Yellow light means plenty of acetone.The gadget is $99 and is good for any number of measurements. I stand for my comment and think Jimmy looks swell and I am also pleased that you cannot any longer attack him for his weight. But as suspected resumption of a standard diet brings the diabetes-2, and weight gain back. While Jimmy Moore has done reasonably well in acheiving and maintaining a healthy weight, considering where he has come from, he is by no means a paragon of health. His LDL lipoprotein numbers are through the roof high, he seems to have worsened his insulin resistance since in his own words he sees very high blood sugars even from a simple salad, he eats a diet that is composed of 97% protein and fat.
I don't know of any but those Okinawans and other members of the Blue Zones seem to be doing quite well. We are all getting older, that said, he looks fantastic.21NSMarch 18 2014 2"Where did you get the figure 97% protein from ? JM has, nothwithstanding your innocence on the matter, been ~vociferously~ promulgating the virtues of his 83-85%+ fat eating regimen ever since he began his "nutritional ketosis" madness more than a year ago.
But isn't it the responsibility of those who advocate high fat diets and defend them publicly on blogs to make themselves familiar with this kind of information already??? My #1 goal has been to reach a ketotic state and not consume anything that would knock me out of that.
I specifically talked about his LDL particle numbers being dangerously high, at last count, over 2700.You may find the following to your interest.
Directly on JM's blog, Dr, Thomas Dayspring wrote the following:“Using all the knowledge we possess today, all of the numbers that you are thrilled about have no meaning in the face of a 99th percentile LDL-P. The cholesterol concentrations that often have no meaning are low levels (where an LDL-P is needed to evaluate risk). No one with an LDL-C of 285 with the exception of a Type III dyslipoproteinemia patient have a low apoB or LDL-P. You need to significantly reduce the saturated fat in your diet and see what happens: repeat the NMR in 3 weeks and you will know if your nightmare LDL-P is sat fat related. JM boasts of the experts, including Dayspring, who is perhaps the world's leading lipidologist, he interviewed for the "Cholesterol Clarity" manifesto he wrote.
One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis. However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma. It is assumed, that if total or LDL-C or non-HDL-C levels are elevated the odds are good that some of that cholesterol will find its way into the arteries, and for sure there, are many studies correlating those measurements with CHD risk. We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C). Because the core lipid content of each and every LDL differs (how many cholesterol molecules it traffics) it takes different numbers of LDLs to traffic a given number of cholesterol molecules: the more depleted an LDL is of cholesterol, the more particles (LDL-P) it will take to carry a given cholesterol mass (LDL-C). The usual causes of cholesterol depleted particles are that the particles are small or they are TG-rich and thus have less room to carry cholesterol molecules. After particle number endothelial integrity is certainly related to atherogenic particle entry: inflamed endothelia have inter-cellular gaps and express receptors that facilitate apoB-particle entry. I don't see why as he is doing really great, showing others the ins and outs of getting out of weight gain into weight loss and loss of the killing visceral fat , the fat that spawns weight gain and diabetes 2. My 5 cents!30NSMarch 18 2014Nonsense on top of further nonsense.Do you have any links on the longevity of the Masai or Inuit or other LCHF-like eating societies? Richard K Bernstein?is this a hidden vegan or vegan like ploy?Ar you promoting Sugar and or grain? If the protein is comparable to the carbs in insulin index, then just 30% of the diet intake is causing insulin surges.
I can tell modest protein is not an insulin issue from measuring blood ketones, which are a good proxy for absence of insulin.
So the rate and intensity of insulin surges at 70-20-10 (30% insulin triggering) is qualitatively much different than at 20-15-65 (80% insulin triggering). Kenyon's work showed reduced insulin remarkable decreased aging, but as usual there was a J-curve, so no one is aiming for zero insulin.And there are numerous metabolic benefits to having less glucose being trafficked in the blood and being shunted into cells, to many to mention in one comment. Then there are the benefits of ketones as more efficient, mitochondria-enhancing fuel and highly beneficial metabolic signalling.As to methods of getting into ketosis without LCHF, surely fasting is LCHF. Indeed, I recall reading Phinney and Volek pointing out there is autophagy of depleted adipose cells. However, the evidence he marshals for the LDL-P argument is statistically arcane at best and does not establish causation. When I reviewed his site last year he conceded that the case of high LDL on keto is new territory. Here he reverts to old prejudice on the basis it has not been proven safe--"just take the damn statins." In the end, I don't find he has made a persuasive case.
The "gradient" hypothesis about more LDL magically penetrating artery walls as if by osmosis is unconvincing.
A friend who is an anesthesiologist sees a lot of operations and, for example, gives an example of a lifelong vegetarian with rock bottom LDL with one heart artery totally blocked and the others totally clear. If the gradient hypothesis were plausible, there would not be one artery blocked and the others clear.As for Inuit and the Maasai, Dr. Weston Price in the 1930s surveyed traditional cultures around the world who were not yet introduced to Western diet (notably starch and sugar).
Price found the Maasai (who live almost entirely on meat, dairy and blood of ruminants) and certain remote Swiss villagers to be the healthiest he found.
Thomas Seyfried calls mitochondrial enhancement therapy, with is essentially calorie restricted low carb high fat.
To this day, if I get a few grey hairs on my chest or head I simply cut out carbs and reduce calories for a couple of days and the grey hairs restore to normal. Many others have reported this.The problem with the genetic determinism hypothesis is that it does not explain the metabolic mechanism.
With diminished mitochondrial output due to oxidative stress, for example, the cells lack sufficient energy to produce pigment. After speaking with several older people with seemingly preternatural non-greying, my wife hit upon low or zero sugar consumption as a near-universal among the non-grey people.
Eliminate the suspected source and if the condition disappears, then reintroduce the source and see if it comes back. Thus I have high confidence what greying indicates, or at least how to control it.Another instructive case for me was the plight of an owner of a small gas and service station.
He had recently acquired the station, but it was obvious to my wife and I that it was a poor location for access reasons. He was extremely eager at the beginning and did all sorts of creative things to draw traffic and we made a point of going there often.
Anyway, within a few months of things going badly and him looking entirely defeated, he went from jet black hair to totally grey. Plainly it was the stress, which is again consistent with weakened mitochondria as the metabolic mechanism behind loss of capacity to produce pigment in hair cells.Do you have reference to a study that shows the mechanism involved in greying of hair?
Do you know where I could order the older model or if anyone else makes these a little cheaper?

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