Diabetes: The differences between types 1 and 2 There are fundamental differences between diabetes type 1 and type 2, including when they might occur, their causes, and how they affect someone's life. Find out here what distinguishes the different forms of the disease, the various symptoms, treatment methods, and how blood tests are interpreted. Read now
The goal of treating metabolic syndrome is to prevent the development of diabetes, heart disease, and stroke. Your doctor will first suggest lifestyle modifications such as exercising for 30 minutes most days of the week. One study showed that individuals who are physically active (30 minutes of activity at least once per week) have half the risk of developing metabolic syndrome than those who are inactive. Your doctor may also suggest eating a healthy diet to promote weight loss and normal blood cholesterol and fat levels. https://www.healthshare.com.au/storage/e2d6972eb9e9fe519fb8847f9afe0d6f.png.60x60_q85_box-0,0,446,446.png
The prevailing opinion is that all of these markers are signs of insulin resistance, meaning the diminished ability of a given amount of insulin to exert its normal effect. When insulin resistance develops, it can impact metabolic processes in many ways, resulting in the specific markers listed above. However, different individuals respond to insulin resistance in different ways. Also, the time frame in which certain signs develop varies. This variability makes defining—and treating—metabolic syndrome tricky.
"Secondary" diabetes refers to elevated blood sugar levels from another medical condition. Secondary diabetes may develop when the pancreatic tissue responsible for the production of insulin is destroyed by disease, such as chronic pancreatitis (inflammation of the pancreas by toxins like excessive alcohol), trauma, or surgical removal of the pancreas.
Hypertension results from a complex interaction of genes and environmental factors. Numerous common genetic variants with small effects on blood pressure have been identified as well as some rare genetic variants with large effects on blood pressure. Also, genome-wide association studies (GWAS) have identified 35 genetic loci related to blood pressure; 12 of these genetic loci influencing blood pressure were newly found. Sentinel SNP for each new genetic locus identified has shown an association with DNA methylation at multiple nearby CpG sites. These sentinel SNP are located within genes related to vascular smooth muscle and renal function. DNA methylation might affect in some way linking common genetic variation to multiple phenotypes even though mechanisms underlying these associations are not understood. Single variant test performed in this study for the 35 sentinel SNP (known and new) showed that genetic variants singly or in aggregate contribute to risk of clinical phenotypes related to high blood pressure.
^ Qaseem, A; Wilt, TJ; Rich, R; Humphrey, LL; Frost, J; Forciea, MA; Clinical Guidelines Committee of the American College of Physicians and the Commission on Health of the Public and Science of the American Academy of Family, Physicians. (21 March 2017). "Pharmacologic Treatment of Hypertension in Adults Aged 60 Years or Older to Higher Versus Lower Blood Pressure Targets: A Clinical Practice Guideline From the American College of Physicians and the American Academy of Family Physicians". Annals of Internal Medicine. 166 (6): 430–437. doi:10.7326/m16-1785. PMID 28135725.
This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.
The undiagnosed/untreated metabolic condition that spreads. Metabolism is an intricate system of organs communicating with one another to do a job. If you have a problem in one area, it will affect other areas as well. The example I use with patients is to picture metabolism as an orchestra playing a song. If the flutes are playing off key or out of time, the other instruments in the band will likely wander off key and timing as well. In the end, everyone is off and the song is a mess. This is how metabolic damage can develop as well. An untreated thyroid condition will negatively affect all other systems and metabolism as a whole.
Nope! Just as Time agreed, other research has shown that the low fat craze directly coincides with the increasing obesity epidemic. As you may have noticed above, fat is not on the list of insulin stimulating foods.. but sugar is! And sugar is just the thing that is added to low fat foods to make them taste better. So not only do you get a heightened insulin response to these low fat, low calorie foods leaving you in fat storing mode, but you are get an altered satiety response. That is right, fat is critical for the regulation of gut hormones and also the hormones that make you feel full after a meal and keep you feeling full between meals.
Hypertension is one of the most common worldwide diseases afflicting humans and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease. Despite extensive research over the past several decades, the etiology of most cases of adult hypertension is still unknown, and control of blood pressure is suboptimal in the general population. Due to the associated morbidity and mortality and cost to society, preventing and treating hypertension is an important public health challenge. Fortunately, recent advances and trials in hypertension research are leading to an increased understanding of the pathophysiology of hypertension and the promise for novel pharmacologic and interventional treatments for this widespread disease.
Epigenetic phenomena, such as DNA methylation and histone modification, have also been implicated in the pathogenesis of hypertension. For example, a high-salt diet appears to unmask nephron development caused by methylation. Maternal water deprivation and protein restriction during pregnancy increase renin-angiotensin expression in the fetus. Mental stress induces a DNA methylase, which enhances autonomic responsiveness. The pattern of serine protease inhibitor gene methylation predicts preeclampsia in pregnant women.