T2 Diabetes is a Voluntary Lifestyle Choice Disease. - Politics Forum.org | PoFo

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Provision of the two UN HDI indicators other than GNP.
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#14893711
(Just like Tobacco smoking related Lung Cancer), T2 Diabetes is a Voluntary Lifestyle Choice Disease.

(Ignorance, Mental-Stress and Ill-discipline are major subsidiary causative factors as well)
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1st principles 1st:
Definition: Diabetes mellitus type 2 is a long-term metabolic disorder that is characterized by high blood sugar, insulin resistance, and relative lack of insulin. https://en.wikipedia.org/wiki/Diabetes_mellitus_type_2

Blood sugar = calories, aka energy. (https://en.wikipedia.org/wiki/Food_energy)
Law of conservation of energy:https://en.wikipedia.org/wiki/Conservation_of_energy*energy can neither be created nor destroyed; rather, it can only be transformed from one form to another

Majority of people with T2 diabetes have a very high % of body fat and a low basal metabolism rate.

The basal metabolism rate is influenced by the % of skeletal muscle a person has, (obviously, the % muscle to fat is lower in people with a high % body fat). People with a low % muscle have a low basal metabolic rate and are thus more likely to get fat (or are already fat).

The purpose of Insulin is to help cells absorb glucose in blood (especially fat and liver cells) since brain and muscle cells admit glucose much more readily where necessary (especially when exercising).

Resistance to Insulin by cells occurs primarily because cellular energy stores (as glucose/ glycogen/ fat) are already full and cannot increase storage any further without bursting or tearing apart the cell wall/ cell architecture. Fat cells have the highest energy storage capacity so usually, insulin resistance happens when fat cells have very low or reduced vacant storage capacity. Just as a bucket filled to the brim with water will overflow upon further influx, diabetes is a condition where the fat cells are filled to capacity and are thus unable to absorb blood glucose (energy) levels further without causing structural damage to themselves. Insulin resistance in this case is thus a product of lassitude and gluttony and not a genetic disease.

Lifestyle and work also plays a big part since only well trained (/skilled) muscles (and perhaps other cells) can utilise fat as an energy source at high stress/ aerobic intensity (higher VO2 max levels etc). Many cosmopolitan denizens have high stress occupations for which they are physically poorly trained to handle, even should it be a white collar job in nature. Just as a 100m sprint (high VO2max activity in midst of high fight/flight hormone levels) consumes mostly glucose as energy source, a high stress/ toxic work environment results in muscle and other cells preferentially using glucose as energy substrate rather than fat as would be the case in a more tranquil/ harmonious work environment (Insufficient sleep/ rest also causes fight/flight hormone action resulting in higher glucose rather than fat metabolism). Low blood glucose causes hunger pangs and in the context of a hectic work environment, means more binging on fatty foods and sugary drinks to cure hunger pangs quickly as well as alcohol and tobacco products which are all short term stimulants but with long term detriment. Such a lifestyle leads to diabetes at best and a heart attack/ stroke/ cancer in most people which will most likely end their careers and perhaps bankrupt either themselves or their country from the stratospheric healthcare costs of providing care and concern for 40-50 years of ignorance, poor lifestyle choices / ill discipline.

PS:
Other consequences of a sedentary lifestyle include:
Obstructive Sleep Apnoea which contributes to diabetes: poor respiratory muscle tone coupled with a big tummy and fat blocking the respiratory tract causes deep sleep to be interrupted by persistently cycling airway blockage (snoring) when muscles relax and the already partially fat blocked airways become completely blocked/ compressed by fatty tissues (suffocation resulting in repeated subconscious micro awakenings during sleep).

The poor state of rest results in increased stress hormones (catecholamines) circulating in the blood which in themselves, besides antagonising insulin action, also raise the blood pressure (Hypertension) and shift the energy metabolism choice from fat to glucose: resulting in poor performance (repeated hunger pangs) and even more fat accumulation since high glucose is extremely toxic to blood vessels and especially the kidney: so fat accumulation becomes a one way street, increasing with every meal but not being expanded off in between.

Diabetes and Hypertension are both partners in crime (mutual accelerants) because they both cause blood vessel inflammation which most likely further increase blood catecholamine levels which both serve to accelerate one another resulting in even more severe (vivious cycle) blood vessel inflammation: both of which are the primary cause of heart attacks, strokes and perhaps even cancer too.

Ignorance, Mental-Stress and Ill-discipline are thus the primary cause of T2 Diabetes and to be blamed for the stratospheric healthcare costs and high morbidity suffered by modern day society citizens today.

In conclusion, all people with a high body fat % (and BMI above 18.5) https://www.builtlean.com/2010/08/03/ideal-body-fat-percentage-chart/ need to do more physical exercise and avoid a sedentary lifestyle to improve their skeletal muscle quantity, quality and tone to improve their basal metabolic rate (and personal productivity levels) and thus keep their % body fat below the prescribed levels of 15% for males and 25% for females to avoid the conditions of obesity, diabetes, hypertension, obstructive sleep apnoea, high cholesterol, high mental/ work stress levels etc which place an increasingly unaffordable burden on healthcare costs for all.


References:
- Image https://www.builtlean.com/2010/08/03/ideal-body-fat-percentage-chart/
- 1 in 3 Singaporeans suffer from sleep apnea: Study: CNA17Mar2016: http://www.channelnewsasia.com/news/singapore/1-in-3-singaporeans-suffer-from-sleep-apnea-study-8137824
- Start now to prevent and manage chronic diseases: ST27Sept2016: "As of 2010, more than half of Singapore's adult population between 18 and 69 years old have high cholesterol, four in 10 are overweight or obese, a quarter have prediabetes or diabetes and about one in five has hypertension." http://www.straitstimes.com/singapore/health/start-now-to-prevent-and-manage-chronic-diseases
- 1 in 10 stroke patients here aged under 50: ST, 19Nov2016: "Medical conditions such as high blood pressure or high cholesterol can make a person more likely to get a stroke, say doctors." http://www.straitstimes.com/singapore/1-in-10-stroke-patients-here-aged-under-50

May not be diabetes, but his symptoms still suggests something wrong with his brain blood flow/blood vessles e.g.: https://en.wikipedia.org/wiki/Transient_ischemic_attack ):
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#14895451
Many naturally die slowly and painfully, albeit at a high healthcare costs to society:
kidneys die= kidney failure needing dialysis.
Eyes die: person goes blind
Blood vessels die: results in anything from strokes to amputations etc
etc etc....

Guess governments should place more investments in exercise promotion and other health enhancing education programmes/ sponsorships etc, that would be a better investment although it takes time since prevention is always better than cure...
#14895526
Changing one's lifestyle cannot cure type 2 diabetes. Genes associated with type 2 diabetes risk are TCF7L2 (insulin secretion and glucose production) and CAPN10, which is associated with type 2 diabetes risk in Mexican-Americans. T2D risk genes are more common among certain populations. There are some inter-ethnic differences in the risk allele frequencies, which are lower in East Asians than those in Europeans and South Asians (Qi et al. 2016).

Abstract
Type 2 diabetes (T2D) is the result of interaction between environmental factors and a strong hereditary component. We review the heritability of T2D as well as the history of genetic and genomic research in this area. Very few T2D risk genes were identified using candidate gene and linkage-based studies, but the advent of genome-wide association studies has led to the identification of multiple genes, including several that were not previously known to play any role in T2D. Highly replicated genes, for example TCF7L2, KCNQ1 and KCNJ11, are discussed in greater detail. Taken together, the genetic loci discovered to date explain only a small proportion of the observed heritability. We discuss possible explanations for this “missing heritability”, including the role of rare variants, gene-environment interactions and epigenetics. The clinical utility of current findings and avenues of future research are also discussed.

TCF7L2: TCF7L2 was discovered as a T2D susceptibility gene after a strong linkage signal was mapped to chromosome 10q in a Mexican-American population[21]. This region was later fine-mapped in the Icelandic population and confirmed in United States and Danish cohorts, where the risk locus was found to be located in intron 3 of the TCF7L2 gene[22]. The association between T2D and a number of single-nucleotide polymorphisms (SNPs) in the TCF7L2 gene has since been strongly confirmed in multiple Genome-wide association studies (GWAS) in different ethnic groups and this gene remains the most replicated and most strongly associated T2D risk gene at this time[23]. We will discuss this gene further in the GWAS section of this review.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746083/

Abstract
Type 2 diabetes (T2D) has become a major health problem throughout the world and the epidemic is particularly severe in Asian countries. Compared with European populations, Asians tend to develop diabetes at a younger age and at much higher incidence rates given the same amount of weight gain. Genome-wide association studies (GWAS) have identified over 70 loci associated with T2D. Although the majority of GWAS results were conducted in populations of European ancestry, recent GWAS in Asians have made important contributions to the identification of T2D susceptibility loci. These studies not only confirmed T2D susceptibility loci initially identified in European populations, but also identified novel susceptibility loci that provide new insights into the pathophysiology of diseases. In this article, we review GWAS results of T2D conducted in East and South Asians and compare them to those of European populations. Currently identified T2D genetic variants do not appear to explain the phenomenon that Asians are more susceptible to T2D than European populations, suggesting further studies in Asian populations are needed.

https://www.ncbi.nlm.nih.gov/pmc/articl ... 5/#S6title

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