25 Matching Annotations
  1. Jul 2024
    1. the question is why are the mitochondria not doing their job why is the self not responding to insulin 00:05:34 that's the issue different tissues different reasons but the main one is the liver

      for - question - health - insulin resistance - why aren't mitochondria within cells not responding to insulin?

      question - health - insulin resistance - why aren't mitochondria within cells not responding to insulin? - The fat cells are being stored in the liver, resulting in - fatty liver disease - The liver stores the fat cells floating in blood (triglycerides) then recirculates it back to the cells. - The cells and liver are caught up in a vicious cycle of "hot potatos" with the fat cells.<br /> - (See Stanford explainer video above)

    2. insulin takes glucose from the blood and also fats from the blood in the form of triglyceride 00:03:11 and stuffs it in cells for a rainy day

      for - health - insulin and insulin resistance - simple explanation - to - insulin resistance - clear and simple explainer video - Stanford University health - insulin - simple explanation - insulin stores sugars and tryglycerides floating around in the blood into cells. - more detailed explanation - when blood glucose rises, then beta cell of pancreas start to secrete insulin to bind to glucose and put into cells for storage - Watch this clear, short video explaining insulin resistance from Stanford University - https://hyp.is/4Ymu4D1ZEe-jFfeB23zicA/docdrop.org/video/U1cr14xffrk/

    3. having a high blood glucose is a manifestation of the problem not the problem itself because if you 00:02:34 didn't have the mitochondrial dysfunction you wouldn't have the high blood glucose so the high blood glucose is Downstream of the actual problem 00:02:45 and insulin is a way to shall we say cover up the problem

      for - key insight - insulin covers up the real problem of mitochondria dysfunction

    4. metabolic syndrome

      for - health - insulin resistance - metabolic syndrome

      health - insulin resistance - metabolic syndrome - When your mitochondria doesn't work, it results in insulin resistance - Metabolic syndrome includes an enormous variety of the major diseases afflicting modernity - up to 75% of the diseases that affect modern humans and - up to 75% of today's health care costs - and includes - type 2 diabetes - hypertension - dyslipidemia - cardiovascular disease - cancer - dementia - fatty liver disease - pollycystic ovarian disease - (he didn't include strokes here but he mentions throughout his talk)

    5. for - personal health - metabolic disease - insulin resistance caused by mitochondria dysfunction - interview - Dr. Robert Lustig - health - dangers of sugar in our diet

      summary - Robert Lustig is a researcher and major proponent for educating the dangers of sugar as the root cause of the majority of preventable western disease - He explains how sugar and carbs are a major variable and root cause of a majority of these diseases - It is useful to look at these bodily dysfunctions from the perspective of Michael Levin, in which all these diseases of the body are problems with lower levels of the multi-scale competency architecture - https://jonudell.info/h/facet/?max=100&expanded=true&user=stopresetgo&exactTagSearch=true&any=michael+levin%2C+multi-scale+competency+architecture

    6. insulin resistance is actually 00:01:14 Downstream of something even more important that we will talk about called mitochondrial dysfunction

      for - health - insulin resistance - a symptom of mitochondria dysfunction

    1. but as the situation continues it may require more and more and more insulin to get the same amount 00:02:40 of glucose into the cells

      for - key insight - health - insulin resistance

      key insight - health - insulin resistance - This is the key to the mechanism by which insulin levels increase in the blood. - As our diet places higher levels of glucose in the blood, the pancreas responds by releasing more and more insulin to process this elevated level of insulin and the cells respond, - but the cells, especially surrounding the organs no longer store fat when a certain threshold of high insulin is reached - high amounts of visceral fat around the organs is then accompanied by fat being released by the cells into the blood stream, elevating triglyceride levels - The liver then starts to take this up and if there are now elevated trigycerides in the bloodstream, the liver and cells get locked into a vicious cycle of fat release

    2. for - explanation - insulin resistance - Stanford University

      explanation - insulin resistance - Standard University - great explanation from Standford University

      from - Prof. Emeritus Robert Lustig on root cause of insulin resistance - https://hyp.is/RFJQrj1aEe-nIQu5Sj1fyw/docdrop.org/video/WVFMyzQE-4w/

    1. the vast majority of hypertension high blood pressure the root cause is insulin resistance metabolic disease

      for - health - heart - majority of hypertension and high blood pressure is caused by insulin resistance metabolic disease

    2. many of these patients had high lipids and high blood pressure and they were given beta 00:28:25 blockers and thide diuretics which as you know also have the same consequence as the statins do in in exacerbating insulin resistance

      for - health - heart - Beta-blocker/thiazide diuretic combos

      health - heart - Beta-blocker/thiazide diuretic combos - This combo lowers the blood pressure by - removing excess water and salt from the body and - slowing the heart rate. - These only mask the symptoms CAUSED BY INSULIN RESISTANCE

    3. you can take these medications you can expose yourself to the risk of the medications 00:26:57 or or you can change the way you eat you can deal with the true underlying problem insulin resistance

      for - health - heart - root cause of heart disease - lifestyle choices - dietary choice

      health - heart - root causes of heart disease - lifestyle choices - dietary choice - root cause of insulin resistance is poor diet with too much sugar and carbs and other variables such as excessive alcohol - dietary changes can shift lipid particles to large, fluffy LD particles - high sugar and carbs is a main factor leading to insulin resistance

      to - Root cause of insulin resistance - interview with Robert Lustig - https://hyp.is/l14UvjzwEe-cUVPwiO6lIg/docdrop.org/video/WVFMyzQE-4w/

  2. Oct 2023
  3. Mar 2022
    1. mTOR (mechanistic target of rapamycin) is an important enzyme that regulates things like cell growth, cell survival, protein synthesis, and autophagy. It also promotes the activation of insulin and IGF-1 receptors. This is why the presence of IGF-1 and insulin increases the amount of mTOR. You need to down-regulate mTOR in order to trigger autophagy. As an additional benefit, decreasing mTOR also causes senescent cells to down-regulate the release of inflammatory secretions. This means even if you don’t kill those cells through autophagy, you at least stop them from inflicting damage to the surrounding cells for months afterwards. IGF-1 has a pretty high half life in your body (about 12 hours) so if you want to keep autophagy running at all on a carnivore diet, you’ll also want to practice intermittent fasting.

      Intermittent fasting here will absolutely help but this problem is largely eliminated simply by following the right ratios for an effective [[Carnivore Diet]], eating [[nose-to-tail]] which will keep insulin levels low so that [[mTOR]] should still be down regulated

  4. Sep 2021
  5. May 2021
  6. Feb 2019
    1. The nomination has sparked criticism, however, over Mr Azar’s own track record at Eli Lilly, a pharmaceuticals giant that was one of several to repeatedly increased the price of insulin, a life-saving drug used to treat diabetes. 

      The man should be prosecuted. Evil!

  7. Jan 2019
    1. Adipose tissue is no longer considered to be an inert tissue that stores fat. This tissue is capable of expanding to accommodate increased lipids through hypertrophy of existing adipocytes and by initiating differentiation of pre-adipocytes. Adipose tissue metabolism exerts an impact on whole-body metabolism. As an endocrine organ, adipose tissue is responsible for the synthesis and secretion of several hormones. These are active in a range of processes, such as control of nutritional intake (leptin, angiotensin), control of sensitivity to insulin and inflammatory process mediators (tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), resistin, visfatin, adiponectin, among others) and pathways (plasminogen activator inhibitor 1 (PAI-1) and acylation stimulating protein (ASP) for example). This paper reviews some of the biochemical and metabolic aspects of adipose tissue and its relationship to inflammatory disease and insulin resistance.
  8. Nov 2018
    1. Objective To determine the effects of diets varying in carbohydrate to fat ratio on total energy expenditure.Design Randomized trial.Setting Multicenter collaboration at US two sites, August 2014 to May 2017.Participants 164 adults aged 18-65 years with a body mass index of 25 or more.Interventions After 12% (within 2%) weight loss on a run-in diet, participants were randomly assigned to one of three test diets according to carbohydrate content (high, 60%, n=54; moderate, 40%, n=53; or low, 20%, n=57) for 20 weeks. Test diets were controlled for protein and were energy adjusted to maintain weight loss within 2 kg. To test for effect modification predicted by the carbohydrate-insulin model, the sample was divided into thirds of pre-weight loss insulin secretion (insulin concentration 30 minutes after oral glucose).Main outcome measures The primary outcome was total energy expenditure, measured with doubly labeled water, by intention-to-treat analysis. Per protocol analysis included participants who maintained target weight loss, potentially providing a more precise effect estimate. Secondary outcomes were resting energy expenditure, measures of physical activity, and levels of the metabolic hormones leptin and ghrelin.Results Total energy expenditure differed by diet in the intention-to-treat analysis (n=162, P=0.002), with a linear trend of 52 kcal/d (95% confidence interval 23 to 82) for every 10% decrease in the contribution of carbohydrate to total energy intake (1 kcal=4.18 kJ=0.00418 MJ). Change in total energy expenditure was 91 kcal/d (95% confidence interval −29 to 210) greater in participants assigned to the moderate carbohydrate diet and 209 kcal/d (91 to 326) greater in those assigned to the low carbohydrate diet compared with the high carbohydrate diet. In the per protocol analysis (n=120, P<0.001), the respective differences were 131 kcal/d (−6 to 267) and 278 kcal/d (144 to 411). Among participants in the highest third of pre-weight loss insulin secretion, the difference between the low and high carbohydrate diet was 308 kcal/d in the intention-to-treat analysis and 478 kcal/d in the per protocol analysis (P<0.004). Ghrelin was significantly lower in participants assigned to the low carbohydrate diet compared with those assigned to the high carbohydrate diet (both analyses). Leptin was also significantly lower in participants assigned to the low carbohydrate diet (per protocol).Conclusions Consistent with the carbohydrate-insulin model, lowering dietary carbohydrate increased energy expenditure during weight loss maintenance. This metabolic effect may improve the success of obesity treatment, especially among those with high insulin secretion
  9. Jan 2018
  10. Dec 2017
  11. Nov 2017
    1. Donohue syndrome and Rabson-Mendenhall syndrome usually have homozygous or compound heterozygous mutations in the IR gene, and patients with these diseases have severe insulin resistance together with various symptoms, such as growth retardation, occasional hypoglycemia from infancy, intrauterine growth retardation, and low birth weight [3–6]

      This is interesting!

  12. Jul 2017
    1. Insulin sends a message to our cells that nutrients are available, meaning it’s time to grow and proliferate. When the levels of the hormones drop, it’s a signal to cells that its time to enter a life-extending mode of conservation. Such a system makes evolutionary sense.

      Very good explanation!

  13. Mar 2017
    1. The most effective approach has been minimizing fat stores located inside the abdominal cavity (visceral body fat) in addition to minimizing total body fat.[46] Visceral fat, which is more metabolically active than subcutaneous fat, has been found to produce many enzymatic signals, e.g. resistin, which increase insulin resistance and circulating VLDL particle concentrations, thus both increasing LDL particle concentrations and accelerating the development of diabetes mellitus.
    1. Polyunsaturated fats protect against cardiovascular disease by providing more membrane fluidity than monounsaturated fats, but they are more vulnerable to lipid peroxidation (rancidity). The large scale KANWU study found that increasing monounsaturated fat and decreasing saturated fat intake could improve insulin sensitivity, but only when the overall fat intake of the diet was low.[1] However, some monounsaturated fatty acids (in the same way as saturated fats) may promote insulin resistance, whereas polyunsaturated fatty acids may be protective against insulin resistance.[2][3] Studies have shown that substituting dietary monounsaturated fat for saturated fat is associated with increased daily physical activity and resting energy expenditure. More physical activity was associated with a higher-oleic acid diet than one of a palmitic acid diet. From the study, it is shown that more monounsaturated fats lead to less anger and irritability.[4]