Have Jews created the Global "Diabetes" Epidemic?

[CrackSmokeRepublican]

This may seem preposterous but take a minute to hear the evidence.  -- CSR

1. Diabetes and Tuberculosis have a relationship with Mycobacteria.

Diabetes mellitus, tuberculosis and the mycobacteria: Two millenia of enigma
Lawrence Broxmeyer *

C/o Med-America Research, 148-14A 11th Avenue, Whitestpme, NY 11357, United States
Received 31 March 2005; accepted 11 April 2005

Summary

The thought that tuberculosis and the mycobacteria could cause diabetes seems farfetched, but is not. The
peculiar relationship and frequent association of diabetes mellitus and tuberculosis has been observed for more than
2000 years, yet the reason for this correlation is, to this day, not known. Before the discovery of insulin, a diagnosis of
diabetes was a death sentence within 5 years, and the usual cause of that death was tuberculosis. Despite this, in the
5th century, tuberculosis was already being portrayed as a ''complication'' of diabetes, a view little changed to this
day, parroting Root's original 1934 description of ''a one-sided relationship'': tuberculosis still seen as a common
complication of diabetes, while diabetes is thought to be no more common among TB patients than in the population at
large. To Nichol's, this was ''not logically tenable'' and in his study of 178 otherwise healthy, non-diabetic military
men with tuberculosis at Fitzsimmons Army Hospital, one-third had abnormal glucose screening tests. But despite his
findings and those of Reaud in New York and others, this was not being recognized elsewhere, and Nichols wanted to
know why. Nichols concluded that the incidence of diabetes among tuberculosis patients was considerably
underestimated and that in tuberculosis patients, diabetes develops quite commonly. Diabetes was easy to detect.
Tuberculosis and the mycobacteria were not.

The evidence for a mycobacterial cause of diabetes is mounting rapidly. Schwartz and Haas both linked Type-2
diabetes to tuberculosis. And the pancreatic islet amyloid deposits that they found as a by-product of systemic
tubercular infection have recently been dissolved by rifampicin, a first line drug against tuberculosis. Engelbach spoke
of ''transitory'' diabetes in TB and Karachunskii noted changes in carbohydrate metabolism in patients with
tuberculosis which commonly led to insulin deficiency with persistent hyperglycemia. Furthermore, mycobacterial
elements have been shown recently not only to cause ''autoimmune'' Type-1 diabetes in NOD (non-obese diabetic)
mice, but act as a vaccine to stop the inevitable diabetes that would otherwise materialize. The documentation of
patient cases where TB has preceded and come before the development of diabetes is extensive yet underplayed and
both Lin's and Tsai's studies speak of tuberculosis complicated by diabetes. Diabetes has been around since the first
century AD, in a perpetual state of coping and managing. It is time, it is long past time, to cure diabetes. But current
models as to its cause are not equipping us to do so.

c 2005 Elsevier Ltd. All rights reserved.

http://www.drbroxmeyer.netfirms.com/diabetes.pdf

2. Example of Goeth contracting diabetes after clearing Ghettos in Poland.

Amon Leopold Goeth


The photo above shows the Commandant of the Plaszow camp, Amon Leopold Goeth (Göth), after he was arrested by the SS Criminal Police for "corruption and brutality" on September 13, 1944 and imprisoned at Breslau.

Amon Leopold Goeth, the villain of the movie Schindler's List, was born in 1908 in Vienna, Austria. At the age of 24, he joined the Nazi party. In 1940, Amon Goeth became a member of the Waffen-SS. He was assigned to the SS headquarters for Operation Reinhard in Lublin in German-occupied Poland in 1942. Operation Reinhard was the plan to evacuate the Jews from the Ghettos in Poland to three death camps: Treblinka, Sobibor and Belzec, all of which were in eastern Poland. Goeth's first task was supervise the liquidation of several of the small ghettos in Lublin.



Amon Goeth in his SS uniform

The photo above shows Amon Goeth before his health deteriorated. After he was arrested and imprisoned by the SS, he was diagnosed with diabetes and sent to an SS sanitarium at Bad Tölz in Germany.

http://www.scrapbookpages.com/poland/pl ... ow03A.html

3. Diabetes was a disease of the Roman world.  Likely related to "Urbanization", dietary changes, like of sunlight (vitamin D), anxiety, related to a life involving Jewish trades.

Conclusion

In 1995, the number of adults with diabetes mellitus
was estimated to be 135 million worldwide; this
number is expected to increase to 300 million by
2025. Diabetes has been around since the first century
AD in a perpetual state of coping and managing.
It is time, it is long past time, to cure
diabetes. Schwartz and Haas's studies, linking diabetes,
tuberculosis and the mycobacteria, laid the
foundation for such a cure and a series of studies
done only within the last decade or two further
solidify that link. Nichols [38] stated outright that

4. The Disease was Genetic as it relates to mycobacteria and tuberculosis. Jews since ancient times, were known as "animal pelt-skins" traders, the place where mycobacteria are harbored:

Genetic Diseases? Yes. But Must We Call Them 'Jewish'? (YES--CSR)

By Sander Gilman
Published August 25, 2006, issue of August 25, 2006.

The extraordinary science of genetics, which is in the process of describing the very nature of our natures, is still in its infancy. The claims made for genetics, a science as narcissistic as any infant, generally outstrip the science's ability to define or treat genetic illnesses. Yet there is an undeniable power in the notion that some people carry within them the seeds of their own and their children's illnesses. But there is also a risk: In a world of interrelated databanks and insurance that can be canceled at a moment's notice, would anyone want to be labeled as "at risk"? Is there any benefit to being a member of a collective that is seen as suffering from its very own genetic diseases?

When it comes to Jews, even the best of the recent work on genetic inheritance is tainted with the idea that Jews constitute a "race" and not a peoplehood. The curse of racial theory and its culmination in the Shoah should make us ever vigilant about the misappropriation of scientific claims as applied to "the Jews," even when it is sweetened with praise. In a much-discussed study published last year, three University of Utah anthropologists suggested that Jewish "superior" intelligence was the result of the selective "inbreeding" of Jews. The study proceeded to link the "genetics of intelligence" with the prevalence of "Jewish genetic diseases." The authors wrote: "Perhaps most of the characteristic Ashkenazi genetic diseases fall into this category. Selection has imposed a heavy human cost: not crippling at the population level, cheaper than the malaria-defence mutations like sickle cell and G6PD deficiency, but tragic nonetheless." Jews may be smart, but the cost is that they are an "ill people." Of course, being an "ill people" was also a charge made by 19th-century antisemitic science.

Are the Jews an "ill people"? Well, there is a history to this. In the United States, the National Foundation for Jewish Genetic Diseases has identified nine genetic diseases as "being the most common among Jews of Eastern European or Ashkenazi descent." The diseases include Tay-Sachs; Bloom's syndrome, in which about 10% of those affected also have diabetes; Canavan disease, a progressive neurological disorder; dystonia, which affects movement control; Fanconi anemia, which often leads to leukemia; familial dysautonomia, a disease of the nervous system; Gaucher disease, a metabolic disorder; Niemann-Pick disease, a neurodegenerative disorder, and the most recently discovered "Jewish" genetic disease, mucolipidosis, a neurological disorder. Labeling these diseases "Jewish," especially in the public press, has created the impression that mainly "Jews" (defined variously as an ethnic, religious or biological group) carry and manifest them. The reality, however, belies this claim. A collective can't carry a disease; only individuals can.

Medical genetics today offers little but the identification of potential risk for such individuals. As Keith Wailoo and Stephen Pemberton show in their new book, "The Troubled Dream of Genetic Medicine: Ethnicity and Innovation in Tay-Sachs, Cystic Fibrosis, and Sickle Cell Disease" (Johns Hopkins), the pitfalls associated with genetic testing (fear, absence of choice) may often outweigh the advantages. The boundaries surrounding these diseases are seen to be absolute, even though there are, for example, regular reports of cases of Tay-Sachs beyond the "Jewish" community, as the disease is also present in non-Jewish communities in Louisiana and Quebec.

Yet there are diseases that do seem to be limited to Eastern European Jews. The case of familial dysautonomia can be taken as almost paradigmatic. The Web site of the Familial Dysautonomia Hope Foundation has made the link explicit: "Our logo shows a small case 'fd' to reflect the medical expression of the autosomal recessive nature of FD genetics. The letters are in an upswept Star of David to symbolize our optimism for the future; the Star of David in recognition of the predominantly Jewish inheritance of this disorder (our 'founder,' who had the first mutation several hundred years ago, undoubtedly lived in a Polish shtetl)." Dysautonomia thus becomes a "Jewish" disease, and all its sufferers become part of an extended family, an imagined community linked by their common ancestor, who happened to be a Jew. But why a Jew? Because in Central Europe and in Russia, Jews rarely, if ever, felt themselves to be Polish or Russian. Had they, would we speak of familial dysautonomia as a "Polish genetic disease"? Probably not. We would speak of it as being limited to the offspring of a specific individual and as a mutation that appeared first in a specific location.

One mother of a child with familial dysautonomia wrote to me that she saw a particularly "Jewish" difficulty in constructing such an extended, public family: "My armchair theory is that Jewish families have some difficulty accepting children who do not have a bright future (as opposed to, in general, Catholic families). In the Hasidic community, kids with FD are often 'hidden' (according to the main doctor who treats the disorder)." This strikes me as a problem intimated in the Utah study. What do you do with genetic diseases that create Jews who are other than "smart"?

A historical model for the dangers of speaking about "Jewish diseases" can be found in the story of diabetes. For hundreds of years it was understood as being transmitted within specific groups (in the scientific language of the 19th century, "races") such as blacks and Jews. Diabetes is a good case study for such questions because it is a disease that has two forms, one of which is clearly transmitted genetically; the other may be present as a genetic predisposition — with a strong environmental factor. In the 19th century, when this distinction was not understood, labeling blacks or Jews as diabetic races was a means of labeling these groups as inferior. Even Jewish scientists at the turn of the century accepted the racial stigmatization of diabetes. Rather than being seen as a disease of individuals, diabetes was the fault of "the Jews." Diabetes as the "Jewish disease" became a curse on all Jews, and part of the anxiety about being Jewish or having Jewish ancestry. These things have a way of shifting; today, the general consensus is that diabetes is not a particularly Jewish illness.

"Race" has reappeared today in categories such as "Jewish genetics diseases," as if the pseudoanthropological definitions of race of the 19th and 20th centuries are identical with the idea of genetic cohorts in contemporary science. While any individual Jew may show the impact of any number of genetically transmitted diseases, "Jewish" or not, binding this evident fact to a homogenous biological definition of a Jew leads to misrepresentations and potentially bad medicine. The desire to draw clear lines between different populations is perhaps intrinsic to human nature. The need to define and control is built into all social groups as central to their self-definition. But, in the long run, it is probably better if Jews are spared the label of being an "ill people," and for all individuals, Jewish or not, to undergo genetic testing to at least identify those potential illnesses that they or their children may have, independent of their self-definition as "Jews."

Sander Gilman, the author of more than 70 books, is a distinguished professor of the liberal arts and sciences at Emory University.


Read more: http://www.forward.com/articles/1471/#ixzz13QlIbh3M

5. Jewish Genetic propensity to auto-immune diseases

ethany L. Niell, Jeffrey C. Long, Gad Rennert, and Stephen B. Gruber. "Genetic Anthropology of the Colorectal Cancer-Susceptibility Allele APC I1307K: Evidence of Genetic Drift within the Ashkenazim." American Journal of Human Genetics 73 (2003): 1250-1260. Abstract excerpts:

    "The adenomatous polyposis coli (APC) I1307K allele is found in 6% of the Ashkenazi Jewish population and in 1%-2% of Sephardi Jews; it confers a relative risk of 1.52.0 for colorectal cancer (CRC) on all carriers. ... A common progenitor haplotype spanned across APC I1307K from the centromeric marker D5S135 to the telomeric marker D5S346 and was observed in individuals of Ashkenazi, Sephardi, and Arab descent. The ancestor of modern I1307K alleles existed 87.9118 generations ago (~2,200-2,950 years ago)."

George E. Ehrlich, M.D. "Genetics of Familial Mediterranean Fever and Its Implications." Annals of Internal Medicine 129 (October 1, 1998): 581-582. Excerpts:

    "Ashkenazi Jews -- those chiefly from the Pale of Poland, Russia, and central European countries -- seem to be genetically different from their Sephardic coreligionists, who mainly stem from the Mediterranean countries of Africa and Europe. Familial Mediterranean fever is rare among Ashkenazi Jews but common among Sephardim.... In the case of Jews, almost two millennia may not be long enough to account for the genetic differences between the Ashkenazi and Sephardic Jews in their inherited disease propensities (such as diabetes mellitus and Tay-Sachs disease in eastern Ashkenazi Jews and familial Mediterranean fever in Sephardim). Professor Heller was among those who believed that Ashkenazi and Sephardic Jews have different origins. Some speculate that Ashkenazi Jews descended from the Khazars, an early medieval empire that straddled the Volga River and dominated the eastern Black Sea and the Caspian Sea. Their rulers and many of their subjects converted to Judaism, probably in the eighth century, and the Khazars were gradually forced westward after successive losses to Muslim armies from the south, Mongols from the east, and the Rus (Scandinavians who gave Russia its name) from the north. The genetic distribution of the missense mutations reported by Eisenberg and colleagues9 adds further detail to the argument: It distinguishes between the Sephardic (M693V) and Ashkenazi (V726A) Jews, grouping the latter with Iraqi Jews and some Armenians and suggesting that all three groups originated in an area contiguous to or encompassing the Khazar empire (which probably incorporated many of the Jews remaining in that area after the Babylonian captivity). In fact, the Khazars were a Turkic people, and it would be of interest to look for this genetic mutation in contemporary Turks with the clinical signs and symptoms of familial Mediterranean fever."
    9. Eisenberg S, Aksentijevich I, Deng Z, Kastner DL, Matzner Y. Diagnosis of familial Mediterranean fever by a molecular genetics method. Ann Intern Med. 1998;129:539-42.
http://www.khazaria.com/genetics/abstra ... eases.html

6.  Jewish Doctors likely made enormous profits by treating diseases (Tuberculosis, Diabetes, hysteria) that their group brought with them via trade. Certain populations had DNA that was not disposed towards Jewish Mycobacteria which resulted in auto-immune diseases.    

THE MIDDLE PERIOD

The medieval period of Jewish history does not coincide exactly with the common historical definition of the Middle Ages in Western civilization, but may be said to extend from the second-third centuries C.E. until the 19th century when, in most Western countries, Jews were granted full emancipation.

The large variety of climates, environments, and customs to which the Jewish people were exposed during their migrations in exile naturally had a profound influence on the development of their medical thought and knowledge. Thus, for example, there is a description of diabetes mellitus in the writings of Maimonides. According to him, this was a disease quite common in the warm Mediterranean countries with which he was acquainted but practically unknown in Northern Europe. Talmudic scholars give a precise description of ratan ("filariasis") and its treatment – a malady unknown in Europe. Similarly, the prevalence of eye diseases in the Orient greatly encouraged the development of ophthalmology and, when Jewish eye doctors migrated to Europe, they quickly acquired an excellent reputation among their Christian colleagues.

However, the merit of Jewish doctors of that period lay not only in their individual achievements as physicians, but in their work as translators and transmitters of Greek medicine to the Arabs and later on of Arab medicine to Europe. Jewish scholars, and among them physicians, had command of the three most important scholastic languages of the time – Latin, Arabic, and Hebrew – and, in some cases, Greek. This enabled them to translate most of the Arab and Greek medical works into Hebrew and Latin or vice versa. Knowledge of Hebrew was considered extremely important in the study of medicine. The English scholar Roger *Bacon (c. 1220–c. 1292) declared that Christian physicians were ignorant in comparison with their Jewish colleagues because they lacked knowledge of the Hebrew and Arabic in which most of the medical works were written. Vesalius, the great 16th-century anatomist, made a point of learning Hebrew to facilitate his studies, and gives Hebrew terms together with their Greek equivalents in his work Fabrica (see also *Frigeis, Lazaro De). Mosellanus, in his rectorial address at the University of Leipzig in 1518, urged Christian medical students to learn Hebrew so that they might study the medical lore "hidden in the libraries of the Jews." The close religious and family ties linking the various Jewish communities also helped to spread medical knowledge and facilitate rapid communication. As merchants and travelers the Jews met the best minds of their period and became acquainted with drugs, plants, and remedies from many parts of the world.

http://www.jewishvirtuallibrary.org/jso ... 13493.html

The ancient Egyptians kicked them out since they were said to have "Diseases".... this requires careful thought.  This may seem over the top but keep in mind that as Jewish culture was introduced into countries... often times people who would have had immune-systems primed for hunting, eating raw foods and working a harvest -- would later find themselves working indoors without ample sunlight.  This often leads to Tuberculosis and  Diabetes...

BCG research

Tumor necrosis factor-alpha, or TNF-α, is part of the immune system. It helps the immune system distinguish self from non-self tissue. People with type 1 diabetes are deficient in this substance. Dr. Denise Faustman theorizes that giving Bacillus Calmette-Guérin (BCG), an inexpensive generic drug used to immunize against Mycobacterium tuberculosis, would have the same impact as injecting diabetic mice with Freund's Adjuvant, which stimulates TNF-α production. TNF-α kills the white blood cells responsible for destroying beta cells, and thus prevents, or reverses diabetes.[33] She has reversed diabetes in laboratory mice with this technique, but was only able to receive funding for subsequent research from The Iaccoca Foundation, founded by Lee Iacocca in honor of his late wife, who died from diabetes complications (likely infected from the Jews behind Lee Iacocca -- CSR). Human trials are set to begin in 2008.

http://en.wikipedia.org/wiki/Diabetes_mellitus_type_1

* Home
    * |
    * Journals
          o The Lancet
          o The Lancet Infectious Diseases
          o The Lancet Neurology
          o The Lancet Oncology
    * |
    * Collections
    * |
    * Audio
    * |
    * Conferences
          o The Lancet Conferences
          o Conference Collaborations
          o Meet the Editors at Conferences
    * |
    * Education
          o At The Limits
          o The Lancet Core Clinical Collection
    * |
    * Resource Centres
          o The Lancet Series
          o The Lancet Student
          o H1N1 Influenza
    * |
    * For Authors
          o Writing for The Lancet
          o Writing for The Lancet Infectious Diseases
          o Writing for The Lancet Neurology
          o Writing for The Lancet Oncology
          o About Protocol Reviews
          o Accepted Protocol Summaries
    * |
    * Careers

outline goes here
The Lancet Infectious Diseases, Volume 9, Issue 12, Pages 737 - 746, December 2009

Tuberculosis and diabetes mellitus: convergence of two epidemics

Kelly E Dooley MD a b, Dr Richard E Chaisson MD

Summary

The link between diabetes mellitus and tuberculosis has been recognised for centuries. In recent decades, tuberculosis incidence has declined in high-income countries, but incidence remains high in countries that have high rates of infection with HIV, high prevalence of malnutrition and crowded living conditions, or poor tuberculosis control infrastructure. At the same time, diabetes mellitus prevalence is soaring globally, fuelled by obesity. There is growing evidence that diabetes mellitus is an important risk factor for tuberculosis and might affect disease presentation and treatment response. Furthermore, tuberculosis might induce glucose intolerance and worsen glycaemic control in people with diabetes. We review the epidemiology of the tuberculosis and diabetes epidemics, and provide a synopsis of the evidence for the role of diabetes mellitus in susceptibility to, clinical presentation of, and response to treatment for tuberculosis. In addition, we review potential mechanisms by which diabetes mellitus can cause tuberculosis, the effects of tuberculosis on diabetic control, and pharmacokinetic issues related to the co-management of diabetes and tuberculosis.

http://www.thelancet.com/journals/lanin ... 8/abstract

Jews carrying Tuberculosis and Diabetes

Tuberculosis was not just a "Jewish disease," as some 20th-century observers would have it, even though it was widely associated with Jewish immigrants. A highly infectious disorder spread by coughing, spitting and handshaking, tuberculosis was an urban phenomenon whose etiology was entirely bound up with the institutions of the modern metropolis: the department store, the movie house, the restaurant, the subway and the well-trafficked street.

But then modernity also made possible its eradication, inspiring health reformers in the years prior to World War I to enlist a wide array of the most up-to-date visual strategies to call attention to the disease. Taking to the streets, the National Tuberculosis Association sponsored parades, prominently displayed "Don't Spit" signs in Yiddish and Italian as well as in English, and mounted exhibitions at several of the nation's most prestigious museums, among them New York City's American Museum of Natural History. Replete with an oversized reproduction of a disease-bearing fly, this 1908 exhibition drew thousands of viewers who were eager to see for themselves how tuberculosis took hold of the body politic.

The nation's leading and most imaginative anti-tuberculosis society even made use of the then-embryonic medium of film to herald preventive health measures. Its 1914 motion picture, "The Temple of Moloch," for instance, melodramatically told of the efforts of a young doctor to assist a working-class family laid low by the disease. In the course of things, movie-going audiences learned about the proper use of the broom and about the most effective forms of ventilation.

For thousands of tuberculars, though, the deployment of inventive health measures came too late. Racked with frequent coughing, too weak to work or eat, these people were encouraged by their doctors to leave the city for more salubrious environments out west where they could restore their bodies and their spirits by spending several months outdoors, doing little else but recuperating. "Sufficient fresh air, sufficient food, and sufficient rest and sleep are the watch-dogs [sic] of health, and where they are on the alert, consumption can never enter," insisted Lawrence Flick, a Pennsylvania physician who authored a pamphlet about the dangers of tuberculosis.

Heeding his message, thousands took to the hills, prompting one Denver nurse to write as early as 1907 of a "vast army of sufferers... continually pouring into Colorado." Some of the American Jews among them sought admission to the National Jewish Hospital, an institution established and administered by Denver's German Jewish community. Others, especially those who kept kosher, preferred the facility maintained by the Jewish Consumptive Relief Society. As historian Alan Kraut documents in "Silent Travelers: Germs, Genes, and the 'Immigrant Menace,'" his pioneering 1994 study of the relationship between immigration and health, the administration of the National Jewish Hospital frowned on the dietary laws, arguing that they were "inadvisable for medical reasons." The powers that be at the Jewish Consumptive Relief Society, on the other hand, endorsed kashruth, dismissing as "mere nonsense" the notion that it might interfere with the recovery process. On the contrary. To their way of thinking, adherence to kashruth and other traditional rituals might actually hasten it.

Left to their own devices, residents at both sanatoria had a lot of free time on their hands. Some idled away the hours by writing letters back home, others by reminiscing and still others by contributing to the Jewish Consumptive Relief Society's official publication, "The Sanatorium," or by creating a newsletter all their own, which they called Hatikvah (The Hope). "The Invalid," a poem written in Yiddish by A. Druskin and published in Hatikvah in 1923, gives voice to the plight of those suffering from tuberculosis so far from home.

    "Chained
    Sickness holds me down
    Tho free, I lie in bed a captive,
    I cannot tear my eyes
    From your bewitching mountains
    That weave in majestic peace,
    With blue transparent light
    Their eternal mountain dreams.

    I stretch out my arms to them
    And it seems to me
    I feel their cool breath
    That brings relief
    To my fever burning body —
    But I drop my hands,
    I cannot reach the far mountains...."

Read more: http://www.forward.com/articles/10873/#ixzz13QtPxNd8

A Jewish life means life indoors... leading to sickness:

August 4, 2010 | 12:03 pm
Cod liver oil, vitamin D and the Jewish mother

Posted by Norman Lavin, M.D, PhD., UCLA Medical School

I was raised in a "shtetl" on the west side of Chicago, where communal life was in large measure under the direction of the Jewish Elders.  Religiosity dominated our daily life, including our interaction with family and friends.  Our community was also concerned about safety and health.  Medical care was expensive and generally inaccessible, so most treatment modalities were learned from family and friends.  One of these was cod liver oil.  With only one exception every year (Yom Kippur), my mother forced down my throat a large tablespoon of the most rancid, smelly oil ever created on this planet.  Motor oil would have probably tasted much better.  In retrospect, this was clearly done with concern and caring for my health and well-being, which was not obvious while I was belching and retching for an hour after the ingestion of this foul-smelling, fishy oil.  It was 30 years later before I ever ate fish again.

Cod liver oil was traditionally manufactured by filling a wooden barrel with fresh cod livers and seawater and allowing the mixture to ferment for up to a year before removing the oil.  Unfortunately, I once had a quick glimpse of this process at the rear of a fish market when I was a young child.  Aaach!  Today, cod liver oil is made by cooking and extracting the liver of this fatty fish during the manufacture of fishmeal.  The Jewish mother felt that this therapeutic product could have a positive effect on the health of the heart and the bone, as well as nourishment for the skin, hair and nails.  It also helped ease the pain and joint stiffness associated with arthritis, and the use of cod liver oil during pregnancy was associated with a lower risk of type I diabetes in the offspring.  In a recent Norwegian study, more than 68,000 female cancer patients who took daily cod liver oil supplements had significantly reduced mortality compared to women who did not take such supplements.

Cod liver oil has been utilized for many centuries.  In addition to their diet, the Vikings used this oil as a lubricant to allow the transport of ships across land – the oil was smeared on logs which acted as rollers beneath the hull of the ship.

The ingredients in cod liver oil that are therapeutic include omega-3 fatty acids, vitamin A, and vitamin D.  Studies have shown that this product has the potential to reduce both the progression of cardiovascular disease and related mortality, including sudden cardiac death.  Researchers also found that people who suffer from depression who received a daily dose of 1 gram of an omega-3 fatty acid (found in cod liver oil) for 12 weeks experienced a decrease in their symptoms, such as anxiety, sadness and sleeping problems.

You now have a choice.  You could continue to take the cod liver oil, but now flavored and often in a capsule form, or you could just simply supplement with Vitamin D tablets (and add omega-3 fatty acids).  Low vitamin D status is extremely common worldwide because of low dietary intake and low skin production.  Suboptimal vitamin D levels contributes to the development of rickets, osteoporosis, falls, fractures and a multitude of other conditions.  Although consensus does not exist, it appears that circulating vitamin D levels greater than 30-32 ng/ml are needed for optimal health.  To achieve this, daily intake of at least 1000 IU of D3 daily are required, and it is probable that substantially higher amounts are needed to achieve normal values in a population basis.  Widespread optimization of Vitamin D status likely will lead to prevention of many diseases with attendant reduction of morbidity, mortality and expense.

LOW VITAMIN D CONSEQUENCES

A. Low vitamin D has long been associated with rickets and has a role in the pathogenesis of osteoporosis by way of calcium malabsorption.  Recent studies show that low Vitamin D levels are associated with higher fracture risk.  In addition, a dose effect was reported with greater Vitamin D intakes and higher achieved vitamin D concentrations, providing superior fracture reduction benefit.  Thus, low vitamin D status leads to adverse bone consequences, which can be corrected with supplementation.

B. Muscle function and falls.  Regardless of the mechanism, patients with osteoporosis/osteomalacia because of vitamin D deficiency develop muscle pain and weakness that is improved with vitamin D therapy.  Muscle biopsy in such people reveals atrophy of the fast twitch fibers, which may explain the increased fall risk in vitamin D deficient individuals.  Vitamin D replacement reduces this risk by more than 20%.

C. Cancer.  Vitamin D has antiproliferative and pro-differentiating effects on many cell types, which may reduce cancer risk.  Consistent with this, there is a body of literature which states that low vitamin D intake and /or less sunlight exposure leads to an increased risk of mortality from multiple types of cancer.  Prospective trials of vitamin D supplementation with cancer as an endpoint are very limited.  However, a small prospective study of postmenopausal women found calcium plus vitamin D3 at 1100 IU daily reduces overall cancer risk by approximately 60%.  To summarize, observational data in one small randomized trial find low vitamin D status to be associated with higher cancer risk.  Additional prospective studies are needed.

D. Other Conditions

1. Immunity. It is likely that vitamin D has immune modulating effects.  It has long been recognized that vitamin D deficiency is associated with respiratory infections, which perhaps contributed to the previous use of cod liver oil in anti-tuberculosis therapy.  Low vitamin D status is associated with an increased risk of autoimmune and potentially infectious diseases.  In addition, inflammation is increasingly becoming recognized as a contributor to the pathogenesis of various diseases, and vitamin D modulates inflammatory cytokine production.

2. Diabetes.  It has been suggested that endemic low vitamin D is contributing to the increased prevalence of diabetes mellitus.  Multiple potential mechanisms have been proposed, including vitamin D increasing insulin production/secretion.  Recent observational studies associate low Vitamin D status with both diabetes type I and type II.  Prospective studies of vitamin D supplementation are clearly indicated; it appears that low vitamin D status impairs glucose metabolism.

3. Heart Disease.  Observational studies report an association between low vitamin D and cardiovascular disease.  Potential mechanisms include a vitamin D effect on theendothelium, vascular smooth muscle, and/or cardiomyocytes – all of which possess the vitamin D receptor.  Prospective studies to further evaluate this reported association are needed.

4. Pain and headaches.  There are a few journal articles suggesting that vitamin D supplementations may help with headaches.

5. Alzheimer's and Parkinson's disease.  Some studies have demonstrated a link between
low vitamin D levels and cognitive dysfunction, and a few studies have shown low vitamin D levels to be linked to Parkinson's disease.
In summary, low vitamin D status has been associated with a variety of diseases, and biologically plausible hypotheses exist to suggest a possible causal role.  However, until confirmed by randomized studies, it is wise to be cautious and recognize that association does not prove causation.

WHEN SHOULD VITAMIN D LEVELS BE ASSESSED?
There are no randomized trials advocating a population screening approach, but it seems reasonable to at least measure 25-hydroxy vitamin D in those identified as being at high risk of vitamin D deficiency, and those for whom a prompt musculoskeletal response to optimization of vitamin D status could be expected.

Such groups include those with osteoporosis, a history of falls or high risk of falls, malabsorption such as with celiac disease, radiation enteritis, bariatric surgery, individuals with liver disease, and those requiring medications known to alter vitamin D levels (certain anticonvulsants).  Given the relationship of low vitamin D status with cancer, it also seems rational to measure vitamin D in those with malignancy.

APPROACHES TO VITAMIN D REPLETION/SUPPLEMENTATION
Increasing exposure to sunlight would be an effective and free approach to improving vitamin D status.  However, this does not seem to be viable given widespread sun avoidance campaigns based on the association of UV exposure with skin cancer.

It could be argued that simple treatment of all individuals with vitamin D should be advocated, therefore making vitamin D measurement unnecessary.  But again, there is no expert consensus regarding this recommendation, nor is there consensus regarding a recommended dose.  Some recommend 800 to 1000IU daily, whereas some vitamin D experts suggest values over 2000IU per day.  Vitamin D dosing may differ by age in that older adults likely require higher vitamin D intake because of the lower capability of their skin to produce vitamin D with advancing age.  Similarly, clear differences exist between races, with African-Americans requiring higher intake than Caucasian-Americans.

Various "high dose" repletion approaches exist, such as 50,000 IU three times weekly or monthly.  There are additional reports of recommendations using more than 600,000 IU administered over two months, plus an additional clinical report of 50,000 IU once weekly for up to three years.

Available data find daily vitamin D supplementation to be less effective than expected at increasing vitamin D status, perhaps because of failure to reliably take the supplements.  A reasonable clinical "rule of thumb" is that the addition of 1000 IU of vitamin D3 daily can be expected to increase circulating vitamin D levels by approximately 10 ng/mL.  Keep in mind that it can take up to three to six months for serum vitamin D
levels to plateau following initiation of supplementation.

Finally, after complaining to my mother about the nauseating taste of cod liver oil, she put this slimy, putrid medicine into a glass of orange juice, which, unfortunately, did not mask the taste.  It was yet another 30 years before I could drink orange juice again.  But just yesterday, I sat down to breakfast and I had a plate of geflite fish and a glass of orange juice.  I did not recall the terrible taste, but I was reminded of the love and concern my Jewish mother had for my health and welfare.

http://www.jewishjournal.com/jewish_diseases


April 2, 2010 | 4:40 pm
SCHMALTZ and GREBENES: A Medical Conspiracy

Posted by Norman Lavin, M.D, PhD., UCLA Medical School

For thousands of years, the Jewish people have faced annihilation — promulgated by evil societies, notorious world leaders and the general passivity of
global citizenry. But as deadly as our enemies have been, our diet has often imperiled us as well. Schmaltz (rendered chicken fat) and grebenes (fried chicken skin) and our generally high-fat, low-exercise lifestyles endanger Jews, and therefore the Jewish people.

It is time we understand and confront these enemies as well: obesity, diabetes and other diet-related diseases .

I remember coming home from school with classmates one afternoon many years ago, and we were starved. My mother, with great love and compassion, spread thick layers of yellowish-brown schmaltz on slices of pumpernickel bread. We gulped down these tasty morsels, which kept us barely satiated until dinnertime, when we attacked bowls of chopped liver saturated with more schmaltz, turkey stuffing mixed with schmaltz and chicken soup loaded with dozens of floating unfertilized egg yolks. If we ate everything, Mother rewarded us with grebenes.

All of the pharaohs failed, and so did Hitler, but could these seemingly harmless foods ultimately annihilate the Jewish people? We now know that these fatty foods — bursting with saturated and trans fats — could easily lead to obesity and, ultimately, diabetes, with its attendant consequences of heart disease, kidney dysfunction and liver failure.

These are most likely not "Jewish diseases." There is, however, a subset of Jews who have a predisposition to obesity and diabetes.

Schmaltz and grebenes have almost disappeared from the Jewish kitchen. Therefore, obesity and diabetes also should have disappeared. But people throughout the world are caught in a quagmire of obesity and, consequently, diabetes. Culture is transformative; we have replaced schmaltz with high-calorie fast foods and grebenes with french fries. We no longer walk, run or ride bikes. We sit at computers, stare at television sets, and exercise our fingers texting and tweeting.

Diabetes is omnipresent — it is endemic, it is epidemic, and it can be deadly. The most common type of diabetes, Type 2, can be prevented, and it can be reversed. Modern treatments keep patients healthy with the goal of obliterating all complications.

In my practice, in future columns and in my daily blog, Jewish Diseases, at jewishjournal.com, I will address the prevention and treatment of obesity and diabetes in greater detail. Also to be discussed are the other diseases that affect the Jews. These include Bloom syndrome, Canavan disease, Tay-Sachs, Gaucher, Niemann-Pick and many more. I invite your questions, suggestions, personal experiences and expert opinions as well as references to specific medical centers, physicians or societies.

In the meantime, think about spreading a thick layer of schmaltz on your bread. Think about it — but don't do it. It is time for us as individuals, and as a people, to take control of our diet, our health and our lives.

Dr. Norman Lavin is a clinical professor of endocrinology and director of endocrinology education at UCLA Medical School. This week, his blog Jewish Diseases launches at jewishjournal.com/jewish_diseases.

[CrackSmokeRepublican]

Medicine and the German Jews: a history
 By John M. Efron

http://books.google.com/books?id=3_0xdaMXrc0C

[Panoptimist]

This is great CSR.

It's amazing how a single strain of filth can grow to transcend all spheres of existence.

[CrackSmokeRepublican]

I was thinking about Mary Tyler Moore contracting it in 1969. I bet she got it at age 30, probably after encountering TV Jews like Ed Asner in NY. I bet there are specific Goyim who have the autoimmune triggers turned on after association with certain mycobacterium carrying Jews, which then leads to Type-1 Diabetes.

====

Mary Tyler Moore More


Date of Birth
29 December 1936, Brooklyn, New York, USA

Height
5' 7" (1.70 m)

Mini Biography

Mary Tyler Moore was born in Flatbush, Brooklyn, on December 29, 1936, though Moore's family relocated to California when she was eight. Her childhood was troubled, due in part to her mother's alcoholism. The oldest of three siblings, she attended a Catholic high school and married upon her graduation, in 1955. Her only child, Richie, was born soon after.

A dancer at first, Moore's first break in show business was in 1955, as a dancing kitchen appliance - Happy Hotpoint, the Hotpoint Appliance elf, in commercials generally broadcast during the popular TV program "The Adventures of Ozzie & Harriet" (1952). She then shifted from dancing to acting, and work soon came, at first a number of guest roles on TV series, but eventually a recurring role as "Sam", Richard Diamond's sultry answering service girl, on "Richard Diamond, Private Detective" (1957), her performance being particularly notorious because her legs (usually dangling a pump on her toe) were shown instead of her face.

Although these early roles often took advantage of her willowy charms (in particular, her famously-beautiful dancer's legs), Moore's career soon took a more substantive turn as she was cast in two of the most highly regarded comedies in television history, which would air first-run for most of the Sixties and Seventies. In the first of these, "The Dick Van Dyke Show" (1961), Moore played "Laura Petrie", the charmingly loopy wife of star Dick Van Dyke. The show became famous for its very clever writing and terrific comic ensemble - Moore and her fellow performers received multiple Emmy awards for their work. Meanwhile, she had separated from her first husband, and later married ad man (and, later, network executive) Grant Tinker.

[Timothy_Fitzpatrick]

Reminds me of the Jewish inventor of lobotomy.