Carbohydrate metabolism and obesity -
A growing body of scientific evidence also points to the role of overweight in the development of both type 1 and type 2 diabetes [18]. On the one hand, weight gain can be considered as a complication of insulin treatment, and on the other hand, it has a significant pathophysiological effect on the occurrence and progression of diabetes stages.
Overweight and obesity are the most important factors in the occurrence of insulin resistance and are primarily compensated by hyperinsulinaemia [18]. The problem of diabetes mellitus is especially acute in people who have a shift work schedule, which aggravates the already existing metabolic changes in this group of patients.
Thus, Shan et al. During about 24 years of follow-up, 10, cases of diabetes mellitus were established, while the multivariate risk coefficients of 5-year night shift work before were 1. Thus, both night shift work and an unhealthy lifestyle were associated with a higher risk of developing diabetes.
These results show that most cases of this disease can be averted with early prevention. It is important to note not only the commonality in the occurrence of these diseases, but also the increased risk of serious complications.
Cardiovascular diseases, apnoea, and peripheral blood flow disorders are especially associated with obesity and diabetes. All patients with metabolic disorders overweight, elevated glucose levels , regardless of the severity and age of occurrence, are recommended to optimise their diet and change eating habits.
As indicated in the recommendations of the American Diabetes Association [21], there is no single universal approach to nutrition for such patients, and the selection of a diet should be individual, considering the current diet model, preferences, and specific glycometabolic goals.
Based on studies by nutritionists, for the prevention of obesity-related diseases, the Mediterranean diet is one of the best diets of [22]. It involves the use of seasonal dishes, the use of extra virgin olive oil, an increase in the amount of legumes, vegetables, fruit, nuts, whole grains, and fish in the daily diet with a restriction on the consumption of sweets, red meat, and dairy products.
Such nutrition, like other plant-based approaches, is associated with positive changes in laboratory parameters, and may even reduce the need for high doses of pharmacological drugs [23]. In particular, Mirabelli et al.
These glyco-metabolic benefits appear to persist over time, regardless of changes in body weight, because they are not apparent in other successful nutritional interventions for weight loss [24]. Milenkovic et al.
The Mediterranean diet in this review has proven to be the best diet for patients with diabetes and overweight.
It helps reduce glycosylated haemoglobin, thereby improving glycaemic control, causing weight loss, and improving lipid exchange [25]. Along with this, HbA1c significantly decreased in patients with overweight and obesity 5.
The use of such methods of early prevention as walking more than 10, steps per day, dosed physical activity in the form of cardio and swimming, and nutrition correction Mediterranean diet with alcohol restriction significantly reduces body weight and optimises carbohydrate metabolism.
Conflict of interest The author declares no conflict of interest. Obesity and overweight. Published online Adilovna ZM, Pazylbekovna KG, Smailkhanovna AN. Prevalence and correlates of insufficient physical activity among diabetic patients in Almaty, Kazakhstan.
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higher-fat diets for weight loss [ , , ]. The USDA has virtually abandoned the public health campaign to reduce total dietary fat [ ]. Food processing. A systematic review of observational data by Poti et al. Although the continuing increases in obesity prevalence might be attributable to lack of public adoption rather than any inherent deficiency of the EBM itself, the results of EBM-guided treatment throughout the last century suggest otherwise.
If the patient lost weight as predicted, this merely confirmed the comfortable feeling that treatment of obesity was really a pretty simple matter. However, if, as so often happened, the patient failed to lose weight, he was dismissed as uncooperative or chastized as gluttonous.
It was the rare physician who entertained the possibility that failure to follow a regimen might in itself be a medical problem. In , the National Institutes of Health sponsored a Consensus Development Conference on Methods for Voluntary Weight Loss and Control, including many of the leading experts in obesity.
However, the Consensus Conference found little evidence that obesity treatment achieved much better outcomes that those reviewed by Stunkard and McLaren-Hume [ ]. Axiomatically, disease treatment focused on causal drivers upstream along the mechanistic pathway should be more effective, and more sustainable for the patient, than those targeting downstream consequences and manifestations.
This treatment would work temporarily if one could convince a febrile patient to try it , but the body would compensate for the heat loss by severe shivering and blood vessel constriction.
Once the patient got out of the cold shower, the fever would return. Antipyretics work more effectively, and more pleasantly for the patient, by addressing the biological driver of heat accumulation. Similarly, if obesity results from a disorder of fuel partitioning, then measures to treat that problem e.
Maintaining the contrast between these competing models is critical to clarify thinking, inform a research agenda, and identify effective means of prevention and treatment. This claim belies the most fundamental possible differences among models: causal direction and mechanisms of causality Fig.
To subsume the CIM in this way requires construing the EBM so broadly as to make it unfalsifiable, and consequently useless as a scientific hypothesis.
However, this characterization was not made by CIM proponents and offers a false distinction. The control of adipose tissue biology by multiple hormonal, autonomic and other influences has been recognized for decades [ 27 ].
Indeed, the physiological actions of high-GL and high-sugar diets have long been conceptualized as involving integrated relationships among multiple organs beyond adipose tissue and numerous hormones beyond insulin [ 6 , 29 ]. For scientific models to remain relevant, they must grow as knowledge accrues.
Even as Hall et al. Lack of explicit testable hypotheses. How will key steps along the causal pathway be interrogated? What studies will differentiate the proposed causal pathway overeating drives chronic weight gain from the contrasting hypothesis in the CIM?
When humans or animals are experimentally overfed, they gain weight initially. But changes in hunger and energy expenditure oppose ongoing weight change; after the force-feeding ends, individuals characteristically undereat until body weight returns to baseline [ , , , , , ].
While arguing that opponents of the EBM confuse physics with pathophysiology, Hall et al. These tautologies provide no mechanistic insight. Paucity of mechanisms involving key model components. How does the new EBM explain the rapid population-level increase in weight, and large variations within individuals over time?
Physiologically regulated variables e. What studies would distinguish the putative mediators e. Moreover, if pleasure-related responses to tasty foods cause chronic overconsumption, why has it been so difficult to demonstrate an independent effect of palatability on obesity [ , , , , , , , ]?
Disregard of well-established metabolic mechanisms. For individuals with obesity, energy restriction elicits hallmarks of the starvation response including reduced energy expenditure long before body fat stores reach a normal level.
How do the hedonic and reward aspects of palatable food trigger metabolic responses? Difficulty accounting for the natural history of obesity. The secular increase in energy intake from to the present in the U. Considering the psychosocial and other burdens of excessive weight, why do so few people successfully compensate by conscious control for these small daily effects?
After all, adults routinely resist pleasurable temptations e. Reliance on assumptions that do not differentiate among models. The new EBM interprets evidence that the brain controls body weight as supporting a causal role of overeating in obesity.
As considered above, the brain also influences virtually all aspects of energy metabolism and adipocyte biology. For intractable public health problems, the purpose of scientific models is to guide the design of informative research and, by helping to elucidate causal mechanisms, suggest effective approaches to prevention or treatment.
The new EBM does neither. At a minimum, future formulations should 1 specify testable, mechanistically oriented predictions that examine the causal pathway; 2 explain why the increased population-level BMI is defended by metabolic responses; and 3 demonstrate how calorie-independent effects of diet suggested by clinical research and demonstrated by animal models can be integrated in this model.
The EBM and its precursors have dominated thinking for nearly a century [ 7 ]—influencing scientific design, interpretation of experimental findings, public health guidelines, and clinical treatment—largely to the exclusion of other views. For instance, the NIH has sponsored numerous multi-center trials of low-fat diets for obesity-related outcomes [ , , ] all with negative primary outcomes , but nothing comparable for low-GL diets.
With the inability of conventional strategies to stem the rising toll of obesity-related disease, new causal models should be studied, not suppressed by hyperbolic claims of having disproven them [ 2 , 9 , 18 , 19 , 57 , 58 , , , ]. Admittedly, debate on complicated scientific questions may polarize, with a tendency for both sides to cite selectively from inconclusive evidence.
This problem is exacerbated by difficulties in studying the small daily effects that characterize the natural history of obesity. In the interests of scientific advancement and public health, all sides of this debate should work together to formulate mutually acceptable versions of competing models and design unbiased studies that would put them to a rigorous test.
A constructive paradigm clash may be facilitated with the recognition that evidence for one model in certain experimental settings does not invalidate the other model in all settings, and that obesity pathogenesis in humans may entail elements of both.
Finally, we would emphasize that this paradigm clash should not delay public health action. Refined grains and added sugars comprise about one-third of energy intake in the US and Europe.
Both models target these highly processed carbohydrates—albeit for different reasons—as major drivers of weight gain. Regardless of how this debate may evolve, common ground now exists on the need to replace these products with minimally processed carbohydrates or healthful fats in the prevention and treatment of obesity.
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die Maßgebliche Mitteilung:)