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Showing posts with the label Blood Pressure

Does a high animal protein/fat diet forestall obesity?

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Don Matesz had an interesting blog post the other day that I tweeted:   Grass-Fed Animal Products Prevent Obesity and Cardiovascular Disease?   He writes: Not for Mongolians. Mongols eat a diet largely composed of milk products, meat, and fat from free-ranging, organic, grass-fed animals. They consume few plant foods because few edible plants grow in the cold continental climate of Mongolia. The climate forced them into a natural experiment in low-carb nutrition based on grass-fed animal products. I have an interest in Mongolians because there's definitely some influence of these people in my husband's ancestral line.   I went looking for any peer review literature that might address the Mongolians and found an interesting article.  But before that, I also found some other info.  Don points out in a note to WAPF (presumably aimed at their promotion of raw milk) that the Mongols boiled their milk and made cheese from it.  But one of the accoun...

Protein, Insulin-like Growth Factor-1 (IGF-1) and Glucose Homeostasis

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I've blogged previously on the LoBAG diets for treatment of diabetes.   These diets are higher in protein that standard recommendations - 30% vs. 15% - with varying carb content (20,30 & 40% have been studied).  With both of the lower carb diets, this group has achieved good improvements in HbA1c levels in relatively short time (5-10 weeks).  In comparing their diets  they observed: Increasing the protein content of the diet from 15 to 30% resulted in an 35% increase in IGF-I regardless of whether the carbohydrate content was 40%, 20%, or 30% as in the present study. Thus the dietary protein-induced increase in IGF-I is independent of the amount of dietary carbohydrate and fat. I believe the near-OCD obsession with insulin in the LC community overshadows the vast body of research on other hormones and peptides that's out there and their role in metabolism.

The Metabolic Advantage of Fructose

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Is fructose making us fat?  Apparently the answer is no if you get your fructose in the form of candy! Thanks to MM for sending me this paper. Candy consumption was not associated with body weight measures, risk factors for cardiovascular disease, or metabolic syndrome in US adults: NHANES 1999-2004 For the purposes of this study, candies were defined as follows: Sugar candy consists of sugar in crystalline form or semisolid (amorphous) forms with other ingredients including flavors and colors; examples include peppermint, lollipops, licorice, and gum drops. Chocolate candy is a mixture of processed cacao, cocoa butter, and sugar and often contains other ingredients, including milk, fruit, nuts, and caramels.  This group analyzed 3 sets of NHANES data to look at candy consumption defined as: Candy consumers were defined as those participants consuming any amounts of candy/confection except gum and were placed in 1of 3 overlappin...

Elevated Free Fatty Acids: Detrimental?

As many of my readers know, I've been challenged lately on my beliefs on NEFA.  So I thought I would summarize my thinking on this in a post rather than having several comments scattered amongst a few threads.   I'm not going to be referencing my post here at this time (it's too time consuming to do so at the moment).  If/when I have the opportunity to do so in the future, I'll do a bumped update.   These are my thoughts based on extensive research of the peer review literature on this topic, in almost all cases, considered review of full text articles including reading as many supporting citations in major reviews as possible.  Over the past year I have read at least a hundred such articles. Elevated non-esterified or free fatty acids (NEFA/FFA) are a symptom associated with insulin resistance, Metabolic Syndrome (aka Syndrome X) and Type II diabetes.  The overwhelming evidence in the literature points to elevated NEFA being more than just associated wit...

Hypertension, Insulin and Free Fatty Acids (Part I)

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Obesity Hypertension Is Related More to Insulin's Fatty Acid Than Glucose Action Although resistance to insulin-mediated glucose disposal has emerged as a link between abdominal obesity and hypertension, abnormalities of nonesterified fatty acid metabolism may play a greater role. ... Fatty acid concentration and turnover were markedly more resistant to suppression by insulin in obese hypertensive than in lean or obese normotensive individuals. ... The data indicate that blood pressure is related to the effects of insulin on fatty acid metabolism. The findings raise the possibility that resistance of hormone-sensitive lipase to insulin participates in elevating the blood pressure of abdominally obese hypertensive subjects by increasing fatty acid concentration and turnover. I'm C&P'ing the entire Introduction because it contains live links to background references some readers may be interested in.

Insulin Is an Anti-inflammatory and Anti-atherosclerotic Hormone

Insulin Is an Anti-inflammatory and Anti-atherosclerotic Hormone   (full text free until end of the month) Fasting hyperinsulinemia is associated with an increased risk of atherosclerotic complications of heart attack and stroke. This has resulted in the concept that insulin may promote atherosclerosis in spite of the absence of any evidence that insulin is atherogenic either in the human or in experimental models. Recent evidence shows that insulin exerts vasodilatory, anti-platelet and anti-inflammatory effects at the cellular level in vitro and in the human in vivo. Since atherosclerosis is a chronic inflammatory process of the arterial wall, insulin may be potentially anti-atherosclerotic in the long term. More recent data on experimental atherosclerosis in the mouse shows that (1) insulin administration reduces the number and the size of atherosclerotic lesions in apo E null mice and (2) in IRS-2 null mice, the interruptio...

Adiposopathy v. Obesity ~ I

I just came across the following article, and haven't quite digested the whole thing just yet.  Still, it is interesting so I thought I would share it here.  This post will be about the most curious topic in this paper, but I hope to revisit this in a series of future blog posts (hence the "I" in the title).   Adiposopathy Is a More Rational Treatment Target for Metabolic Disease than Obesity Alone Near as I can tell, the lead author, Harold Bays, is the doctor who coined the term "adiposopathy" or "sick fat".   Adiposopathy is pathologic adipose tissue dysfunction that may be initiated and/or exacerbated by fat accumulation (adiposity) in genetically susceptible patients [1••].  Adipocytes are metabolically active and adipose tissue is an important endocrine organ (Table 1) [2••]. Abnormalities of adipocyte factors contribute to dysmetabolism (Fig. 1), and adiposopathy [1••,3•] promotes some of the most...

The Progression of Insulin Resistance

Vascular function, insulin resistance and fatty acids   (I'll blog on the vascular focus of this paper shortly, but this post is focusing on the bolded statements in the abstract). Abstract Over the past 10 years it has become clear that intact vascular function, especially at the level of the endothelium {cells lining the blood vessels}, is paramount in the prevention or delay of cardiovascular disease. It has also become clear that insulin itself, in addition to its metabolic actions, directly effects vascular endothelium and smooth muscle.  Insulin, at normal physiologic concentrations, causes changes in skeletal muscle blood flow in healthy, insulin-sensitive subjects. Insulin’s effect on the endothelium is mediated through its own receptor and insulin signalling pathways, resulting in the increased release of nitric oxide. Insulin’s vascular actions are impaired in insulin-resistant conditions such as obesity...

Sudden Cardiac Death and Free Fatty Acids

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Here is the Heart Rhythm Society's Definition: Sudden cardiac death (SCD), also called cardiac arrest, is used to describe a situation in which the heart abruptly and without warning stops working, so no blood can be pumped to the rest of the body. It is responsible for half of all heart disease deaths. Sudden cardiac death occurs when the heart’s electrical system malfunctions. It is not a heart attack (also known as a myocardial infarcation). A heart attack is when a blockage in a blood vessel interrupts the flow of oxygen-rich blood to the heart, causing heart muscle to die. So if the heart can be compared to a house, SCD occurs when there is an electrical problem and a heart attack – when the problem is the plumbing. Later in that summary it is stated that 75% showed evidence of prior heart attack, and 80% evidence of CVD.  So that leaves 25% with no evidence of prior heart attack and 20% with no CVD. So I do a little math: *  SCD deaths occurring in people with no pr...

Insulin resistance and the regulation of vascular tone: is insulin a vasodilator?

Insulin resistance and the regulation of vascular tone: is insulin a vasodilator? This is a review article that discusses an action of insulin that is not normally considered, it's possible function as a vasodilator.  I wonder if this might not be the reason why some low carbers still struggle with high blood pressure even after achieving a lower weight. ... insulin-induced glucose uptake was associated with a striking increase in leg blood flow; the insulin dose-responses of blood flow and glucose extraction were very similar. These findings raised the possibility that insulin is a vasodilator hormone. In addition, the effect of insulin on leg blood flow was blunted in obese insulin-resistant patients, suggesting that vascular (in)sensitivity is a component of insulin resistance. My summary:  There appears to be a vasodilating action of insulin, however it is unclear whether this is a direct action of insulin or through an indirect...