden cardiac death. Design.—Prospective cohort study. Setting.—The US Physicians’ Health Study. Patients.—A total of 20,551 US male physicians 40 to 84 years of age and free of myocardial infarction, cerebrovascular disease, and cancer at baseline who completed an abbreviated, semiquantitative food frequency questionnaire on fish consumption and were then followed up to 11 years. Main Outcome Measure.—Incidence of sudden cardiac death (death within 1 hour of symptom onset) as ascertained by hospital records and reports of next of kin. Results.—There were 133 sudden deaths over the course of the study. After controlling for age, randomized aspirin and beta carotene assignment, and coronary risk factors, dietary fish intake was associated with a reduced risk of sudden death, with an apparent threshold effect at a consumption level of 1 fish meal per week (P for trend=.03). For men who consumed fish at least once per week, the multivariate relative risk of sudden death was 0.48 (95% confidence interval, 0.24-0.96;P=.04) compared with men who consumed fish less than monthly. Estimated dietary n-3 fatty acid intake from seafood also was associated with a reduced risk of sudden death but without a significant trend across increasing categories of intake. Neither dietary fish consumption nor n-3 fatty acid intake was associated with a reduced risk of total myocardial infarction, nonsudden cardiac death, or total cardiovascular mortality. However, fish consumption was associated with a significantly reduced risk of total mortality. Conclusion.—These prospective data suggest that consumption of fish at least once per week may reduce the risk of sudden cardiac death in men

γ-Glutamyltransferase and Risk of Sudden Cardiac Death in Middle-Aged Finnish Men: A New Prospective Cohort Study Free full text

BACKGROUND: γ-Glutamyltransferase (GGT) has been linked to an increased risk of several cardiovascular outcomes; however, the relationship of GGT with sudden cardiac death (SCD) has not been investigated previously. We aimed to assess the association of GGT with risk of SCD. METHODS AND RESULTS: Serum GGT activity was assessed at baseline in the Kuopio Ischemic Heart Disease prospective cohort of 1780 men, and 136 SCDs were recorded during 22 years of follow-up. Correction for within-person variability was made using data from repeated measurements taken several years apart. The regression dilution ratio of loge GGT adjusted for age was 0.68 (95% CI 0.61-0.74). Serum GGT was log-linearly associated with risk of SCD. The hazard ratio for SCD per 1 SD higher baseline loge GGT values (2-fold higher) was 1.30 (95% CI 1.10-1.54; P=0.002) after adjustment for several established risk factors and remained consistent with further adjustment for alcohol consumption, resting heart rate, lipids, and C-reactive protein (hazard ratio 1.26, 95% CI 1.05-1.50; P=0.014). The corresponding hazard ratios were 1.48 (95% CI 1.15-1.89; P=0.002) and 1.40 (95% CI 1.07-1.82; P=0.014) after correction for within-person variability. Hazard ratios remained unchanged after accounting for incident coronary events and did not vary importantly by levels or categories of prespecified conventional risk factors. CONCLUSIONS: GGT is positively, log-linearly, and independently associated with future risk of SCD in the general male population. Further research is needed to replicate these findings.  [Health-e-Iron Notewe have earlier described the relationship of elevated GGT with environmental toxins such as mercury. The study below was an earlier study also based on GGT levels and sudden cardiac death among the subjects of the Kuopio Ischemic Hearth Disease Risk Factor Study. This study quantified hair mercury content as an interactive measure in SCD.]

Serum Long-Chain n-3 Polyunsaturated Fatty Acids, Mercury, and Risk of Sudden Cardiac Death in Men: A Prospective Population-Based Study Free full text

Objectives: Fish consumption has been associated with reduced risk of cardiovascular diseases (CVD), especially sudden cardiac death (SCD). Fish is the major source of long-chain n-3 polyunsaturated fatty acids (PUFA) eicosapentaenoic acid and docosahexaenoic acid. It is also a major source of methylmercury, which was associated with increased risk of CVD in this
study population
. Impact of interaction between long-chain n-3 PUFA and methylmercury on the SCD risk is unknown. Methods: A total of 1,857 men from the prospective, population-based Kuopio Ischaemic Heart Disease Risk Factor study, aged 42–60 years and free of CVD at baseline in 1984–1989, were studied. Serum long-chain n-3 PUFA was used as the marker for long-chain n-3 PUFA intake and hair mercury as the marker for mercury exposure. Results: During the mean follow-up of 20.1 years, 91 SCD events occurred. In the multivariate Cox proportional hazards
regression models, serum long-chain n-3 PUFA concentration was not associated with the risk of SCD until hair mercury was accounted for; then the hazard ratio (HR) in the highest vs. lowest tertile was 0.54 [95% confidence interval (CI) 0.32 to 0.91, p for trend = 0.046]. When the analyses were stratified by hair mercury content, among those with lower hair mercury, each 0.5 percentage unit increase in the serum long-chain n-3 PUFA was associated with HR of 0.77 (95% CI 0.64 to 0.93), whereas no association was seen among those with higher hair mercury (p for interaction = 0.01). Among the individual long-chain n-3 PUFA, docosahexaenoic acid was most strongly associated with the risk. 
Conclusion: High exposure to mercury may reduce the benefits of long-chain n-3 PUFA on SCD. [Health-e-Iron Note: the study below is an earlier study from the same cohort of Finnish men.As the above study and the one above link elevated GGT levels to SCD, the below study links elevated serum ferritin levels to myocardial infarction.]  

High Stored Iron Levels Are Associated With Excess Risk of Myocardial Infarction in Eastern Finnish Men  Free full text

BACKGROUND: Iron can induce lipid peroxidation in vitro and in vivo in humans and has promoted ischemic myocardial injury in experimental animals. We tested the hypothesis that high serum ferritin concentration and high dietary iron intake are associated with an excess risk of acute myocardial infarction. METHODS AND RESULTS: Randomly selected men (n = 1,931), aged 42, 48, 54, or 60 years, who had no symptomatic coronary heart disease at entry, were examined in the Kuopio Ischaemic Heart Disease Risk Factor Study (KIHD) in Eastern Finland between 1984 and 1989. Fifty-one of these men experienced an acute myocardial infarction during an average follow-up of 3 years. On the basis of a Cox proportional hazards model adjusting for age, examination year, cigarette pack-years, ischemic ECG in exercise test, maximal oxygen uptake, systolic blood pressure, blood glucose, serum copper, blood leukocyte count, and serum high density lipoprotein cholesterol, apolipoprotein B, and triglyceride concentrations, men with serum ferritin greater than or equal to 200 micrograms/l had a 2.2-fold (95% CI, 1.2-4.0; p less than 0.01) risk factor-adjusted risk of acute myocardial infarction compared with men with a lower serum ferritin. An elevated serum ferritin was a strong risk factor for acute myocardial infarction in all multivariate models. This association was stronger in men with serum low density lipoprotein cholesterol concentration of 5.0 mmol/l (193 mg/dl) or more than in others. Also, dietary iron intake had a significant association with the disease risk in a Cox model with the same covariates. CONCLUSIONS: Our data suggest that a high stored iron level, as assessed by elevated serum ferritin concentration, is a risk factor for coronary heart disease.[Health-e-Iron Note: we next supply a study that shows that Americans living in the U.S. are generally grossly deficient in their intake of omega-3 fatty acids.]

U.S. adults are not meeting recommended levels for fish and omega-3 fatty acid intake: results of an analysis using observational data from NHANES 2003–2008 Free full text

[Health-e-Iron Note: we supply the conclusion of this study here: CONCLUSION: "Our current observational findings show that a significant number of American adults are not meeting recommendations for omega-3 fatty acid intake. This dietary behavior may have negative consequences to CVD risk. CVD builds over a lifetime, with initiation and progression commencing during the pediatric years, strengthening the argument to focus on nutrition behavior and select food consumption during childhood. As we are approaching the development and release of the 2015 DGA, specific strategies to increase consumption of omega-3 fatty acids in the U.S. population need to be addressed. As omega-3 fatty acids are deemed important from authoritative bodies, a collaborative strategy of dietary supplementation (i.e., fish oil supplements), food fortification, in addition to food sources (i.e., fish consumption) may need to be considered to achieve recommendations in the American population and to have significant and beneficial public health impact." [Health-e-Iron Note: these data raise a question: how much of health and survival disparities seen in the U.S. can be attributed to the dietary insufficiency of omega-3 fatty acid intake? The study directly below might point to an answer.]

Survival Differences among Native-Born and Foreign-Born Older Adults in the United States Free full text

BACKGROUND: Studies show that the U.S. foreign-born population has lower mortality than the native-born population before age 65. Until recently, the lack of data prohibited reliable comparisons of U.S. mortality by nativity at older ages. This study provides reliable estimates of U.S. foreign-born and native-born mortality at ages 65 and older at the end of the 20(th) century. Life expectancies of the U.S. foreign born are compared to other developed nations and the foreign-born contribution to total life expectancy (TLE) in the United States is assessed. METHODS: Newly available data from Medicare Part B records linked with Social Security Administration files are used to estimate period life tables for nearly all U.S. adults aged 65 and older in 1995. Age-specific survival differences and life expectancies are examined in 1995 by sex, race, and place of birth. RESULTS: Foreign-born men and women had lower mortality at almost every age from 65 to 100 compared to native-born men and women. Survival differences by nativity were substantially greater for blacks than whites. Foreign-born blacks had the longest life expectancy of all population groups (18.73 [95% confidence interval {CI}, 18.15-19.30] years at age 65 for men and 22.76 [95% CI, 22.28-23.23] years at age 65 for women). The foreign-born population increased TLE in the United States at older ages, and by international comparison, the U.S. foreign born were among the longest-lived persons in the world. CONCLUSION: Survival estimates based on reliable Medicare data confirm that foreign-born adults have longer life expectancy at older ages than native-born adults in the United States. [Health-e-Iron Notewe will next try to find out what's behind this "survival advantage" gained by foreigners moving to the U.S. Interestingly, a similar survival advantage has been reported among infants born in the U.S. to foreign-born mothers. This "paradox" is detailed in the below abstract.]

Differing first year mortality rates of term births to White, African-American, and Mexican-American US-born and foreign-born mothers

To determine whether maternal nativity (US-born versus foreign-born) is associated with the first year mortality rates of term births. Stratified and multivariable binomial regression analyses were performed on the 2003-2004 National Center for Health Statistics linked live birth-infant death cohort files. Only term (37-42 weeks) infants with non-Latina White, African-American, and Mexican-American mothers were studiedThe infant mortality rate (<365 days, IMR) of births to US-born non-Latina White mothers (n = 3,684,569) exceeded that of births to foreign-born White mothers (n = 226,621): 2.4/1,000 versus 1.3/1,000, respectively; relative risk (RR) = 1.8 [95 % confidence interval (CI) 1.6-2.0]. The IMR of births to US-born African-American mothers (n = 787,452) exceeded that of births to foreign-born African-American mothers (n = 118,246): 4.1/1,000 versus 2.2/1,000, respectivelyRR = 1.8 (1.6-2.1). The IMR of births to US-born Mexican-American mothers (n = 338,337) exceeded that of births to Mexican-born mothers (n = 719,837): 2.4/1,000 versus 1.8/1,000, respectivelyRR = 1.3 (1.2-1.4)These disparities were not limited to a singular cause of death and were widest among deaths due to Sudden Infant Death Syndrome. In multivariable binomial regression models, the adjusted RR of infant mortality for non-LBW, term births to US-born (compared to foreign-born) for WhiteAfrican-American, and Mexican-American mothers equaled 1.5 (1.3-1.7), 1.7 (1.5-2.1) and 1.6 (1.4-1.8), respectivelyThe IMR of term births to White, African-American, and Mexican-American mothers exceeds that of their counterparts with foreign-born mothers independent of traditional individual level risk factors.  [Health-e-Iron Notethese disturbing reports are reflective of the dismal ranking of the United States compared to all industrial countries in Infant Mortality Rates (IMRs). Compared to all countries in which IMRs are measured, the U.S. (as of 2015) ranks number 57 from the top (or the best ranking) country. For example, Japan's IMR was only 35% that of the U.S. in 2015, and the IMR of Cuba was 78% that of the U.S. in the same year. The below abstract reports another troubling trend, increasing "age-adjusted' death rates for certain diseases, particularly Alzheimer's disease.]

Trends in Disparity by Sex and Race/Ethnicity for the Leading Causes of Death in the United States—1999-2010

CONTEXT: Temporal trends in disparities in the leading causes of death within and between US demographic subgroups indicate the need for and success of interventions to prevent premature death in vulnerable populations. Studies that report recent trends are limited and outdated. OBJECTIVE: To describe temporal trends in disparities in death rates by sex and race/ethnicity for the 10 leading causes of death in the United States during 1999-2010. DESIGN: We used underlying cause of death data and population estimates from the National Vital Statistics System to calculate age-adjusted death rates for the 10 leading causes of death during 1999-2010. We measured absolute and relative disparities by sex and race/ethnicity for each cause and year of death; we used weighted linear regression to test for significance of trends over time. RESULTS: Of the 10 leading causes of death, age-adjusted death rates by sex and race/ethnicity declined during 1999-2010 for 6 causes and increased for 4 causes. But sex and racial/ethnic disparities between groups persisted for each year and cause of death. In the US population, the decreasing trend during 1999-2010 was greatest for cerebrovascular disease (-36.5%) and the increasing trend was greatest for Alzheimer disease (52.4%). For each sex and year, the disparity in death rates between Asian/Pacific Islanders (API) and other groups varied significantly by cause of death. In 2010, the API-non-Hispanic black disparity was largest for heart disease, malignant neoplasms, cerebrovascular diseases, and nephritis; the API-American Indian/Alaska Native disparity was largest for unintentional injury, diabetes mellitus, influenza and pneumonia, and suicide; and the API-non-Hispanic white disparity was largest for chronic lower respiratory diseases and Alzheimer disease. CONCLUSIONS: Public health practitioners can use these findings to improve policies and practices and to evaluate progress in eliminating disparities and their social determinants in vulnerable populations. [Health-e-Iron Noteour working hypothesis has been that the grossly disparate disease and mortality rates between black Americans and other American racial groups is, in part, related to their higher measures of both serum ferritin and GGT, a fact that is very apparent when age-matched population are compared. And further, that those disparate biochemical measures might be largely caused by dietary differences inclusive of "Omega-3" deficiencies, which might comprise the largest responsible component, and is one that affects all life spans inclusive of maternity through infancy and beyond through child development and all ages of adulthood. We believe that the reason for the consistently higher serum ferritin measures in American blacks compare to whites is most aptly described below, in this abstract summary of related findings recently reported by Zacharski, et al.]

Racial Health Disparities, and Variant Red Cell and Iron Homeostasis

Oxidative stress from excess iron may contribute to racial health disparities. Previously we reported improved clinical outcomes with lower ferritin and higher percent transferrin saturation (%TS) levels in White but not Black participants with peripheral arterial disease entered to a clinical trial. This report demonstrates racially variant interactions between hemoglobin, ferritin, and %TS levels. Lower hemoglobin and %TS levels, and higher ferritin levels were documented in Black compared with White participants within cardiovascular disease risk categories. Ferritin levels near 80 ng/mL related to higher hemoglobin levels in White but not Black participants. Higher %TS levels with ferritin levels above 80 ng/mL in White participants were blunted in Black participants. Ferritin/%TS ratios were significantly higher in Black than White participants. Iron incorporation into hemoglobin and scavenging by transferrin may buffer iron toxicity more effectively in White than in Black individuals. Metabolic vulnerability to iron excess may explain, in part, racial health disparities.



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