how APGAR became a Backronym

Apgar score (AP-gar skor) noun

A method of assessing a newborn's health.

[After anesthesiologist Virginia Apgar (1909-1974) who devised it.]


This is a judging world and we get evaluated right from birth (Apgar score) to death (how many people came to the funeral). In 1953, Dr. Virginia Apgar devised a quick way to measure the health of a newborn child. She assigned 0, 1, or 2 points for each of the five criteria: heart rate, respiration, muscle tone, skin color, and reflex response. The Apgar score is typically calculated at one minute and five minutes after birth. Ten years after the debut of the Apgar score, Dr. L. Joseph Butterfield introduced an acronym as a mnemonic aid for the term: Appearance, Pulse, Grimace, Activity, Respiration. Also see backronym.

"The baby, a 6-pound, 14-ounce boy, appeared so healthy that doctors who delivered him gave him an Apgar score of 9 on a scale of 1 to 10."
Delthia Ricks; Congenital Malaria Case is First For NY; Newsday (New York); Apr 23, 2005.



X-Bonus
Oh to have a lodge in some vast wilderness. Where rumors of oppression and deceit, of unsuccessful and successful wars may never reach me anymore. -William Cowper, poet (1731-1800)

Not very encouraging news for doctors in private practice

Reduction of diabetes risk in routine clinical practice: Are Physical Activity and Nutrition Interventions feasible and are the outcomes from reference trials replicable? A Systematic Review and meta-analysis

Magnolia Cardona-Morrell email, Lucie Rychetnik email, Stephen L Morrell email, Paola T Espinel email and Adrian Bauman email

BMC Public Health 2010, 10:653doi:10.1186/1471-2458-10-653
Published: 29 October 2010
Abstract (provisional)

Background

The clinical effectiveness of intensive lifestyle interventions in preventing or delaying diabetes development in people at high risk has been established from randomised trials of structured, intensive interventions conducted over the past two decades in several countries. The challenge is to translate them into routine clinical settings. The objective of this review was to determine whether lifestyle interventions delivered to high-risk adult patients in routine clinical care settings are feasible and effective in achieving reductions in risk factors for diabetes.
Methods

Data sources: MEDLINE (PubMed), EMBASE, CINAHL, The Cochrane Library, Google Scholar, and grey literature were searched for English-language articles published from January 1990 to August 2009. The reference lists of all articles collected were checked to ensure that no relevant suitable studies were missed. Study selection: We included RCTs or before-and-after (with or without a control group) studies of lifestyle interventions with the stated aim of diabetes risk reduction or diabetes prevention conducted in routine clinical settings and delivered by healthcare providers such as family physicians, practice nurses, allied health personnel, or other healthcare staff associated with a health service. Outcomes of interest were weight loss, reduction in waist circumference, improvement of impaired fasting glucose or oral glucose tolerance test (OGTT) results, improvements in fat and fibre intakes, increased level of engagement in physical activity and reduction in diabetes incidence.
Results

Twelve from 41 potentially relevant studies were included in the review. Four studies were suitable for meta-analysis. A significant positive effect of the interventions on weight was reported by all study types. The meta-analysis showed that lifestyle interventions achieved weight and waist circumference reductions after one year. However, no clear effects on biochemical or clinical parameters were observed, possibly due to short follow-up periods or lack of power of the studies meta-analysed. Changes in dietary parameters or physical activity were generally not reported. Most studies assessing feasibility were supportive of implementation of lifestyle interventions in routine clinical care.
Conclusion

Lifestyle interventions for patients at high risk of diabetes, delivered by a variety of clinical health care providers in routine clinical settings, are feasible but appear to be of limited clinical benefit one year after intervention. Despite convincing evidence from structured intensive trials, this systematic review showed that translation into routine practice has less effect on diabetes risk reduction.

Vitamin D deficiency and Diabetic Retinopathy

Vitamin D Has Retinopathy Link
By John Gever, Senior Editor, MedPage Today
Published: October 20, 2010
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
Action Points

* Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.


* Note that the study cannot determine causality, and that whether vitamin D supplementation can reduce the risk of diabetic complications is not known.

CHICAGO -- Diabetic retinopathy may be added to the list of conditions potentially related to vitamin D insufficiency, a researcher said here.

A study of 123 diabetic individuals with varying degrees of retinopathy, along with two groups of controls, showed that low vitamin D levels were significantly more common in those with the diabetic complication, according to John F. Payne, MD, of Emory University in Atlanta.

In a poster presentation here at the American Academy of Ophthalmology's annual meeting, Payne also reported that multivitamin use appeared to be helpful in preventing vitamin D insufficiency -- at least as currently defined.

"If you were taking a daily multivitamin, your mean vitamin D [25-hydroxyvitamin D] was about 31 [ng/mL] versus about 22 if you weren't taking a multivitamin," he told MedPage Today. Because 30 ng/mL was the cutoff Payne and colleagues had used to define insufficiency, "now you're up to the optimum level."

But he acknowledged that some researchers have begun to advocate for higher levels of daily vitamin D intake and serum levels of the 25-OH-D metabolite, relative to current norms, as necessary for health.

Payne and colleagues gathered a total of 221 individuals in five groups: 47 volunteers without diabetes or any eye disease; 51 without diabetes who had uveitis, macular degeneration, or other ocular diseases; 41 diabetics without eye disease; 40 diabetics with nonproliferative diabetic retinopathy; and 42 diabetics with proliferative disease.

Serum 25-OH-D levels were measured from December 2009 to March 2010, which eliminated seasonal effects on vitamin D levels.

Mean levels in the five groups were as follows (P<0.001 for diabetics versus nondiabetics):

* Healthy controls: 28.8 ng/mL
* Nondiabetics with eye disease: 24.7 ng/mL
* Diabetics without eye disease: 23.2 ng/mL
* Diabetics with nonproliferative retinopathy: 21.5 ng/mL
* Diabetics with proliferative retinopathy: 18.0 ng/mL

Vitamin D insufficiency was found in 81% of the proliferative retinopathy group and about 70% of the two other diabetic groups, versus 55% of the two nondiabetic groups (P=0.048).

Black participants, who made up about half the overall sample, had lower mean 25-OH-D levels than whites, at 23.7 versus 29.2 ng/mL -- a difference found in most studies, as melanin in the skin interferes with the vitamin D-boosting effect of sunlight.

But in multivariate analysis, which accounted for body mass index, glycated hemoglobin levels, and two measures of renal function, only the presence or absence of self-reported daily multivitamin use was significantly associated with 25-OH-D level (mean 31.1 versus 22.0 ng/mL).

Vitamin D insufficiency was seen in 44% of those taking daily multivitamins, versus 83% of those not taking them (P<0.001).

Payne said the big unanswered question remains whether vitamin D supplementation can reduce the risk of diabetic complications, or any of the wide range diseases that have been linked to vitamin insufficiency in previous studies. These have included breast cancer, heart failure, multiple sclerosis, GI infections, and age-related cognitive decline, among others.

He noted that in this cohort, there was not a significant relationship between reported multivitamin use and the presence or severity of diabetic retinopathy.

Payne added that a randomized, placebo-controlled trial of supplements might be impossible because withholding them from patients known to have vitamin insufficiency could be considered unethical.

"We may have to go about getting that data a bit differently than we normally would," he said.

Nevertheless, Payne recommended that patients and physicians should consider vitamin D supplements in the meantime, since they are safe and could very well be helpful.

The study was supported by Research to Prevent Blindness and the National Eye Institute.

Payne and colleagues declared they had no competing financial interests.

Primary source: American Academy of Ophthalmology
Source reference:
Payne J, et al "Vitamin D insufficiency in diabetic retinopathy" AAO 2010; Abstract PO223

Coke or Pepsi a day can bring on Diabetes

'Sugary beverages' increase risk of Type 2 diabetes


According to a new study, regular consumption of sugar-sweetened beverages is linked with a clear and consistently greater risk of metabolic syndrome and Type 2 diabetes. Picture: Agency
WASHINGTON
Friday, October 29, 2010 - Page B02
A NEW study has found that regular consumption of soda and other sugar-sweetened beverages is associated with a clear and consistently greater risk of metabolic syndrome and Type 2 diabetes.

According to the Harvard School of Public Health (HSPH) researchers, the study provides empirical evidence that intake of sugary beverages should be limited to reduce risk of these conditions.

The study appears online Wednesday in the journal Diabetes Care and will appear in the November print edition.

"Many previous studies have examined the relationship between sugar-sweetened beverages and risk of diabetes, and most have found positive associations but our study, which is a pooled analysis of the available studies, provides an overall picture of the magnitude of risk and the consistency of the evidence," said lead author Vasanti Malik, a research fellow in the HSPH Department of Nutrition.

Consumption of sugary drinks, the majority of which are sodas, has increased substantially in the US and across the globe and previous scientific studies have shown consistent associations with weight gain and risk of obesity.

However, this study is the first meta-analysis to quantitatively review the evidence linking sugar-sweetened beverages with type two diabetes and metabolic syndrome.

Metabolic syndrome is a group of risk factors, such as high blood pressure and excess body fat around the waist, that increase the risk of coronary artery disease, stroke and diabetes.

The researchers, led by Malik and senior author Frank Hu, professor of nutrition and epidemiology at HSPH, did a meta-analysis that pooled 11 studies that examined the association between sugar-sweetened beverages and those conditions. The studies included more than 300,000 participants and 15,043 cases of Type 2 diabetes and 19,431 participants and 5,803 cases of metabolic syndrome.

The findings showed that drinking one to two sugary drinks per day increased the risk of Type 2 diabetes by 26 per cent and the risk of metabolic syndrome by 20 per cent compared with those who consumed less than one sugary drink per month.

Drinking one 12-ounce serving per day increased the risk of Type 2 diabetes by about 15 per cent.

"The association that we observed between soda consumption and risk of diabetes is likely a cause-and-effect relationship because other studies have documented that sugary beverages cause weight gain, and weight gain is closely linked to the development of Type 2 diabetes," said Hu.

While a number of factors are at work in the development of Type 2 diabetes and metabolic syndrome, sugar-sweetened beverages represent one easily modifiable risk factor that if reduced will likely make an important impact, say the researchers. "People should limit how much sugar-sweetened beverages they drink and replace them with healthy alternatives, such as water, to reduce risk of diabetes as well as obesity, gout, tooth decay, and cardiovascular disease," said Malik.

DIABETES AS A SOCIAL ILLNESS

DIABETES AS A SOCIAL ILLNESS
Generational Trauma, Exile, Desperation, Marginalization as causes of Diabetes
Sudah Yehuda Kovesh Shaheb
M.D, M.Sc, M.S
Visiting Professor of Medical Anthropology, University of Havana, Department of Philosophy, La Habana, Cuba
Consultant Endocrinologist to various Indian tribes in the USA.
The often stressed paradigm, based firmly on the biomedical model of body as a machine, uses terminology to blame the indigenous peoples and the peoples of emergent economies for their increasing rates of suffering from Diabetes.
I would like to demonstrate, with various examples from around the world that trauma, exile, oppression, alienation lay at the roots of the endemic Diabetes, which is only a symptomatic representation in the body of the sufferer, of spiritual disruption, marginalization and poverty. The solution, treatment and especially prevention of this epidemic should focus on the root causes, rather than the eradication or hiding symptoms, this reflected in the lack of successful national diabetes programmes in richer countries such as USA, UK or Australia, where rates of Diabetes continue to soar despite latest technology, increasing number of Endocrinologists, Diabetologists, Nutritionists and Educators, and increasing amount of money spent on Diabetes.
Models, with practical advice to translate culturally relevant tools to comprehend social illnesses and their treatment in community and clinical settings will be alluded to, such as the successful programme of prevention of obesity among the indigenous children among some Plains Indian tribes.

If you are interested you can get in touch with me
cochinjew@yahoo.com

Diabetes in Cambodia.. Another Explanation

Cambodia 30 years Later..
Foetal Origins of Adult Disease
The Barker Hypothesis
A leading Academic Nephrologist was once asked: is there a physiological explanation for the susceptibility of renal disease among the native populations?
It is possible that they have a lesser number of nephrons, 800 000 per kidney rather than the usual one million, which may predispose them to later kidney disease.
In the kidney, maternal dietary imbalance may lead to developmentally induced deviations from the optimal ratio of body mass to nephron number. A relative deficiency in the number of nephrons is thought to create an increased risk of inadequate renal function and hypertension in later life31,53 and, ultimately, a predisposition to renal failure and a potentially reduced life span.54 The severity of the hypertension in rodent models appears to depend on sex, with males having higher risk.43 The molecular mechanisms are incompletely understood. In the rat, the intrarenal renin–angiotensin system appears to be critical for normal nephrogenesis and may be altered by maternal dietary imbalance, both during the neonatal stage55 and at later time points.56
There is no doubt in my mind that Renin Angiotensin System is important, from a clinical stand point. One is able to protect the life of the individual by protecting the kidney by Angiotensin Converting Enzyme Inhibition ( such as Lisinopril, Enalapril )
Other studies have implicated reduced activity of the antiapoptotic homeobox gene product paired box 2 (Pax-2) in reduced number of nephrons57,58
The propensity of all native peoples: American Indians, Australian Aboriginals, Polynesians could be a genetic protective or genetic modified mechanism.
In all hunting and gathering societies, the intake of meat was sporadic but when it did occur, large amounts of meat were eaten. It is well known that meat, products from the meat, increases renal flow and that an expansion of existing glomerular filtration would become necessary, thus a decreased number of nephrons could balloon themselves periodically to accommodate the sporadic event. When the sporadic events become regular, as the native communities adjust to a European Diet, there may be weakening of this mechanism, leading to a propensity for renal dysfunction ( this is just my theory!)
or have suggested that hypertension in later life caused by maternal dietary imbalance results from up-regulated sodium transport in the distal nephron, possibly triggered by increased oxidative stress.59
the Normal Blood pressure is a point of contention. The current 130/90 was formulated by Insurance Actuaries in Connecticut, and is possibly suited for Europeans, even that I am not sure. Certainly Asians and indigenous people have a normal BP readings in the range of 120/70 and we should aim at that. Overweight possibly is the single most common reason for an increase of BP of about 5 mm Hg.
Nutritional stress in pregnant rats reduces the growth of the endocrine pancreas during organogenesis and increases beta-cell apoptosis,60 leading to hyperglycemia and impaired insulin secretion when the offspring become adults. Glucocorticoids may be involved in inducing phenotypic changes and have been shown to inhibit the transcription factor pancreatic and duodenal homeobox 1 (Pdx-1) in beta-cell precursors, which may affect the resultant number of beta cells.61 In the adult male rat offspring of mothers on a protein-restricted diet, low birth weight is associated with reduced expression of components of the insulin signal-transduction pathway in skeletal muscle (including the protein kinase C zeta isoform, the p85 regulatory subunit of phosphoinositide-3 kinase, and the insulin-sensitive glucose transporter type 4 [GLUT4]).62 Similar abnormalities have been reported in infants of low birth weight,62 and together with the developmentally induced reduction in skeletal muscle mass,3 these abnormalities might contribute to later insulin resistance.
I have seen a number of cases, of young men presenting with Hyperglycaemia, who are thin and presentation mistaken for Type 1 Diabetes. Unlike ketosis prone Type 2 Diabetes, these young people do not revert to normal or not able to get by using oral hypoglycaemic agents.
Review of the histories of these patients revealed two common features:
Intra Uterine Pancreatic Insult
Adult Pancreatic Insult.
Both with excessive alcohol.
It is possible that the intrauterine pancreas were insulted with alcohol and stunted ( other chemicals possibly could do the same), and limping by the glucostasis when further insult to the pancreas decrease their ability to maintain homeostasis of Glucose.
In the rat model of nutritional imbalance, the offspring of rats fed an imbalanced diet during pregnancy later had elevated blood pressure, reduced nephron number, and increased responses to salt loading55 as well as reduced vasodilator function in the systemic arteries.40 Rat pups subjected to hypoxic conditions during gestation appear to have fewer but larger cardiomyocytes than pups exposed to normal oxygen levels and are more susceptible to infarction during periods of ischemia and reperfusion as adults.63 Increased blood pressure in fetal sheep stimulates cardiomyocytes to leave the cell cycle prematurely and hypertrophy,64 which may affect cardiac function in adult life. Cardiac hypertrophy is also evident in lambs born to ewes undernourished during early gestation.65 Chronic fetal anemia alters the developing coronary vascular tree in the near-term sheep fetus, and the remodeled coronary tree persists into adulthood.66 In one study, carotid intima–media thickness at 9 years of age in 216 children of European ancestry whose mothers had energy intake in the lowest quartile during early or late pregnancy was higher than that of children whose mothers had intake in the highest quartile, a finding that implies that maternal nutrition within an unexceptional range during pregnancy can affect the subsequent risk of atherogenesis in the offspring.67
THE ABOVE INFORMATION IS OF EXTREME IMPORTANCE FOR THOSE WORKING IN THE FIELD OF DIABETES IN CAMBODIA. I WOULD LIKE A SOCIAL COMMENTARY OF THE SITUATION DURING THE ERA 30 YEARS AGO, DETAILING THE NUTRITIONAL DEFICIENCIES TO BE ADDED TO THIS.
I BELONG TO A GROUP OF PEOPLE WHO SIXTY FIVE TO SEVENTY YEARS AGO UNDERWENT A MOST BRUTAL HOLOCAUST KNOWN IN EUROPE. WE REMEMBER IT AS SHOAH..
The term holocaust originally derived from the Greek word holókauston, meaning a "completely (holos) burnt (kaustos)" sacrificial offering to a god. Its Latin form (holocaustum) was first used with specific reference to a massacre of Jews by the chroniclers Roger of Howden[8] and Richard of Devizes in the 1190s. Since the late 19th century, it has been used primarily to refer to disasters or catastrophes.
The biblical word Shoah (שואה) (also spelled Sho'ah and Shoa), meaning "calamity," became the standard Hebrew term for the Holocaust as early as the 1940s.[9] Shoah is preferred by many Jews for a number of reasons, including the theologically offensive nature of the original meaning of "holocaust
HOWEVER PAINFUL IT MAY BE, IT IS IMPORTANT TO REMEMBER..

Yet another Fraud by Drug Companies to the Fore

GlaxoSmithKline to pay $750m fine in fraud case
By Robert Weisman
Globe Staff / October 27, 2010



Federal prosecutors in Boston yesterday said British drug giant GlaxoSmithKline PLC agreed to pay $750 million to settle civil and criminal charges that it made and sold adulterated drugs, including the antidepressant Paxil, to Medicaid and other government payers.

The settlement, one of the largest ever in a health care fraud case, burnished the reputation of the US attorney’s office in Boston as the premier federal office for investigating health care fraud. It has been responsible for recovering about $6 billion in health care fines and claims in the past decade, about 25 percent of all recoveries nationally.

“A settlement of this size will help build confidence in the public that health care fraud will be prosecuted,’’ said US Attorney Carmen Ortiz, who oversaw the office’s civil and criminal investigations.

The case began when a whistle-blower, Cheryl Eckard, global quality assurance manager for London-based GlaxoSmithKline, filed a complaint in 2004 under the False Claims Act about the company’s manufacturing processes at a Puerto Rican subsidiary. Eckard, who does not live in Massachusetts, filed the complaint under seal in a Boston court because of the expertise of the US attorney’s office, which decided to intervene in the case, according to her lawyer and Ortiz.

Under the settlement unveiled yesterday, GlaxoSmithKline admitted to operating its SB Phamco Puerto Rico Inc. unit “in a manner that was inconsistent with current good manufacturing practice requirements,’’ P.D. Villarreal, senior vice president and head of global litigation, said in a statement issued by the company.

GlaxoSmithKline, which gained a foothold in the Boston area when it purchased Sirtris Pharmaceuticals two years ago, said it would take a charge of $750 million against its second-quarter earnings to account for the settlement. Its shares edged down 14 cents, or 0.3 percent, to $40.17 yesterday on the New York Stock Exchange.

The settlement covered four drugs manufactured at a Cidra, Puerto Rico, plant that has since been shuttered: Kytril, an antinausea medication; Bactroban, a topical anti-infection skin ointment; Paxil CR, a controlled release formulation of the company’s antidepressant drug Paxil; and Avandamet, a combination Type II diabetes drug.

According to criminal information filed in the case, prosecutors alleged that the manufacturing plant failed to ensure its Kytril and Bactroban products were free of micro-organism contamination. They also alleged the plant’s processes caused the two-layer Paxil CR tablets to split and that Avandamet tablets didn’t always have the mix of active ingredients approved by the Food and Drug Administration.

Under the civil settlement, GlaxoSmithKline agreed to pay $600 million to the federal government and to states based on a percentage of the Medicaid claims they filed for the four drugs, including more than $8 million that will go to Massachusetts’ Medicaid program. Eckard, the whistle-blower, will receive about $96 million.

In a separate plea agreement in the criminal case, the company agreed to pay a $150 million fine. “The success of this whistle-blower case will change the way drug companies run their manufacturing facilities,’’ said New York lawyer Neil Getnick, Eckard’s attorney. “The takeaway for corporate America is that dedicated employees who try to do the right thing can’t be silenced and made to go away.’’