Monday, October 02, 2006

Diabetes, not obesity, increases risk of developing critical illness and early death

Diabetes puts people at risk of developing critical illness and dying early, but obesity without diabetes does not. A study published today in the open access journal Critical Care reveals that individuals suffering from diabetes are three times more at risk of developing critical illness and dying young than individuals who do not have diabetes. Obese individuals who do not have diabetes, by contrast, have the same risk of dying or of falling critically ill as non-obese patients who do not have diabetes. These results are surprising, as obesity is linked to diabetes. The authors of the study conclude that the relationship between obesity, diabetes and critical illness is complex and that obesity, per se, does not predict poor outcomes.

Katarina Slynkova and colleagues from the University of Kentucky Chandler Hospital collaborated with colleagues from Emory University School of Medicine to analyse data from 15,408 subjects aged 44 to 66, coming from four different US communities, who had originally been studied between 1986 and 1989. The authors analysed the subjects' body mass index (BMI), presence of diabetes (either type 1 or type 2) and the subjects' history of critical illness (acute organ failure) and mortality within 3 years.

Slynkova et al.'s results show that, in the absence of diabetes, obese individuals do not have an increased risk of suffering from acute organ failure, and of dying from acute organ failure, than non-obese individuals. By contrast, patients with diabetes are three times more likely to become critically ill with acute organ failure and they are three times more likely to die from acute organ failure, or from any cause, than patients who do not have diabetes, regardless of their BMI. Slynkova et al. conclude that diabetes is a strong independent predictor of acute organ failure and subsequent death, or death from any cause.


Journal abstract follows:

The role of body mass index and diabetes in the development of acute organ failure and subsequent mortality in an observational cohort

By: Katarina Slynkova , David M Mannino , Greg S Martin , Richard S Morehead and Dennis E Doherty


Several studies have shown a correlation between body mass index (BMI) and both the development of critical illness and adverse outcomes in critically ill patients. The goal of our study was to examine this relationship prospectively with particular attention to the influence of concomitant diabetes mellitus (DM).


We analyzed data from 15,408 participants in the Atherosclerosis Risk in Communities (ARIC) study for this analysis. BMI and the presence of DM were defined at baseline. We defined acute organ failure as those subjects who met a standard definition with diagnostic codes abstracted from hospitalization records. Outcomes assessed included the following: risk of the development of acute organ failure within three years of the baseline examination; in-hospital death while ill with acute organ failure; and death at three years among all subjects and among those with acute organ failure.


At baseline, participants with a BMI of at least 30 were more likely than those in lower BMI categories to have DM (22.4% versus 7.9%, p < 0.01). Overall, BMI was not a significant predictor of developing acute organ failure. The risk for developing acute organ failure was increased among subjects with DM in comparison with those without DM (2.4% versus 0.7%, p < 0.01). Among subjects with organ failure, both in-hospital mortality (46.5% versus 12.2%, p < 0.01) and 3-year mortality (51.2% versus 21.1%, p < 0.01) was higher in subjects with DM.


Our findings suggest that obesity by itself is not a significant predictor of either acute organ failure or death during or after acute organ failure in this cohort. However, the presence of DM, which is related to obesity, is a strong predictor of both acute organ failure and death after acute organ failure.



A recent study suggests thwarting vitamin K's function could hinder bone health and contribute to the development of osteoporosis, results that call into question a need for increased vitamin K supplementation. The University of Michigan School of Nursing study found that typical intake of vitamin K may in fact not be enough to support bone health in the perimenopausal years. The finding could spur formulators to more actively promote vitamin K for pre-menopausal women, although the ingredient can cause complications for those on blood thinners.

Vitamin K is found in green and green leafy vegetables as well as vegetable oils, however most individuals do not consume sufficient amounts to promote bone health. Few multivitamins contain vitamin K, and those that do have minimal amounts of the nutrient. According to lead author Jane Lukacs, the current intake is recommended to be 1 ug/kg/d, based on Vitamin K's influence on blood clotting. "What is becoming apparent, is that what is adequate for blood clotting may not be adequate for bone health," said Lukacs .

In the UK, the average age at which women reach menopause is 51 years, according to the National Osteoporosis Society. Menopause is characterized by a loss of oestrogen production, which accelerates bone loss. At worst, this can lead to osteoporosis, a disease characterized by brittle bones.

The study, published in the current issue of the journal Menopause (13(5):799-808, September/October 2006), noted that one of the early effects of declining oestrogen is the impairment of vitamin K function in bones even before bone loss from menopause can be measured. Fifty-nine healthy women participated in the study funded by pharmaceutical giant Pfizer. The women were divided into three groups: 19 women aged 40-52; 21 women aged 20-30; and 19 untreated women between 40-52 years. The study included blood tests, interviews and food frequency quesionnaires to determine dietary habits, calculation of the body mass index as well as measurement of bone mineral density of the lumbar spine and the non-dominant hip.

"Our study suggests that the generally accepted level of vitamin K in healthy women is inadequate to maintain bone health just at the onset of menopause," said lead author Jane Lukacs, she did not express an opinion on optimum vitamin K intake.

With the help of vitamin K, the protein osteocalcin can bind to calcium in the bone. This protein becomes part of the bone structure when it is chemically modified to bind to calcium through a carboxylization. In the study, the percentage of undercarboxylated osteocalcin was higher in the untreated early postmenopause cohort compared with all the other women (21.9+/-1.7 percent vs 17.4+/-0.9 percent, n=40; P = 0.02). This implies these women were deficient in vitamin K.

"Percentage of undercarboxylated osteocalcin may be a specific bone marker of the early postmenopause in healthy women," concluded the study. Lukacs said it is necessary to explore whether vitamin K supplementation in the early postmenopause will offer an additional intervention for women concerned about their future risk of fracture. Those who take anticoagulant medicine for hypercoagulation however are generally advised not to take vitamin K because it is thought to play a role in blood clotting.



Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.


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