Diabetes is a medical condition that is NOT due solely to overfeeding

 

Diabetes, the medical condition of persistently high blood sugar, is driven by critical deficiencies in five things: genes, nourishment, sleep, exercise, and stress management and diabetes is exacerbated by various excesses. Ironically, one such excess is the high sugar diet [300 grams of carbohydrate a day!] recommended by the American Diabetes Association.

In the etiology of diabetes, while deficiencies drive the process, one possible contributing excess is the consumption of vast amounts of sugars in brief periods of time, forcing the body to process sparingly soluble amylin precursor proteins faster than it can safely do so; as insoluble junk accumulates, insulin producing cells can be killed off prematurely, one of many routes to type II diabetes.

Undernourishment is one of the 5 drivers of medical conditions, the precursors of disease and death.

In America, undernourishment is often accompanied by overfeeding. Undernourishment fails to shut off the hunger drive until the next meal, and when food is readily available, this awakened hunger (along with stress, lack of sleep, and insufficient exercise) contributes to overfeeding.

Hence the mistaken notion of American doctors that obesity is a risk factor for type II diabetes, a notion that often borders on the ludicrous assertion that obesity causes diabetes. No Indian doctor would that mistake because:

In India, undernourishment is rarely accompanied by overfeeding.

Consider this article:

Incidence of diabetes highest, progression fastest among Asian Indians

Anjana RM, et al. Diabetes Care. 2015;doi:10.2337/dc14-2814.

April 30, 2015
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Asian Indians with prediabetes exhibit one of the highest incidence rates for diabetes, despite being younger and having a much lower average BMI than other high-risk populations, according to research in Diabetes Care.

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The follow-up study of a large population-based epidemiologic study of adults in south India also showed that progression from prediabetes to diabetes occurs much faster in Asian Indians than in other ethnic groups, according to researchers.

Ranjit Mohan Anjana, MD, vice president of Madras Diabetes Research Foundation in Chennai, India, and colleagues at other institutions analyzed data from 1,376 participants of the Chennai Urban Rural Epidemiology Study (CURES) cohort with a normal glucose tolerance (n = 1,077) or prediabetes (n = 299) at baseline, who were followed for a median of 9.1 years. Participants completed interviewer-administered questionnaires at both baseline (between 2001 and 2003) and follow-up (between 2012 and 2013) regarding their socioeconomic status, medical and family history, physical activity, and tobacco and alcohol use. Researchers measured BMI, waist and hip circumference, blood pressure and glucose levels. Researchers checked cases of self-reported diabetes against medical records for accuracy.

Among participants with normal glucose tolerance at baseline, 19.4% developed diabetes and 25.7% developed prediabetes. Among participants with existing prediabetes, 58.9% went on to develop diabetes.

The incidence rate of diabetes for the cohort was 33.1 per 1,000 person-years (95% CI, 29.9-36.5), whereas the incidence rate for prediabetes among those with a normal glucose tolerance at baseline was 29.5 per 1,000 person-years (95% CI, 26.1-33.1).

The incidence rate for prediabetes for the cohort was 78.9 per 1,000 person-years — higher than rates reported in small, isolated populations, such as the Pima Indians, the Micronesian population of Nauru and Native Americans participating in the Strong Heart Study, according to researchers.

“Part of this could be explained by the high prevalence of family history [of diabetes] in our population,” the researchers wrote. “It also represents rapid epidemiological transition in our population.”

Those in the cohort with normal glucose tolerance who went on to develop diabetes were significantly older and had a higher BMI, waist circumference, systolic and diastolic BP and insulin resistance compared with those who did not develop the disease. Those in the cohort with prediabetes who developed diabetes had a significantly higher fasting plasma glucose, 2-hour plasma glucose and HbA1c level, and they were more likely to have a family history of the disease than those who did not progress to diabetes, according to researchers.

“Awareness of the predictors of incident diabetes will help in the identification of individuals at highest risk so that appropriate preventive measures could be taken to slow down the epidemic of diabetes in this population,” the researchers wrote. – by Regina Schaffer

Disclosure: The researchers report no relevant financial disclosures.

The beneficial effect of sugar on stress

Sugar-sweetened beverages suppress cortisol, stress responses in brain

Tyron MS, et al. J Clin Endocrinol Metab. 2015;doi:10.1210/jc.2014-4353.

April 16, 2015
The hormone cortisol and stress responses were suppressed with the consumption of sugar-sweetened beverages, according to recent study findings published in The Journal of Clinical Endocrinology & Metabolism.

Diet beverages sweetened with aspartame did not produce the same effects, according to the researchers.

“This is the first evidence that high sugar — but not aspartame — consumption may relieve stress in humans,” Kevin D. Laugero, PhD, of the University of California, Davis, and the U.S. Department of Agriculture’s Agricultural Research Service, said in a press release. “The concern is psychological or emotional stress could trigger the habitual overconsumption of sugar and amplify sugar’s detrimental effects, including obesity.”

Laugero and colleagues evaluated 19 women aged 18 to 40 years with a BMI range of 20 kg/m2 to 34 kg/m2 to determine the effect of sucrose- or aspartame-sweetened beverage consumption on the effect of cortisol and responses to stress. Eight participants were assigned to consume aspartame-sweetened beverages, and 11 were assigned to sucrose-sweetened beverages.

Participants drank one of the assigned beverages at breakfast, lunch and dinner and were instructed not to consume other sugar-sweetened beverages for a 12-day period. Participants consumed a standardized low-sugar diet and stayed at a clinical research center for 3.5 days before and after the study. After the 12-day period, participants underwent MRI screening after performing math tests to gauge the brain’s stress response. Saliva samples also were provided to measure cortisol levels.

Higher stress-induced activity in the left hippocampus was revealed after 2 weeks of consumption of sucrose-sweetened beverages compared with aspartame-sweetened beverages (P = .001). Cortisol response was diminished after 2 weeks of consumption of sucrose-sweetened beverages and was elevated after consumption of aspartame-sweetened beverages.

“The results suggest differences in dietary habits may explain why some people underreact to stressful situations and others overreact,” Laugero said. “Although it may be tempting to suppress feelings of stress, a normal reaction to stress is important to good health. Research has linked over- and under-reactivity in neural and endocrine stress systems to poor mental and physical health.” – by Amber Cox

Disclosure: The researchers report no relevant financial disclosures.

Another example of the failure of mutations cause aging

Science 20 March 2015:
Vol. 347 no. 6228 p. 1326
DOI: 10.1126/science.347.6228.1326-d

  • Editors’ Choice

Aging

Aging

DNA mutations do not age yeast

The molecular basis of aging—just what it is that wears out and causes the functional decline of an aged cell or organism—remains unclear. In hope of better understanding this, Kaya et al. monitored individual yeast cells and sequenced their DNA to test whether accumulated DNA mutations are a cause of replicative aging in yeast. The number of daughter cells produced before a mother yeast cell dies defines the replicative life span of the mother cell. But the cells accumulated only 0.4 mutations over the life span of an average cell. Thus, at least in yeast, DNA mutations do not seem to cause aging.

Aging Cell 10.1111/acel.12290 (2015).

Dr Brash’s findings may uncover some serious accessory nutrient deficiencies in the diets of mice and men

 

Consider the following article about Dr. Douglas Brash’s research:
You can still get skin cancer in the shade

Stepping under the shade of an umbrella after soaking in some sun might feel like an instant cool, but your skin cells have a postsunshine hangover that lasts for hours. In fact, molecules excited by the ultraviolet (UV) rays keep on damaging the DNA in skin cells even in complete darkness, researchers have discovered. The finding could lead to a new generation of skin cancer preventives that are applied after a day in the sun and block these delayed effects.

“This is an interesting, unexpected, and very important new mechanism of skin damage by UV radiation,” says dermatologist David Fisher of Massachusetts General Hospital in Boston, who was not involved in the work.

When UV rays from sunlight—or a tanning bed—hit skin cells, the radiation damages genes, causing extra chemical bonds to form between the building blocks of DNA. Over time, these genetic changes accumulate and can make cells more prone to the skin cancer melanoma. But when radiology researcher Douglas Brash of Yale University tracked the timing of these genetic changes in isolated skin cells, he found that the extra bonds in the DNA didn’t stop forming when UV rays stopped. For more than 3 hours after cells were exposed to UV light, the DNA damage kept increasing.

“What this means is that we’ve been underestimating the amount of DNA damage that people are getting from UV exposure,” Brash says.

He and his collaborators went on to show, in both mouse and human skin cells, that the lingering damaging effects of UV rays were dependent on melanin, the pigment that gives skin its color. High levels of melanin in dark-skinned people are typically associated with protection against melanoma, because the melanin absorbs UV energy, preventing it from causing DNA damage. But Brash found a second role for the pigment. When UV rays hit skin cells, they cause a cascading reaction that puts melanin in an excited state. For hours afterward, even if the cells are in darkness, the energy from the excited melanin can keep damaging DNA, the scientists report online today in Science.

The new paper is “extraordinarily important and elegantly done,” says Frank Meyskens, a melanoma researcher at the University of California, Irvine. It finally explains a longtime clinical observation that has stumped researchers, he says: why black albinos in Africa have such low rates of melanoma. Without any melanin in their skin, they don’t get the protective effects of the pigment, yet they also don’t have the long-term damage after sun exposure that comes with excited melanin.

The research also suggests a new way to prevent melanoma. “If we can divert the energy from the excited melanin before it gets transferred, we might be able to intervene,” Brash says. In the new study, his group found that vitamin E lotion diminished some of the delayed effects of UV rays, but he suspects there are other compounds that could work even better. “If you look at the data out there on current sunscreens and skin cancer prevention, it’s not so great,” Fisher says. “But this new finding could really give us new opportunities to improve.”

Posted in Biology, Chemistry, Health

————–

This finding suggests that something important is deficient in mouse and human skin cells: molecules that quench excited melanin and radiate heat harmlessly. The essential nutrient vitamin E may the molecule, but I wonder if it is a network of accessory nutrients like the carotenes, squalene, and many other polyenes like them. If mice and humans ate a healthier diet, we may not be so vulnerable to the aftershocks of excited melanin. A network of nutrients could serve as a shuttle to carry the energy ever farther from DNA, until it is dissipated harmlessly as heat.

Chronic Fatigue Syndrome is Toxic Lifestyle Syndrome

Chronic fatigue Syndrome (CFS) is a symptom of our sad and clueless times. Now scientists are proposing a new name that obfuscates its etiology. CFS is a toxic lifestyle syndrome driven by major deficiencies in the four controllable health parameters: nutrition, stress-control, sleep, and exercise, deficiencies that are exacerbated by too much toxicity. And the uncontrollable deficiency that plagues our health is our lousy genes.
Here is the article:
Goodbye chronic fatigue syndrome, hello SEID

A committee convened by the Institute of Medicine (IOM) has proposed a new name for a condition known variously as chronic fatigue syndrome or myalgic encephalomyelitis. The unwieldy new moniker: systemic exertion intolerance disease, or SEID. In a report released today, the committee also suggests a new set of diagnostic criteria for SEID.

After reviewing more than 9000 scientific studies, hearing testimony from experts, and soliciting input from the public, the committee concluded that “the name ‘chronic fatigue syndrome’ has done a disservice to many patients,” calling it  “stigmatizing and trivializing.” Myalgic encephalomyelitis (ME), they noted, “does not accurately describe the major features of the disease.”

At least 20 sets of diagnostic criteria exist, the committee noted, which has confused patients, clinicians, and their families, as well as researchers studying the disease. The proposed diagnostic criteria are more focused on “the central symptoms” such as a reduced or impaired ability to work and study, malaise after exertion, and “unrefreshing” sleep.  The report, “Beyond Myalgic Encephalitis/Chronic Fatigue Syndrome: Redefining an Illness,” runs 235 pages.

Peter Rowe, who heads the Chronic Fatigue Clinic at the Johns Hopkins Children’s Center in Baltimore, Maryland, and was one of 15 committee members, had high praise for the process and the product. “This is a phenomenal report,” Rowe said, noting that it had unanimous support. “It has the best summary of the evidence that I’ve ever read.” The U.S. Department of Health and Human Services and the Social Security Administration sponsored the IOM study and report.

Systemic exertion intolerance disease does not exactly roll off the tongue. IOM committee member Ronald Davis, a biochemist who heads the genome center at Stanford University in Palo Alto, California, says the group considered about 100 options. “Boy, did we  struggle with that,” he said. “It’s hard to come up with a good name, and I don’t think this is a perfect name.”

But Davis thinks its essential to do away with chronic fatigue syndrome. “My son is sick with it, and when I tell people, they say, ‘I had that once,’ because they were tired once,” he said. “ME is a better name, but there are no real data that fit the name.”

Davis hopes the report will convince all clinicians that they can diagnose the disease and that it is real. “I hope it will get rid of those who may not believe it,” Davis said. “They’ll have to keep it to themselves. It’s incompetence and it’s malpractice.”

The new diagnostic criteria build on what are known as the Canadian Consensus Criteria, first put forward in 2003. But the report offers a distinct, simpler definition that focuses on “the central element of this disorder,” said committee chair Ellen Wright Clayton at “public release event” held at IOM this morning. “The essence of this disorder is that if patients with this disorder engage in exertion—cognitive, emotional, physical, whatever—that their symptoms are made much worse and often for a prolonged period of time,” said Clayton, a law professor at Vanderbilt University in Nashville. The name, she said, reflects this. “We want to name it for what it is,” she said. “This is what the patients experience.”

The committee was  “struck by the relative paucity of research” that has gone into SEID. “Remarkably little research funding has been made available to study the etiology, pathophysiology, and effective treatment of this disease, especially given the number of people afflicted,” the report noted. (It cited estimates that said between 836,000 and 2.5 million Americans have chronic fatigue syndrome or ME, but Davis points out that some popular diagnostic criteria have far too liberal definitions of the condition.)

The report recommends that a multidisciplinary committee review the diagnostic criteria for SEID within 5 years. Rowe says they may want to review the name, too. “We don’t believe it’s going to be the name forever, but it’s a step forward,” he says.

Posted in Health, Scientific Community

It is not all about calcium: Trace minerals strengthen tooth enamel toward decay

Science 13 February 2015:
Vol. 347 no. 6223 p. 732
DOI: 10.1126/science.347.6223.732-a

  • This Week in Science

Dental Materials

Dental Materials

Key trace minerals greatly strengthen teeth

Figure

Rodent skull shows pigmented and regular tooth enamel

CREDIT: MICHAEL GRAYDON

The outer layers of teeth are made up of nanowires of enamel that are prone to decay. Gordon et al. analyzed the composition of tooth enamel from a variety of rodents at the nanometer scale (see the Perspective by Politi). In regular and pigmented enamel, which contain different trace elements at varying boundary regions, two intergranular phases—magnesium amorphous calcium phosphate or a mixed-phase iron oxide—control the rates of enamel demineralization. This suggests that there may be alternative options to fluoridation for strengthening teeth against decay.

Common sense says stop stuffing sugar down diabetics’ throats

Here is some common sense re: Fructose and Diabetes:

Type 2 diabetes fueled by added fructose

Current dietary guidelines allowing 25% of total daily calories as added sugars are being challenged by researchers who are proposing reductions in the amount of added sugars people consume, according to recent review published in Mayo Clinic

“At current levels, added-sugar consumption, and added-fructose consumption in particular, are fueling a worsening epidemic of type 2 diabetes,” James J. DiNicolantonio, PharmD, a cardiovascular research scientist at Saint Luke’s Mid America Heart Institute in Kansas City, Mo., said in a press release. “Approximately 40% of US adults already have some degree of insulin resistance, with projections that nearly the same percentage will eventually develop frank diabetes.”

End-organ damage and diabetic complications have been linked to fructose consumption, particularly high-fructose corn syrup and sucrose.

DiNicolantonio and colleagues performed a comprehensive literature review that showed significant adverse metabolic harms (ie, worsening of glucose and insulin levels, glucose tolerance, blood pressure, fast storage, and lipids) when glucose-only starch or lactose is replaced with fructose-containing sucrose (even when calories were held constant), and these effects are greater when higher proportions of fructose are added to the diet.

DiNicolantonio suggests that added sugar levels should be more in line with the American Heart Association’s recommendations of no more than 6 teaspoons per day for women and no more than 9 teaspoons per day for men. Currently, there is no recommended restriction on fructose-containing added sugar in the American Diabetes Association guidelines or the 2010 Dietary Guidelines for Americans.

“Clearly a calorie is not a calorie,” DiNicolantonio told Endocrine Today. “To say this differently, a calorie coming from added sugars is much more harmful than a calorie coming from starch or lactose for promoting diabetes.” – by Amber Cox

For more information:

James J. DiNicolantonio, PharmD, can be reached at jjdinicol@gmail.com.